Physiology

2016 NEET PG

Chapter: General Physiology; Topic: Body Fluids; Subtopic: Measurement of Body Fluid Compartments

Key Definitions & Concepts

Indicator Dilution Principle: The method used to measure the volume of a fluid compartment. Formula: Volume = (Amount of indicator injected - Amount excreted) / Concentration of indicator.
Total Body Water (TBW): Measured using substances that distribute freely in all body fluids, such as Deuterium Oxide (D2O), Tritium Oxide, or Antipyrine.
Extracellular Fluid (ECF): Measured using substances that cross capillaries but not cell membranes, such as Inulin, Mannitol, or Sucrose.
Intracellular Fluid (ICF): Cannot be measured directly because no substance distributes exclusively in the ICF. It is calculated as: ICF = Total Body Water - Extracellular Fluid.
Plasma Volume: Measured using substances that remain in the vessels, such as Evans Blue dye (T-1824) or Radio-labeled Albumin (131I-Albumin).
Blood Volume: Calculated from Plasma Volume and Hematocrit: Blood Volume = Plasma Volume / (1 - Hematocrit). Alternatively measured with Cr-51 labeled RBCs.
Interstitial Fluid (ISF): Cannot be measured directly. Calculated as: ISF = Extracellular Fluid - Plasma Volume.
Inulin: A polymer of fructose used as the gold standard for measuring ECF volume and GFR because it is neither metabolized nor secreted.
Evans Blue (T-1824): A dye that binds avidly to plasma albumin; used to measure plasma volume.
Deuterium Oxide (Heavy Water): An isotope of water used to measure Total Body Water.

Lead Question - 2016

Measurement of intracellular fluid in a 50 years old male is done by?

a) Dilution method

b) Evans blue

c) D20

d) Indirectly

Explanation: The measurement of body fluid volumes relies on the Indicator Dilution Principle. However, this method requires a substance that distributes *exclusively* into the specific compartment being measured. For the Intracellular Fluid (ICF), there is no known substance that can be injected into the blood and will distribute *only* into cells without remaining in the extracellular space. Therefore, the ICF volume cannot be measured directly. Instead, it is calculated Indirectly. We measure Total Body Water (using D2O/Tritium) and Extracellular Fluid (using Inulin/Mannitol), and then subtract the ECF from the TBW (ICF = TBW - ECF). Therefore, the correct answer is d) Indirectly.

1. Which substance is considered the "Gold Standard" for measuring Extracellular Fluid (ECF) volume?

a) Sodium thiosulfate

b) Inulin

c) Deuterium Oxide

d) Evans Blue

Explanation: To measure the ECF, a substance must pass freely through capillary walls (to leave plasma) but must not cross cell membranes (to avoid entering the ICF). It should also not be metabolized rapidly. Inulin, a large polysaccharide (polymer of fructose), fits these criteria perfectly. It distributes into the plasma and interstitial fluid but does not enter cells. While other substances like Mannitol, Sucrose, and radioactive Sodium are used, Inulin is widely regarded as the physiological standard. D2O measures TBW. Evans Blue measures plasma. Therefore, the correct answer is b) Inulin.

2. To measure Plasma Volume specifically, the indicator substance must possess which property?

a) It must be a small, non-polar molecule

b) It must bind tightly to plasma proteins

c) It must cross the capillary membrane freely

d) It must be actively secreted by the renal tubules

Explanation: Plasma volume is the intravascular part of the ECF. To measure it, the indicator must stay within the blood vessels and not leak out into the interstitial space. Capillaries are generally permeable to small molecules but impermeable to large proteins (albumin). Therefore, dyes like Evans Blue (which binds to albumin) or Radio-iodinated Albumin (I-131 Albumin) are used. By binding to proteins, these indicators are effectively trapped in the vascular compartment, allowing for the calculation of plasma volume via dilution. Small non-polar molecules would measure TBW. Therefore, the correct answer is b) It must bind tightly to plasma proteins.

3. Total Body Water (TBW) constitutes approximately what percentage of body weight in a healthy young adult male?

a) 40%

b) 50%

c) 60%

d) 80%

Explanation: The standard reference value for Total Body Water in a young adult male is 60% of body weight. This percentage varies with age, gender, and adiposity. Females generally have a lower percentage (~50%) due to higher adipose tissue content (fat is hydrophobic, so higher fat = lower water percentage). Infants have a much higher water content (~75-80%). In the elderly, TBW decreases to about 50-55% in males. The 60-40-20 rule helps remember the distribution: 60% TBW, 40% ICF, 20% ECF. Therefore, the correct answer is c) 60%.

4. A patient has a Hematocrit of 40% and a Plasma Volume measured as 3 Liters. What is the calculated Total Blood Volume?

a) 4 Liters

b) 5 Liters

c) 6 Liters

d) 7.5 Liters

Explanation: Blood is composed of Plasma and Cells (RBCs). Hematocrit (Hct) represents the fraction of blood volume occupied by cells. Therefore, the fraction occupied by plasma is (1 - Hct). Formula: Total Blood Volume = Plasma Volume / (1 - Hematocrit). Given: Plasma Volume = 3 L, Hematocrit = 0.40 (40%). Calculation: Blood Volume = 3 / (1 - 0.40) = 3 / 0.6 = 5 Liters. This calculation is crucial clinically when only plasma volume can be measured directly using dye dilution. Therefore, the correct answer is b) 5 Liters.

5. Which of the following fluid compartments cannot be measured directly by any exogenous marker?

a) Plasma Volume

b) Extracellular Fluid

c) Interstitial Fluid

d) Total Body Water

Explanation: There are two major compartments that are measured indirectly because no substance distributes exclusively into them. 1. Intracellular Fluid (ICF): No substance goes only into cells. (ICF = TBW - ECF). 2. Interstitial Fluid (ISF): No substance stays only in the interstitium without entering plasma or cells. Indicators for ECF (like Inulin) enter both plasma and ISF. Indicators for plasma (Evans Blue) stay in plasma. Thus, Interstitial Fluid is calculated as the difference: ISF = ECF - Plasma Volume. Therefore, the correct answer is c) Interstitial Fluid.

6. In the indicator dilution method, if the substance injected is metabolized or excreted by the kidney before equilibrium is reached, the calculated volume will be:

a) Correct

b) Falsely Low

c) Falsely High

d) Zero

Explanation: The formula is Volume = Amount Injected / Final Concentration. If the indicator is metabolized or excreted, the Final Concentration in the blood will be lower than it should be (numerator stays same, denominator decreases). Mathematically, dividing by a smaller number yields a larger result. Therefore, the calculated volume will be Falsely High (overestimated). To correct for this, serial measurements are taken and extrapolated back to time zero, or substances that are not metabolized (like radioactive isotopes or inulin) are preferred. Therefore, the correct answer is c) Falsely High.

7. Which compartment contains the smallest volume of fluid in the body?

a) Intracellular Fluid

b) Plasma

c) Interstitial Fluid

d) Transcellular Fluid

Explanation: The body fluids are divided as follows (for a 70kg man): TBW = 42 L. ICF = 28 L (2/3 of TBW). ECF = 14 L (1/3 of TBW). ECF is subdivided into Interstitial Fluid (~10.5 L or 3/4 of ECF) and Plasma (~3.5 L or 1/4 of ECF). However, there is a specialized "third space" called Transcellular Fluid (CSF, synovial, pleural, pericardial, intraocular fluids). This compartment is the smallest, normally constituting only about 1-2 Liters (~1.5% of body weight). Therefore, the correct answer is d) Transcellular Fluid.

8. The "20-40-60 Rule" is a useful mnemonic for body fluid distribution. What does the "40" represent?

a) Percentage of body weight that is Extracellular Fluid

b) Percentage of Total Body Water that is Intracellular

c) Percentage of body weight that is Intracellular Fluid

d) Percentage of body weight that is solid tissue

Explanation: The "60-40-20 Rule" helps estimate fluid volumes as a percentage of total body weight: 60% = Total Body Water (TBW). 40% = Intracellular Fluid (ICF). 20% = Extracellular Fluid (ECF). This rule applies to a standard "reference man." It highlights that the majority of our body weight is water, and the majority of that water (2/3) is located inside our cells. Therefore, the "40" stands for the percentage of body weight that is Intracellular Fluid. Therefore, the correct answer is c) Percentage of body weight that is Intracellular Fluid.

9. Tritiated Water (3H2O) is used to measure which body fluid compartment?

a) Plasma Volume

b) Total Body Water

c) Extracellular Fluid

d) Blood Volume

Explanation: To measure Total Body Water (TBW), the indicator must be a substance that behaves exactly like water: it must cross capillary walls AND cell membranes freely to distribute evenly throughout the entire aqueous space of the body. Isotopes of water are the ideal candidates. Tritiated Water (3H2O) (radioactive) and Deuterium Oxide (D2O) (heavy water, non-radioactive) are chemically equivalent to water and distribute in the total water pool. Antipyrine is another lipid-soluble substance used for this purpose. Therefore, the correct answer is b) Total Body Water.

10. Which condition leads to a decrease in the percentage of Total Body Water relative to body weight?

a) Increased muscle mass

b) Infancy

c) Obesity

d) Male gender

Explanation: The percentage of Total Body Water is inversely proportional to the amount of body fat. Adipose tissue contains very little water compared to lean muscle tissue. Therefore, as body fat increases, the relative fraction of the body composed of water decreases. Obesity significantly lowers the TBW percentage (sometimes to as low as 45%). Infants have very little fat and high water content (75%). Males typically have more lean muscle than females, so they have a higher water percentage. Therefore, the correct answer is c) Obesity.

Chapter: General Physiology; Topic: Transport Across Cell Membranes; Subtopic: Primary Active Transport and ATPase Pumps

Key Definitions & Concepts

Primary Active Transport: Transport of solutes against their electrochemical gradient utilizing energy derived directly from the hydrolysis of ATP.
ATPase (Adenosine Triphosphatase): An enzyme class that catalyzes the decomposition of ATP into ADP and a free phosphate ion, releasing energy to drive transport.
Electrogenic Pump: A pump that generates a net flow of charge across the membrane (unequal movement of cations/anions), contributing directly to the membrane potential.
Na+/K+ ATPase: The ubiquitous P-type ATPase that maintains the resting membrane potential and cell volume by pumping 3 Na+ out and 2 K+ in.
P-type ATPase: A family of pumps that form a phosphorylated intermediate during the transport cycle (e.g., Na+/K+ pump, Ca2+ pump, H+/K+ pump).
SERCA (Sarcoplasmic Endoplasmic Reticulum Calcium ATPase): A pump responsible for sequestering Ca2+ back into the sarcoplasmic reticulum during muscle relaxation.
Cardiac Glycosides (Digoxin/Ouabain): Drugs that specifically inhibit the Na+/K+ ATPase by binding to the extracellular domain of the alpha subunit.
ABC Transporters (ATP-Binding Cassette): A large superfamily of primary active transporters that transport a wide variety of substrates (e.g., MDR1, CFTR).
H+/K+ ATPase (Proton Pump): Located in gastric parietal cells, responsible for acid secretion; inhibited by Omeprazole.
Secondary Active Transport: Uses the energy stored in an ion gradient (created by primary active transport) rather than direct ATP hydrolysis (e.g., SGLT).

[Image of Na-K ATPase pump mechanism]

Lead Question - 2016

ATPase is which type of pump?

a) Secondary active

b) Electrogenic

c) Symport

d) All of the above

Explanation: The question refers to the general properties of ion-motive ATPases, most notably the Na+/K+ ATPase. These pumps function via Primary Active Transport because they directly hydrolyze ATP to move ions against gradients. Therefore, option (a) is incorrect. They are generally antiports (moving ions in opposite directions), not symports, so (c) is incorrect. A key feature of the Na+/K+ ATPase is that it moves 3 positive charges (Na+) out for every 2 positive charges (K+) in. This net movement of positive charge out of the cell creates an electrical potential difference, making the pump Electrogenic. It contributes directly to the negative resting membrane potential. Therefore, the correct answer is b) Electrogenic.

1. The Na+/K+ ATPase pump consists of alpha and beta subunits. The specific binding site for ATP is located on the:

a) Extracellular side of the alpha subunit

b) Intracellular side of the alpha subunit

c) Extracellular side of the beta subunit

d) Intracellular side of the beta subunit

Explanation: The Na+/K+ ATPase is a heterodimer. The large Alpha subunit is the catalytic unit responsible for the transport activity. It spans the membrane and has binding sites for Na+ and ATP on the Intracellular side and binding sites for K+ and cardiac glycosides (like ouabain) on the extracellular side. The Beta subunit is a glycoprotein essential for the proper folding and trafficking of the pump to the plasma membrane but does not bind ATP. Phosphorylation of the alpha subunit is the key step in the transport cycle. Therefore, the correct answer is b) Intracellular side of the alpha subunit.

2. Which of the following is a classic P-type ATPase found in the Sarcoplasmic Reticulum of muscle cells, essential for relaxation?

a) Na+/H+ Exchanger

b) H+/K+ ATPase

c) SERCA pump

d) MDR1 protein

Explanation: Muscle relaxation requires the rapid removal of Calcium (Ca2+) from the cytosol. This is achieved primarily by pumping Ca2+ back into the Sarcoplasmic Reticulum (SR) against a massive concentration gradient. The pump responsible for this is the SERCA (Sarcoplasmic Endoplasmic Reticulum Calcium ATPase) pump. It is a P-type ATPase that consumes ATP to transport 2 Ca2+ ions per cycle from the cytosol into the SR lumen. Dysfunction of this pump can lead to delayed relaxation (Brody's disease) or altered contractility in heart failure. Therefore, the correct answer is c) SERCA pump.

3. Digoxin increases cardiac contractility (positive inotropy) by inhibiting the Na+/K+ ATPase. The immediate consequence of this inhibition that leads to increased contractility is:

a) Increased intracellular K+

b) Decreased intracellular Ca2+

c) Increased intracellular Na+

d) Membrane hyperpolarization

Explanation: Digoxin inhibits the Na+/K+ ATPase. Normally, this pump keeps intracellular Sodium low. When inhibited, Intracellular Na+ accumulates. This rise in [Na+]in reduces the gradient for the Na+/Ca2+ Exchanger (NCX), which normally pumps Ca2+ out by bringing Na+ in. With a reduced Na+ gradient driving it, the NCX slows down, leading to an accumulation of Intracellular Calcium. This extra Ca2+ is stored in the SR and released during subsequent beats, increasing the force of contraction (inotropy). Thus, the primary effect is increased Na+. Therefore, the correct answer is c) Increased intracellular Na+.

4. The gastric H+/K+ ATPase (Proton Pump) is responsible for acid secretion. It is an electroneutral pump because it exchanges:

a) 1 H+ for 1 K+

b) 2 H+ for 1 K+

c) 1 H+ for 2 K+

d) 3 H+ for 2 K+

Explanation: The H+/K+ ATPase located in the parietal cells of the stomach is responsible for the final step of acid secretion. It pumps Hydrogen ions (H+) into the gastric lumen and Potassium ions (K+) into the cell, using ATP hydrolysis. The stoichiometry of this exchange is 1 H+ for 1 K+ (some sources say 2:2, but the ratio is 1:1). Because equal amounts of positive charge are moved in opposite directions, there is no net movement of charge across the membrane. Thus, unlike the Na+/K+ pump, the proton pump is Electroneutral. Therefore, the correct answer is a) 1 H+ for 1 K+.

5. Multidrug Resistance Protein 1 (MDR1 or P-glycoprotein) pumps chemotherapeutic agents out of cancer cells. It belongs to which family of primary active transporters?

a) P-type ATPases

b) V-type ATPases

c) F-type ATPases

d) ABC Transporters

Explanation: Transporters are classified by structure and mechanism. The P-type ATPases (Na/K, Ca, H/K) involve phosphorylation. The ABC (ATP-Binding Cassette) Transporters utilize the energy of ATP binding and hydrolysis to transport a wide variety of substrates (lipids, drugs, ions) across membranes without being phosphorylated themselves. MDR1 (P-glycoprotein) and CFTR (Cystic Fibrosis Transmembrane Conductance Regulator) are prominent members of the ABC Transporter superfamily. Overexpression of MDR1 causes resistance to chemotherapy by actively pumping the drugs out of the tumor cells. Therefore, the correct answer is d) ABC Transporters.

6. In addition to maintaining membrane potential, the Na+/K+ ATPase is critical for regulating:

a) Cell division

b) Cell volume

c) DNA replication

d) Protein synthesis

Explanation: Cells contain high concentrations of imperatnt organic molecules (proteins, phosphates) that are negatively charged and osmotically active. This creates a "Donnan effect" that tends to pull water into the cell, threatening to burst it. The Na+/K+ ATPase acts as a functional "pump-leak" mechanism. By actively pumping 3 Na+ out (and keeping the membrane effectively impermeable to Na+), it removes osmotically active particles from the cytoplasm. This counteracts the osmotic pull of intracellular proteins, preventing cellular swelling and maintaining Cell Volume. Inhibition of the pump leads to cell swelling and lysis. Therefore, the correct answer is b) Cell volume.

7. Which class of ATPases is primarily responsible for acidifying intracellular organelles like lysosomes and endosomes?

a) P-type ATPases

b) V-type ATPases

c) F-type ATPases

d) ABC Transporters

Explanation: The acidification of intracellular compartments (lysosomes, endosomes, secretory vesicles) is achieved by proton pumps. These pumps are structurally distinct from the P-type pumps of the plasma membrane. They are classified as V-type (Vacuolar) ATPases. V-type ATPases pump protons (H+) from the cytoplasm into the organelle lumen, consuming ATP. They do not undergo phosphorylation during the cycle. F-type ATPases are the mitochondrial ATP synthases (running in reverse to synthesize ATP). P-type are the ion pumps like Na/K. Therefore, the correct answer is b) V-type ATPases.

8. The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is unique among ABC transporters because it functions as:

a) An active pump for Chloride

b) An ion channel for Chloride

c) An active pump for Sodium

d) An exchanger for Bicarbonate

Explanation: Most ABC transporters (like MDR1) use ATP to actively pump substrates against a gradient. CFTR is a notable exception. Although it possesses the structural Nucleotide Binding Domains (NBDs) characteristic of the ABC family and binds/hydrolyzes ATP, it does not function as an active pump. Instead, ATP binding/hydrolysis regulates the opening and closing (gating) of the protein, allowing it to function as a passive Ion Channel for Chloride. Cl- flows down its electrochemical gradient. This unique "broken pump" mechanism is vital for epithelial fluid secretion. Therefore, the correct answer is b) An ion channel for Chloride.

9. A significant portion of the body's Basal Metabolic Rate (BMR) is accounted for by the energy consumption of the:

a) Ca2+ ATPase

b) H+ ATPase

c) Na+/K+ ATPase

d) Myosin ATPase

Explanation: The maintenance of ion gradients is a metabolically expensive process. The Na+/K+ ATPase is constitutively active in almost all cells of the body. In neurons and kidney tubules, its activity is particularly high. It is estimated that the Na+/K+ pump consumes approximately 20-40% of the total ATP produced in a resting individual. Consequently, it is a major contributor to the Basal Metabolic Rate (BMR) and basal thermogenesis. Thyroid hormones increase BMR in part by upregulating the expression of Na+/K+ pump units. Therefore, the correct answer is c) Na+/K+ ATPase.

10. Omeprazole and Pantoprazole are clinically used to treat GERD. They function by forming a covalent disulfide bond with, and irreversibly inhibiting, which pump?

a) Gastric Na+/K+ ATPase

b) Gastric H+/K+ ATPase

c) Esophageal Ca2+ ATPase

d) Intestinal Na+/Glucose Symport

Explanation: Proton Pump Inhibitors (PPIs) like Omeprazole are prodrugs that are activated in the acidic environment of the parietal cell canaliculus. Once activated, they bind irreversibly to cysteine residues on the alpha subunit of the Gastric H+/K+ ATPase (Proton Pump). This inhibition blocks the final common pathway of acid secretion, regardless of the stimulus (histamine, gastrin, or acetylcholine). Because the inhibition is irreversible, acid secretion is suppressed until new pump molecules are synthesized, allowing for once-daily dosing. Therefore, the correct answer is b) Gastric H+/K+ ATPase.

Chapter: General Physiology; Topic: Body Fluids and Membranes; Subtopic: Gibbs-Donnan Equilibrium

Key Definitions & Concepts

Gibbs-Donnan Equilibrium: The behavior of charged particles near a semi-permeable membrane that typically fails to distribute evenly across the two sides due to the presence of a non-diffusible charged substance (usually protein).
Non-Diffusible Anions: Large intracellular proteins ($Pr^-$) and organic phosphates that cannot cross the cell membrane; they carry a net negative charge at physiological pH.
Donnan Product Rule: At equilibrium, the product of the concentrations of diffusible cations and anions on one side equals the product on the other side ($[K^+]_{in} \times [Cl^-]_{in} = [K^+]_{out} \times [Cl^-]_{out}$).
Donnan Excess: The phenomenon where the total concentration of diffusible ions is greater in the compartment containing the non-diffusible ion (ICF) than in the compartment without it (ECF).
Osmotic Effect: Because total ions are higher in the ICF due to the Donnan effect, water tends to enter the cell; the Na+/K+ pump acts as a functional "anti-Donnan" mechanism to prevent cell swelling.
Intracellular pH: Due to the Donnan distribution, $H^+$ ions are slightly more concentrated inside the cell, making the ICF slightly more acidic than the ECF.
Chloride Shift: An example of passive anionic redistribution (Hamburger phenomenon) that respects Donnan principles across the RBC membrane.
Resting Membrane Potential: The Donnan effect contributes to the negative charge inside the cell, although the K+ leak channels and Na/K pump are the primary determinants.
Electroneutrality: Despite the unequal distribution of individual ions, each compartment (ICF and ECF) remains electrically neutral macroscopically.
Colloid Osmotic Pressure: In capillaries, plasma proteins create a Donnan effect that contributes to the oncotic pressure keeping fluid in the vessels.

[Image of Gibbs Donnan Equilibrium diagram]

Lead Question - 2016

Due to Donnan-Gibbs effect?

a) Concentration of K. is greater in ECF

b) Concentration of cl is greater in ECF

c) Total ions are more in ICF

d) All are true

Explanation: The Gibbs-Donnan effect occurs because non-diffusible anions (proteins) are trapped inside the cell (ICF). To maintain electrical neutrality, these proteins attract diffusible cations ($K^+$) into the cell and repel diffusible anions ($Cl^-$) out of the cell. Mathematically, to satisfy the equilibrium product ($[Cat]_{in} \times [An]_{in} = [Cat]_{out} \times [An]_{out}$), the sum of the concentrations of diffusible ions inside the compartment with the protein must be greater than the sum of ions in the outer compartment. This is known as the "Donnan Excess." Therefore, the total number of osmotically active particles is higher in the ICF. While Cl- is indeed greater in ECF, option (c) describes the fundamental thermodynamic consequence of the effect regarding total osmolarity. Therefore, the correct answer is c) Total ions are more in ICF.

1. According to the Gibbs-Donnan equilibrium principle, which of the following mathematical relationships is true regarding diffusible ions K+ and Cl-?

a) $[K^+]_{in} = [K^+]_{out}$

b) $[K^+]_{in} \times [Cl^-]_{out} = [K^+]_{out} \times [Cl^-]_{in}$

c) $[K^+]_{in} \times [Cl^-]_{in} = [K^+]_{out} \times [Cl^-]_{out}$

d) $[K^+]_{in} + [Cl^-]_{in} = [K^+]_{out} + [Cl^-]_{out}$

Explanation: The Gibbs-Donnan equilibrium dictates that at equilibrium, the product of the concentrations of the diffusible cation and anion on one side of the membrane must equal the product of their concentrations on the other side. This ensures that the chemical potential gradients are balanced by the electrical potential. Therefore, the correct relationship is the product of the internal ions equals the product of the external ions. Option (d) is incorrect because the sums are unequal (Donnan excess). Therefore, the correct answer is c) $[K^+]_{in} \times [Cl^-]_{in} = [K^+]_{out} \times [Cl^-]_{out}$.

2. The presence of intracellular non-diffusible anions results in the intracellular pH being:

a) Slightly more acidic than ECF

b) Slightly more alkaline than ECF

c) Exactly equal to ECF

d) Independent of the Donnan effect

Explanation: Hydrogen ions ($H^+$) are diffusible cations. The Donnan effect predicts that diffusible cations will be attracted to the compartment containing the non-diffusible anions (the ICF). Therefore, $H^+$ tends to accumulate inside the cell, following the same distribution pattern as $K^+$. A higher concentration of $H^+$ corresponds to a lower pH. Consequently, the intracellular fluid is typically slightly more acidic (pH ~7.0-7.2) compared to the extracellular fluid (pH ~7.4), partly due to this passive distribution. Therefore, the correct answer is a) Slightly more acidic than ECF.

3. Which cellular mechanism functions as a "functional anti-Donnan pump" to prevent cell swelling and lysis?

a) Na+-H+ Exchanger

b) Cl--HCO3- Exchanger

c) Na+-K+ ATPase

d) Ca2+ ATPase

Explanation: The Donnan effect creates a situation where the total concentration of ions (osmolarity) is higher inside the cell than outside. This creates an osmotic gradient that favors water entry, which would naturally cause the cell to swell and burst. To counteract this, the cell uses the Na+-K+ ATPase. By actively pumping 3 $Na^+$ ions out for every 2 $K^+$ ions in, the pump effectively makes the membrane functionally impermeable to Sodium (keeping $Na^+$ out). This removal of osmotically active particles ("double Donnan effect") maintains cell volume. Therefore, the correct answer is c) Na+-K+ ATPase.

4. In a system where proteins are negatively charged inside the cell, what is the expected distribution of Chloride (Cl-) ions?

a) $[Cl^-]_{in} > [Cl^-]_{out}$

b) $[Cl^-]_{in} = [Cl^-]_{out}$

c) $[Cl^-]_{out} > [Cl^-]_{in}$

d) Chloride is impermeable

Explanation: Chloride is a diffusible anion. The intracellular proteins are non-diffusible anions ($Pr^-$). Since like charges repel, the negative charge of the intracellular proteins repels the Chloride ions, driving them out of the cell. Additionally, to maintain the Donnan equilibrium product, if cations ($K^+$) are high inside, anions ($Cl^-$) must be low inside. Thus, the concentration of Chloride is significantly higher in the Extracellular Fluid (ECF) than in the Intracellular Fluid (ICF). Therefore, the correct answer is c) $[Cl^-]_{out} > [Cl^-]_{in}$.

5. The Gibbs-Donnan effect contributes approximately how much to the Resting Membrane Potential (RMP) of a nerve fiber?

a) -90 mV (The entire potential)

b) -60 mV

c) -10 mV to -20 mV

d) 0 mV

Explanation: The Resting Membrane Potential (typically -70 to -90 mV) is primarily determined by the selective permeability of the membrane to Potassium (Nernst potential of K+) and the electrogenic Na+/K+ pump. The passive distribution of ions due to the Donnan effect (fixed protein anions) does contribute to the negativity, but it is not the sole generator. If the Na+/K+ pump stops, the potential eventually collapses to the Donnan potential, which is much smaller, roughly -10 mV to -20 mV. The active pump is required to reach physiological RMP. Therefore, the correct answer is c) -10 mV to -20 mV.

6. In the capillaries, the Donnan effect involving plasma proteins (Albumin) creates an extra osmotic pressure that is approximately what percentage of the total oncotic pressure?

a) 1%

b) 50%

c) 33-50%

d) 99%

Explanation: Plasma oncotic pressure (Colloid Osmotic Pressure) is crucial for retaining fluid in capillaries. It is roughly 28 mmHg. About 19 mmHg of this is caused by the dissolved proteins themselves (van 't Hoff component). However, because proteins are negative (at pH 7.4), they hold extra cations (mostly $Na^+$) in the plasma due to the Donnan effect. These extra trapped cations exert their own osmotic pressure, which accounts for the remaining ~9 mmHg. Thus, the Donnan effect contributes roughly 33-50% (specifically about 1/3) of the total effective oncotic pressure. Therefore, the correct answer is c) 33-50%.

7. Which ion acts as the "Non-diffusible" ion in the Donnan equilibrium established across the Red Blood Cell membrane?

a) Sodium

b) Hemoglobin

c) Bicarbonate

d) Potassium

Explanation: In the context of the Red Blood Cell (RBC), the membrane is permeable to water and small anions (Cl-, HCO3-) via the Band 3 exchanger, but it is impermeable to large proteins. The primary large, negatively charged protein trapped inside the RBC is Hemoglobin. The negative charge on hemoglobin dictates the passive distribution of diffusible ions like Chloride (the Chloride shift) according to Donnan principles. Sodium and Potassium are regulated by pumps, not just passive Donnan forces. Therefore, the correct answer is b) Hemoglobin.

8. If $[K^+]_{out} = 5$ mM and $[Cl^-]_{out} = 100$ mM, and due to the Donnan effect the $[Cl^-]_{in} = 5$ mM, what must be the concentration of $[K^+]_{in}$ at equilibrium?

a) 5 mM

b) 20 mM

c) 100 mM

d) 500 mM

Explanation: Apply the Donnan product rule: $[K^+]_{in} \times [Cl^-

Chapter: General Physiology; Topic: Membrane Potentials; Subtopic: The Nernst Equation and Equilibrium Potentials

Key Definitions & Concepts

Nernst Equation: A mathematical relationship used to calculate the equilibrium potential for a single ion based on its concentration gradient across a membrane.
Equilibrium Potential (E): The electrical potential difference that exactly balances the concentration gradient for a specific ion, resulting in no net flux.
Valence (z): The electrical charge of an ion (e.g., +1 for Na+, -1 for Cl-, +2 for Ca2+); a critical variable in the Nernst equation.
Concentration Gradient: The difference in ion concentration between the intracellular and extracellular fluid (Cin/Cout); the driving force for diffusion.
Electrochemical Gradient: The net driving force acting on an ion, combining both the electrical potential difference and the concentration difference.
Driving Force: Mathematically defined as (Vm - Eion); determines the magnitude and direction of current flow when channels are open.
Reversal Potential: Another term for Equilibrium Potential; the voltage at which the current direction reverses.
Temperature (T): The Nernst potential is directly proportional to absolute temperature; typically calculated at 37°C (310 K) in physiology.
Faraday's Constant (F): Represents the magnitude of electric charge per mole of electrons.
Non-ionic Solutes: Substances like glucose or urea that lack charge (z=0); the Nernst equation cannot be applied to them as they do not generate diffusion potentials.

[Image of Nernst equation formula]

Lead Question - 2016

Nernnst equation related to equilibrium potential does not depend upon?

a) Concentration gradient

b) Electric gradient

c) Non-ionic solution

d) Concentration of ions in two solution

Explanation: The Nernst equation ($E = -61/z \times \log([C]_{in}/[C]_{out})$) describes the condition of equilibrium for charged particles (ions). It calculates the Electrical gradient (voltage) required to balance a specific Concentration gradient (ratio of ions in two solutions). The variables strictly required are Temperature, Gas Constant, Faraday's Constant, Valence ($z$), and the Concentrations inside and outside. If a solute is Non-ionic (uncharged, $z=0$), the denominator in the equation becomes zero (or the concept becomes physically meaningless in this context), as uncharged molecules diffuse solely based on concentration and do not generate an opposing electrical potential. Therefore, the correct answer is c) Non-ionic solution.

1. In the Nernst equation, the equilibrium potential is inversely proportional to which property of the ion?

a) Lipid solubility

b) Valence (Charge)

c) Molecular weight

d) Extracellular concentration

Explanation: The simplified Nernst equation at 37°C is $E = -61.5/z \times \log([C]_{in}/[C]_{out})$. The variable '$z$' represents the valence (charge) of the ion. Because '$z$' is in the denominator of the constant factor, the magnitude of the equilibrium potential is inversely proportional to the valence. For example, a divalent ion like Calcium ($z=+2$) will have a smaller Nernst slope factor ($\approx 30.7$) compared to a monovalent ion like Sodium ($z=+1$, factor $\approx 61.5$) for the same concentration ratio magnitude. Molecular weight and lipid solubility are not variables in the Nernst equation. Therefore, the correct answer is b) Valence (Charge).

2. A patient with severe burns develops acute hyperkalemia (high extracellular K+). According to the Nernst prediction, how does this affect the Equilibrium Potential for Potassium ($E_K$)?

a) $E_K$ becomes more negative (Hyperpolarized)

b) $E_K$ becomes less negative (Depolarized)

c) $E_K$ becomes positive

d) $E_K$ remains unchanged

Explanation: Under normal conditions, $[K^+]_{in}$ is high ($\approx 140$) and $[K^+]_{out}$ is low ($\approx 4$), resulting in an $E_K$ of about -90 mV. In hyperkalemia, $[K^+]_{out}$ increases. This decreases the concentration ratio ($[K^+]_{in}/[K^+]_{out}$). Mathematically, as the ratio approaches 1, the logarithm approaches 0. Consequently, the equilibrium potential moves closer to 0 mV (i.e., it becomes less negative or depolarized). This shift in $E_K$ (and consequently the Resting Membrane Potential) moves the cell closer to the firing threshold, increasing excitability and risk of cardiac arrhythmias. Therefore, the correct answer is b) $E_K$ becomes less negative (Depolarized).

3. Which factor is NOT considered in the Nernst Equation but IS included in the Goldman-Hodgkin-Katz (GHK) equation?

a) Temperature

b) Membrane Permeability

c) Ion Concentration

d) Ion Valence

Explanation: The Nernst equation calculates the potential for a single ion assuming the membrane is fully permeable to it (or at equilibrium). However, real cell membranes are permeable to multiple ions simultaneously (Na+, K+, Cl-) to varying degrees. The Goldman-Hodgkin-Katz (GHK) equation calculates the actual Resting Membrane Potential by taking into account the Membrane Permeability ($P$) of each ion in addition to their concentrations. For example, the resting membrane is dominated by K+ because $P_K$ is much higher than $P_{Na}$. Nernst assumes ideal, single-ion conditions. Therefore, the correct answer is b) Membrane Permeability.

4. If the concentration of Sodium inside the cell is 14 mM and outside is 140 mM, the Nernst potential for Sodium (log 10 = 1) is approximately:

a) -61 mV

b) +90 mV

c) +61 mV

d) 0 mV

Explanation: Using the Nernst equation: $E_{Na} = -61/z \times \log([C]_{in}/[C]_{out})$. $z$ for Sodium is +1. Ratio is $14/140 = 0.1$ (or $1/10$). $\log(0.1) = -1$. $E_{Na} = -61 \times (-1) = +61 mV$. Alternatively, using the "61 log (Out/In)" form: $61 \times \log(140/14) = 61 \times \log(10) = 61 \times 1 = +61$ mV. Sodium has a strong electrochemical drive to enter the cell, creating a positive equilibrium potential. Therefore, the correct answer is c) +61 mV.

5. The "Driving Force" for an ion to move across the membrane is mathematically defined as:

a) $Vm - E_{ion}$

b) $E_{ion} - Vm$

c) Permeability $\times$ Concentration

d) Nernst Potential $\times$ Valence

Explanation: The direction and magnitude of ionic current (I) flow through an open channel depend on the Driving Force. This is defined as the difference between the actual Membrane Potential ($Vm$) and the ion's Equilibrium Potential ($E_{ion}$). Formula: Driving Force = $Vm - E_{ion}$. If $Vm$ equals $E_{ion}$, the driving force is zero and there is no net current (equilibrium). If $Vm$ is -70 mV and $E_{Na}$ is +60 mV, the driving force is -130 mV, representing a very strong force pulling Na+ into the cell. Therefore, the correct answer is a) $Vm - E_{ion}$.

6. A patient with renal failure presents with hypocalcemia (low extracellular Calcium). How does this affect neuronal excitability, and what is the mechanism?

a) Decreased excitability due to hyperpolarized Nernst potential

b) Increased excitability due to lowering of the threshold potential

c) No change in excitability

d) Increased excitability due to Na+ pump inhibition

Explanation: This is a high-yield clinical correlation. While the Nernst potential for Ca2+ changes, the primary effect of Hypocalcemia is on the Voltage-Gated Sodium Channels. Extracellular calcium normally binds to the outer surface of Na+ channels, stabilizing them and making them harder to open. When extracellular Ca2+ is low, this stabilizing effect is lost. Consequently, the threshold voltage required to open Na+ channels becomes more negative (closer to the resting potential). This lowers the threshold for firing, leading to Increased excitability and tetany (Chvostek's/Trousseau's signs). Therefore, the correct answer is b) Increased excitability due to lowering of the threshold potential.

7. If the membrane potential is clamped at +61 mV, and the equilibrium potential for Sodium is +61 mV, what is the net flux of Sodium ions?

a) Net influx

b) Net efflux

c) Zero net flux

d) Dependent on ATP availability

Explanation: This scenario describes the definition of the Nernst/Equilibrium potential. At +61 mV, the electrical repulsion of positive sodium ions from inside the positive cell exactly balances the chemical force driving sodium down its concentration gradient into the cell. Because the electrical and chemical forces are equal and opposite, the system is in equilibrium. Although individual ions may move, there is Zero net flux of sodium. This potential is also called the "Reversal Potential" because movement would reverse direction if the voltage went higher or lower. Therefore, the correct answer is c) Zero net flux.

8. What effect does increasing the temperature of the solution have on the Nernst Equilibrium Potential?

a) It decreases the potential magnitude

b) It increases the potential magnitude

c) It has no effect

d) It reverses the polarity

Explanation: The Nernst equation includes the term $RT/zF$, where $T$ is the absolute temperature in Kelvin. Since $T$ is in the numerator, the magnitude of the equilibrium potential is Directly proportional to the temperature. As temperature increases, the kinetic energy of the ions increases, leading to a stronger diffusion tendency. Consequently, a larger electrical potential is required to oppose this increased diffusion force and maintain equilibrium. Thus, the potential magnitude Increases. Therefore, the correct answer is b) It increases the potential magnitude.

9. The resting membrane potential of a neuron (-70 mV) is closest to the Nernst potential of Potassium (-90 mV) rather than Sodium (+60 mV) because:

a) Potassium has the highest concentration gradient

b) The membrane has high resting permeability to Potassium

c) The Sodium-Potassium pump moves more Potassium

d) Potassium is a divalent ion

Explanation: According to the GHK equation, the membrane potential is a weighted average of the equilibrium potentials of all permeant ions, weighted by their permeabilities. In a resting neuron, the membrane possesses numerous "leak channels" that are highly selective for Potassium. Thus, the resting membrane Permeability to Potassium ($P_K$) is about 50-100 times higher than that for Sodium ($P_{Na}$). This high permeability "pulls" the resting membrane potential towards $E_K$. If Na+ channels open (increasing $P_{Na}$), the potential moves towards $E_{Na}$. Therefore, the correct answer is b) The membrane has high resting permeability to Potassium.

10. If the concentration gradient of a monovalent cation is reversed (i.e., higher concentration inside than outside becomes higher outside than inside), the new Nernst potential will:

a) Change in magnitude only

b) Change in sign (polarity) only

c) Become zero

d) Remain exactly the same

Explanation: The Nernst equation depends on the log of the concentration ratio ($C_{in}/C_{out}$). If the gradient is reversed (e.g., swapping the values of $C_{in}$ and $C_{out}$), the ratio becomes the reciprocal (inverted). The logarithm of a reciprocal ($\log(1/x)$) is equal to the negative logarithm ($-\log(x)$). Therefore, reversing the gradient simply reverses the sign of the calculated voltage. For example, if high inside gives -90 mV (like K+), high outside (with same ratio) would give +90 mV. The magnitude remains the same (assuming the ratio value is the same), but the Polarity reverses. Therefore, the correct answer is b) Change in sign (polarity) only.

Chapter: General Physiology; Topic: Nerve-Muscle Physiology; Subtopic: Resting Membrane Potential and Nernst Equation

Key Definitions & Concepts

Nernst Equation: Used to calculate the equilibrium potential for a single ion. Formula: E = -61 x log(Cin/Cout) at 37°C.
Equilibrium Potential (E): The membrane potential at which the electrical gradient exactly balances the chemical concentration gradient for a specific ion, resulting in no net flow.
Potassium (K+): The primary ion determining the Resting Membrane Potential (RMP). High concentration inside (ICF ~140-150 mEq/L), low outside (ECF ~4-5 mEq/L).
Sodium (Na+): High concentration outside (ECF ~140-150 mEq/L), low inside (ICF ~10-14 mEq/L). Equilibrium potential is roughly +60 mV.
Resting Membrane Potential (RMP): The baseline potential difference across the membrane, typically -70 to -90 mV in neurons/muscle, largely due to K+ leak channels.
Goldman-Hodgkin-Katz Equation: Calculates membrane potential taking into account the permeability and concentration of multiple ions (K+, Na+, Cl-).
Gibbs-Donnan Effect: The unequal distribution of permeant charged ions caused by the presence of non-permeant charged ions (like proteins) on one side of the membrane.
Na+-K+ ATPase: An electrogenic pump that maintains the ion gradients by moving 3 Na+ out and 2 K+ in against their gradients.
Depolarization: The membrane potential becomes less negative (moves towards 0 or positive), often driven by Na+ influx.
Hyperpolarization: The membrane potential becomes more negative than RMP, often driven by K+ efflux or Cl- influx.

Lead Question - 2016

ECF concentration of 1C. is 150 meq/L and ICF concentration of le is 5 meq/L. What is the equilibrium potential for K+ is?

a) +60 mV

b) -60 mV

c) -90 mV

d) +90 mV

Explanation: The question asks for the equilibrium potential of Potassium (K+). Standard physiological values for K+ are high intracellularly (~150 mEq/L) and low extracellularly (~5 mEq/L). The text "ECF concentration of 1C...150" and "ICF...5" likely contains typos ("1C" for ICF, "le" for ECF, or swapped values), as the question specifically asks for K+. Applying the Nernst Equation: E = -61 x log (Cin / Cout). Using standard K+ values (Cin=150, Cout=5): E = -61 x log(150/5) = -61 x log(30) = -61 x 1.477 ≈ -90 mV. If the numbers 150 (outside) and 5 (inside) were strictly used for a cation, the result would be +90 mV (resembling Na+ gradients), but since the question asks for K+, the negative potential is the physiological answer. Therefore, the correct answer is c) -90 mV.

1. Which ion has the highest permeability across the resting neuronal cell membrane, thereby contributing most to the Resting Membrane Potential?

a) Sodium (Na+)

b) Chloride (Cl-)

c) Potassium (K+)

d) Calcium (Ca2+)

Explanation: The Resting Membrane Potential (RMP) is determined by the ion to which the membrane is most permeable. In the resting state, the cell membrane contains numerous "leak channels" that are open. The majority of these are Potassium (K+) leak channels. Because the membrane is much more permeable to K+ than to Na+ or other ions (roughly 50-100 times more), K+ flows out of the cell down its concentration gradient, carrying positive charge out and leaving the inside negative. This drives the RMP close to the Nernst equilibrium potential of Potassium (-90 mV). Therefore, the correct answer is c) Potassium (K+).

2. If the extracellular concentration of Potassium [K+]out is acutely increased (hyperkalemia), what happens to the Resting Membrane Potential?

a) It becomes more negative (Hyperpolarization)

b) It becomes less negative (Depolarization)

c) It remains unchanged

d) It reaches the Sodium equilibrium potential

Explanation: The RMP is sensitive to the gradient of Potassium. According to the Nernst equation (E = -61 log [Cin/Cout]), increasing the denominator ([K+]out) makes the ratio smaller, the log value smaller, and thus the equilibrium potential less negative (closer to zero). Physiologically, a high external K+ reduces the concentration gradient for K+ to leave the cell. Less K+ leaving means less positive charge is removed, making the inside of the cell less negative compared to the outside. This shift towards a more positive potential is called Depolarization, making excitable cells more prone to firing initially. Therefore, the correct answer is b) It becomes less negative (Depolarization).

3. The equilibrium potential for Chloride (Cl-) in most neurons is approximately -70 mV. If the Resting Membrane Potential is also -70 mV, what is the net flow of Chloride ions?

a) Net influx

b) Net efflux

c) No net flow

d) Active transport out of the cell

Explanation: The "Equilibrium Potential" (Nernst potential) is defined as the voltage at which the electrical driving force exactly balances the chemical concentration driving force. If the membrane potential (Vm) is exactly equal to the equilibrium potential for Chloride (E-Cl), the electrochemical forces acting on Chloride are equal and opposite. Consequently, there is No net flow of the ion across the membrane, even if channels are open. This state of equilibrium is why inhibitory postsynaptic potentials (IPSPs) mediated by Cl- (like GABA-A receptors) often "clamp" the membrane potential at -70 mV. Therefore, the correct answer is c) No net flow.

4. During the upstroke of the nerve action potential, the membrane potential transiently approaches the equilibrium potential of which ion?

a) Potassium (+90 mV)

b) Sodium (+60 mV)

c) Chloride (-70 mV)

d) Calcium (+130 mV)

Explanation: During the depolarization phase (upstroke) of an action potential, Voltage-Gated Sodium Channels open, dramatically increasing the membrane's permeability to Sodium (Na+). According to the Goldman equation, the membrane potential shifts towards the equilibrium potential of the most permeant ion. Since Na+ permeability (P-Na) becomes dominant, the potential rushes towards the Sodium equilibrium potential (E-Na), which is approximately +60 mV. It usually peaks around +30 to +40 mV due to the simultaneous/delayed opening of K+ channels and inactivation of Na+ channels preventing it from fully reaching +60 mV. Therefore, the correct answer is b) Sodium (+60 mV).

5. Which factor has a value of approximately -61 mV in the Nernst equation at body temperature (37°C)?

a) RT/zF

b) 2.303 RT/zF

c) Faraday's Constant

d) Gas Constant

Explanation: The full Nernst equation is E = -(RT/zF) * ln(Cin/Cout). To convert the natural logarithm (ln) to the base-10 logarithm (log), we multiply by 2.303. The constants are: Gas constant (R), Temperature (T in Kelvin), Valency (z), and Faraday's constant (F). At body temperature (37°C or 310 K), the combined factor 2.303 RT/F equals approximately 61.5 mV. For a monovalent ion (z=1), this is simplified to -61 mV (or +61 mV depending on the log ratio inversion). This constant is essential for quick calculations. Therefore, the correct answer is b) 2.303 RT/zF.

6. The sodium-potassium pump (Na+-K+ ATPase) is described as "electrogenic" because it:

a) Moves equal amounts of charge in both directions

b) Creates a net positive charge inside the cell

c) Moves 3 positive charges out for every 2 positive charges in

d) Consumes ATP to generate an action potential

Explanation: The Na+-K+ pump moves 3 Sodium ions (Na+) out of the cell and 2 Potassium ions (K+) into the cell for every cycle using 1 ATP. Both ions are positively charged. By pumping 3 cations out and only bringing 2 cations in, there is a net loss of 1 positive charge from the intracellular space. This net movement of charge creates a small electrical potential (making the inside more negative), contributing about -4 mV directly to the Resting Membrane Potential. This capability to generate a potential difference makes the pump Electrogenic. Therefore, the correct answer is c) Moves 3 positive charges out for every 2 positive charges in.

7. Calculate the equilibrium potential for Calcium (Ca2+) if [Ca2+]out = 2 mM and [Ca2+]in = 0.0002 mM. (Use the factor 61).

a) +122 mV

b) -122 mV

c) +61 mV

d) +244 mV

Explanation: Using the Nernst Equation: E = -61/z * log(Cin/Cout). Calcium is a divalent cation, so z = +2. The factor becomes -61/2 = -30.5. Concentration ratio: Cin/Cout = 0.0002 / 2 = 0.0001 (which is 10^-4). Log(10^-4) = -4. Calculation: E = -30.5 * (-4) = +122 mV. Alternatively, E = +61/z * log(Cout/Cin) = +30.5 * log(10000) = 30.5 * 4 = +122 mV. Calcium has a very large gradient driving it into the cell, resulting in a highly positive equilibrium potential. Therefore, the correct answer is a) +122 mV.

8. In the Goldman-Hodgkin-Katz equation, the contribution of Chloride (Cl-) is entered differently from Na+ and K+ because:

a) Chloride is divalent

b) Chloride has a negative valence (anion)

c) Chloride is not permeable

d) Chloride is actively transported into the cell

Explanation: The Goldman equation calculates Vm based on permeability (P) and concentrations. For cations (Na+, K+), the term is log([C]out / [C]in). However, Chloride is an Anion (negative valence, z = -1). Due to the properties of logarithms (log(A/B) = -log(B/A)), the negative charge allows the term to be inverted to maintain the positive sign of the equation's structure. Thus, for Chloride, the concentrations are inverted: [Cl-]in is in the numerator and [Cl-]out is in the denominator. This accounts for the valence difference. Therefore, the correct answer is b) Chloride has a negative valence (anion).

9. The absolute refractory period of a neuron is primarily due to the:

a) Opening of Voltage-gated K+ channels

b) Inactivation of Voltage-gated Na+ channels

c) Hyperpolarization of the membrane

d) Closure of leak channels

Explanation: During the absolute refractory period, no new action potential can be generated, regardless of the stimulus strength. This occurs during the depolarization and early repolarization phases. The molecular basis is the state of the Voltage-gated Sodium Channels. After opening to cause depolarization, these channels enter an Inactivated state (ball-and-chain mechanism closes the pore). They cannot reopen until the membrane repolarizes and the channels reset to the "closed but ready" state. This prevents back-propagation and limits firing frequency. Hyperpolarization causes the relative refractory period. Therefore, the correct answer is b) Inactivation of Voltage-gated Na+ channels.

10. Which transport mechanism is responsible for establishing the high concentration of Potassium inside the cell?

a) Simple Diffusion

b) Secondary Active Transport

c) Primary Active Transport

d) Facilitated Diffusion

Explanation: While K+ leak channels allow K+ to exit (creating the RMP), the high intracellular concentration of K+ is established and maintained against its concentration gradient. Moving ions "uphill" (from low extracellular to high intracellular concentration) requires metabolic energy. The Na+-K+ ATPase pump performs this function by using ATP hydrolysis to actively pump K+ into the cell (and Na+ out). This is Primary Active Transport. Without this pump, the gradients would dissipate via diffusion, and the cell would lose its excitability. Therefore, the correct answer is c) Primary Active Transport.

Chapter: General Physiology; Topic: Transport Across Cell Membranes; Subtopic: Modes of Membrane Transport

Key Definitions & Concepts

Simple Diffusion: Passive movement of substances (like gases, water, lipophilic drugs) down a concentration gradient directly through the lipid bilayer; generally considered the most common mechanism overall.
Primary Active Transport: Transport against a gradient utilizing direct energy from ATP hydrolysis (e.g., Na+/K+ ATPase, Ca2+ ATPase).
Secondary Active Transport: Transport driven by the energy stored in the electrochemical gradient of another molecule (usually Na+), not direct ATP usage.
Symport (Cotransport): A type of secondary active transport where two substances move in the same direction (e.g., SGLT1 moving Na+ and Glucose into the cell).
Antiport (Counter-transport): Secondary active transport where substances move in opposite directions (e.g., Na+/Ca2+ exchanger).
Facilitated Diffusion: Passive transport aided by carrier proteins or channels, exhibiting saturation kinetics (e.g., GLUT transporters).
Pinocytosis: "Cell drinking"; a form of endocytosis where the cell engulfs extracellular fluid and dissolved solutes non-specifically.
Phagocytosis: "Cell eating"; engulfment of large particles (bacteria, debris) by specialized cells like macrophages.
Receptor-Mediated Endocytosis: Highly specific uptake of ligands (like LDL or Transferrin) involving clathrin-coated pits.
Aquaporins: Specialized channel proteins that facilitate the rapid passive diffusion of water molecules.

[Image of Cell membrane transport mechanisms summary]

Lead Question - 2016

Most common mechanism for transport into the cell?

a) Diffusion

b) Primary active transport

c) Antiport

d) Cotransport

Explanation: When considering the sheer volume of molecules moving across cell membranes generally (including water, oxygen, carbon dioxide, nitrogen, and lipophilic substances), the most common mechanism is Diffusion (specifically Simple Diffusion). This process is passive, requires no energy, and follows the concentration gradient. In the context of pharmacology, the vast majority of drugs are absorbed and enter cells via passive diffusion (following Fick's Law). While nutrient uptake (glucose, amino acids) often relies on carrier-mediated transport (cotransport), diffusion remains the fundamental and most prevalent baseline process for cellular life and gas exchange. Therefore, the correct answer is a) Diffusion.

1. The Na+/K+ ATPase pump maintains the transmembrane potential by moving ions against their gradients. For every ATP molecule hydrolyzed, what is the stoichiometry of ion movement?

a) 3 Na+ in, 2 K+ out

b) 2 Na+ out, 3 K+ in

c) 3 Na+ out, 2 K+ in

d) 1 Na+ out, 1 K+ in

Explanation: The Na+/K+ ATPase is the quintessential example of primary active transport. It is ubiquitous in animal cells. Its function is to maintain the low intracellular sodium and high intracellular potassium concentrations. The pump operates by hydrolyzing one molecule of ATP to pump 3 Sodium ions (Na+) OUT of the cell and 2 Potassium ions (K+) INTO the cell. Because 3 positive charges leave and only 2 enter, the pump is electrogenic, contributing slightly (about -4mV) to the negative resting membrane potential. Therefore, the correct answer is c) 3 Na+ out, 2 K+ in.

2. A diabetic patient is prescribed an SGLT2 inhibitor (flozin) to lower blood glucose. This drug targets a transporter in the proximal renal tubule. The physiological mechanism of glucose reabsorption via SGLT2 is an example of:

a) Facilitated Diffusion

b) Primary Active Transport

c) Secondary Active Transport (Symport)

d) Simple Diffusion

Explanation: Glucose is reabsorbed from the renal tubule lumen against its concentration gradient. To achieve this uphill transport, the cell utilizes the energy stored in the inward Sodium gradient (established by the Na+/K+ pump). The Sodium-Glucose Linked Transporter (SGLT) binds both Na+ and Glucose and transports them together into the cell. Since both move in the same direction, this is Symport (or Cotransport). Because the energy comes from the ion gradient rather than direct ATP hydrolysis at the transporter, it is classified as Secondary Active Transport. Therefore, the correct answer is c) Secondary Active Transport (Symport).

3. Insulin stimulates glucose uptake in skeletal muscle and adipose tissue by inducing the translocation of which transporter to the cell membrane?

a) GLUT1

b) GLUT2

c) GLUT4

d) SGLT1

Explanation: Glucose transporters (GLUTs) mediate facilitated diffusion of glucose. GLUT4 is unique because it is the insulin-sensitive transporter. In the basal state, GLUT4 is sequestered in intracellular vesicles. Upon insulin binding to its receptor, a signaling cascade causes these vesicles to fuse with the plasma membrane, inserting GLUT4 and increasing glucose uptake by 10-20 fold. This is the mechanism for postprandial glucose clearance. GLUT1 is ubiquitous (blood-brain barrier). GLUT2 is in the liver/pancreas (glucose sensor). SGLT1 is in the intestine. Therefore, the correct answer is c) GLUT4.

4. In cardiac muscle cells, Calcium extrusion during relaxation is partially achieved by the Na+/Ca2+ Exchanger (NCX). This transporter moves 3 Na+ in and 1 Ca2+ out. This is an example of:

a) Uniport

b) Antiport (Counter-transport)

c) Primary Active Transport

d) Passive Diffusion

Explanation: The Na+/Ca2+ Exchanger (NCX) is crucial for preventing calcium overload in cardiac myocytes. It uses the energy of the Na+ gradient (sodium wanting to enter the cell) to push Calcium out of the cell against its massive concentration gradient. Since the two species move in opposite directions (Na+ in, Ca2+ out), this mechanism is defined as Antiport or Counter-transport. It is a form of secondary active transport. The drug Digitalis inhibits the Na+/K+ pump, accumulating intracellular Na+, which weakens the NCX gradient, keeping Ca2+ inside to increase contractility. Therefore, the correct answer is b) Antiport (Counter-transport).

5. A patient with familial hypercholesterolemia has extremely high levels of LDL cholesterol due to a defect in cellular uptake. The mechanism by which cells normally internalize LDL particles is:

a) Pinocytosis

b) Phagocytosis

c) Receptor-Mediated Endocytosis

d) Simple Diffusion

Explanation: Low-Density Lipoprotein (LDL) is too large to pass through channels or carriers. Its uptake is highly regulated. The LDL particle binds to specific LDL Receptors concentrated in Clathrin-coated pits on the cell membrane. This binding triggers the invagination of the membrane to form a coated vesicle, internalizing the LDL-Receptor complex. This specific, high-affinity process is Receptor-Mediated Endocytosis. Defects in the LDL receptor or the protein apolipoprotein B-100 impair this binding, leading to elevated serum cholesterol. Pinocytosis is non-specific "drinking." Therefore, the correct answer is c) Receptor-Mediated Endocytosis.

6. The MDR1 (Multi-Drug Resistance) protein, often overexpressed in cancer cells, pumps chemotherapeutic drugs out of the cell. Structurally and functionally, this transporter belongs to the:

a) ABC Transporter superfamily

b) Solute Carrier (SLC) family

c) Ion Channel family

d) Aquaporin family

Explanation: P-glycoprotein (MDR1) is an efflux pump that removes toxins and drugs from cells. It functions by binding ATP and using the energy of hydrolysis to pump substrates against their gradient. This ATP-dependence classifies it as a Primary Active Transporter. Structurally, it contains ATP-Binding Cassettes, placing it in the ABC Transporter superfamily. The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is another famous member of this family (though it functions as a chloride channel, it is structurally an ABC protein). Therefore, the correct answer is a) ABC Transporter superfamily.

7. Which transport mechanism exhibits the property of Transport Maximum (Tm), where the rate of transport plateaus at high substrate concentrations?

a) Simple Diffusion through lipid bilayer

b) Simple Diffusion through channels

c) Carrier-Mediated Transport

d) Osmosis

Explanation: Saturation kinetics is a hallmark of processes requiring a specific binding site. In Carrier-Mediated Transport (both Facilitated Diffusion and Active Transport), there are a finite number of transporter proteins in the membrane. As substrate concentration increases, the rate of transport increases until all binding sites are occupied (saturated). At this point, the rate reaches a maximum velocity (Vmax) or Transport Maximum (Tm) and cannot increase further. Simple diffusion does not saturate; its rate is linear with concentration. Therefore, the correct answer is c) Carrier-Mediated Transport.

8. Omeprazole is used to treat peptic ulcers by inhibiting the H+/K+ ATPase in gastric parietal cells. This pump is responsible for the secretion of acid. What type of transport does this pump perform?

a) Secondary Active Transport

b) Primary Active Transport

c) Facilitated Diffusion

d) Passive leak channel

Explanation: The proton pump (H+/K+ ATPase) in the stomach must concentrate H+ ions in the lumen by a factor of over a million compared to the intracellular space. This massive gradient requires significant energy input. The pump hydrolyzes ATP directly to drive H+ out into the lumen and K+ into the cell (electroneutral 1:1 exchange). Since it uses ATP directly, it is a Primary Active Transporter. Proton Pump Inhibitors (PPIs) like Omeprazole irreversibly bind to and inhibit this pump. Therefore, the correct answer is b) Primary Active Transport.

9. The "Chloride Shift" in Red Blood Cells involves the exchange of Bicarbonate (HCO3-) leaving the cell for Chloride (Cl-) entering the cell. This anion exchange is mediated by Band 3 protein via:

a) Facilitated Diffusion (Antiport)

b) Active Transport

c) Simple Diffusion

d) Pinocytosis

Explanation: The Band 3 protein (AE1) is an Anion Exchanger. It facilitates the movement of HCO3- and Cl- across the RBC membrane. This movement is passive; it does not consume ATP. The direction is driven by the concentration gradients of the ions (which change between tissues and lungs). However, because it involves a carrier protein moving two ions in opposite directions, it is mechanistically an Antiport. Since it is passive (no energy), it is technically a form of Facilitated Diffusion acting as an exchanger. In standard classification, it's often grouped under Antiport/Exchangers. Therefore, the correct answer is a) Facilitated Diffusion (Antiport).

10. In nerve axons, the rapid depolarization phase of the action potential is mediated by the influx of Sodium. Through which type of membrane protein does this Sodium enter?

a) Voltage-Gated Ion Channel

b) Ligand-Gated Ion Channel

c) Leak Channel

d) Na+/K+ Pump

Explanation: Ion channels provide a watery pore for ions to diffuse passively down their electrochemical gradients. They are gated to control flow. During an action potential, the membrane potential reaches a threshold, triggering the opening of Voltage-Gated Sodium Channels. Na+ rushes into the cell (down its gradient), causing depolarization. This is simple diffusion through a channel protein. Ligand-gated channels open in response to neurotransmitters (like ACh). Leak channels are always open (responsible for resting potential). The pump builds the gradient but doesn't create the spike. Therefore, the correct answer is a) Voltage-Gated Ion Channel.

Chapter: General Physiology; Topic: Transport Across Cell Membranes; Subtopic: Modes of Membrane Transport

Key Definitions & Concepts

Simple Diffusion: Passive movement of substances (like gases, water, lipophilic drugs) down a concentration gradient directly through the lipid bilayer; generally considered the most common mechanism overall.
Primary Active Transport: Transport against a gradient utilizing direct energy from ATP hydrolysis (e.g., Na+/K+ ATPase, Ca2+ ATPase).
Secondary Active Transport: Transport driven by the energy stored in the electrochemical gradient of another molecule (usually Na+), not direct ATP usage.
Symport (Cotransport): A type of secondary active transport where two substances move in the same direction (e.g., SGLT1 moving Na+ and Glucose into the cell).
Antiport (Counter-transport): Secondary active transport where substances move in opposite directions (e.g., Na+/Ca2+ exchanger).
Facilitated Diffusion: Passive transport aided by carrier proteins or channels, exhibiting saturation kinetics (e.g., GLUT transporters).
Pinocytosis: "Cell drinking"; a form of endocytosis where the cell engulfs extracellular fluid and dissolved solutes non-specifically.
Phagocytosis: "Cell eating"; engulfment of large particles (bacteria, debris) by specialized cells like macrophages.
Receptor-Mediated Endocytosis: Highly specific uptake of ligands (like LDL or Transferrin) involving clathrin-coated pits.
Aquaporins: Specialized channel proteins that facilitate the rapid passive diffusion of water molecules.

[Image of Cell membrane transport mechanisms summary]

Lead Question - 2016

Most common mechanism for transport into the cell?

a) Diffusion

b) Primary active transport

c) Antiport

d) Cotransport

1. The Na+/K+ ATPase pump maintains the transmembrane potential by moving ions against their gradients. For every ATP molecule hydrolyzed, what is the stoichiometry of ion movement?

a) 3 Na+ in, 2 K+ out

b) 2 Na+ out, 3 K+ in

c) 3 Na+ out, 2 K+ in

d) 1 Na+ out, 1 K+ in

a) Facilitated Diffusion

b) Primary Active Transport

c) Secondary Active Transport (Symport)

d) Simple Diffusion

3. Insulin stimulates glucose uptake in skeletal muscle and adipose tissue by inducing the translocation of which transporter to the cell membrane?

a) GLUT1

b) GLUT2

c) GLUT4

d) SGLT1

4. In cardiac muscle cells, Calcium extrusion during relaxation is partially achieved by the Na+/Ca2+ Exchanger (NCX). This transporter moves 3 Na+ in and 1 Ca2+ out. This is an example of:

a) Uniport

b) Antiport (Counter-transport)

c) Primary Active Transport

d) Passive Diffusion

5. A patient with familial hypercholesterolemia has extremely high levels of LDL cholesterol due to a defect in cellular uptake. The mechanism by which cells normally internalize LDL particles is:

a) Pinocytosis

b) Phagocytosis

c) Receptor-Mediated Endocytosis

d) Simple Diffusion

6. The MDR1 (Multi-Drug Resistance) protein, often overexpressed in cancer cells, pumps chemotherapeutic drugs out of the cell. Structurally and functionally, this transporter belongs to the:

a) ABC Transporter superfamily

b) Solute Carrier (SLC) family

c) Ion Channel family

d) Aquaporin family

7. Which transport mechanism exhibits the property of Transport Maximum (Tm), where the rate of transport plateaus at high substrate concentrations?

a) Simple Diffusion through lipid bilayer

b) Simple Diffusion through channels

c) Carrier-Mediated Transport

d) Osmosis

a) Secondary Active Transport

b) Primary Active Transport

c) Facilitated Diffusion

d) Passive leak channel

9. The "Chloride Shift" in Red Blood Cells involves the exchange of Bicarbonate (HCO3-) leaving the cell for Chloride (Cl-) entering the cell. This anion exchange is mediated by Band 3 protein via:

a) Facilitated Diffusion (Antiport)

b) Active Transport

c) Simple Diffusion

d) Pinocytosis

10. In nerve axons, the rapid depolarization phase of the action potential is mediated by the influx of Sodium. Through which type of membrane protein does this Sodium enter?

a) Voltage-Gated Ion Channel

b) Ligand-Gated Ion Channel

c) Leak Channel

d) Na+/K+ Pump

Chapter: General Physiology; Topic: Transport Across Cell Membranes; Subtopic: Mechanisms of Passive Transport (Simple Diffusion)

Key Definitions & Concepts

Simple Diffusion: The passive movement of solute molecules across a semipermeable membrane from an area of higher concentration to an area of lower concentration without the aid of transport proteins.
Fick's Law of Diffusion: States that the rate of diffusion (J) is directly proportional to the surface area (A), concentration gradient (ΔC), and lipid solubility, and inversely proportional to the thickness of the membrane (Δx).
Lipid Solubility (Partition Coefficient): A measure of how easily a substance dissolves in lipids; substances with high lipid solubility (non-polar) diffuse rapidly through the lipid bilayer.
Channel Proteins: Transmembrane proteins that form water-filled pores (e.g., aquaporins, ion channels) allowing specific hydrophilic substances to cross the membrane; distinct from simple diffusion through the lipid matrix.
Facilitated Diffusion: Passive transport mediated by carrier proteins that undergo conformational changes; unlike simple diffusion, it exhibits saturation kinetics (Tm).
Concentration Gradient: The driving force for simple diffusion; net flux stops when the concentration is equal on both sides (equilibrium).
Permeability Coefficient: A value representing the ease with which a specific molecule crosses a specific membrane; depends on lipid solubility and molecular size.
Meyer-Overton Correlation: Specifically relates the potency of general anesthetics to their lipid solubility; a clinical application of simple diffusion principles.
Diffusion Capacity (DLCO): A clinical measure of the lung's ability to transfer gas (CO) from alveoli to blood; reduced in fibrosis (thickened membrane) and emphysema (lost surface area).
Brownian Motion: The random thermal motion of molecules that underlies the physical process of diffusion.

[Image of Simple diffusion vs Facilitated diffusion graph]

Lead Question - 2016

Following is a feature of simple diffusion?

a) Against a concentration gradient

b) Easy for non-polar substance

c) More in thick membrane

d) Requires carrier protein

Explanation: Simple diffusion describes the movement of molecules directly through the lipid bilayer of the cell membrane. The core of the membrane is hydrophobic (lipid). Therefore, non-polar (lipophilic) substances like Oxygen (O2), Carbon Dioxide (CO2), nitrogen, steroid hormones, and anesthetics can dissolve in this lipid matrix and pass through easily. Diffusion is a passive process driven by thermal energy, moving substances down their concentration gradient (high to low), not against it. According to Fick's Law, the rate of diffusion is inversely proportional to membrane thickness (thicker = slower) and does not require carrier proteins (which characterizes facilitated diffusion or active transport). Therefore, the correct answer is b) Easy for non-polar substance.

1. According to Fick's Law of diffusion, the rate of net diffusion (J) is inversely proportional to which of the following parameters?

a) Concentration gradient

b) Surface area of the membrane

c) Thickness of the membrane

d) Lipid solubility of the solute

Explanation: Fick's Law mathematically describes passive diffusion: J = (D * A * ΔC) / Δx. Here, 'J' is the rate of diffusion. 'A' (Surface Area) and 'ΔC' (Concentration Gradient) are in the numerator, meaning diffusion increases as these increase. Lipid solubility also increases the diffusion coefficient (D). However, 'Δx' represents the diffusion distance or the Thickness of the membrane and is in the denominator. This means that as the membrane becomes thicker, the rate of diffusion decreases. This is clinically relevant in conditions like pulmonary fibrosis, where a thickened respiratory membrane impairs gas exchange. Therefore, the correct answer is c) Thickness of the membrane.

2. A scuba diver suffering from "the bends" (decompression sickness) has nitrogen bubbles forming in the blood. Nitrogen gas crosses cell membranes primarily by:

a) Facilitated diffusion via gas transporters

b) Simple diffusion through the lipid bilayer

c) Active transport

d) Solvent drag

Explanation: Respiratory gases such as Oxygen, Carbon Dioxide, and Nitrogen are small, non-polar, uncharged molecules. Because of their lipophilic nature, they do not require specific transporters, channels, or energy to cross cell membranes. Instead, they move via Simple diffusion through the lipid bilayer. This allows for rapid equilibration between the alveoli and pulmonary capillaries. In decompression sickness, the rapid decrease in ambient pressure causes nitrogen (which had diffused into tissues under high pressure) to come out of solution faster than it can diffuse back into the lungs to be exhaled. Therefore, the correct answer is b) Simple diffusion through the lipid bilayer.

3. Which graphical representation best characterizes the relationship between the rate of transport and substrate concentration in simple diffusion?

a) Sigmoidal curve

b) Rectangular hyperbola (saturation kinetics)

c) Linear relationship

d) Exponential decay

Explanation: This is a key distinguishing feature between simple and carrier-mediated transport. In simple diffusion, the rate of transport is directly proportional to the concentration gradient. As long as the concentration difference increases, the rate of diffusion increases without limit. This produces a straight Linear relationship on a graph (non-saturable). In contrast, carrier-mediated transport (like facilitated diffusion) relies on a limited number of protein carriers. Once all carriers are occupied (Vmax), the rate plateaus, showing saturation kinetics (rectangular hyperbola). Therefore, the correct answer is c) Linear relationship.

4. A premature infant develops Respiratory Distress Syndrome (RDS) due to surfactant deficiency. This leads to alveolar collapse (atelectasis). Physiologically, this hypoxia is primarily caused by a reduction in which factor of Fick's Law?

a) Membrane thickness

b) Diffusion coefficient

c) Surface area

d) Concentration gradient

Explanation: Fick's Law states diffusion is proportional to Surface Area (A). The lungs normally have a massive surface area for gas exchange provided by millions of open alveoli. In Neonatal RDS, the lack of surfactant leads to high surface tension and the collapse of alveoli (atelectasis). This collapse drastically reduces the total functional Surface area available for oxygen diffusion from the air into the blood. While the membrane might thicken later due to damage, the primary immediate physical deficit causing hypoxia is the loss of surface area. Therefore, the correct answer is c) Surface area.

5. Which of the following substances has the highest permeability coefficient across a pure phospholipid bilayer?

a) Glucose

b) Sodium ion (Na+)

c) Water

d) Steroid hormones (e.g., Cortisol)

Explanation: Permeability depends on size, charge, and lipid solubility. Ions like Sodium (Na+), despite being small, are highly charged and surrounded by a hydration shell, making them essentially impermeable to the hydrophobic lipid core without channels. Glucose is large and polar, requiring transporters (GLUTs). Water is small and polar; it can diffuse slowly but relies mostly on aquaporins. Steroid hormones are lipids (cholesterol derivatives). Being non-polar and lipophilic, they have the highest partition coefficient and diffuse most readily directly through the bilayer to reach intracellular receptors. Therefore, the correct answer is d) Steroid hormones (e.g., Cortisol).

6. The "Partition Coefficient" of a solute is a measure of its:

a) Molecular weight

b) Water solubility relative to its size

c) Lipid solubility relative to water solubility

d) Electrical charge density

Explanation: The Partition Coefficient (K) is a physicochemical property that predicts how easily a substance can cross a biological membrane via simple diffusion. It is defined as the ratio of a substance's solubility in oil (lipid) to its solubility in water. A high partition coefficient means the substance is more soluble in lipids than in water (lipophilic). Since the cell membrane core is lipid, substances with a high partition coefficient (like general anesthetics) enter cells very rapidly. This concept is central to the Meyer-Overton rule in anesthesiology. Therefore, the correct answer is c) Lipid solubility relative to water solubility.

7. A patient with severe pneumonia has fluid accumulation in the alveoli (pulmonary edema). This impairs oxygenation because the presence of fluid essentially increases the:

a) Membrane surface area

b) Diffusion distance (path length)

c) Solubility of Oxygen

d) Partial pressure of Oxygen in alveoli

Explanation: Gas exchange involves diffusion through the respiratory membrane (alveolar epithelium, interstitium, capillary endothelium). In pulmonary edema, fluid accumulates in the interstitial space and within the alveoli. Oxygen molecules must now diffuse not only through the tissue barriers but also through a layer of fluid to reach the red blood cells. This effectively increases the Diffusion distance (path length) or membrane thickness (Δx in Fick's Law). Since diffusion time is proportional to the square of the distance, even small increases in fluid thickness cause significant hypoxemia. Therefore, the correct answer is b) Diffusion distance (path length).

8. Which variable determines the direction of net simple diffusion of an uncharged solute?

a) The chemical concentration gradient only

b) The electrical gradient only

c) The electrochemical gradient

d) ATP availability

Explanation: For charged particles (ions), movement is dictated by both the chemical gradient (concentration difference) and the electrical gradient (potential difference), collectively known as the electrochemical gradient. However, for uncharged solutes (like glucose, urea, O2), the electrical potential across the membrane exerts no force on the molecule. Therefore, the driving force for net diffusion is governed solely by the Chemical concentration gradient (difference in concentration) across the membrane. Diffusion continues until the concentrations on both sides are equal. Therefore, the correct answer is a) The chemical concentration gradient only.

9. Unlike simple diffusion, facilitated diffusion is characterized by:

a) Transport against the concentration gradient

b) Non-specific transport of any molecule

c) Requirement for metabolic energy (ATP)

d) Competitive inhibition and stereospecificity

Explanation: Both simple and facilitated diffusion are passive (downhill) processes requiring no ATP. However, facilitated diffusion uses specific carrier proteins (like GLUT4 for glucose). Because it involves binding to a protein, it shares properties with enzymes: 1) Stereospecificity (e.g., transporting D-glucose but not L-glucose), 2) Saturation (Tm), and 3) Competitive inhibition (structurally similar molecules can block the transporter). Simple diffusion, being a physical process through the lipid bilayer, does not display stereospecificity or competitive inhibition in the classical sense. Therefore, the correct answer is d) Competitive inhibition and stereospecificity.

10. In a laboratory setting, increasing the temperature of a solution will have what effect on the rate of simple diffusion?

a) It will decrease linearly

b) It will increase

c) It will remain unchanged

d) It will stop completely

Explanation: Diffusion is driven by the random thermal motion (Brownian motion) of molecules. The kinetic energy of molecules is directly related to temperature. As temperature increases, the kinetic energy of the solute molecules increases, causing them to move and collide more frequently and vigorously. This results in an Increase in the rate of diffusion. Conversely, cooling a solution slows down molecular motion and the rate of diffusion. This is a fundamental physical principle applicable to biological systems as well. Therefore, the correct answer is b) It will increase.

Chapter: Cell Biology; Topic: Cell Membrane Structure; Subtopic: Lipid Rafts and Membrane Microdomains

Key Definitions & Concepts

Lipid Rafts: Specialized, dynamic microdomains within the plasma membrane that are rich in cholesterol and sphingolipids, creating a "liquid-ordered" phase.
Fluid Mosaic Model: The classical model of the cell membrane described by Singer and Nicolson; lipid rafts represent a modification to this model by introducing heterogeneity.
Caveolae: A specific type of lipid raft characterized by flask-shaped invaginations of the plasma membrane, stabilized by the protein Caveolin.
Sphingolipids: A class of lipids containing a backbone of sphingoid bases; they possess long, saturated fatty acid chains that pack tightly with cholesterol.
GPI-anchored proteins: Proteins attached to the outer leaflet of the membrane via a Glycosylphosphatidylinositol anchor; they preferentially partition into lipid rafts.
Signal Transduction: A primary function of lipid rafts is to concentrate signaling receptors and effector molecules to facilitate efficient cellular communication.
Detergent-Resistant Membranes (DRMs): Lipid rafts are often operationally defined by their insolubility in non-ionic detergents (like Triton X-100) at low temperatures.
Cholesterol: The "glue" of lipid rafts; it fills the spaces between the saturated fatty acid tails of sphingolipids, increasing membrane thickness and order.
Caveolin-1: An integral membrane protein essential for the formation of caveolae; it acts as a scaffold for signaling complexes.
Viral Entry: Many pathogens (e.g., HIV, Influenza) utilize lipid rafts as platforms for binding to and entering or exiting host cells.

[Image of Lipid raft structure in plasma membrane]

Lead Question - 2016

Lipid rafts are seen in?

a) Ribosomes

b) Mitochondria

c) Plasma membrane

d) ER

Explanation: Lipid rafts are specialized, dynamic microdomains located within the Plasma membrane. While the endoplasmic reticulum (ER) is the site of lipid synthesis, the specific assembly of cholesterol and sphingolipids into the tightly packed, ordered structures characteristic of "rafts" occurs primarily in the Golgi and is maintained in the plasma membrane. Ribosomes are protein synthesis machinery and lack membranes. Mitochondria have membranes but do not typically exhibit the classic cholesterol-rich lipid rafts found on the cell surface (though mitochondrial-associated membranes exist). The high concentration of cholesterol and sphingolipids in the plasma membrane allows these rafts to function as platforms for signaling and sorting. Therefore, the correct answer is c) Plasma membrane.

1. Which biochemical property principally distinguishes the lipids found in lipid rafts from those in the surrounding fluid membrane?

a) Shorter fatty acid chains

b) High content of polyunsaturated fatty acids

c) High degree of saturation in fatty acyl chains

d) Absence of cholesterol

Explanation: The structural integrity of lipid rafts relies on the tight packing of lipid molecules. The phospholipids and sphingolipids within rafts typically possess long, straight, High degree of saturation in fatty acyl chains. Saturated fats lack double bonds (kinks), allowing them to pack closely together. This is in contrast to the surrounding "liquid-disordered" membrane, which is rich in unsaturated (kinked) fatty acids (like phosphatidylcholine) that create fluidity. Cholesterol intercalates between these saturated chains, further cementing the "liquid-ordered" phase. This saturation is what makes rafts thicker and more resistant to solubilization than the rest of the membrane. Therefore, the correct answer is c) High degree of saturation in fatty acyl chains.

2. A researcher is studying the entry mechanism of the Simian Virus 40 (SV40). They find that the virus binds to a receptor localized in flask-shaped invaginations of the plasma membrane. Which protein is the primary structural component of these specific lipid rafts?

a) Clathrin

b) Caveolin

c) Actin

d) Dynamin

Explanation: The flask-shaped invaginations described are a specific subtype of lipid raft known as Caveolae ("little caves"). Unlike planar lipid rafts, caveolae are stabilized by the integral membrane protein Caveolin (specifically Caveolin-1, -2, or -3). Caveolins form oligomers that insert into the inner leaflet of the plasma membrane, inducing curvature. These domains are hotspots for endocytosis (potocytosis) and signal transduction. SV40 is a classic example of a virus that utilizes caveolae for cell entry. Clathrin coats coated pits, which are distinct from lipid rafts. Actin is cytoskeletal. Dynamin pinches off vesicles. Therefore, the correct answer is b) Caveolin.

3. Which class of membrane-associated proteins is most preferentially targeted to lipid rafts?

a) Transmembrane proteins with short alpha-helices

b) GPI-anchored proteins

c) Peripheral proteins attached via electrostatic interactions

d) Proteins with prenyl groups

Explanation: Lipid rafts serve as sorting platforms for specific proteins. The most classic association is with GPI-anchored proteins (Glycosylphosphatidylinositol-anchored proteins). These proteins lack a transmembrane domain and are anchored to the outer leaflet of the plasma membrane by a lipid tail. The saturated fatty acid chains of the GPI anchor have a high affinity for the ordered, cholesterol-rich environment of the lipid raft. Consequently, GPI-anchored proteins (like CD55, CD59, and Alkaline Phosphatase) are highly concentrated in these microdomains. Transmembrane proteins are generally excluded unless they have specific raft-targeting sequences (like palmitoylation). Therefore, the correct answer is b) GPI-anchored proteins.

4. In a laboratory experiment, a cell membrane sample is treated with cold 1% Triton X-100 detergent. After centrifugation, a floating fraction is isolated that is insoluble in the detergent. This fraction is most likely to contain:

a) The entire plasma membrane

b) Lipid rafts

c) Cytoskeletal elements only

d) Soluble cytosolic proteins

Explanation: This describes the operational definition of lipid rafts in biochemistry. Because of the tight packing of saturated sphingolipids and cholesterol, lipid rafts are resistant to solubilization by non-ionic detergents (like Triton X-100) at low temperatures (4°C). The rest of the fluid membrane dissolves. The rafts remain intact and, due to their high lipid content, have a low buoyant density. Upon sucrose gradient centrifugation, they float to the top. Thus, these isolated fractions are often called "Detergent-Resistant Membranes" (DRMs), which correspond to Lipid rafts. Therefore, the correct answer is b) Lipid rafts.

5. Cholera toxin exerts its pathological effect by binding to a specific ganglioside receptor located on the intestinal epithelium. This receptor is enriched in lipid rafts. Which ganglioside is it?

a) GM1

b) GM2

c) GD1a

d) GT1b

Explanation: Gangliosides are glycosphingolipids containing sialic acid. They are major components of lipid rafts, residing in the outer leaflet. The B-subunit of the Cholera Toxin binds with extremely high affinity to the GM1 ganglioside. Since GM1 is concentrated in lipid rafts, the toxin hijacks this microdomain to enter the cell (via raft-dependent endocytosis) and activate adenylate cyclase. This interaction is a classic example of how pathogens exploit the specific lipid composition of host membrane rafts for pathogenesis. GM2 is associated with Tay-Sachs disease. Therefore, the correct answer is a) GM1.

6. Paroxysmal Nocturnal Hemoglobinuria (PNH) is caused by a defect in the PIG-A gene, leading to a deficiency of GPI anchors. As a result, protective proteins like CD55 and CD59 are missing from the cell surface. Normally, these proteins would be located in:

a) Clathrin-coated pits

b) Lipid rafts

c) The inner mitochondrial membrane

d) The nuclear envelope

Explanation: CD55 (Decay Accelerating Factor) and CD59 (Membrane Inhibitor of Reactive Lysis) are complement regulatory proteins. They are anchored to the red blood cell membrane via GPI anchors. As established, GPI-anchored proteins preferentially partition into Lipid rafts. In PNH, the failure to synthesize the GPI anchor means these proteins cannot attach to the membrane (and thus cannot localize to rafts). Without these protective proteins, the red blood cells are susceptible to complement-mediated lysis, leading to hemolysis. This links the clinical pathology directly to raft-associated protein sorting. Therefore, the correct answer is b) Lipid rafts.

7. Which intracellular modification is commonly used to target cytoplasmic proteins, such as Src family kinases (e.g., Lck, Fyn), to the inner leaflet of lipid rafts?

a) Phosphorylation

b) Ubiquitination

c) Palmitoylation

d) Glycosylation

Explanation: While GPI anchors target proteins to the outer leaflet of rafts, intracellular signaling proteins must attach to the inner leaflet. This is often achieved through dual acylation: myristoylation and Palmitoylation. Palmitoylation involves the reversible attachment of a saturated 16-carbon fatty acid (palmitate) to a cysteine residue. This saturated lipid tail has a high affinity for the ordered lipid environment of the raft. Src family kinases like Lck and Fyn rely on palmitoylation to reside in rafts, which is crucial for T-cell receptor signaling. Therefore, the correct answer is c) Palmitoylation.

8. In the context of Alzheimer's disease, the processing of Amyloid Precursor Protein (APP) by Beta-secretase (BACE1) to form the toxic Amyloid-beta peptide is thought to occur primarily in:

a) The Nucleolus

b) Lipid rafts

c) The fluid (non-raft) phase of the membrane

d) Proteasomes

Explanation: The "Amyloidogenic pathway" involves the cleavage of APP by BACE1 (beta-secretase) and gamma-secretase. Research suggests that BACE1 and gamma-secretase are preferentially located within Lipid rafts. Consequently, the production of the neurotoxic A-beta peptide occurs within these microdomains. Conversely, Alpha-secretase (which cleaves APP into non-toxic fragments) is typically found in the non-raft (disordered) regions. This spatial separation suggests that cholesterol levels and raft integrity play a significant role in the pathogenesis of Alzheimer's, making raft modulation a potential therapeutic target. Therefore, the correct answer is b) Lipid rafts.

9. The T-cell immunological synapse involves the clustering of T-cell Receptors (TCR) and costimulatory molecules. This clustering and subsequent signal transduction are dependent on the coalescence of:

a) Mitochondria

b) Lipid rafts

c) Lysosomes

d) Ribosomes

Explanation: Activation of a T-cell requires the formation of an "immunological synapse" at the point of contact with an antigen-presenting cell. Before activation, TCRs and signaling kinases (like Lck) are dispersed. Upon ligand binding, small, individual Lipid rafts containing these signaling components aggregate to form larger, stable signaling platforms (macrodomains). This clustering brings the kinase (Lck) into proximity with its substrate (ITAMs on the TCR complex), initiating the phosphorylation cascade. Disruption of lipid rafts (e.g., by depleting cholesterol) abolishes T-cell activation. Therefore, the correct answer is b) Lipid rafts.

10. Which molecule is considered the "glue" that keeps lipid rafts together by filling the voids between the sphingolipids?

a) Integral proteins

b) Unsaturated fatty acids

c) Cholesterol

d) Glycerol

Explanation: The structure of a lipid raft is chemically defined by the interaction between sphingolipids and cholesterol. Sphingolipids have long, saturated hydrocarbon chains. Cholesterol is a rigid, planar molecule. It intercalates between the saturated tails of the sphingolipids. Because of its shape, cholesterol fills the voids effectively, promoting tight packing and increasing the thickness of the bilayer. It acts as a dynamic "glue" or spacer that stabilizes the ordered phase. Removing cholesterol (using cyclodextrins) causes lipid rafts to disintegrate and lose their function. Therefore, the correct answer is c) Cholesterol.

2015 NEET PG

Chapter: Physiology; Topic: Renal Physiology; Subtopic: Epithelial Sodium Channels (ENaC)

Keyword Definitions:
• Epithelial sodium channel (ENaC): Sodium-selective channel present in renal collecting ducts, lungs, colon, and sweat glands.
• Alpha subunit (α): Functional pore-forming ENaC unit required for channel activation.
• Beta subunit (β): Regulatory subunit modifying channel kinetics and surface stability.
• Gamma subunit (γ): Enhances channel opening probability and increases sodium conductance.
• Aldosterone: Hormone stimulating ENaC synthesis and increasing sodium reabsorption.
• Pseudohypoaldosteronism: Disorder caused by ENaC mutations impairing sodium regulation.

Lead Question – 2015
Epithelial sodium channels has ?
a) 2α, 2β
b) 1α, 1β
c) 2α, 2β, 2γ
d) 2α, 1β, 2γ

Explanation (Answer: c) 2α, 2β, 2γ)
ENaC consists of six subunits assembled as 2α, 2β, 2γ. Each α unit contributes to channel pore structure, while β and γ regulate gating and stability. Channel expression is regulated by aldosterone, enhancing sodium uptake in renal collecting ducts. Dysfunction causes electrolyte imbalance, hyperkalemia, hypotension, and acid-base disorders, highlighting ENaC’s physiological relevance in sodium homeostasis.

1. ENaC channels are primarily located in:
a) Proximal tubule
b) Thick ascending limb
c) Collecting duct
d) Loop of Henle

Explanation (Answer: c) Collecting duct)
ENaC channels are present mainly in the principal cells of the collecting duct, where they control fine sodium reabsorption. Aldosterone increases ENaC expression and activity, affecting sodium retention and potassium secretion. Proximal tubule reabsorbs sodium via other transporters but not ENaC. Collecting duct dysfunction causes salt wasting and volume depletion.

2. Aldosterone increases sodium reabsorption by increasing:
a) Na⁺/K⁺ pump synthesis
b) ENaC channel insertion
c) K⁺ channel activation
d) Water reabsorption alone

Explanation (Answer: b) ENaC channel insertion)
Aldosterone stimulates increased ENaC insertion in collecting duct cell membranes, enhancing sodium reabsorption. It also stimulates Na⁺/K⁺ ATPase activity indirectly. Enhanced sodium uptake increases osmotic water movement. Reduced ENaC response contributes to pseudohypoaldosteronism and impaired sodium conservation in hypovolemic states.

3. Mutation of ENaC leads to:
a) Liddle syndrome
b) Gitelman syndrome
c) Bartter syndrome
d) Diabetes insipidus

Explanation (Answer: a) Liddle syndrome)
Liddle syndrome is caused by gain-of-function mutation of ENaC leading to excessive sodium reabsorption, volume expansion, hypertension, and hypokalemia. Unlike hyperaldosteronism, aldosterone levels are low. Treatment involves amiloride or triamterene, ENaC blockers. Other syndromes affect different segments of renal tubules, not ENaC.

4. Which diuretic blocks ENaC channels?
a) Furosemide
b) Thiazides
c) Amiloride
d) Mannitol

Explanation (Answer: c) Amiloride)
Amiloride blocks ENaC directly, reducing sodium reabsorption and preventing potassium loss. It is used in Liddle syndrome and as potassium-sparing diuretic in hypertension. Furosemide acts on NKCC2 in loop of Henle; thiazides inhibit Na-Cl transport in distal tubule; mannitol increases osmotic diuresis without channel interaction.

5. ENaC activity is highest in which physiological state?
a) Hypernatremia
b) Volume depletion
c) Hyperkalemia
d) Metabolic acidosis

Explanation (Answer: b) Volume depletion)
During volume depletion, aldosterone surges, increasing ENaC synthesis and sodium retention to restore blood volume. Hyperkalemia also stimulates aldosterone but ENaC activation primarily aims to conserve sodium. In metabolic acidosis or hypernatremia, ENaC regulation is not the dominant corrective mechanism.

6. Dysfunction of ENaC results in:
a) Hyponatremia
b) Salt-wasting crisis
c) Hypercalcemia
d) Hypermagnesemia

Explanation (Answer: b) Salt-wasting crisis)
Loss-of-function ENaC mutations cause pseudohypoaldosteronism type I, leading to impaired sodium reabsorption and severe salt-wasting. Symptoms include hypotension, dehydration, hyperkalemia, and metabolic acidosis. Hyponatremia occurs secondarily but core problem is salt loss. Calcium and magnesium levels remain unaffected directly by ENaC dysfunction.

7. ENaC is regulated by which hormone?
a) Vasopressin
b) Aldosterone
c) Cortisol
d) Thyroxine

Explanation (Answer: b) Aldosterone)
Aldosterone is the principal regulator of ENaC. It increases transcription and translation of ENaC subunits and enhances surface expression. Vasopressin affects aquaporins, not ENaC. Cortisol binds glucocorticoid receptors with minimal sodium transport effect, while thyroxine influences metabolism but not direct ENaC regulation.

8. In cystic fibrosis, epithelial sodium channel activity is:
a) Decreased
b) Absent
c) Increased
d) Normal

Explanation (Answer: c) Increased)
In cystic fibrosis, absence of functional CFTR leads to increased ENaC activity, causing excessive sodium and water reabsorption, leading to thick mucus. Hyperactive ENaC worsens airway obstruction. Treatments target airway hydration and correction of mucus viscosity, indirectly reducing ENaC impact on respiratory tissues.

9. ENaC channel malfunction leads to:
a) Hyperkalemia
b) Hypokalemia
c) Hypercalcemia
d) Hypoglycemia

Explanation (Answer: a) Hyperkalemia)
ENaC dysfunction reduces sodium entry into principal cells, lowering electrical gradient needed for potassium secretion. This leads to hyperkalemia, metabolic acidosis, and hypotension in salt-wasting states. Conversely, ENaC hyperactivity in Liddle syndrome can cause hypokalemia due to excessive K⁺ secretion driven by enhanced sodium uptake.

10. ENaC activity is clinically assessed using:
a) Sweat chloride test
b) Blood glucose test
c) Liver function test
d) Thyroid profile

Explanation (Answer: a) Sweat chloride test)
Sweat chloride test identifies CFTR dysfunction, indirectly reflecting ENaC hyperactivity in cystic fibrosis. CFTR normally inhibits ENaC; absence results in excessive sodium uptake, reducing chloride secretion. Elevated sweat chloride indicates defective CFTR, associated with overactive ENaC and thickened secretions.

Chapter: Physiology; Topic: Body Fluid Compartments; Subtopic: Total Body Water Variations

Keyword Definitions:
• Total Body Water (TBW): Combined intracellular and extracellular fluid making up body water content.
• Extracellular fluid: Fluid outside cells including plasma and interstitial fluid.
• Intracellular fluid: Fluid contained within cells forming majority of TBW.
• Neonatal body water: High water composition present at birth decreasing with age.
• Body weight percentage: Proportion of TBW relative to total body mass.
• Fluid distribution: Proportioning of water into functional compartments in the human body.

Lead Question - 2015
Percentage of total body water to body weight at birth?
a) 90%
b) 80%
c) 60%
d) 50%

Explanation (Answer: b) 80%
At birth, total body water is approximately 80% of body weight. Neonates have a much higher water content due to increased extracellular fluid and reduced fat stores. Over the first year of life, water content declines as fat stores increase and intracellular fluid expands proportionally. Adults maintain around 60% TBW. This high neonatal TBW influences drug distribution and dehydration susceptibility.

1. Total body water in adult males is approximately:
a) 70%
b) 65%
c) 60%
d) 50%

Explanation (Answer: c) 60%
Adult males have around 60% TBW due to higher muscle mass and lower fat compared to females. Muscle contains more water, while fat holds less. TBW decreases with age as lean body mass decreases. Understanding TBW is vital for fluid therapy, electrolyte balance evaluation, and pharmacokinetic calculations in clinical settings.

2. Extracellular fluid constitutes what percentage of TBW?
a) 10%
b) 20%
c) 33%
d) 50%

Explanation (Answer: b) 20%
Extracellular fluid constitutes roughly 20% of TBW, including plasma and interstitial fluid. The remaining 80% is intracellular fluid. ECF shifts play major roles in dehydration, edema, and shock. Loss of ECF volume leads to hypovolemia affecting plasma volume, and sudden ECF changes influence blood pressure regulation and electrolyte stability.

3. Intracellular fluid forms approximately:
a) 20% of TBW
b) 40% of TBW
c) 50% of TBW
d) 80% of TBW

Explanation (Answer: b) 40% of TBW)
Intracellular fluid (ICF) forms about 40% of body weight, making it the largest body fluid compartment. It contains high potassium and phosphate concentrations essential for cellular metabolism. Severe acidosis, hyperkalemia, or fluid shifts can disturb ICF balance, affecting cell function and neuromuscular stability in clinical conditions.

4. Newborns are more prone to dehydration because:
a) Low metabolic rate
b) High total body water
c) Low kidney concentration ability
d) Low respiratory rate

Explanation (Answer: c) Low kidney concentration ability)
Newborn kidneys have limited ability to concentrate urine, making them prone to dehydration. Although they have high TBW (80%), rapid water turnover and immature renal function contribute to quick dehydration. They require careful monitoring of fluid intake, especially in diarrheal illnesses or fever where fluid loss increases rapidly.

5. Body water decreases with age due to:
a) Increased bone density
b) Increased fat content
c) Increased muscle mass
d) Increased blood volume

Explanation (Answer: b) Increased fat content)
With aging, body fat increases and muscle decreases, reducing total body water. Fat contains low water content compared to muscle. Elderly individuals therefore have reduced TBW and are more prone to dehydration, electrolyte imbalance, and exaggerated effects of medications due to altered volume of distribution.

6. Which fluid compartment expands most in edema?
a) Intracellular fluid
b) Plasma
c) Interstitial fluid
d) Blood cells

Explanation (Answer: c) Interstitial fluid)
Edema results from expansion of interstitial fluid compartment. Causes include increased capillary hydrostatic pressure, decreased oncotic pressure, lymphatic obstruction, or increased capillary permeability. Fluid accumulates outside cells and vasculature, leading to swelling. Prompt evaluation is essential to diagnose underlying cardiac, renal, hepatic, or inflammatory causes.

7. In severe dehydration, which compartment loses water first?
a) Intracellular fluid
b) Extracellular fluid
c) Bone marrow
d) Blood cells

Explanation (Answer: b) Extracellular fluid)
Extracellular fluid is lost first in dehydration. As plasma volume drops, tissue perfusion decreases leading to tachycardia and hypotension. If fluid loss continues, intracellular fluid is lost next as cells compensate osmolarity differences. Rapid fluid therapy is essential to restore perfusion and prevent shock and organ failure.

8. Which group has the lowest percentage of body water?
a) Neonates
b) Adult males
c) Adult females
d) Elderly females

Explanation (Answer: d) Elderly females)
Elderly females have the lowest TBW due to higher body fat composition and reduced muscle mass with age. This makes them more susceptible to dehydration, electrolyte imbalance, drug toxicity, and hypotension. Fluid therapy in elderly requires careful management to avoid overload or depletion.

9. A child with diarrhea loses primarily:
a) Intracellular fluid
b) Extracellular fluid
c) Intravascular proteins
d) Fat-soluble vitamins

Explanation (Answer: b) Extracellular fluid)
Diarrhea results in rapid extracellular fluid loss leading to dehydration, sunken eyes, prolonged capillary refill, and low urine output. Children compensate poorly due to high body water turnover. Oral rehydration specifically replenishes ECF with balanced electrolytes to restore plasma and interstitial volume effectively.

10. Body water percentage increases in:
a) Obesity
b) Pregnancy
c) Aging
d) Malnutrition

Explanation (Answer: d) Malnutrition)
In malnutrition, body fat reduces and lean mass proportion increases, raising TBW percentage relative to body weight despite absolute deficit. This altered distribution affects drug dosing and fluid therapy. Pregnancy increases plasma volume but not TBW percentage, while obesity and aging decrease TBW due to high fat content.

Chapter: Physiology; Topic: Membrane Transport Mechanisms; Subtopic: Pore-Mediated Diffusion

Keyword Definitions:
• Pores: Small aqueous openings in membrane allowing selective passage of ions/molecules.
• Diffusion: Passive movement of particles from high to low concentration through pores/channels.
• Transcytosis: Vesicular transport across cells via endocytosis and exocytosis.
• Endocytosis: ATP-dependent process where cell engulfs material into vesicles.
• Active transport: Movement against concentration gradient needing ATP and carrier proteins.
• Channel proteins: Allow rapid ion movement across membrane via pores.

Lead Question - 2015
Transport through pores in cell membranes is ?
a) Active transport
b) Transcytosis
c) Diffusion
d) Endocytosis

Explanation (Answer: c) Diffusion)
Diffusion through membrane pores is a passive process relying on concentration gradient. Pores allow small ions, water, and molecules to pass without ATP. Active transport needs energy and carriers, not pores. Endocytosis and transcytosis involve vesicles, not pores. Channel proteins act as pores facilitating ion flow based on electrochemical gradients, making diffusion the correct mechanism.

1. Ion movement through voltage-gated channels occurs by:
a) Active transport
b) Diffusion
c) Osmosis
d) Transcytosis

Explanation (Answer: b) Diffusion)
Ions move through voltage-gated channels by diffusion, driven by electrochemical gradients. Channels open/close in response to voltage but the movement itself remains passive. Active transport involves ATP, while osmosis is for water and transcytosis involves vesicles. Neuronal action potentials rely on rapid ion diffusion across membranes through opened channels.

2. Aquaporin-mediated water flow is an example of:
a) Active transport
b) Osmosis
c) Endocytosis
d) Vesicular transport

Explanation (Answer: b) Osmosis)
Aquaporins facilitate osmosis, allowing rapid passive water movement through membrane pores along osmotic gradients. No ATP is required. This mechanism is critical in kidney collecting ducts and RBC homeostasis. Endocytosis uses vesicles and ATP, and active transport moves against gradient, not applicable for water.

3. Which factor increases rate of pore diffusion?
a) Increased membrane thickness
b) Higher concentration gradient
c) Reduced surface area
d) Lower temperature

Explanation (Answer: b) Higher concentration gradient)
A steep concentration gradient increases pore-mediated diffusion. Rate rises because more molecules move from higher to lower concentration locations. Membrane thickness and lower temperature reduce diffusion, while reduced surface area decreases rate. Channel number also influences transport through pores significantly.

4. Sodium influx during depolarization occurs by:
a) Active transport
b) Facilitated diffusion through channels
c) Endocytosis
d) Transcytosis

Explanation (Answer: b) Facilitated diffusion through channels)
During nerve depolarization, Na⁺ enters via voltage-gated sodium channels through facilitated diffusion. No ATP is consumed; movement follows electrochemical gradient. Active transport is responsible for restoring gradients later via Na⁺/K⁺ pump. Endocytosis and transcytosis involve vesicle pathways, not ion flow.

5. Which substance diffuses fastest through membrane pores?
a) Glucose
b) K⁺ ion
c) Large protein
d) Lipoprotein

Explanation (Answer: b) K⁺ ion)
K⁺ ions diffuse rapidly due to channel proteins providing selective pore pathways. Glucose requires carrier-mediated transport, not pores. Proteins and lipoproteins are too large to pass through pores. Ion diffusion is fast and essential for electrical activity in muscles and neurons.

6. A patient with channelopathy affecting Na⁺ channels may present with:
a) Paralysis
b) Excess sweating
c) Hyperglycemia
d) Leukopenia

Explanation (Answer: a) Paralysis)
Channelopathies impair Na⁺ diffusion through membrane pores, affecting nerve conduction and muscle depolarization. This results in episodic weakness or paralysis. Diffusion failure prevents proper action potential propagation. Hyperglycemia and leukopenia are unrelated. Sweating involves autonomic control, not sodium channel defects directly.

7. Which statement regarding pore diffusion is TRUE?
a) Requires ATP
b) Is selective for specific ions
c) Moves substances against gradient
d) Stops when vesicles form

Explanation (Answer: b) Is selective for specific ions)
Ion channels function as pores with selectivity filters allowing only specific ions (Na⁺, K⁺, Ca²⁺, Cl⁻) to pass. Transport follows gradient, requires no ATP, and does not rely on vesicles. Selectivity ensures precise physiological regulation during depolarization, repolarization, and synaptic transmission.

8. Which condition affects pore-mediated diffusion most?
a) Increase in channel number
b) ATP depletion
c) Lysosomal rupture
d) DNA mutation

Explanation (Answer: a) Increase in channel number)
Increasing channel number increases diffusion rate because more pores allow higher flow of ions. ATP depletion affects active transport but not diffusion through pores. Lysosomal rupture and DNA mutation have indirect effects and do not directly change pore diffusion capacity. Ion channel expression levels regulate membrane conductance.

9. Which process uses pores to equalize solute movement?
a) Active transport
b) Simple diffusion
c) Endocytosis
d) Microtubule transport

Explanation (Answer: b) Simple diffusion)
Simple diffusion through membrane pores equalizes solute concentration. Driven by gradient, movement continues until equilibrium is achieved. No carriers or ATP required. Endocytosis and microtubule transport involve intracellular mechanisms unrelated to pore transport. Active transport works against gradient, not leveling it.

10. In dehydration, water enters cells through:
a) Vesicles
b) Aquaporin pores
c) ATP pumps
d) Co-transporters

Explanation (Answer: b) Aquaporin pores)
During dehydration, osmotic gradients drive water movement into cells through aquaporin pores. This is passive transport requiring no ATP. Co-transporters and pumps do not carry water directly. Aquaporins maintain fluid balance in kidneys, brain, and RBCs, helping regulate osmolarity rapidly and efficiently.

Chapter: Physiology; Topic: Membrane Transport; Subtopic: Carrier-Mediated Transport Mechanisms

Keyword Definitions:
• Active transport: Carrier-mediated movement of substances against concentration gradient using ATP.
• Facilitated diffusion: Carrier-mediated movement of substances along concentration gradient without ATP.
• Carrier protein: Membrane transport protein assisting movement across membrane.
• Concentration gradient: Difference in solute concentration across membrane driving diffusion.
• Transport saturation: Maximum transport rate reached when all carriers are occupied.
• Specificity: Property by which carriers bind specific solutes for movement.

Lead Question - 2015
Similarity between active transport and facilitated diffusion?
a) Energy requirement
b) Against concentration gradient
c) Carrier protein
d) All of the above

Explanation (Answer: c) Carrier protein)
Both active transport and facilitated diffusion require carrier proteins embedded in the membrane. Facilitated diffusion is passive and moves substances along concentration gradients, while active transport requires ATP to move substances against gradient. Despite differences in energy usage and direction of flow, their primary similarity is reliance on specific carriers, showing saturation and specificity.

1. Saturation of membrane transport occurs due to:
a) Excess ATP
b) Limited carrier proteins
c) Breakdown of receptors
d) Increased osmosis

Explanation (Answer: b) Limited carrier proteins)
Saturation occurs when all carrier proteins become fully occupied, preventing transport rate from increasing further. This applies to active transport and facilitated diffusion. The fixed number of carriers limits rate despite increasing substrate concentration. This principle explains glucose spill in diabetes when renal carriers saturate, causing glucosuria due to overflow of filtered glucose.

2. Which characteristic is shared by both active transport and facilitated diffusion?
a) ATP dependence
b) Movement against gradient
c) Specificity
d) Vesicular formation

Explanation (Answer: c) Specificity)
Specificity is a hallmark of both processes because carrier proteins bind particular molecules. Specific interactions allow selective transport of ions, glucose, or amino acids. Active transport differs in ATP requirement and direction; facilitated diffusion does not use energy. Vesicular formation pertains to endocytosis, not carrier mechanisms.

3. Which process demonstrates saturation kinetics?
a) Simple diffusion
b) Carrier-mediated transport
c) Osmosis
d) Filtration

Explanation (Answer: b) Carrier-mediated transport)
Carrier-mediated processes such as active transport and facilitated diffusion show saturation because carrier proteins reach maximum turnover rate. Simple diffusion continues to increase proportionally with gradient and does not saturate. Filtration and osmosis depend on pressure gradients and membrane permeability but not on carriers, so they do not saturate.

4. Insulin increases glucose uptake by increasing:
a) ATP production
b) GLUT-4 carriers
c) Membrane thickness
d) Osmotic pressure

Explanation (Answer: b) GLUT-4 carriers)
Insulin promotes translocation of GLUT-4 carriers to cell membrane in muscle and adipose tissue, enabling facilitated diffusion of glucose. More carriers increase transport rate until saturation is reached. ATP does not directly drive glucose uptake. Osmotic pressure changes occur after glucose entry, not controlling the mechanism itself.

5. Which feature distinguishes active transport from facilitated diffusion?
a) Carrier specificity
b) Saturation kinetics
c) ATP requirement
d) Reversibility

Explanation (Answer: c) ATP requirement)
ATP requirement is the major difference. Active transport consumes ATP to pump molecules against gradient. Facilitated diffusion does not require ATP and moves molecules down their gradient. Both show specificity and saturation, and both exhibit reversible binding, but only active transport uses metabolic energy.

6. In sodium-glucose cotransport, similarity with facilitated diffusion includes:
a) ATP consumption
b) Carrier involvement
c) Energy independence
d) Movement along gradient

Explanation (Answer: b) Carrier involvement)
Both processes involve carrier proteins. Sodium-glucose cotransport uses secondary active transport requiring Na⁺ gradient indirectly dependent on ATP. Facilitated diffusion uses no ATP. Both involve specific carrier binding and saturation kinetics. Movement along gradient applies only to glucose movement in facilitated diffusion, not cotransport itself.

7. Which factor affects both active transport and facilitated diffusion?
a) Membrane cholesterol
b) Carrier affinity
c) ATP level
d) Vesicular fusion

Explanation (Answer: b) Carrier affinity)
The degree of carrier affinity for the transported molecule influences both active transport and facilitated diffusion. Higher affinity enhances transport rate until saturation. ATP level affects only active transport. Vesicular fusion pertains to exocytosis not carrier-mediated mechanisms. Cholesterol influences membrane fluidity but not carrier specificity directly.

8. Glucose reabsorption in kidneys is impaired when:
a) Carriers are absent
b) Carriers reach saturation
c) Osmosis increases
d) Urinary pressure rises

Explanation (Answer: b) Carriers reach saturation)
When glucose concentration exceeds renal threshold, carriers saturate and cannot reabsorb all glucose, leading to glucosuria. This illustrates shared saturation kinetics of facilitated diffusion and secondary active transport. Osmosis and urinary pressure do not directly regulate glucose carriers. Absence of carriers occurs only in rare genetic conditions like SGLT2 defects.

9. Sodium-potassium pump differs from facilitated diffusion because it:
a) Uses carrier proteins
b) Shows saturation
c) Requires direct ATP
d) Is reversible

Explanation (Answer: c) Requires direct ATP)
The Na⁺/K⁺ ATPase pump requires direct ATP hydrolysis to transport ions against gradient. Facilitated diffusion does not use ATP. Both use carrier proteins and display saturation, but their energy requirements and direction of transport differ. Pump failure leads to cell swelling and impaired membrane potential balance.

10. Which shared characteristic makes transport specific?
a) Binding sites on carrier protein
b) Osmotic gradient
c) ATP hydrolysis
d) Membrane thickness

Explanation (Answer: a) Binding sites on carrier protein)
Carrier proteins have specific binding sites determining what molecules they transport. This specificity underlies both active transport and facilitated diffusion. By matching substrate size, shape, and charge, carriers ensure selectivity. ATP hydrolysis is relevant only to active transport. Membrane thickness affects diffusion rate but not specificity.

Chapter: Physiology; Topic: Cell Membrane Transport; Subtopic: Carrier-Mediated Transport Systems

Keyword Definitions:
• Concentration gradient: Difference in solute concentration across membrane that drives transport.
• Carrier-mediated transport: Membrane proteins assist movement of substances across cell membrane.
• Active transport: ATP-dependent process moving substances against concentration gradient.
• Facilitated diffusion: Carrier-mediated passive transport along gradient, no ATP used.
• Osmosis: Passive movement of water across membrane based on solute concentration.
• Endocytosis: Vesicular process involving membrane engulfing particles into cell.

Lead Question - 2015
Transport process which is against concentration gradient and carrier mediated is ?
a) Facilitated diffusion
b) Osmosis
c) Active transport
d) Endocytosis

Explanation (Answer: c) Active transport)
Active transport is the only process that moves substances against the concentration gradient while being carrier-mediated with ATP utilization. Carrier proteins undergo conformational changes powered by ATP to push molecules from low to high concentration. Facilitated diffusion is carrier-mediated but not ATP dependent. Osmosis is passive water movement and endocytosis is vesicular, not gradient-based.

1. Na⁺/K⁺ ATPase pump is an example of:
a) Primary active transport
b) Secondary active transport
c) Facilitated diffusion
d) Osmosis

Explanation (Answer: a) Primary active transport)
The Na⁺/K⁺ ATPase pump uses ATP directly to transport 3 Na⁺ out and 2 K⁺ into the cell, ensuring membrane potential stability. This process works against concentration gradients and is carrier-mediated. It is essential for neuronal excitability, muscle contraction, and cellular volume maintenance. Secondary active transport relies on gradient created by this pump.

2. Glucose transport in renal tubules occurs by:
a) Simple diffusion
b) Na⁺-glucose cotransport
c) Osmosis
d) Exocytosis

Explanation (Answer: b) Na⁺-glucose cotransport)
Glucose reabsorption in renal tubules occurs via secondary active transport where Na⁺-glucose cotransporters use Na⁺ gradient generated by Na⁺/K⁺ pump. This mechanism is carrier-mediated but does not directly use ATP. The driving force is Na⁺ electrochemical gradient. Failure of this process leads to glucosuria in renal tubular disorders.

3. Which does NOT require ATP?
a) Active transport
b) Facilitated diffusion
c) Secondary active transport
d) Vesicular transport

Explanation (Answer: b) Facilitated diffusion)
Facilitated diffusion moves molecules along concentration gradient using carrier proteins but does not require ATP. In contrast, active transport uses ATP directly or indirectly (secondary active transport). Vesicular transport such as endocytosis and exocytosis involves energy use for membrane remodeling and vesicle formation.

4. Drug efflux pumps in bacteria use:
a) Passive diffusion
b) Secondary active transport
c) Simple diffusion
d) Enzymatic breakdown

Explanation (Answer: b) Secondary active transport)
Drug resistance in bacteria often involves secondary active transport using proton-motive force. Efflux pumps expel antibiotics against gradient without direct ATP hydrolysis but depend on ion gradients established by primary transporters. This enables bacterial survival by reducing intracellular drug concentration.

5. Movement of Ca²⁺ out of sarcoplasm into sarcoplasmic reticulum requires:
a) Passive diffusion
b) Ca²⁺-ATPase pump
c) Osmosis
d) Facilitated diffusion

Explanation (Answer: b) Ca²⁺-ATPase pump)
The SERCA pump actively transports Ca²⁺ back into sarcoplasmic reticulum using ATP energy. This allows muscle relaxation and maintains Ca²⁺ homeostasis. This is classic primary active transport working against gradient, essential in cardiac and skeletal muscle physiology. Passive diffusion would not clear Ca²⁺ efficiently against gradient direction.

6. Which transport mechanism becomes saturated at high substrate concentration?
a) Simple diffusion
b) Facilitated diffusion
c) Osmosis
d) Filtration

Explanation (Answer: b) Facilitated diffusion)
Facilitated diffusion exhibits saturation kinetics because carrier proteins reach maximum capacity (Tm). Simple diffusion has no transport maximum and increases linearly with gradient. Saturation is clinically important in diabetes where glucose exceeds renal tubular Tm and spills into urine, producing glucosuria due to overload of transporters.

7. A patient with low ATP levels will have impaired:
a) Active transport
b) Simple diffusion
c) Osmosis
d) Water filtration

Explanation (Answer: a) Active transport)
Low ATP levels affect active transport because the process relies on ATP for pumping molecules against gradients. For example, Na⁺/K⁺ ATPase slows, leading to accumulation of Na⁺ inside cells and swelling. Passive processes like diffusion and osmosis still occur without ATP, but active transport stops when ATP is depleted.

8. Glucose uptake in brain occurs by:
a) Active transport
b) GLUT-1 transporters
c) Endocytosis
d) Na⁺-dependent cotransport

Explanation (Answer: b) GLUT-1 transporters)
The brain uses GLUT-1 facilitated diffusion for glucose uptake. GLUT-1 is insulin-independent and works along concentration gradient, ensuring constant supply. Even during hypoglycemia, brain uptake is prioritized. No ATP is used in this carrier-mediated process. Na⁺-dependent mechanisms are used in renal and intestinal transport but not in CNS.

9. Which process is vesicular in nature and not carrier-mediated?
a) Endocytosis
b) Active transport
c) Facilitated diffusion
d) Secondary active transport

Explanation (Answer: a) Endocytosis)
Endocytosis involves engulfing extracellular particles via membrane invagination forming vesicles. It is not carrier-mediated and does not rely on gradients. It requires ATP for vesicle formation. Examples include receptor-mediated endocytosis and phagocytosis. Carrier-mediated processes are specific and saturable, unlike vesicular mechanisms.

10. In intestinal epithelium, amino acid uptake occurs via:
a) Na⁺-dependent cotransport
b) Simple diffusion
c) Endocytosis
d) Osmosis

Explanation (Answer: a) Na⁺-dependent cotransport)
Amino acids are absorbed by secondary active transport using Na⁺-dependent cotransport. The Na⁺ gradient generated by Na⁺/K⁺ ATPase drives amino acid uptake into enterocytes. This process is carrier-mediated, energy-linked indirectly, and saturable. Defects in transporters result in disorders like Hartnup disease where amino acid absorption is impaired.

Chapter: Physiology; Topic: Cell Membrane Physiology; Subtopic: Mechanisms of Membrane Transport

Keyword Definitions:
• Concentration gradient: Difference in solute concentration across a membrane driving passive transport.
• Membrane permeability: Ability of membrane to allow specific substances to pass through.
• Passive transport: Movement of substances without ATP, dependent on gradient and membrane properties.
• Charge of particle: Determines how ions interact with membrane channels and electrochemical gradients.
• Membrane thickness: Affects diffusion rate inversely according to Fick’s law.
• Particle size: Influences diffusion speed; smaller particles cross faster in simple diffusion.

Lead Question - 2015
Most important factor in transport across a membrane?
a) Charge of particle
b) Membrane thickness
c) Size of particle
d) Concentration gradient

Explanation (Answer: d) Concentration gradient)
The concentration gradient is the primary factor influencing passive transport across a membrane. When the gradient is steep, movement of molecules occurs rapidly from high concentration to low concentration. While particle size, charge, and membrane thickness influence permeability, diffusion relies most strongly on gradient magnitude. Fick’s law mathematically supports this dominance in biological membrane transport.

1. Simple diffusion depends primarily on:
a) ATP energy
b) Concentration gradient
c) DNA content
d) tRNA availability

Explanation (Answer: b) Concentration gradient)
Simple diffusion requires no ATP and occurs when a concentration gradient drives molecules from high to low concentration. The steeper the gradient, the faster the diffusion. Temperature, membrane surface area, and particle size play secondary roles. DNA or tRNA have no direct involvement. Diffusion continues until equilibrium is reached in the cell.

2. Ions cross the cell membrane mainly through:
a) Lipid bilayer
b) Protein channels
c) Nucleus
d) Lysosomes

Explanation (Answer: b) Protein channels)
Charged ions cannot penetrate lipid bilayers easily; they require protein channels or transporters. Ion channels control movement according to electrochemical gradients. Sodium, potassium, calcium, and chloride flow through selective channels. The lipid bilayer blocks charged molecules, making channels vital in nerve conduction and muscle depolarization.

3. According to Fick’s law, rate of diffusion decreases if:
a) Surface area increases
b) Membrane thickness increases
c) Concentration gradient increases
d) Membrane permeability increases

Explanation (Answer: b) Membrane thickness increases)
Fick’s law states diffusion rate varies directly with surface area and concentration gradient and inversely with membrane thickness. Thicker membranes slow diffusion because molecules travel a longer distance. This principle explains delayed gas exchange in pulmonary fibrosis where thickened alveolar membranes impair oxygen diffusion.

4. Facilitated diffusion differs from simple diffusion in that it:
a) Requires ATP
b) Uses carrier proteins
c) Moves against gradient
d) Stops at equilibrium

Explanation (Answer: b) Uses carrier proteins)
Facilitated diffusion uses carrier proteins or channel proteins to transport large or charged molecules along concentration gradients. It does not require ATP, unlike active transport. It saturates when carrier proteins are fully occupied. The process halts at equilibrium just like simple diffusion, distinguishing it from pump-driven active transport.

5. The most important determinant of ion movement through membrane is the:
a) Proton gradient
b) Electrochemical gradient
c) Hydration status
d) Gene expression

Explanation (Answer: b) Electrochemical gradient)
Ions cross membranes based on electrochemical gradients, consisting of two components—concentration gradient and electrical potential difference. Both influence ion direction and speed. Sodium entry during depolarization, potassium efflux during repolarization, and calcium influx in muscle contraction are all driven by this combined force.

6. A patient with pulmonary fibrosis has reduced oxygen diffusion due to:
a) Increased membrane thickness
b) Lower oxygen solubility
c) Increased surface area
d) Increased gradient

Explanation (Answer: a) Increased membrane thickness)
Pulmonary fibrosis thickens alveolar-capillary membranes, thereby reducing diffusion rate according to Fick’s law. Even with high oxygen concentration gradient, transfer is impaired because diffusion distance increases. Resulting symptoms include hypoxia, dyspnea, and reduced oxygen saturation. Treatment aims to reduce inflammation and improve effective lung surface area.

7. Glucose enters muscle cells via:
a) Simple diffusion
b) Facilitated diffusion
c) Osmosis
d) Active transport pump

Explanation (Answer: b) Facilitated diffusion)
Glucose entry into muscle occurs through GLUT-4 transporters, which perform facilitated diffusion. Insulin stimulates transporter translocation to membrane. Once gradient exists, glucose moves down gradient without ATP. In insulin resistance, GLUT-4 fails to respond, impairing glucose uptake and causing hyperglycemia characteristic of type 2 diabetes.

8. Increasing membrane permeability will:
a) Increase rate of diffusion
b) Decrease concentration gradient
c) Stop particle movement
d) Block osmosis

Explanation (Answer: a) Increase rate of diffusion)
Higher membrane permeability increases diffusion because membrane offers less resistance. Permeability is influenced by lipid solubility, channel availability, and membrane composition. Lipophilic molecules diffuse rapidly while hydrophilic molecules require channels or carriers. Gradients still determine direction and magnitude of net flow.

9. Which process requires ATP to move molecules against gradient?
a) Osmosis
b) Simple diffusion
c) Facilitated diffusion
d) Active transport

Explanation (Answer: d) Active transport)
Active transport consumes ATP to move substances against their concentration gradient. The sodium-potassium pump is the classic example, exchanging 3 sodium ions out and 2 potassium ions in. This maintains membrane potential and cellular homeostasis. Other processes—osmosis, simple diffusion, and facilitated diffusion—do not use energy.

10. Water crosses the cell membrane mainly by:
a) Sodium channels
b) Aquaporins
c) Lysosomes
d) Mitochondria

Explanation (Answer: b) Aquaporins)
Water transport mostly occurs through specialized channels called aquaporins. These protein channels allow rapid water movement following osmotic gradients. Aquaporin defects cause disorders like nephrogenic diabetes insipidus. Passive osmotic movement continues until equilibrium is reached. Their function highlights importance of gradient-driven membrane transport.

2014 NEET PG

Chapter: Physiology Topic: Nervous System; Subtopic: Pain Pathways and Nerve Fiber Types

Keyword Definitions:

Pain: An unpleasant sensory and emotional experience associated with actual or potential tissue damage.
Nociceptors: Specialized sensory receptors that detect damaging or potentially damaging stimuli.
Aδ fibers: Thinly myelinated fibers transmitting sharp, localized “first pain.”
C fibers: Unmyelinated fibers transmitting dull, burning “second pain.”
Myelination: Fatty insulation of axons increasing conduction velocity.
Dorsal horn: Region in spinal cord receiving sensory input from nociceptors.
Spinothalamic tract: Major ascending pathway conveying pain and temperature sensations to the brain.

Lead Question – 2014

Sharp pain is transmitted by which type of fibres?
a) Aα
b) Aβ
c) Aδ
d) C

Explanation: The correct answer is Aδ fibers. These are thinly myelinated nerve fibers that transmit sharp, localized, and fast pain sensations. They conduct impulses at a velocity of 5–30 m/s. The pain they mediate is often called “first pain.” In contrast, unmyelinated C fibers transmit dull, burning, and poorly localized “second pain” at slower speeds.

1) Which fibers transmit slow, burning pain?
a) Aα
b) Aβ
c) Aδ
d) C
Explanation: The correct answer is C fibers. These are unmyelinated, small-diameter fibers that conduct impulses at 0.4–2 m/s. They carry dull, throbbing, and persistent pain known as “second pain.” Their slow conduction allows prolonged perception of tissue injury and contributes to protective behavior and healing awareness.

2) Which part of the brain perceives pain intensity and localization?
a) Thalamus
b) Cerebellum
c) Hypothalamus
d) Hippocampus
Explanation: The correct answer is Thalamus. The thalamus acts as a relay center for sensory impulses, including pain, directing them to the somatosensory cortex. It helps localize and interpret pain intensity before emotional components are processed in the limbic system.

3) Which neurotransmitter is primarily involved in transmission of pain in the spinal cord?
a) Dopamine
b) Glutamate
c) Acetylcholine
d) GABA
Explanation: The correct answer is Glutamate. It is the main excitatory neurotransmitter in nociceptive pathways, particularly in Aδ fiber synapses within the dorsal horn. Substance P is also involved, particularly in chronic pain transmission via C fibers and secondary sensory neurons.

4) Which fibers are responsible for tactile sensations like touch and pressure?
a) Aα
b) Aβ
c) Aδ
d) C
Explanation: The correct answer is Aβ fibers. These are large, heavily myelinated fibers that conduct sensory impulses rapidly. They are primarily responsible for transmitting non-noxious stimuli like touch, pressure, and vibration, helping differentiate pain from normal tactile sensations.

5) Which tract transmits pain and temperature sensations to the brain?
a) Dorsal column
b) Corticospinal tract
c) Spinothalamic tract
d) Vestibulospinal tract
Explanation: The correct answer is Spinothalamic tract. This ascending pathway originates in the dorsal horn of the spinal cord and carries pain and temperature sensations to the thalamus and somatosensory cortex, enabling conscious pain perception and localization.

6) A patient reports sharp pain immediately after a needle prick. Which fibers are involved?
a) Aδ fibers
b) C fibers
c) Aβ fibers
d) B fibers
Explanation: The correct answer is Aδ fibers. These fibers rapidly transmit the initial sharp pain from mechanical or thermal stimuli. Their conduction speed allows quick withdrawal reflexes, helping prevent further tissue damage before slow C fiber pain begins.

7) A patient with peripheral neuropathy loses sharp pain sensation but retains dull pain. Which fibers are affected?
a) C fibers
b) Aδ fibers
c) Aβ fibers
d) Aα fibers
Explanation: The correct answer is Aδ fibers. Damage to thinly myelinated Aδ fibers causes loss of sharp pain and temperature discrimination, while unmyelinated C fibers still transmit burning or aching sensations, preserving slow pain response.

8) Which of the following is true regarding pain transmission by Aδ fibers?
a) They are unmyelinated
b) They transmit dull pain
c) They conduct impulses rapidly
d) They mediate visceral pain
Explanation: The correct answer is They conduct impulses rapidly. Aδ fibers are thinly myelinated, allowing faster conduction (5–30 m/s) compared to unmyelinated C fibers. They are responsible for acute, localized pain sensations from somatic structures like skin and muscles.

9) A burn patient reports persistent throbbing pain hours after injury. Which fibers are responsible?
a) Aδ fibers
b) C fibers
c) Aβ fibers
d) Aα fibers
Explanation: The correct answer is C fibers. They mediate slow, prolonged pain that persists after initial injury. This continuous pain aids in wound protection. C fibers are unmyelinated, slow-conducting, and important in chronic pain and inflammatory responses.

10) A patient with spinal cord injury loses pain and temperature sensation but retains touch and vibration. Which tract is damaged?
a) Dorsal column
b) Spinothalamic tract
c) Corticospinal tract
d) Vestibulospinal tract
Explanation: The correct answer is Spinothalamic tract. It carries pain and temperature sensations from the opposite side of the body. Its damage results in loss of these sensations below the lesion, while touch and vibration (carried by dorsal columns) remain intact.

Chapter: Physiology; Topic: Hypothalamic Regulation of Appetite; Subtopic: Neuroendocrine Control of Feeding Behavior

Keyword Definitions:

Appetite: Desire for food regulated by hypothalamic centers, influenced by hormones and neurotransmitters.
Arcuate nucleus: A hypothalamic region that contains neurons regulating hunger and satiety.
NPY (Neuropeptide Y): A potent appetite stimulant found in the hypothalamus.
AGRP (Agouti-related peptide): A neuropeptide that increases food intake by antagonizing melanocortin receptors.
CART (Cocaine- and amphetamine-regulated transcript): A peptide that suppresses appetite.
α-MSH (Alpha-melanocyte-stimulating hormone): A peptide that decreases appetite via MC4 receptors.
Insulin: Hormone that decreases appetite by acting on hypothalamic centers.

Lead Question – 2014

Which of the following increases appetite?
a) CART
b) α - MSH
c) AGPP
d) Insulin

Explanation: The correct answer is AGRP (Agouti-related peptide). AGRP stimulates appetite by inhibiting melanocortin receptors (MC3 and MC4) in the hypothalamus, promoting feeding behavior. It acts synergistically with Neuropeptide Y, both secreted from arcuate nucleus neurons. CART and α-MSH suppress appetite, while insulin also inhibits food intake via satiety signaling pathways.

1) Which hormone secreted from the stomach stimulates appetite?
a) Ghrelin
b) Leptin
c) Insulin
d) CCK
Explanation: The answer is Ghrelin. It is a peptide hormone produced by the stomach that increases appetite by acting on hypothalamic neurons, especially the NPY/AGRP group. Ghrelin levels rise before meals and fall afterward, signaling hunger to maintain energy balance through hypothalamic stimulation of feeding behavior.

2) Which center of the hypothalamus is known as the hunger center?
a) Ventromedial nucleus
b) Lateral hypothalamic area
c) Arcuate nucleus
d) Paraventricular nucleus
Explanation: The correct answer is Lateral hypothalamic area. It contains neurons that stimulate feeding when activated. Damage to this region leads to anorexia. It integrates peripheral signals like ghrelin and glucose levels, modulating neuronal activity to promote hunger sensations and maintain energy homeostasis in the body.

3) Which hypothalamic nucleus acts as the satiety center?
a) Lateral hypothalamus
b) Ventromedial nucleus
c) Arcuate nucleus
d) Posterior hypothalamus
Explanation: The correct answer is Ventromedial nucleus. It inhibits feeding behavior when stimulated. Lesions in this area cause hyperphagia and obesity. It receives leptin and insulin signals, reducing food intake by suppressing hunger-promoting neurons in the lateral hypothalamus and maintaining energy balance.

4) Which neurotransmitter promotes satiety and reduces appetite?
a) Dopamine
b) Serotonin
c) Norepinephrine
d) Glutamate
Explanation: The correct answer is Serotonin. It acts on hypothalamic receptors to reduce appetite and food intake, particularly carbohydrates. Serotonin increases satiety through activation of POMC neurons and inhibition of NPY/AGRP neurons. Drugs enhancing serotonin activity can help reduce appetite and support weight management.

5) Which of the following is an anorexigenic hormone?
a) Ghrelin
b) Neuropeptide Y
c) Leptin
d) AGRP
Explanation: The correct answer is Leptin. Secreted by adipose tissue, it signals energy sufficiency to the hypothalamus, reducing appetite. It inhibits NPY and AGRP neurons while stimulating POMC/CART neurons, promoting satiety. Leptin deficiency or resistance is associated with obesity and altered energy homeostasis in humans.

6) A 45-year-old obese patient shows leptin resistance. Which mechanism explains his persistent hunger?
a) Increased CART activity
b) Impaired hypothalamic leptin signaling
c) Enhanced α-MSH sensitivity
d) Decreased ghrelin secretion
Explanation: The answer is Impaired hypothalamic leptin signaling. Leptin resistance prevents satiety signaling, causing continued food intake despite energy sufficiency. It leads to altered neuronal responses in the arcuate nucleus, persistent hunger, and weight gain due to failure of leptin-mediated appetite suppression mechanisms.

7) A person deprived of sleep for several days reports increased hunger. Which hormone likely increased?
a) Leptin
b) Ghrelin
c) Insulin
d) CART
Explanation: The answer is Ghrelin. Sleep deprivation increases ghrelin and decreases leptin, stimulating appetite and preference for high-calorie foods. This imbalance promotes weight gain. Ghrelin acts on hypothalamic centers, enhancing NPY and AGRP activity, which trigger hunger signals during energy deficit or sleep loss.

8) Which hypothalamic peptide increases appetite during fasting?
a) CART
b) AGRP
c) CRH
d) Somatostatin
Explanation: The correct answer is AGRP. Fasting increases AGRP expression in arcuate neurons, stimulating appetite. AGRP inhibits melanocortin receptors that normally suppress feeding. This compensatory mechanism helps restore energy balance during caloric restriction or prolonged fasting conditions.

9) A patient with hypothalamic tumor affecting the lateral hypothalamus presents with weight loss and loss of appetite. What is the likely mechanism?
a) Overactivation of AGRP neurons
b) Damage to hunger center
c) Hyperleptinemia
d) Ghrelin excess
Explanation: The answer is Damage to hunger center. The lateral hypothalamus is responsible for stimulating appetite. Tumor-induced damage leads to anorexia, weight loss, and decreased feeding behavior, demonstrating its critical role in energy intake regulation.

10) A child presents with hyperphagia and obesity due to a mutation in the leptin receptor gene. What happens to appetite control?
a) Increased leptin sensitivity
b) Impaired satiety signaling
c) Reduced ghrelin secretion
d) Enhanced α-MSH response
Explanation: The correct answer is Impaired satiety signaling. Mutation in leptin receptor prevents leptin from inhibiting appetite-regulating neurons in the hypothalamus, leading to uncontrolled hunger, hyperphagia, and early-onset obesity despite high leptin levels in circulation.

Chapter: Physiology; Topic: Thermoregulation; Subtopic: Mechanism of Fever

Keyword Definitions:

• Endogenous Pyrogens: Cytokines like IL-1, IL-6, and TNF-α produced by immune cells that mediate fever.

• Hypothalamic Set Point: Temperature level regulated by the preoptic area of the hypothalamus.

• PGE2: Prostaglandin E2, a lipid mediator that raises hypothalamic temperature set point during fever.

• Thermoregulation: Physiological process maintaining internal temperature through heat production and loss mechanisms.

Lead Question - 2014

Endogenous pyrogens act by ?

a) Increasing heat generation

b) Raising thermostat point of hypothalamus

c) Causing vasoconstriction

d) By Non-shivering thermogenesis

Answer & Explanation: Correct answer is b) Raising thermostat point of hypothalamus. Endogenous pyrogens such as IL-1, IL-6, and TNF-α trigger the synthesis of PGE2 in the hypothalamic preoptic area, elevating the temperature set point. The body perceives its normal temperature as low and activates heat-generating mechanisms like shivering and vasoconstriction to raise temperature. This process continues until the body temperature reaches the new set point, resulting in fever. This mechanism aids immune function by inhibiting microbial growth. When pyrogenic signals subside, antipyretic mechanisms like sweating and vasodilation restore normal temperature.

1) Which cytokine is the most potent endogenous pyrogen?

a) IL-1

b) IL-10

c) Interferon-gamma

d) TNF-beta

Answer & Explanation: Correct answer is a) IL-1. IL-1 is a major endogenous pyrogen released by macrophages. It stimulates hypothalamic PGE2 production, elevating the set point for temperature regulation, thereby initiating the febrile response.

2) Fever differs from hyperthermia because:

a) Both are caused by external heat

b) Set-point increases in fever

c) Set-point decreases in fever

d) Fever has no hypothalamic control

Answer & Explanation: Correct answer is b) Set-point increases in fever. In fever, hypothalamic set-point rises due to PGE2, while in hyperthermia, body temperature rises above the set-point due to external or metabolic causes without hypothalamic involvement.

3) The main site of PGE2 synthesis during fever is:

a) Hippocampus

b) Preoptic area of hypothalamus

c) Cerebellum

d) Medulla oblongata

Answer & Explanation: Correct answer is b) Preoptic area of hypothalamus. PGE2 acts here to elevate the set-point temperature, resulting in activation of heat conservation and production mechanisms that induce fever.

4) During fever, the body initiates heat conservation by:

a) Vasodilation

b) Vasoconstriction

c) Perspiration

d) Sweating

Answer & Explanation: Correct answer is b) Vasoconstriction. To conserve heat, cutaneous vessels constrict, reducing blood flow to skin and minimizing heat loss, which helps elevate core temperature to the new hypothalamic set-point.

5) Exogenous pyrogens cause fever by:

a) Directly raising hypothalamic set-point

b) Stimulating endogenous cytokine release

c) Activating sweat glands

d) Inhibiting IL-6 production

Answer & Explanation: Correct answer is b) Stimulating endogenous cytokine release. Exogenous pyrogens like bacterial lipopolysaccharides induce immune cells to produce IL-1 and TNF-α, which in turn raise the hypothalamic set-point through PGE2 synthesis.

6) A patient with infection develops chills before fever. The chills are due to:

a) Decreased body temperature

b) Set-point rising above body temperature

c) Sweating

d) Vasodilation

Answer & Explanation: Correct answer is b) Set-point rising above body temperature. The hypothalamus perceives current temperature as low and activates shivering and vasoconstriction to generate heat, causing chills before the actual rise in temperature.

7) Which of the following is not an endogenous pyrogen?

a) IL-6

b) TNF-α

c) IL-10

d) IL-1

Answer & Explanation: Correct answer is c) IL-10. IL-10 is an anti-inflammatory cytokine that suppresses immune activation and downregulates proinflammatory mediators, thereby reducing fever and inflammation.

8) Which antipyretic drug inhibits prostaglandin synthesis?

a) Paracetamol

b) Atropine

c) Dopamine

d) Epinephrine

Answer & Explanation: Correct answer is a) Paracetamol. Paracetamol (acetaminophen) inhibits cyclooxygenase enzymes in the CNS, thereby reducing PGE2 synthesis in the hypothalamus and lowering the elevated set-point temperature.

9) Which organ detects and controls body temperature changes?

a) Hypothalamus

b) Thalamus

c) Medulla

d) Pituitary gland

Answer & Explanation: Correct answer is a) Hypothalamus. The hypothalamus integrates signals from thermoreceptors and controls autonomic responses to maintain body temperature within physiological limits during fever or cold exposure.

10) Clinical case: A 45-year-old male develops fever after bacterial infection. The fever subsides after taking ibuprofen. What is the mechanism?

a) Increased vasoconstriction

b) Inhibition of PGE2 synthesis

c) Decreased IL-6 secretion

d) Activation of sweat glands

Answer & Explanation: Correct answer is b) Inhibition of PGE2 synthesis. Ibuprofen inhibits COX enzymes, reducing PGE2 production in the hypothalamus, thereby lowering the elevated temperature set-point and promoting heat loss through sweating and vasodilation.

Chapter: Physiology; Topic: Thermoregulation; Subtopic: Fever Mechanism

Keyword Definitions:

• Fever: Elevation of body temperature due to pyrogenic response to infection or inflammation.

• Prostaglandins (PGs): Lipid mediators derived from arachidonic acid, involved in inflammation, fever, and vascular tone.

• PGE2: Key prostaglandin produced in hypothalamus, mediates fever by elevating set-point.

• PGF2α, PGI2, PGD2: Other prostaglandins with roles in smooth muscle contraction, vasodilation, platelet function, and sleep regulation.

Lead Question - 2014

Fever is produced by ?

a) PGF2α

b) PGE2

c) PGI2

d) PGD2

Answer & Explanation: Correct answer is b) PGE2. Fever occurs when pyrogens (endogenous or exogenous) trigger prostaglandin E2 synthesis in the preoptic area of the anterior hypothalamus. PGE2 elevates the hypothalamic set-point, causing heat-conserving mechanisms like vasoconstriction and shivering, which raise body temperature. Other prostaglandins, such as PGF2α, PGI2, and PGD2, have distinct physiological roles including smooth muscle contraction, vasodilation, platelet inhibition, and sleep regulation, and do not directly mediate fever. Understanding PGE2’s role is crucial for therapeutic interventions with antipyretics like NSAIDs that inhibit cyclooxygenase, thereby reducing PGE2 and fever.

1) Endogenous pyrogens include:

a) IL-1, IL-6, TNF-α

b) PGE2 only

c) Histamine

d) Bradykinin

Answer & Explanation: Correct answer is a) IL-1, IL-6, TNF-α. These cytokines are produced by activated leukocytes in infection or inflammation. They stimulate hypothalamic PGE2 production, raising the temperature set-point and causing fever.

2) NSAIDs reduce fever by inhibiting:

a) Lipoxygenase

b) Cyclooxygenase

c) Phospholipase A2

d) Adenylate cyclase

Answer & Explanation: Correct answer is b) Cyclooxygenase. NSAIDs block COX enzymes, preventing conversion of arachidonic acid to prostaglandins, including PGE2. Reduced PGE2 synthesis lowers hypothalamic set-point, thus decreasing fever.

3) Pyrogen-induced PGE2 acts on which hypothalamic region?

a) Posterior hypothalamus

b) Preoptic anterior hypothalamus

c) Suprachiasmatic nucleus

d) Lateral hypothalamus

Answer & Explanation: Correct answer is b) Preoptic anterior hypothalamus. PGE2 in this region increases the thermoregulatory set-point, leading to heat conservation and generation mechanisms that elevate core body temperature during fever.

4) Fever helps the body by:

a) Reducing metabolic rate

b) Enhancing immune response

c) Causing hypothermia

d) Decreasing leukocyte activity

Answer & Explanation: Correct answer is b) Enhancing immune response. Moderate fever improves leukocyte mobility, enhances phagocytosis, and inhibits growth of certain pathogens, serving as a protective physiological response.

5) Exogenous pyrogens are:

a) Bacterial toxins

b) Cytokines

c) PGE2

d) Histamine

Answer & Explanation: Correct answer is a) Bacterial toxins. Lipopolysaccharide (LPS) and other bacterial products act as exogenous pyrogens, stimulating cytokine release which induces hypothalamic PGE2 synthesis, leading to fever.

6) Which prostaglandin is involved in vasodilation but not fever?

a) PGE2

b) PGI2

c) PGF2α

d) None

Answer & Explanation: Correct answer is b) PGI2. PGI2 (prostacyclin) is mainly produced by endothelial cells, inhibits platelet aggregation, and causes vasodilation. It does not directly mediate hypothalamic set-point elevation or fever.

7) Shivering during fever is triggered by:

a) Decreased set-point

b) Increased hypothalamic set-point

c) Peripheral vasodilation

d) Reduced PGE2

Answer & Explanation: Correct answer is b) Increased hypothalamic set-point. When PGE2 raises the hypothalamic set-point above body temperature, heat-generating mechanisms like shivering and vasoconstriction are activated to reach the new set-point.

8) Antipyretics target fever by:

a) Reducing IL-1 production

b) Inhibiting PGE2 synthesis

c) Stimulating TNF-α

d) Activating PGF2α

Answer & Explanation: Correct answer is b) Inhibiting PGE2 synthesis. Drugs like aspirin and ibuprofen inhibit cyclooxygenase, preventing PGE2 formation, thereby lowering the hypothalamic set-point and alleviating fever.

9) Fever-producing prostaglandin is synthesized from:

a) Cholesterol

b) Arachidonic acid

c) Phosphatidylcholine

d) Linoleic acid

Answer & Explanation: Correct answer is b) Arachidonic acid. Arachidonic acid is released from membrane phospholipids and converted by COX enzymes to PGE2, the key mediator elevating hypothalamic set-point and causing fever.

10) Which prostaglandin is mainly involved in sleep regulation, not fever?

a) PGD2

b) PGE2

c) PGI2

d) PGF2α

Answer & Explanation: Correct answer is a) PGD2. PGD2 is synthesized in the brain, particularly by leptomeninges, promoting sleep and modulating circadian rhythm. Unlike PGE2, it does not induce hypothalamic fever response.

2013 NEET PG

Topic: Cellular Respiration

Subtopic: Shuttles for Reducing Equivalents in Glycolysis

Keyword Definitions:

• Reducing equivalents: Electrons carried mainly by NADH or FADH₂ for ATP production.

• Malate shuttle: Pathway transferring cytosolic NADH electrons into mitochondria via malate-oxaloacetate.

• Glutamate shuttle: Transfers reducing equivalents using glutamate-aspartate transaminases.

• Carnitine: Molecule required for fatty acid transport into mitochondria, not NADH transport.

• Creatine: Energy buffer compound, not used in NADH shuttling.

Lead Question - 2013

Reducing equivalants produced in glycolysis are transported from cytosol to mitochondria by ?

a) Carnitine

b) Creatine

c) Malate shuttle

d) Glutamate shuttle

Answer & Explanation:

Cytosolic NADH cannot directly enter mitochondria. Instead, electrons are transferred by specific shuttles. The malate-aspartate shuttle is the main mechanism in most tissues, while glycerol-3-phosphate shuttle is used in some. Carnitine and creatine are unrelated. Correct answer is c) Malate shuttle for NADH transport across mitochondrial membranes.

1) In skeletal muscle, the major shuttle for NADH transfer is?

a) Malate-aspartate shuttle

b) Glycerol-3-phosphate shuttle

c) Carnitine shuttle

d) Citrate shuttle

Explanation:

Skeletal muscle primarily uses the glycerol-3-phosphate shuttle, which transfers electrons from NADH to FADH₂ at the mitochondrial membrane. This results in slightly less ATP yield compared to the malate shuttle. Correct answer is b) Glycerol-3-phosphate shuttle as the major system in skeletal muscle glycolysis.

2) Malate-aspartate shuttle transfers reducing equivalents into mitochondria as?

a) NADH

b) Malate

c) Succinate

d) Lactate

Explanation:

The malate-aspartate shuttle converts oxaloacetate into malate, which carries reducing equivalents across the mitochondrial inner membrane. Once inside, malate is reconverted to oxaloacetate, regenerating NADH in the mitochondrial matrix. Correct answer is b) Malate as the transported intermediate.

3) Which shuttle is more energy efficient?

a) Malate-aspartate shuttle

b) Glycerol-3-phosphate shuttle

c) Carnitine shuttle

d) Citrate shuttle

Explanation:

The malate-aspartate shuttle is more energy efficient because it regenerates NADH inside mitochondria, yielding ~3 ATP per NADH. The glycerol-3-phosphate shuttle regenerates FADH₂, yielding ~2 ATP per electron pair. Correct answer is a) Malate-aspartate shuttle, which maximizes ATP production.

4) A neonate with defective malate-aspartate shuttle will show?

a) Reduced ATP generation from glycolysis

b) Increased creatine levels

c) Impaired fatty acid transport

d) Enhanced gluconeogenesis

Explanation:

Defective malate-aspartate shuttle prevents cytosolic NADH reoxidation, leading to impaired ATP yield from glycolysis and possible lactic acidosis. Fatty acid transport involves carnitine, not this shuttle. Correct answer is a) Reduced ATP generation from glycolysis due to blocked NADH utilization.

5) Glutamate-aspartate shuttle is active in?

a) Liver and heart

b) Skeletal muscle only

c) Adipose tissue only

d) RBCs

Explanation:

The glutamate-aspartate shuttle is most active in liver, kidney, and heart where efficient NADH transfer is crucial for aerobic metabolism. RBCs lack mitochondria, so shuttles are absent. Correct answer is a) Liver and heart.

6) Carnitine shuttle mainly transports?

a) Fatty acids into mitochondria

b) NADH into mitochondria

c) ATP out of mitochondria

d) CO₂ into mitochondria

Explanation:

The carnitine shuttle transfers long-chain fatty acids into mitochondria for β-oxidation. It does not transport reducing equivalents. Correct answer is a) Fatty acids into mitochondria.

7) Clinical defect in carnitine shuttle presents with?

a) Hypoketotic hypoglycemia

b) Lactic acidosis

c) Hyperammonemia

d) Ketoacidosis

Explanation:

Deficiency of carnitine or CPT enzymes impairs fatty acid entry into mitochondria, preventing β-oxidation and ketone body formation. This leads to hypoketotic hypoglycemia during fasting. Correct answer is a) Hypoketotic hypoglycemia.

8) In neurons, which shuttle is predominant for NADH transfer?

a) Malate-aspartate shuttle

b) Glycerol-3-phosphate shuttle

c) Carnitine shuttle

d) Pyruvate shuttle

Explanation:

Neurons depend on the malate-aspartate shuttle to maximize ATP generation. This shuttle ensures high-energy yield for neuronal function. Correct answer is a) Malate-aspartate shuttle.

9) During hypoxia, which effect occurs due to failure of shuttles?

a) Accumulation of NADH in cytosol

b) Increased ATP from oxidative phosphorylation

c) Increased fatty acid β-oxidation

d) Enhanced electron transport chain function

Explanation:

In hypoxia, NADH reoxidation is impaired, leading to cytosolic NADH accumulation and lactate production. Correct answer is a) Accumulation of NADH in cytosol with lactic acidosis.

10) Which shuttle links glycolysis to oxidative phosphorylation most efficiently?

a) Malate-aspartate shuttle

b) Glycerol-3-phosphate shuttle

c) Carnitine shuttle

d) Citrate shuttle

Explanation:

The malate-aspartate shuttle directly couples cytosolic NADH with mitochondrial NADH, efficiently linking glycolysis to oxidative phosphorylation. Correct answer is a) Malate-aspartate shuttle.

Topic: Mitochondrial Physiology

Subtopic: Physiological Uncouplers of Oxidative Phosphorylation

Keyword Definitions:

• Uncoupler: Compound that dissipates the proton gradient across the inner mitochondrial membrane, generating heat instead of ATP.

• Thyroxine: Thyroid hormone that increases basal metabolic rate partly by mild mitochondrial uncoupling.

• Free fatty acids: Substrates that act as natural uncouplers enhancing proton leakage.

• Thermogenin: Uncoupling protein (UCP1) in brown fat responsible for non-shivering thermogenesis.

• Oxidative phosphorylation: Process coupling electron transport chain to ATP production via ATP synthase.

Lead Question - 2013

Physiological uncoupler is ?

a) Thyroxine

b) Free fatty acids

c) Thermogenin

d) All of the above

Answer & Explanation:

Physiological uncouplers include thyroid hormone, free fatty acids, and thermogenin. They naturally increase metabolic rate and thermogenesis by dissipating proton gradient in mitochondria. Thermogenin in brown fat is the most prominent, but thyroxine and fatty acids also contribute. Correct answer is d) All of the above as physiological uncouplers.

1) Clinical effect of thermogenin activity?

a) Heat generation

b) ATP accumulation

c) Hypothermia

d) Hypometabolism

Explanation:

Thermogenin (UCP1) in brown adipose tissue uncouples oxidative phosphorylation, generating heat instead of ATP. This non-shivering thermogenesis is important in neonates and cold adaptation. It prevents hypothermia by converting stored energy into body heat. Correct answer is a) Heat generation through proton gradient dissipation and enhanced oxygen consumption in mitochondria.

2) Thyroxine causes mild uncoupling by?

a) Inhibiting cytochrome oxidase

b) Enhancing proton leak across inner mitochondrial membrane

c) Inhibiting glycolysis

d) Blocking ATP synthase directly

Explanation:

Thyroxine increases basal metabolic rate by stimulating mitochondrial biogenesis and enhancing proton leakage across the inner mitochondrial membrane. This mild uncoupling raises oxygen consumption and heat production. It does not directly inhibit ATP synthase or glycolysis. Correct answer is b) Enhancing proton leak across the inner mitochondrial membrane physiologically.

3) Free fatty acids act as uncouplers by?

a) Increasing proton conductance

b) Blocking complex III

c) Inhibiting adenylate kinase

d) Reducing NADH supply

Explanation:

Free fatty acids insert into the mitochondrial inner membrane and increase proton conductance, leading to dissipation of proton motive force. This reduces ATP synthesis and increases heat generation. Thus, they act as physiological uncouplers at high concentrations. Correct answer is a) Increasing proton conductance across inner mitochondrial membrane gradients.

4) A neonate kept in cold room resists hypothermia due to?

a) White adipose tissue

b) Brown adipose tissue with thermogenin

c) Skeletal muscle glycogen

d) Liver gluconeogenesis

Explanation:

Neonates resist hypothermia through non-shivering thermogenesis mediated by thermogenin (UCP1) in brown adipose tissue. This specialized fat generates heat by uncoupling oxidative phosphorylation, protecting against cold stress. White adipose tissue mainly stores energy, not heat. Correct answer is b) Brown adipose tissue with thermogenin-mediated heat production in neonates.

5) Excess thyroxine in hyperthyroidism leads to?

a) Hypothermia

b) Increased metabolic rate and heat intolerance

c) Decreased oxygen consumption

d) Decreased heart rate

Explanation:

Hyperthyroidism increases basal metabolic rate due to mitochondrial uncoupling effects of thyroxine. Patients develop heat intolerance, weight loss despite increased appetite, tachycardia, and sweating. Correct answer is b) Increased metabolic rate and heat intolerance due to physiological uncoupling induced by elevated thyroxine hormone levels chronically.

6) In brown adipose tissue, thermogenin is located in?

a) Outer mitochondrial membrane

b) Inner mitochondrial membrane

c) Cytosol

d) Nucleus

Explanation:

Thermogenin (UCP1) is specifically located in the inner mitochondrial membrane of brown adipocytes. It acts as a proton channel, bypassing ATP synthase, dissipating proton gradient, and generating heat. Correct answer is b) Inner mitochondrial membrane where thermogenin uncoupling occurs during adaptive thermogenesis in mammals, especially infants and hibernating animals.

7) Which of the following is NOT a physiological uncoupler?

a) Thyroxine

b) Thermogenin

c) Free fatty acids

d) Cyanide

Explanation:

Cyanide is not a physiological uncoupler but a poison that inhibits cytochrome oxidase (Complex IV), halting electron transport and ATP production. Physiological uncouplers include thermogenin, thyroxine, and free fatty acids. Correct answer is d) Cyanide, which causes histotoxic hypoxia and cellular asphyxia, not uncoupling activity.

8) A patient overdosed with DNP develops hyperthermia. The mechanism is similar to?

a) Thermogenin in brown fat

b) Cyanide toxicity

c) Oligomycin inhibition

d) Rotenone inhibition

Explanation:

DNP is a chemical uncoupler that collapses the proton gradient similar to thermogenin action. It increases oxygen consumption and heat production without ATP synthesis. Cyanide and rotenone inhibit ETC complexes, while oligomycin blocks ATP synthase. Correct answer is a) Thermogenin in brown fat physiology.

9) Clinical importance of physiological uncouplers?

a) Heat production and metabolic regulation

b) ATP overproduction

c) Reduced oxygen requirement

d) Protein synthesis regulation

Explanation:

Physiological uncouplers regulate energy balance by generating heat instead of ATP, critical in neonates, hibernating animals, and adaptation to cold. They also modulate oxygen consumption and free radical generation. Correct answer is a) Heat production and metabolic regulation as their main physiological importance in humans and animals.

10) Which hormone acts as a mild physiological uncoupler by stimulating metabolism?

a) Cortisol

b) Insulin

c) Thyroxine

d) Aldosterone

Explanation:

Thyroxine increases metabolic rate partly via mitochondrial uncoupling, enhancing oxygen consumption and heat generation. This hormone elevates basal metabolic rate and energy expenditure. Insulin, cortisol, and aldosterone act by other mechanisms. Correct answer is c) Thyroxine, a mild physiological uncoupler important in metabolic and thermal regulation mechanisms naturally.

Topic: Cell Signaling
Subtopic: G Protein Coupled Receptors (GPCRs) and Neurotransmission

Keyword Definitions:
• GPCR (G Protein Coupled Receptor): Membrane receptor activating intracellular G proteins upon ligand binding.
• Muscarinic receptors: Cholinergic receptors acting via GPCRs, affecting heart, smooth muscle, and glands.
• Nicotinic receptors: Ligand-gated ion channels, not GPCRs, mediating fast synaptic transmission.
• Insulin receptor: Tyrosine kinase receptor, not GPCR, regulating glucose uptake.
• GABA-A receptor: Ligand-gated chloride channel, mediating inhibitory neurotransmission.

Lead Question - 2013
Which of the following act through G protein coupled receptors?
a) Ach Muscarinic receptors
b) Insulin receptors
c) Ach Nicotinic receptors
d) GABA-A receptors

Explanation:
Muscarinic acetylcholine receptors are classic GPCRs, mediating parasympathetic effects via G proteins. Insulin receptors are tyrosine kinases, nicotinic receptors and GABA-A are ligand-gated ion channels. Therefore, only muscarinic receptors act through GPCRs. Answer: a) Ach Muscarinic receptors.

1) Which second messenger is increased by M2 muscarinic receptor activation in heart?
a) cAMP decrease
b) cAMP increase
c) IP3 increase
d) DAG increase
Explanation:
M2 muscarinic receptors are Gi-coupled in the heart. Activation inhibits adenylate cyclase, decreasing cAMP, slowing heart rate and contractility. Answer: a) cAMP decrease.

2) Which receptor type is involved in fast skeletal muscle contraction?
a) Nicotinic Ach receptor
b) Muscarinic Ach receptor
c) β1 adrenergic receptor
d) GABA-B receptor
Explanation:
Nicotinic acetylcholine receptors are ligand-gated ion channels at the neuromuscular junction, allowing rapid sodium influx, depolarization, and muscle contraction. Answer: a) Nicotinic Ach receptor.

3) A patient with bradycardia is given atropine. Which receptor is blocked?
a) M2 muscarinic receptor
b) β1 receptor
c) Nicotinic receptor
d) α1 receptor
Explanation:
Atropine is a muscarinic antagonist that blocks M2 receptors in the heart, preventing parasympathetic-mediated slowing of heart rate. Answer: a) M2 muscarinic receptor.

4) Which receptor mediates parasympathetic glandular secretion via GPCR?
a) M3 muscarinic receptor
b) Nicotinic receptor
c) β2 adrenergic receptor
d) GABA-A receptor
Explanation:
M3 muscarinic receptors are Gq-coupled GPCRs, stimulating phospholipase C, IP3 production, and intracellular Ca²⁺ increase, leading to glandular secretion. Answer: a) M3 muscarinic receptor.

5) Which GPCR mediates bronchodilation by sympathetic stimulation?
a) β2 adrenergic receptor
b) M3 receptor
c) Nicotinic receptor
d) GABA-A receptor
Explanation:
β2 adrenergic receptors are Gs-coupled GPCRs in bronchial smooth muscle. Activation increases cAMP, causing relaxation and bronchodilation. Answer: a) β2 adrenergic receptor.

6) Clinical: A patient has hypotension due to septic shock. Which GPCR pathway is targeted by norepinephrine infusion?
a) α1 receptor
b) M2 receptor
c) Nicotinic receptor
d) GABA-B receptor
Explanation:
Norepinephrine acts on α1 adrenergic receptors (Gs/PLC-coupled) causing vasoconstriction, raising blood pressure. These are GPCR-mediated effects. Answer: a) α1 receptor.

7) GABA-B receptor is coupled to:
a) Gi protein
b) Gs protein
c) Gq protein
d) Ion channel
Explanation:
GABA-B receptors are GPCRs coupled to Gi/o proteins, inhibiting adenylate cyclase, opening K⁺ channels, and producing slow inhibitory postsynaptic potentials. Answer: a) Gi protein.

8) Which GPCR mediates vasopressin’s antidiuretic effect?
a) V2 receptor
b) V1 receptor
c) Nicotinic receptor
d) M3 receptor
Explanation:
V2 vasopressin receptors in renal collecting ducts are Gs-coupled GPCRs. Activation increases cAMP, promoting insertion of aquaporin-2 channels and water reabsorption. Answer: a) V2 receptor.

9) Which subunit of G protein activates adenylate cyclase?
a) Gαs
b) Gαi
c) Gβ
d) Gγ
Explanation:
Gαs subunit of stimulatory G protein activates adenylate cyclase, increasing cAMP levels. Gαi inhibits adenylate cyclase. Beta and gamma subunits regulate signaling but do not directly activate adenylate cyclase. Answer: a) Gαs.

10) Clinical: A patient with overactive parasympathetic activity shows bradycardia and hypotension. Which receptor blockade can correct this?
a) Muscarinic receptor antagonist
b) Nicotinic receptor antagonist
c) β1 receptor blocker
d) GABA-A antagonist
Explanation:
Muscarinic antagonists like atropine block M2 receptors in the heart, preventing excessive parasympathetic slowing, correcting bradycardia and hypotension. Nicotinic, β1, and GABA-A are not involved in parasympathetic heart rate regulation. Answer: a) Muscarinic receptor antagonist.

Topic: Cell Signaling
Subtopic: G Protein Coupled Receptors (GPCRs)

Keyword Definitions:
• G Protein: Guanine nucleotide-binding protein involved in signal transduction.
• GPCR: Membrane receptor coupled with G proteins to transmit extracellular signals.
• Alpha subunit: Determines stimulatory or inhibitory action by binding GTP or GDP.
• Second messenger: Intracellular mediator like cAMP or IP3.
• Signal transduction: Process of converting extracellular signals into cellular responses.

Lead Question - 2013
True about G protein coupled receptors is:
a) G proteins bind to hormones on the cell surface
b) All the three subunits alpha, beta and gamma should bind to each other for G protein to act
c) G proteins act as inhibitory and excitatory because of difference in alpha subunit
d) G protein is bound to GTP in resting state

Explanation:
G proteins are inactive in the GDP-bound state. On activation, GDP is exchanged for GTP on alpha subunit. Depending on alpha subunit type (Gs, Gi), they stimulate or inhibit target enzymes. They do not bind hormones directly. Answer: c) G proteins act as inhibitory and excitatory because of difference in alpha subunit.

1) Which second messenger is increased by Gs protein activation?
a) IP3
b) DAG
c) cAMP
d) cGMP
Explanation:
Gs protein stimulates adenylate cyclase, which converts ATP to cAMP. Increased cAMP activates protein kinase A, leading to multiple cellular responses. Answer: c) cAMP.

2) Which of the following hormones acts via Gq protein?
a) ADH (V2 receptor)
b) TSH
c) Angiotensin II
d) ACTH
Explanation:
Angiotensin II acts through Gq protein, stimulating phospholipase C, generating IP3 and DAG, leading to Ca²⁺ release and smooth muscle contraction. Answer: c) Angiotensin II.

3) A 40-year-old woman develops flushing and watery diarrhea. Lab shows elevated VIP levels. Which receptor pathway is involved?
a) Tyrosine kinase
b) GPCR with Gs
c) GPCR with Gi
d) Nuclear receptor
Explanation:
VIP acts via Gs protein-coupled receptors, increasing cAMP and stimulating secretion. VIPoma causes watery diarrhea, hypokalemia, and achlorhydria (WDHA syndrome). Answer: b) GPCR with Gs.

4) Which of the following uses Gi protein mechanism?
a) Glucagon
b) Dopamine D2 receptor
c) ACTH
d) Vasopressin (V2)
Explanation:
Dopamine D2 receptors act via Gi proteins, which inhibit adenylate cyclase, reducing cAMP levels. This leads to inhibitory signaling. Answer: b) Dopamine D2 receptor.

5) Which intracellular change occurs after β-adrenergic receptor stimulation?
a) Increase in cAMP
b) Decrease in IP3
c) Increase in cGMP
d) Increase in DAG
Explanation:
β-adrenergic receptors act via Gs protein, stimulating adenylate cyclase, increasing cAMP levels, which activate PKA and enhance heart rate and contractility. Answer: a) Increase in cAMP.

6) A 32-year-old male ingests cholera toxin. Which step is affected?
a) Inhibition of adenylate cyclase
b) Activation of Gs by ADP ribosylation
c) Stimulation of Gi
d) Inhibition of cAMP
Explanation:
Cholera toxin ADP ribosylates Gs protein, locking it in active form, causing persistent activation of adenylate cyclase and massive cAMP increase, leading to fluid secretion. Answer: b) Activation of Gs by ADP ribosylation.

7) Which receptor is NOT mediated by GPCR?
a) Muscarinic receptor
b) β-adrenergic receptor
c) Insulin receptor
d) Dopamine receptor
Explanation:
Insulin receptor is a receptor tyrosine kinase, not a GPCR. GPCRs mediate muscarinic, β-adrenergic, and dopamine receptors. Answer: c) Insulin receptor.

8) A patient presents with whooping cough. Pertussis toxin inhibits which function?
a) Gi protein function
b) Gs protein activation
c) Tyrosine kinase activity
d) Nuclear receptor action
Explanation:
Pertussis toxin ADP ribosylates Gi protein, preventing inhibition of adenylate cyclase, resulting in persistently high cAMP. Answer: a) Gi protein function.

9) Which G protein subunit binds GTP during activation?
a) Alpha
b) Beta
c) Gamma
d) Delta
Explanation:
The alpha subunit binds GDP in inactive state and GTP in active state, leading to dissociation from beta and gamma subunits and activation of downstream signaling. Answer: a) Alpha.

10) A 55-year-old man with pheochromocytoma shows hypertension and tachycardia due to catecholamine excess. Which receptor is involved in heart stimulation?
a) α1 receptor
b) β1 receptor
c) β2 receptor
d) α2 receptor
Explanation:
β1 adrenergic receptors in the heart mediate increased heart rate and contractility via Gs protein and cAMP pathway, contributing to symptoms of pheochromocytoma. Answer: b) β1 receptor.

Topic: Calcium Signaling

Subtopic: Calmodulin and Enzyme Activation K

Keyword Definitions:

• Calmodulin: A calcium-binding messenger protein regulating many enzymes and cellular processes.

• Protein Kinase: Enzyme that phosphorylates proteins, altering activity.

• Phosphorylase: Enzyme breaking glycogen into glucose-1-phosphate.

• 2,3-DPG: Regulator of hemoglobin’s oxygen affinity.

• Glucokinase: Enzyme phosphorylating glucose in hepatocytes and pancreatic β-cells.

Lead Question – 2013

Calmodulin activates?

a) Muscle phosphorylase

b) Protein kinase

c) 2, 3 DPG

d) Glucokinase

Explanation: Calmodulin is a calcium-binding protein that activates several enzymes, most notably protein kinases. It does not directly activate phosphorylase, glucokinase, or 2,3-DPG. Calmodulin works by binding Ca²⁺ and changing shape to activate target proteins. The correct answer is Protein kinase.

1) Which of the following is a direct target of calmodulin?

a) Myosin light chain kinase

b) Hexokinase

c) Pyruvate dehydrogenase

d) Glycogen synthase

Explanation: Calmodulin directly activates myosin light chain kinase (MLCK) in smooth muscle. This leads to phosphorylation of myosin light chains and contraction. Other listed enzymes are not directly activated by calmodulin. The correct answer is Myosin light chain kinase.

2) Clinical: A patient has defective smooth muscle contraction. Which calmodulin-dependent enzyme is most likely impaired?

a) Myosin light chain kinase

b) Pyruvate carboxylase

c) Lactate dehydrogenase

d) Adenylate cyclase

Explanation: Smooth muscle contraction requires MLCK activation by Ca²⁺-calmodulin. A defect here impairs contraction. Other enzymes are not directly involved in this process. The correct answer is Myosin light chain kinase.

3) Calmodulin regulates which of the following?

a) Adenylate cyclase

b) Glycogen phosphorylase

c) Pyruvate kinase

d) Fructose bisphosphatase

Explanation: Calmodulin can regulate adenylate cyclase in some tissues by binding Ca²⁺ and altering cyclic AMP production. Other enzymes listed are not directly regulated by calmodulin. The correct answer is Adenylate cyclase.

4) Clinical: A hypertensive patient is treated with calcium channel blockers. Which calmodulin-mediated process is most affected?

a) Smooth muscle contraction

b) Glycolysis

c) Urea cycle

d) Beta-oxidation

Explanation: Calcium entry is needed to activate calmodulin and MLCK, leading to smooth muscle contraction. Blocking calcium channels decreases contraction, lowering blood pressure. Correct answer is Smooth muscle contraction.

5) Which secondary messenger works in conjunction with calmodulin?

a) Cyclic AMP

b) Cyclic GMP

c) Calcium ions

d) Inositol triphosphate

Explanation: Calmodulin is activated by calcium ions (Ca²⁺). IP₃ can release calcium from stores, indirectly aiding calmodulin. But the direct activator is calcium. The correct answer is Calcium ions.

6) Clinical: A mutation in calmodulin would primarily affect which system?

a) Calcium-mediated signaling

b) Glycogen synthesis

c) DNA replication

d) Fatty acid synthesis

Explanation: Calmodulin mediates calcium signaling and regulates kinases and enzymes. A mutation would disrupt many calcium-dependent pathways, including muscle contraction and secretion. The correct answer is Calcium-mediated signaling.

7) Calmodulin-dependent protein kinase II is important in:

a) Memory and learning

b) Lipid metabolism

c) Urea synthesis

d) Cholesterol transport

Explanation: CaMKII is a calmodulin-dependent protein kinase important in neuronal plasticity, memory, and learning. This highlights calmodulin’s role in the nervous system. Correct answer is Memory and learning.

8) Clinical: A patient has defective neurotransmitter release. Which calmodulin-related mechanism may be impaired?

a) Synaptic vesicle exocytosis

b) Glycogen storage

c) Fatty acid oxidation

d) DNA repair

Explanation: Calmodulin regulates exocytosis of neurotransmitters by activating calcium-dependent proteins. A defect impairs synaptic transmission. Correct answer is Synaptic vesicle exocytosis.

9) Which enzyme is calmodulin-dependent?

a) Phosphodiesterase

b) Succinyl-CoA synthetase

c) Enolase

d) Aldolase

Explanation: Calmodulin activates certain phosphodiesterases that degrade cyclic nucleotides, regulating signaling. Other enzymes listed are not dependent on calmodulin. The correct answer is Phosphodiesterase.

10) Clinical: A patient with asthma benefits from a drug reducing calmodulin activity. Which effect helps relieve symptoms?

a) Decreased smooth muscle contraction

b) Increased glycolysis

c) Enhanced fatty acid metabolism

d) Increased urea cycle activity

Explanation: Calmodulin is crucial for smooth muscle contraction via MLCK. Inhibiting calmodulin decreases airway smooth muscle contraction, relieving bronchospasm in asthma. The correct answer is Decreased smooth muscle contraction.

Topic: Plasma Proteins

Subtopic: Half-life of Plasma Proteins

Keyword Definitions:

• Prealbumin: Plasma protein also called transthyretin, transports thyroxine and retinol-binding protein.

• Albumin: Most abundant plasma protein, maintains oncotic pressure and transports molecules.

• Half-life: Time taken for half of the protein amount to degrade or be eliminated.

• Plasma Proteins: Proteins circulating in blood, important in transport, immunity, and clotting.

Lead Question – 2013

Half life of Prealbumin is?

a) 2 days

b) 10 days

c) 20 days

d) 40 days

Explanation: The half-life of prealbumin (transthyretin) is approximately 2 days. This short half-life makes it a sensitive marker for acute changes in nutritional status, unlike albumin, which has a longer half-life of around 20 days. Hence, the correct answer is 2 days.

1) Half-life of Albumin is:

a) 5 days

b) 10 days

c) 20 days

d) 40 days

Explanation: Albumin has a half-life of approximately 20 days. It is a major plasma protein synthesized in the liver, responsible for oncotic pressure maintenance and substance transport. Its long half-life makes it unsuitable for acute nutritional assessment. Correct answer is 20 days.

2) Half-life of Fibrinogen is:

a) 1 day

b) 3 days

c) 7 days

d) 14 days

Explanation: Fibrinogen, a coagulation factor, has a half-life of about 3 to 5 days. It plays a key role in blood clotting by being converted to fibrin during hemostasis. The correct answer is 3 days, making it an important acute phase reactant.

3) Half-life of Transferrin is:

a) 2 days

b) 8 days

c) 20 days

d) 40 days

Explanation: Transferrin is an iron-binding plasma protein with a half-life of about 8 days. It transports iron in circulation and is used as an indicator in nutritional and iron metabolism assessment. The correct answer is 8 days.

4) Clinical: A malnourished patient is monitored for improvement. Which plasma protein with the shortest half-life is the best marker?

a) Albumin

b) Prealbumin

c) Transferrin

d) Fibrinogen

Explanation: Prealbumin, with a half-life of 2 days, is the best marker for short-term changes in nutritional status. Albumin has a longer half-life, thus not suitable for acute monitoring. Hence, the correct answer is Prealbumin.

5) Clinical: In liver failure, which plasma protein level decreases first due to its short half-life?

a) Albumin

b) Prealbumin

c) Transferrin

d) Ceruloplasmin

Explanation: Prealbumin is synthesized in the liver and has a short half-life. In liver failure, its level drops quickly, making it an early marker. The correct answer is Prealbumin.

6) Which protein has the longest half-life among plasma proteins?

a) Albumin

b) Transferrin

c) Immunoglobulin G

d) Prealbumin

Explanation: Immunoglobulin G (IgG) has the longest half-life, approximately 23 days, which helps in maintaining long-term immunity. This property also makes IgG suitable for passive immunization. The correct answer is IgG.

7) Clinical: A child with protein-energy malnutrition is treated. Which plasma protein will reflect improvement within 48 hours?

a) Albumin

b) Prealbumin

c) IgG

d) Transferrin

Explanation: Prealbumin responds rapidly due to its 2-day half-life, showing improvement within 48 hours. Albumin, with a longer half-life, changes slowly. Thus, the correct answer is Prealbumin.

8) Which protein has a half-life of around 5 days?

a) Retinol-binding protein

b) Fibrinogen

c) Albumin

d) Transferrin

Explanation: Retinol-binding protein (RBP) has a very short half-life of around 12 hours, not 5 days. Fibrinogen half-life is 3–5 days, so the closest is Fibrinogen with 5 days. Correct answer: Fibrinogen.

9) Clinical: Which plasma protein is used as a sensitive marker for protein-calorie malnutrition because of its short half-life?

a) Albumin

b) Prealbumin

c) Transferrin

d) Ceruloplasmin

Explanation: Prealbumin, due to its very short half-life, is a sensitive marker for protein-calorie malnutrition. Its levels reflect recent nutritional status better than albumin or transferrin. The correct answer is Prealbumin.

10) Which plasma protein has the shortest half-life?

a) Prealbumin

b) Albumin

c) Fibrinogen

d) Transferrin

Explanation: Among plasma proteins, prealbumin has the shortest half-life (2 days), making it useful in clinical monitoring. Albumin and transferrin have longer half-lives, hence are less sensitive for acute nutritional changes. The correct answer is Prealbumin.

Topic: Liver and Plasma Proteins

Subtopic: Albumin Metabolism

Keyword Definitions

• Albumin – major plasma protein synthesized by the liver, maintaining oncotic pressure.

• Half-life – time required for half of a substance to be eliminated from plasma.

• Plasma Proteins – proteins present in plasma, mainly albumin, globulins, fibrinogen.

• Liver – organ responsible for synthesis of albumin and other plasma proteins.

• Oncotic Pressure – osmotic pressure exerted by plasma proteins, preventing edema.

Lead Question (2013)

Half-life of albumin is:

a) 5 days

b) 10 days

c) 20 days

d) 40 days

Explanation: Albumin is synthesized in the liver and has an average plasma half-life of 20 days. Its relatively long half-life reflects stability and slow catabolism. Conditions like malnutrition, chronic liver disease, or nephrotic syndrome affect albumin turnover. Hence, the correct answer is 20 days, indicating albumin’s metabolic persistence.

1) Guessed Question

Which organ is primarily responsible for albumin synthesis?

a) Kidney

b) Spleen

c) Liver

d) Bone marrow

Explanation: Albumin is exclusively synthesized in the liver hepatocytes. It represents the most abundant plasma protein, maintaining osmotic balance and transporting hormones, fatty acids, and drugs. Any impairment of liver function directly decreases albumin production. Therefore, the correct answer is Liver, which plays a central role in protein synthesis.

2) Guessed Question

A patient with cirrhosis presents with low albumin and edema. Cause of edema is?

a) Increased hydrostatic pressure

b) Decreased oncotic pressure

c) Increased lymphatic drainage

d) Increased protein intake

Explanation: Hypoalbuminemia due to liver failure reduces plasma oncotic pressure, leading to movement of fluid into interstitial spaces causing edema and ascites. This clinical manifestation is typical of cirrhosis and chronic liver disease. Hence, the correct answer is Decreased oncotic pressure, directly linked to reduced plasma albumin levels.

3) Guessed Question

Normal serum albumin level in adults is:

a) 1–2 g/dL

b) 2–3 g/dL

c) 3.5–5.5 g/dL

d) 6–8 g/dL

Explanation: The normal serum albumin concentration in adults is 3.5–5.5 g/dL. Levels below 3.5 g/dL indicate hypoalbuminemia, often associated with malnutrition, nephrotic syndrome, or liver disease. Maintaining this concentration is essential for fluid balance and nutrient transport. Thus, the correct answer is 3.5–5.5 g/dL.

4) Guessed Question

Which vitamin deficiency decreases albumin synthesis?

a) Vitamin A

b) Vitamin B12

c) Vitamin C

d) Vitamin K

Explanation: Protein synthesis, including albumin, is impaired in Vitamin B12 deficiency due to defective DNA synthesis and ineffective erythropoiesis. Although other vitamins influence metabolism, Vitamin B12 deficiency is strongly linked with reduced albumin production in chronic deficiency states. Therefore, the correct answer is Vitamin B12, highlighting its metabolic importance.

5) Guessed Question

A nephrotic syndrome patient has albuminuria. What happens to oncotic pressure?

a) Increases

b) Decreases

c) Remains unchanged

d) Doubles

Explanation: In nephrotic syndrome, albumin is lost in urine, resulting in hypoalbuminemia. The decline in plasma albumin reduces oncotic pressure, causing edema and fluid accumulation. This is a hallmark of nephrotic syndrome pathophysiology. Hence, the correct answer is Decreases, demonstrating the direct relationship between albumin and oncotic balance.

6) Guessed Question

Albumin binds and transports all except:

a) Bilirubin

b) Calcium

c) Thyroxine

d) Hemoglobin

Explanation: Albumin transports bilirubin, calcium, fatty acids, and hormones like thyroxine. However, hemoglobin is not carried by albumin; it is bound by haptoglobin when free in plasma. Therefore, the correct answer is Hemoglobin, as albumin is not responsible for its transport. This highlights albumin’s selective transport functions.

7) Guessed Question

Patient with protein-energy malnutrition (kwashiorkor) presents with edema. Cause is?

a) Hypoalbuminemia

b) Hypernatremia

c) Increased vascular resistance

d) Hyperkalemia

Explanation: In kwashiorkor, inadequate dietary protein reduces hepatic albumin synthesis, causing hypoalbuminemia. This decreases plasma oncotic pressure, leading to edema despite adequate caloric intake. Therefore, the correct answer is Hypoalbuminemia, a classic mechanism explaining edema in malnourished children. This condition exemplifies the vital role of albumin in nutrition.

8) Guessed Question

Which test is most specific for assessing hepatic synthetic function?

a) Serum bilirubin

b) Serum albumin

c) Prothrombin time

d) ALT/AST

Explanation: Serum albumin reflects chronic hepatic synthetic capacity, but prothrombin time is more sensitive for acute changes. Since albumin has a long half-life, its fall indicates prolonged liver dysfunction. Therefore, the correct answer is Serum albumin, which is a reliable marker of chronic liver synthetic function over time.

9) Guessed Question

Which of the following increases albumin catabolism?

a) Burns

b) Hypothyroidism

c) Renal artery stenosis

d) Addison’s disease

Explanation: Severe burns increase vascular permeability, leading to albumin leakage and accelerated catabolism. This results in hypoalbuminemia and edema, complicating patient recovery. Hence, the correct answer is Burns, which significantly increase albumin breakdown and loss from circulation. This emphasizes albumin’s vulnerability in catabolic stress states.

10) Guessed Question

Which plasma protein has the longest half-life?

a) Albumin

b) Fibrinogen

c) Transferrin

d) Immunoglobulin G

Explanation: Immunoglobulin G (IgG) has the longest half-life among plasma proteins, around 23 days. Albumin has a shorter half-life of about 20 days. This long half-life makes IgG suitable for passive immunity through maternal transfer and therapeutic use. Thus, the correct answer is Immunoglobulin G, not albumin.

Chapter: General Physiology

Topic: Cell Communication

Subtopic: Gap Junctions and Intercellular Signaling

Keyword Definitions:

• Gap junctions: Specialized intercellular connections allowing ions and molecules to pass directly between cells.

• Connexins: Protein subunits forming channels in gap junctions.

• Cardiac myocytes: Muscle cells of the heart responsible for contraction.

• Smooth muscle: Involuntary, non-striated muscle found in visceral organs.

• Impulse transmission: Movement of action potentials between cells for coordinated function.

Lead Question - 2013

Gap junctions?

a) Are absent in cardiac muscles

b) Are absent in smooth muscles

c) Are present in cardiac muscles to transmit impulse from one to another myocyte

d) Are present in cardiac muscles but no role

Explanation: Gap junctions, made of connexins, are crucial for electrical coupling in cardiac myocytes. They allow action potentials to spread rapidly, ensuring coordinated contraction. Correct answer: c) Are present in cardiac muscles to transmit impulse from one to another myocyte. They are also found in smooth muscle for synchronous contraction.

1) Which protein forms the structural unit of gap junctions?

a) Integrin

b) Connexin

c) Cadherin

d) Selectin

Explanation: Gap junctions are composed of connexin proteins. Six connexins form a connexon, and two connexons align to create a functional gap junction channel. Correct answer: b) Connexin. Cadherins and integrins are adhesion proteins, not channel-forming proteins.

2) A patient with atrial fibrillation shows impaired intercellular electrical coupling. Which structure is most likely defective?

a) Desmosomes

b) Tight junctions

c) Gap junctions

d) Hemidesmosomes

Explanation: Atrial fibrillation often involves dysfunction in gap junctions, which mediate cell-to-cell conduction of impulses. Their alteration leads to arrhythmias. Correct answer: c) Gap junctions. Tight junctions regulate paracellular permeability but not impulse spread.

3) Gap junctions allow passage of which molecules?

a) Proteins

b) DNA

c) Ions and small molecules

d) Large lipids

Explanation: Gap junctions permit ions and small molecules (less than 1 kDa) like calcium, ATP, and second messengers to pass between cells. Correct answer: c) Ions and small molecules. Large macromolecules like proteins and DNA cannot pass.

4) A neonate presents with arrhythmias and skin abnormalities due to connexin mutation. This syndrome reflects dysfunction in?

a) Gap junctions

b) Desmosomes

c) Adherens junctions

d) Hemidesmosomes

Explanation: Mutations in connexins impair gap junctions, leading to defective impulse conduction in the heart and abnormal keratinocyte communication in skin. Correct answer: a) Gap junctions. Other junctions primarily mediate adhesion, not ion flow.

5) Which of the following is NOT a function of gap junctions?

a) Electrical coupling

b) Synchronous contraction

c) Paracellular absorption

d) Metabolic cooperation

Explanation: Gap junctions mediate electrical coupling, synchronous activity, and metabolic cooperation. They do not participate in paracellular absorption, which is regulated by tight junctions. Correct answer: c) Paracellular absorption. Gap junctions are key for coordinated function in heart and smooth muscle.

6) A patient with heart failure has reduced connexin-43 expression. Which physiological process will be most impaired?

a) Cardiac impulse propagation

b) Sodium-potassium pump activity

c) Calcium release from SR

d) Myosin cross-bridge cycling

Explanation: Connexin-43 is a major gap junction protein in ventricular myocardium. Its reduction decreases impulse propagation, causing conduction delays and arrhythmias. Correct answer: a) Cardiac impulse propagation. Pump activity and contractile proteins remain intact.

7) Which junction is most important for maintaining barrier integrity of epithelial cells?

a) Gap junction

b) Tight junction

c) Desmosome

d) Adherens junction

Explanation: Tight junctions seal epithelial cells, preventing leakage of solutes across paracellular spaces. Correct answer: b) Tight junction. Gap junctions communicate signals, not barrier integrity. Desmosomes provide strength, and adherens junctions link actin filaments.

8) A 40-year-old man presents with smooth muscle dysfunction and impaired uterine contractions. Which junction defect could explain this?

a) Gap junction

b) Tight junction

c) Focal adhesion

d) Desmosome

Explanation: Smooth muscle contraction synchronization depends on gap junctions. In uterus, they increase near term to enable labor. Defects impair contractions. Correct answer: a) Gap junction. Tight junctions regulate barriers, not muscle function.

9) Which dye transfer experiment demonstrates functional gap junction communication?

a) Lucifer yellow

b) Hematoxylin

c) Eosin

d) Safranin

Explanation: Lucifer yellow is a small fluorescent dye that diffuses through gap junctions, demonstrating intercellular communication. Correct answer: a) Lucifer yellow. Other dyes stain tissues but do not assess junctional transfer.

10) A patient with ventricular arrhythmia has gap junctional uncoupling due to ischemia. Which mechanism explains this finding?

a) Acidosis closes gap junctions

b) Calcium influx strengthens gap junctions

c) Hypoxia opens more connexons

d) ATP depletion activates channels

Explanation: During ischemia, acidosis and calcium overload close gap junctions, impairing conduction and predisposing to arrhythmias. Correct answer: a) Acidosis closes gap junctions. Hypoxia and ATP depletion worsen function but do not directly open channels.

Topic: Membrane Physiology

Subtopic: Ion Channels and Patch-Clamp Technique

Keyword Definitions:

• Patch-clamp: Technique to measure ionic currents through single ion channels.

• Voltage-gated channels: Ion channels opening/closing in response to membrane potential changes.

• Resting Membrane Potential (RMP): Electrical potential difference across resting cell membranes.

• Facilitated diffusion: Passive transport across membranes via carrier proteins.

• Osmotic pressure: Pressure exerted by solutes across semipermeable membranes.

Lead Question - 2013

'Patch-clamp' is used for ?

a) To record facilitated diffusion

b) To record flow in voltage gated channel

c) To record osmotic pressure around semipermeable membrane

d) To record RMP

Explanation: Patch-clamp is a powerful electrophysiological technique for recording ionic currents in individual ion channels, particularly voltage-gated channels. It helps study gating, conductance, and drug effects. Correct answer: b) To record flow in voltage gated channel. Other options relate to different physiological processes not studied by patch-clamp.

1) Which ion channel is primarily responsible for upstroke of neuronal action potential?

a) K+ channels

b) Na+ channels

c) Ca2+ channels

d) Cl- channels

Explanation: The rapid depolarization in neuronal action potential is mediated by opening of voltage-gated Na+ channels, allowing influx of sodium ions. This phase defines the action potential upstroke. Correct answer: b) Na+ channels. Potassium channels act later in repolarization, while calcium channels play supportive roles.

2) A patient with Lambert-Eaton syndrome has impaired neurotransmission due to antibodies against ?

a) Voltage-gated Na+ channels

b) Voltage-gated K+ channels

c) Voltage-gated Ca2+ channels

d) Ligand-gated Cl- channels

Explanation: Lambert-Eaton myasthenic syndrome involves antibodies against presynaptic voltage-gated Ca2+ channels, reducing acetylcholine release at neuromuscular junction. This causes muscle weakness improving with exercise. Correct answer: c) Voltage-gated Ca2+ channels. It differs from myasthenia gravis which affects postsynaptic receptors.

3) Which technique is used to measure membrane potential directly?

a) Patch-clamp

b) Microelectrode insertion

c) Radioisotope flux

d) Fluorescent dyes

Explanation: Microelectrode insertion technique allows direct measurement of membrane potential by impaling a cell and recording voltage difference across its membrane. Correct answer: b) Microelectrode insertion. Patch-clamp mainly records ionic currents, while dyes and isotopes give indirect estimates.

4) A 55-year-old hypertensive patient develops muscle weakness. Patch-clamp study shows reduced Na+ channel activity. Which phase of action potential will be most affected?

a) Depolarization

b) Repolarization

c) Hyperpolarization

d) Resting potential

Explanation: Voltage-gated sodium channels mediate depolarization of the action potential. Reduced activity impairs this initial phase, slowing or blocking excitation. Correct answer: a) Depolarization. Repolarization is mediated by K+ channels, unaffected by sodium channel dysfunction.

5) In cardiac pacemaker cells, which ion channel is critical for spontaneous depolarization?

a) Na+ fast channels

b) K+ channels

c) Funny (If) channels

d) Cl- channels

Explanation: Pacemaker cells rely on funny channels (If), which conduct slow Na+ influx during diastolic depolarization. This automatic activity initiates heartbeats. Correct answer: c) Funny (If) channels. Fast Na+ channels dominate atrial/ventricular depolarization, not pacemaker activity.

6) A young man presents with periodic paralysis triggered by high carbohydrate meals. Patch-clamp shows K+ channel inactivation. What is the diagnosis?

a) Myasthenia gravis

b) Hypokalemic periodic paralysis

c) Hyperkalemic periodic paralysis

d) Lambert-Eaton syndrome

Explanation: Hypokalemic periodic paralysis involves episodic weakness after carbohydrate load or rest, due to defective voltage-gated calcium or potassium channels. Correct answer: b) Hypokalemic periodic paralysis. Patch-clamp aids in confirming channel dysfunction in such disorders.

7) Which ion channel is blocked by tetrodotoxin (puffer fish toxin)?

a) Na+ channels

b) K+ channels

c) Ca2+ channels

d) Cl- channels

Explanation: Tetrodotoxin selectively blocks voltage-gated sodium channels, preventing depolarization and action potential conduction. This causes paralysis and can be fatal. Correct answer: a) Na+ channels. Potassium and calcium channels are unaffected by tetrodotoxin.

8) A patient with cystic fibrosis has defective ion transport due to mutation in ?

a) Voltage-gated Na+ channel

b) CFTR chloride channel

c) Potassium leak channel

d) Calcium channel

Explanation: Cystic fibrosis is caused by mutations in the CFTR gene encoding a chloride channel important for epithelial fluid transport. This leads to thick mucus secretions. Correct answer: b) CFTR chloride channel. Patch-clamp can study defective chloride channel activity.

9) Which ligand-gated channel is activated at the neuromuscular junction?

a) GABA receptor channel

b) Acetylcholine receptor channel

c) NMDA receptor channel

d) Glycine receptor channel

Explanation: At the neuromuscular junction, acetylcholine binds to nicotinic receptors, opening ligand-gated sodium and potassium channels, causing depolarization. Correct answer: b) Acetylcholine receptor channel. Other receptors are inhibitory or central nervous system-specific.

10) A 70-year-old man with Alzheimer’s disease has reduced cholinergic neurotransmission. Which channel activity is most impaired at synapse?

a) Nicotinic receptor channel

b) Voltage-gated Na+ channel

c) Voltage-gated K+ channel

d) Ca2+ leak channel

Explanation: Alzheimer’s disease involves loss of cholinergic neurons, reducing acetylcholine release and nicotinic receptor activity at synapses. Correct answer: a) Nicotinic receptor channel. This underlies cognitive deficits and explains why cholinesterase inhibitors are used in therapy.

Topic: Body Fluid Compartments

Subtopic: Measurement of Plasma Volume

Keyword Definitions:

• Plasma volume: Volume of plasma in blood, measured using dye dilution techniques.

• Evans blue: Dye binding to plasma proteins, used to measure plasma volume.

• Inulin: Polysaccharide used for GFR measurement, not plasma volume.

• Mannitol: Used to measure extracellular fluid volume.

• D2O (Deuterium oxide): Used to measure total body water.

Lead Question - 2013

Plasma volume is measured by ?

a) Inulin

b) Evans blue

c) Mannitol

d) D2O

Explanation: Plasma volume is best measured by Evans blue dye, which binds to plasma proteins like albumin, remaining confined within the vascular compartment. Inulin is for GFR, Mannitol for ECF, and D2O for total body water. Correct answer: Evans blue.

1) Plasma osmolality is mainly determined by?

a) Sodium

b) Potassium

c) Calcium

d) Glucose

Explanation: Plasma osmolality primarily depends on sodium and its associated anions, as sodium is the major extracellular cation. Glucose and urea contribute less significantly under normal conditions. Correct answer: Sodium.

2) A patient receives IV mannitol infusion. What compartment expands most?

a) Plasma volume

b) Extracellular fluid

c) Intracellular fluid

d) Total body water

Explanation: Mannitol distributes only in extracellular fluid, not intracellular fluid. Thus, it expands ECF volume, increasing osmotic gradient and drawing water out of cells. Correct answer: Extracellular fluid.

3) Extracellular fluid volume is measured using?

a) Mannitol

b) Inulin

c) Evans blue

d) D2O

Explanation: Mannitol, sucrose, or thiosulfate can be used to measure extracellular fluid volume since they distribute in both plasma and interstitial fluid compartments but not intracellularly. Correct answer: Mannitol.

4) A patient presents with edema. Plasma volume estimation is best done by?

a) Radio-iodinated albumin

b) Inulin

c) Mannitol

d) D2O

Explanation: Plasma volume is accurately measured by dyes like Evans blue or radio-iodinated albumin, which bind plasma proteins. They do not cross into interstitial fluid. Correct answer: Radio-iodinated albumin.

5) Total body water is best measured by?

a) Inulin

b) D2O

c) Evans blue

d) Mannitol

Explanation: Deuterium oxide (D2O) or tritiated water distributes throughout all compartments, making them ideal for total body water measurement. Correct answer: D2O.

6) A child with diarrhea and dehydration is admitted. Which compartment is lost most?

a) Plasma volume

b) Interstitial fluid

c) Intracellular fluid

d) Extracellular fluid

Explanation: Diarrhea causes loss of extracellular fluid (plasma + interstitial fluid). Severe dehydration may later involve intracellular fluid. Correct answer: Extracellular fluid.

7) Interstitial fluid volume is calculated as?

a) Total body water – Plasma volume

b) Extracellular fluid – Plasma volume

c) Intracellular fluid – Plasma volume

d) Plasma volume – ECF

Explanation: Interstitial fluid cannot be measured directly but is calculated as extracellular fluid volume minus plasma volume. Correct answer: Extracellular fluid – Plasma volume.

8) A burn patient develops hypovolemia. Which compartment is primarily lost?

a) Intracellular fluid

b) Plasma volume

c) Interstitial fluid

d) Extracellular fluid

Explanation: Burns cause increased capillary permeability, leading to plasma protein and fluid loss into interstitial space, reducing plasma volume and overall ECF. Correct answer: Plasma volume.

9) Inulin clearance is used to measure?

a) Plasma volume

b) GFR

c) ECF volume

d) Total body water

Explanation: Inulin is freely filtered by glomeruli, not reabsorbed or secreted. Its clearance accurately measures glomerular filtration rate (GFR), not body fluid compartments. Correct answer: GFR.

10) A 65-year-old hypertensive patient on diuretics shows hyponatremia. Which compartment shrinks most?

a) Intracellular fluid

b) Extracellular fluid

c) Plasma volume

d) Interstitial fluid

Explanation: Diuretic use with sodium loss primarily reduces extracellular fluid volume, including plasma and interstitial compartments, leading to hypovolemia and electrolyte imbalance. Correct answer: Extracellular fluid.

11) D2O method helps in calculating which compartment?

a) Plasma volume

b) Extracellular fluid

c) Total body water

d) Interstitial fluid

Explanation: D2O distributes across all fluid compartments (plasma, interstitial, intracellular). Therefore, it is used to measure total body water. Correct answer: Total body water.

Topic: Acid-Base Balance

Subtopic: Extracellular Buffer Systems

Keyword Definitions:

- Buffer: Substance that resists changes in pH upon addition of acid or base.

- Extracellular Fluid (ECF): Fluid outside cells, including plasma and interstitial fluid.

- Bicarbonate (HCO3-): A major component in the bicarbonate buffering system, neutralizes excess acids.

- Phosphate Buffer: Buffer system more important intracellularly than extracellularly.

- Ammonia: Weak base involved in renal acid-base regulation.

Lead Question - 2013

Most important extracellular buffer ?

a) Phosphate

b) Plasma proteins

c) Ammonia

d) Bicarbonates

Answer and Explanation:

Correct answer is d) Bicarbonates. Bicarbonate buffer system is the most important extracellular buffer. It maintains blood pH within a narrow range by reacting with hydrogen ions to form carbonic acid, which is then converted to CO₂ and water, preventing drastic pH changes essential for normal cellular function.

Guessed Questions for NEET PG:

1. Primary organ regulating bicarbonate concentration?

a) Liver

b) Kidney

c) Lung

d) Pancreas

Explanation: Correct answer is b) Kidney. Kidneys regulate bicarbonate concentration by reabsorbing bicarbonate and excreting hydrogen ions, crucial for acid-base homeostasis.

2. Henderson-Hasselbalch equation relates?

a) pH, pKa, bicarbonate

b) Osmolarity and solute concentration

c) CO₂ pressure and pH

d) pH and protein concentration

Explanation: Correct answer is a) pH, pKa, bicarbonate. It calculates pH based on bicarbonate concentration and CO₂ partial pressure, essential in acid-base physiology.

3. Respiratory compensation corrects?

a) Metabolic acidosis

b) Respiratory alkalosis

c) Metabolic alkalosis

d) None

Explanation: Correct answer is a) Metabolic acidosis. Respiratory system increases ventilation to expel CO₂ and compensate acidosis.

4. In metabolic alkalosis, expected HCO3- level?

a) Decreased

b) Increased

c) Unchanged

d) Zero

Explanation: Correct answer is b) Increased. Metabolic alkalosis causes elevated bicarbonate levels due to acid loss or alkali gain.

5. Which is a volatile acid?

a) Sulfuric acid

b) Hydrochloric acid

c) Carbonic acid

d) Lactic acid

Explanation: Correct answer is c) Carbonic acid. CO₂ from metabolism forms carbonic acid, removable via lungs, making it volatile.

6. Plasma protein buffer works by?

a) Binding hydrogen ions

b) Excreting acids

c) Producing bicarbonate

d) Increasing respiration

Explanation: Correct answer is a) Binding hydrogen ions. Plasma proteins, especially albumin, buffer acids by binding free H+ ions.

7. Main buffer of intracellular fluid?

a) Bicarbonate

b) Phosphate

c) Ammonia

d) Protein

Explanation: Correct answer is d) Protein. Intracellular proteins serve as major buffers by binding hydrogen ions.

8. Normal plasma bicarbonate concentration?

a) 24-28 mEq/L

b) 15-20 mEq/L

c) 30-35 mEq/L

d) 10-15 mEq/L

Explanation: Correct answer is a) 24-28 mEq/L. This range maintains physiological pH in plasma.

9. In respiratory acidosis, cause is?

a) Hypoventilation

b) Hyperventilation

c) Excess bicarbonate

d) Loss of acid

Explanation: Correct answer is a) Hypoventilation. Reduced breathing causes CO₂ accumulation, increasing carbonic acid and lowering pH.

10. Ammonia buffer system mainly operates in?

a) Liver

b) Kidney

c) Lung

d) Plasma

Explanation: Correct answer is b) Kidney. Ammonia is produced and secreted by renal tubular cells, combining with H+ to facilitate acid excretion.

Chapter: Respiratory Physiology

Topic: Pulmonary Function Tests

Subtopic: Dead Space Measurement

Keywords:

Physiological Dead Space: The total volume of the lungs that does not participate in gas exchange, including anatomical and alveolar dead space.
Bohr Equation: A formula used to calculate the physiological dead space based on CO₂ concentration differences between alveolar gas and expired air.
Dalton’s Law: States that the total pressure exerted by a mixture of non-reacting gases is equal to the sum of the partial pressures of individual gases.
Boyle's Law: Describes the inverse relationship between pressure and volume of gas at constant temperature (PV = constant).

Lead Question - 2013:

Physiological dead space is calculated by ?

a) Boyle's law
b) Dalton's law
c) Bohr equation
d) Charle's law

Answer & Explanation:
Correct answer: c) Bohr equation.
Explanation: Physiological dead space is calculated using the Bohr equation, which evaluates the fraction of tidal volume that does not participate in gas exchange by comparing CO₂ concentrations in alveolar and expired air. This calculation is crucial in assessing ventilation efficiency, especially in pulmonary diseases.

MCQ 1:

What does the Bohr equation primarily measure?

a) Lung compliance
b) Physiological dead space
c) Airway resistance
d) Tidal volume

Answer & Explanation:
Correct answer: b) Physiological dead space.
Explanation: The Bohr equation calculates physiological dead space, representing the portion of inspired air not engaged in gas exchange. It compares alveolar and expired CO₂ concentrations, serving as an important index in evaluating respiratory disorders and mechanical ventilation efficiency.

MCQ 2 (Clinical):

In which condition is physiological dead space expected to be significantly increased?

a) Pulmonary embolism
b) Asthma
c) Bronchitis
d) Normal lungs

Answer & Explanation:
Correct answer: a) Pulmonary embolism.
Explanation: Pulmonary embolism blocks pulmonary blood flow, resulting in alveoli that are ventilated but not perfused. This increases physiological dead space and impairs gas exchange efficiency, leading to hypoxemia and requiring urgent diagnosis and treatment in clinical practice.

MCQ 3:

Which is NOT a component of physiological dead space?

a) Anatomical dead space
b) Alveolar dead space
c) Residual volume
d) Both anatomical and alveolar dead space

Answer & Explanation:
Correct answer: c) Residual volume.
Explanation: Physiological dead space consists of anatomical dead space (airways not participating in gas exchange) and alveolar dead space (non-perfused alveoli). Residual volume is the air remaining in the lungs after maximal expiration and is not part of dead space calculation.

MCQ 4 (Clinical):

Why is measuring physiological dead space clinically useful?

a) To assess lung compliance
b) To detect airway obstruction
c) To evaluate gas exchange inefficiency
d) To measure blood oxygen content

Answer & Explanation:
Correct answer: c) To evaluate gas exchange inefficiency.
Explanation: Measuring physiological dead space helps assess the efficiency of ventilation and gas exchange. Elevated dead space suggests ventilation-perfusion mismatch, which can be caused by diseases like pulmonary embolism, chronic obstructive pulmonary disease, or acute respiratory distress syndrome.

MCQ 5:

Which law is used to describe the relationship between gas pressure and volume?

a) Bohr equation
b) Dalton’s law
c) Boyle’s law
d) Charles’s law

Answer & Explanation:
Correct answer: c) Boyle’s law.
Explanation: Boyle's Law states that pressure and volume of a gas are inversely proportional at constant temperature. This principle explains lung inflation and deflation during breathing but is not used to calculate physiological dead space.

MCQ 6 (Clinical):

How does COPD affect physiological dead space?

a) Decreases it
b) No change
c) Increases it
d) Eliminates it

Answer & Explanation:
Correct answer: c) Increases it.
Explanation: COPD leads to destruction of alveolar walls and poor perfusion, causing more alveoli to be ventilated but not perfused, increasing physiological dead space. This worsens gas exchange and contributes to hypoxia, making dead space measurement crucial in clinical assessments.

MCQ 7:

Dalton’s law pertains to?

a) Volume and pressure
b) Gas solubility
c) Partial pressures of gases in a mixture
d) Gas temperature relationship

Answer & Explanation:
Correct answer: c) Partial pressures of gases in a mixture.
Explanation: Dalton’s Law states that the total pressure of a gas mixture equals the sum of the partial pressures of individual gases. This principle is important in understanding gas exchange but does not calculate physiological dead space.

MCQ 8 (Clinical):

Which clinical tool helps measure expired CO₂ for Bohr equation calculation?

a) Spirometer
b) Capnograph
c) Pulse oximeter
d) Peak flow meter

Answer & Explanation:
Correct answer: b) Capnograph.
Explanation: A capnograph continuously measures the CO₂ concentration in exhaled air, allowing clinicians to calculate physiological dead space using the Bohr equation. It provides important data about ventilation and perfusion status, especially during anesthesia and in critically ill patients.

MCQ 9:

Physiological dead space fraction (VD/VT) in healthy adults is approximately?

a) 0.1
b) 0.3
c) 0.5
d) 0.7

Answer & Explanation:
Correct answer: b) 0.3.
Explanation: In healthy adults, the physiological dead space fraction (VD/VT) is typically around 0.3, meaning about 30% of each breath does not participate in gas exchange. Higher fractions indicate impaired ventilation efficiency and are observed in various respiratory disorders.

MCQ 10 (Clinical):

In which situation would physiological dead space decrease?

a) Pulmonary embolism
b) Severe emphysema
c) Hyperventilation
d) Acute respiratory distress syndrome

Answer & Explanation:
Correct answer: c) Hyperventilation.
Explanation: During hyperventilation, increased respiratory rate reduces the relative proportion of dead space compared to tidal volume, temporarily lowering the dead space fraction. However, chronic respiratory diseases typically increase physiological dead space due to ventilation-perfusion mismatch and alveolar destruction.

Chapter: Respiratory Physiology

Topic: Gas Laws in Respiration

Subtopic: Boyle’s Law

Keywords:

Boyle’s Law: States that at constant temperature, the pressure and volume of a gas are inversely proportional (P × V = constant).
Charles’s Law: States that the volume of a gas is directly proportional to its absolute temperature at constant pressure (V/T = constant).
Ideal Gas Law: PV = nRT, relates pressure, volume, number of moles, gas constant, and temperature of a gas.
Pressure (P): The force exerted by gas molecules per unit area of container walls.
Volume (V): The space occupied by the gas.

Lead Question - 2013:

Boyle's Law states that ?

a) P/T = constant
b) PV = constant
c) PV = nRT
d) V/T = constant

Answer & Explanation:
Correct answer: b) PV = constant.
Explanation: Boyle's Law describes the inverse relationship between pressure (P) and volume (V) of a gas at constant temperature: when volume decreases, pressure increases proportionally, and vice versa. This principle explains the mechanics of lung inflation and deflation during breathing cycles in respiratory physiology.

MCQ 1:

Charles’s Law states that ?

a) P/T = constant
b) PV = constant
c) V/T = constant
d) P + V = constant

Answer & Explanation:
Correct answer: c) V/T = constant.
Explanation: Charles's Law states that the volume (V) of a gas is directly proportional to its absolute temperature (T) when pressure is constant. This explains how lung volume changes during breathing, especially in temperature regulation and understanding gas behavior in different respiratory conditions.

MCQ 2 (Clinical):

In emphysema, the lung compliance is:

a) Increased due to alveolar wall destruction
b) Decreased due to fibrosis
c) Normal
d) Increased due to bronchoconstriction

Answer & Explanation:
Correct answer: a) Increased due to alveolar wall destruction.
Explanation: In emphysema, destruction of alveolar walls reduces elastic recoil, increasing lung compliance. Boyle's Law helps explain how alveolar expansion occurs easily but leads to inefficient ventilation due to poor elastic recoil, causing air trapping and impaired gas exchange.

MCQ 3:

Which law relates to pressure, volume, and temperature of gas together?

a) Boyle’s Law
b) Charles’s Law
c) Ideal Gas Law
d) Avogadro’s Law

Answer & Explanation:
Correct answer: c) Ideal Gas Law.
Explanation: The Ideal Gas Law (PV = nRT) relates pressure, volume, and temperature of a gas together, considering the number of moles and gas constant. It applies to respiratory gas exchange and mechanical ventilation, providing a comprehensive understanding of gas behavior in the lungs.

MCQ 4 (Clinical):

Which condition reduces lung compliance?

a) Pulmonary fibrosis
b) Emphysema
c) Bronchiectasis
d) Asthma

Answer & Explanation:
Correct answer: a) Pulmonary fibrosis.
Explanation: Pulmonary fibrosis stiffens lung tissue due to collagen deposition, reducing compliance. Boyle's Law explains that increased stiffness resists volume changes despite pressure variations, leading to difficulty in lung expansion during inspiration and causing breathlessness.

MCQ 5:

At constant temperature, when lung volume increases, pressure inside the alveoli:

a) Increases
b) Remains constant
c) Decreases
d) Fluctuates randomly

Answer & Explanation:
Correct answer: c) Decreases.
Explanation: According to Boyle's Law, during inspiration, diaphragm contracts, thoracic volume increases, and alveolar pressure decreases below atmospheric pressure. This pressure gradient drives air into the lungs, illustrating the inverse relationship between pressure and volume at constant temperature.

MCQ 6 (Clinical):

Which of the following is true during mechanical ventilation?

a) Boyle's Law does not apply
b) Volume is constant despite pressure changes
c) Pressure and volume changes follow Boyle's Law
d) Temperature varies significantly

Answer & Explanation:
Correct answer: c) Pressure and volume changes follow Boyle's Law.
Explanation: Mechanical ventilators apply pressure to inflate lungs; Boyle's Law governs how pressure increases lead to proportional volume expansion. Understanding this helps optimize ventilator settings, prevent barotrauma, and ensure adequate alveolar ventilation without damaging lung tissues.

MCQ 7:

Which is NOT a key variable in Boyle’s Law?

a) Pressure
b) Volume
c) Temperature
d) Gas constant

Answer & Explanation:
Correct answer: c) Temperature.
Explanation: Boyle's Law applies when temperature is constant (isothermal conditions). It only relates pressure and volume inversely. Temperature changes are considered in Charles’s Law or the Ideal Gas Law, so Boyle's Law focuses purely on pressure-volume relationship in the lungs during normal breathing.

MCQ 8 (Clinical):

Why is Boyle's Law significant during anesthesia?

a) It helps calculate drug dosage
b) Explains gas expansion in body cavities
c) Predicts cardiac output
d) Determines renal filtration rate

Answer & Explanation:
Correct answer: b) Explains gas expansion in body cavities.
Explanation: Boyle’s Law explains how gas expands when pressure decreases, crucial in anesthesia where gas-filled spaces (e.g., pneumothorax, intestines) may expand dangerously. Proper understanding prevents complications by adjusting ventilator pressures to avoid overexpansion.

MCQ 9:

In which situation does Boyle’s Law apply during respiration?

a) Airflow during forced expiration
b) Air entering lungs during inspiration
c) Blood flow in pulmonary circulation
d) Oxygen binding to hemoglobin

Answer & Explanation:
Correct answer: b) Air entering lungs during inspiration.
Explanation: During inspiration, thoracic cavity volume increases, alveolar pressure decreases, and air flows from higher to lower pressure. Boyle’s Law (P × V = constant) precisely describes this fundamental principle of normal breathing mechanics in pulmonary physiology.

MCQ 10 (Clinical):

In pneumothorax, Boyle’s Law explains that:

a) Lung volume increases due to external pressure
b) Air enters pleural space lowering intrapleural pressure
c) Loss of negative intrapleural pressure causes lung collapse
d) Gas laws are irrelevant

Answer & Explanation:
Correct answer: c) Loss of negative intrapleural pressure causes lung collapse.
Explanation: Boyle’s Law explains that when intrapleural pressure rises (air enters pleural space), pressure difference disappears, and lungs collapse as volume can’t expand. This understanding is crucial in diagnosing and managing pneumothorax with chest tube drainage to restore negative pressure and lung function.

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2012 NEET PG

Chapter: Gastrointestinal Physiology
Topic: Gastric Secretion and Vitamin Absorption
Subtopic: Intrinsic Factor and Cobalamin (Vitamin B12)

Keyword Definitions:

Intrinsic factor: Glycoprotein secreted by gastric parietal cells essential for vitamin B12 absorption.
Parietal cells: Gastric cells secreting hydrochloric acid and intrinsic factor.
Achlorhydria: Absence of gastric acid impairing release of B12 from dietary proteins.
Cobalamin (B12): Vitamin requiring intrinsic factor for ileal absorption; deficiency causes megaloblastic anemia and neuropathy.
Terminal ileum: Specific intestinal site for intrinsic factor–B12 complex uptake.

Lead Question - 2012

Gastric secretions are essential for absorption of -
a) Cobalmin
b) Fat
c) Thiamine
d) Folic acid

Explanation: Gastric acid and intrinsic factor are essential for vitamin B12 absorption. Acid releases B12 from dietary proteins; intrinsic factor from parietal cells binds B12 enabling ileal uptake. Without gastric secretion (achlorhydria or gastrectomy) cobalamin malabsorption occurs, causing pernicious anemia. Correct answer: a) Cobalamin. This is clinically important in elderly patients.

Guessed Question 1

Intrinsic factor is secreted by which gastric cell type?
a) Chief cells
b) Parietal cells
c) G cells
d) D cells

Explanation: Intrinsic factor is secreted by gastric parietal cells and is indispensable for vitamin B12 absorption in the terminal ileum. Loss of parietal cell function through autoimmune gastritis or gastrectomy eliminates intrinsic factor, producing cobalamin deficiency despite adequate intake. Correct answer: parietal cells. Monitor B12 in at-risk patients clinically.

Guessed Question 2

Pernicious anemia results from deficiency of which gastric product?
a) Pepsin
b) Intrinsic factor
c) Gastrin
d) Hydrochloric acid only

Explanation: Pernicious anemia results from autoimmune destruction of gastric parietal cells causing intrinsic factor deficiency and impaired vitamin B12 absorption. Clinical features include megaloblastic anemia, neurologic deficits, and elevated methylmalonic acid. Treatment requires parenteral or high-dose oral B12 replacement. Correct answer: pernicious anemia (intrinsic factor deficiency). Monitor hematologic and neurologic recovery.

Guessed Question 3

Long-term proton pump inhibitor use affects B12 how?
a) Increases absorption
b) Reduces release of dietary B12
c) Converts B12 to active form
d) No effect

Explanation: Acid suppression from long-term proton pump inhibitor therapy or atrophic gastritis reduces release of dietary B12 from proteins, impairing subsequent intrinsic factor binding and absorption. Over years this can cause B12 deficiency especially in elderly. Correct answer: acid suppression reduces vitamin B12 bioavailability causing deficiency risk. Monitor levels periodically.

Guessed Question 4

Vitamin B12–intrinsic factor complexes are absorbed in the:
a) Duodenum
b) Jejunum
c) Terminal ileum
d) Colon

Explanation: Vitamin B12 bound to intrinsic factor is specifically absorbed in the terminal ileum via receptor-mediated endocytosis. Ileal disease, resection, or bacterial overgrowth disrupts this process causing malabsorption despite normal intrinsic factor. Schilling test historically localized defects. Correct answer: terminal ileum. Clinically check B12, MMA, homocysteine levels and start replacement promptly.

Guessed Question 5

Which laboratory marker is most specific for early B12 deficiency?
a) Serum folate
b) Methylmalonic acid (MMA)
c) Serum iron
d) Alkaline phosphatase

Explanation: Methylmalonic acid and homocysteine accumulate in vitamin B12 deficiency; elevated methylmalonic acid is particularly specific for cobalamin deficiency versus folate deficiency. These biochemical markers detect early deficiency before hematologic changes appear. Treatment with B12 normalizes these metabolites. Correct answer: elevated methylmalonic acid indicates B12 deficiency. Order testing in suspected patients.

Guessed Question 6

Autoimmune gastritis increases risk of which condition related to B12?
a) Peptic ulcer only
b) Gastric carcinoma and carcinoid
c) Pancreatic insufficiency
d) Small bowel bacterial overgrowth only

Explanation: Autoimmune gastritis causing parietal cell loss and intrinsic factor deficiency increases risk of gastric carcinoid and adenocarcinoma due to chronic atrophic gastritis and hypergastrinemia. Vigilant surveillance and B12 replacement are necessary. Correct answer: autoimmune gastritis leads to pernicious anemia and increases gastric cancer risk. Monitor endoscopy periodically in such patients.

Guessed Question 7

Best initial therapy for pernicious anemia with neurologic signs is:
a) Oral folate
b) Parenteral vitamin B12
c) Iron supplements
d) High-dose vitamin C

Explanation: Parenteral intramuscular vitamin B12 bypasses the need for intrinsic factor and corrects hematologic and neurologic deficits; typical regimen includes loading doses then monthly injections. High-dose oral therapy may work by passive diffusion but is less reliable in severe deficiency. Correct answer: parenteral B12 therapy for pernicious anemia. Initiate promptly always.

Guessed Question 8

Which historical test localized cause of B12 malabsorption?
a) Breath test
b) Schilling test
c) Glucose tolerance test
d) D-xylose test

Explanation: The Schilling test historically distinguished malabsorption causes of B12 deficiency using radiolabeled cobalamin with and without intrinsic factor. It localized defects to pernicious anemia versus ileal disease or bacterial overgrowth, but availability ceased. Today clinicians rely on biochemical markers and imaging. Correct answer: Schilling test historically localized absorption defects now.

Guessed Question 9

Which anesthetic practice can precipitate neurologic deterioration in undiagnosed B12 deficiency?
a) Propofol infusion
b) Nitrous oxide exposure
c) Local anesthesia only
d) Spinal anesthesia

Explanation: Exposure to nitrous oxide oxidizes cobalt in cobalamin, inactivating methionine synthase and precipitating neuropathy and megaloblastic anemia in susceptible individuals. This risk increases with preexisting B12 deficiency. Avoid nitrous oxide anesthesia or supplement B12 when deficiency suspected. Correct answer: nitrous oxide inactivates vitamin B12 causing neurologic harm, particularly in elderly.

Guessed Question 10

Neurologic signs (eg, paresthesia, ataxia) distinguish which deficiency?
a) Folate deficiency only
b) Vitamin B12 deficiency
c) Iron deficiency only
d) Vitamin C deficiency

Explanation: Vitamin B12 deficiency produces neurologic manifestations such as peripheral neuropathy, dorsal column dysfunction, and cognitive changes, unlike folate deficiency which causes hematologic abnormalities without neurologic injury. Early recognition and treatment with B12 can reverse symptoms; delayed therapy may leave permanent deficits. Correct answer: neurologic signs are specific to B12 deficiency.

Chapter: Gastrointestinal Physiology
Topic: Lipid Digestion and Absorption
Subtopic: Pancreatic Lipase and Intestinal Fat Handling

Keyword Definitions:

Pancreatic lipase: Enzyme that hydrolyses triglycerides to free fatty acids and monoglycerides.
Co-lipase: Protein required for lipase binding to lipid droplets in the presence of bile salts.
Bile salts: Amphipathic molecules that emulsify fats and form micelles.
Micelle: Mixed bile salt aggregate that transports lipolytic products to enterocytes.
Chylomicron: Lipoprotein formed in enterocytes to carry re-esterified triglycerides via lymphatics.

Lead Question - 2012

Pancreatic lipase hydrolyses ester linkage of triacid glycerides at position?
a) 1 & 2
b) 1 & 3
c) 2 & 3
d) Only 3

Explanation:

Pancreatic lipase cleaves the ester bonds at the primary positions of triacylglycerols producing two free fatty acids and a 2-monoglyceride; this occurs at sn-1 and sn-3 positions and is essential for lipid absorption after emulsification. This specificity influences micelle formation and pancreatic insufficiency causes steatorrhea. Answer: b) 1 & 3.

Guessed Question 1

Co-lipase is required to?
a) Enhance lipase binding to lipid interface
b) Inhibit lipase activity
c) Phosphorylate lipase
d) Substitute for bile salts

Explanation:

Pancreatic co-lipase, secreted as procolipase activated by trypsin, anchors pancreatic lipase to lipid-water interfaces overcoming bile salt inhibition, facilitating triglyceride hydrolysis and efficient fat digestion; absence impairs fat absorption. Clinically significant in cystic fibrosis where co-lipase deficiency contributes to steatorrhea often. Answer: a) Enhance lipase binding.

Guessed Question 2

Bile salts primarily function to?
a) Emulsify fats and form micelles
b) Inhibit pancreatic lipase permanently
c) Hydrolyse triglycerides enzymatically
d) Absorb proteins

Explanation:

Bile salts, amphipathic molecules synthesized from cholesterol and secreted into duodenum, emulsify dietary lipids, increase surface area for pancreatic lipase action, and form mixed micelles carrying monoglycerides and fatty acids to enterocytes for absorption; impaired bile salt secretion causes fat malabsorption. Answer: a) Emulsify fats and form micelles, clinically significant.

Guessed Question 3

Orlistat treats obesity by?

a) Inhibiting pancreatic lipase
b) Stimulating bile production
c) Blocking micelle formation
d) Increasing chylomicron secretion

Explanation:

Orlistat irreversibly inhibits gastric and pancreatic lipases in the intestinal lumen, preventing hydrolysis of triglycerides into absorbable free fatty acids and monoglycerides; unabsorbed fats cause oily stools and reduced caloric uptake aiding weight loss, but may provoke fat-soluble vitamin deficiency. Answer: a) Inhibiting pancreatic lipase, monitor vitamins and supplement accordingly.

Guessed Question 4

Gastric lipase preferentially hydrolyses which position on triglycerides?
a) 1 & 2
b) 1 & 3
c) 2 & 3
d) Only 3

Explanation:

Gastric lipase, secreted by chief cells, begins triglyceride digestion in the stomach by hydrolyzing ester bonds preferentially at the sn-3 position, producing diglycerides and free fatty acids; its activity is acid-stable and complements pancreatic lipase, particularly in neonates and individuals with pancreatic insufficiency. Answer: d) Only 3, clinically relevant for infants.

Guessed Question 5

Long-chain fatty acids are mainly absorbed in the?
a) Ileum
b) Jejunum
c) Colon
d) Stomach

Explanation:

Long-chain fatty acids and monoglycerides form mixed micelles with bile salts in the intestinal lumen, facilitating diffusion into jejunal enterocytes where they are re-esterified to triglycerides, packaged into chylomicrons and secreted via lymphatics; ileal bile salt reabsorption maintains enterohepatic circulation. Answer: b) Jejunum, critical for fat nutrition and lipid disorders.

Guessed Question 6

Fat malabsorption with steatorrhea is classically seen in?
a) Cystic fibrosis
b) Iron deficiency anemia
c) Lactose intolerance
d) Ulcerative colitis

Explanation:

Pancreatic exocrine insufficiency, as seen in cystic fibrosis, reduces pancreatic lipase secretion causing fat malabsorption and steatorrhea; patients present with bulky foul-smelling stools, weight loss, and fat-soluble vitamin deficiencies requiring pancreatic enzyme replacement and nutritional support to prevent growth failure. Answer: a) Cystic fibrosis, particularly in homozygous CFTR mutations patients.

Guessed Question 7

Bile salts at high concentration affect lipase how?
a) Inhibit lipase unless co-lipase present
b) Always activate lipase
c) Hydrolyse lipids independently
d) Convert lipase to inactive form permanently

Explanation:

High bile salt concentrations can inhibit pancreatic lipase binding to lipid droplets; colipase displaces bile salts and anchors lipase enabling triglyceride hydrolysis. Bile salt deficiency causes malabsorption; this mechanism explains impaired fat digestion in cholestasis. Answer: a) Inhibit lipase, clinically important in surgical and hepatic disease today often.

Guessed Question 8

Short and medium chain fatty acids are absorbed via?
a) Chylomicrons into lymphatics
b) Portal vein into liver directly
c) Remain in lumen
d) Excreted unchanged

Explanation:

Short-chain fatty acids and medium-chain triglyceride products are absorbed directly into the portal circulation without incorporation into chylomicrons, providing more rapid hepatic delivery and utility in patients with lymphatic or fat malabsorption; this property underlies use of medium-chain triglyceride formulas in certain clinical settings. Answer: b) Portal vein absorption clinically.

Guessed Question 9

Fat soluble vitamins require what for absorption?
a) Presence of dietary fat and micelles
b) Free water only
c) Protein carriers only
d) Bacterial fermentation

Explanation:

Fat-soluble vitamins A, D, E, and K are incorporated into micelles with dietary lipids and require bile salts and pancreatic lipase activity for efficient absorption; fat malabsorption or cholestasis leads to deficiencies necessitating supplementation, often using water-miscible or parenteral forms. Answer: a) Presence of dietary fat in clinical practice.

Guessed Question 10

Chylomicrons are secreted into?
a) Portal vein
b) Intestinal lymphatics (lacteals)
c) Directly into bloodstream at capillaries
d) Bile

Explanation:

Enterocytes re-esterify absorbed long-chain fatty acids into triglycerides, incorporate them into chylomicrons, and secrete these lipoproteins into intestinal lacteals (lymphatic capillaries), bypassing the portal vein; lymphatic transport delivers dietary lipids to the systemic circulation via thoracic duct. Answer: b) Lymphatics (lacteals) for chylomicron transport important in surgical resection of nodes.

Chapter: Gastrointestinal Physiology
Topic: Intestinal Absorption of Carbohydrates
Subtopic: Monosaccharide Transport and Clinical Correlates

Keyword Definitions:

Hexose: Six-carbon monosaccharides (eg, glucose, fructose) absorbed rapidly from intestine.
Pentose: Five-carbon sugars (eg, ribose) less relevant for dietary absorption.
Disaccharide: Two monosaccharide units (eg, sucrose, lactose) requiring brush border hydrolysis.
Polysaccharide: Long carbohydrate polymers (eg, starch) broken down to monosaccharides before absorption.
SGLT1 / GLUT5 / GLUT2: Key intestinal transporters for glucose/galactose and fructose and basolateral exit.

Lead Question - 2012

Which is maximally absorbed from GIT ?
a) Pentose
b) Hexose
c) Disaccharide
d) Polysaccharide

Explanation: Hexoses such as glucose are maximally absorbed as monosaccharides via specific transporters; they undergo brush border hydrolysis if from disaccharides and then enter enterocytes by sodium dependent and facilitated transporters. This efficient uptake underlies oral rehydration therapy. Answer: b) Hexose.

Question 2

Primary apical transporter for glucose and galactose absorption is?
a) SGLT1
b) GLUT2
c) Na+/K+ ATPase
d) GLUT5

Explanation: Sodium glucose cotransporter 1 (SGLT1) on the apical membrane mediates active uptake of glucose and galactose using the sodium gradient; basolateral GLUT2 completes exit to blood. SGLT1 function is crucial for nutrient absorption and oral rehydration effectiveness. Answer: a) SGLT1.

Question 3

Fructose uptake across apical membrane is mediated by?
a) SGLT1
b) GLUT2
c) GLUT5
d) Na+/K+ ATPase

Explanation: Fructose is absorbed by facilitated diffusion via GLUT5 on the apical membrane and exits via GLUT2 basolaterally; unlike glucose, fructose uptake is sodium independent. Fructose malabsorption causes osmotic diarrhoea and bloating. Answer: c) GLUT5.

Question 4

Lactose intolerance results from deficiency of which enzyme?
a) Sucrase
b) Lactase
c) Maltase
d) Amylase

Explanation: Lactase deficiency in the brush border prevents lactose hydrolysis, allowing unabsorbed disaccharide to reach colon where bacteria ferment it producing gas and osmotic diarrhoea; hydrogen breath test confirms diagnosis. Management includes lactase enzyme replacement or dairy restriction. Answer: b) Lactase deficiency.

Question 5

Oral rehydration therapy primarily depends on which mechanism?
a) Passive diffusion of glucose
b) Fructose facilitated diffusion
c) Active Na+ pump alone
d) Sodium-glucose cotransport

Explanation: Oral rehydration therapy exploits sodium glucose cotransport in the small intestine to enhance passive water absorption, effectively treating diarrhoeal dehydration. Glucose must be present at optimal concentration; hypotonic or hypertonic solutions are less effective. Answer: d) Sodium-glucose cotransport.

Question 6

Sucrase-isomaltase deficiency leads to intolerance of which sugar?
a) Sucrose
b) Glucose
c) Fructose
d) Lactose

Explanation: Sucrase-isomaltase deficiency impairs brush-border hydrolysis of sucrose and some starch breakdown products, causing sucrose intolerance with abdominal pain and osmotic diarrhoea when sucrose is ingested. Genetic testing confirms diagnosis; treatment is dietary sucrose avoidance and probiotics. Answer: a) Sucrase-isomaltase deficiency.

Question 7

SGLT2 inhibitors treat diabetes by acting on which site/process?
a) Enhance SGLT2 activity
b) Inhibit SGLT1
c) Inhibit SGLT2
d) Block GLUT2

Explanation: SGLT2 inhibitors block renal proximal tubule glucose reabsorption, promoting glycosuria to lower blood glucose in diabetes; intestinal absorption unaffected but systemic glucose handling changes. Side effects include urinary infections and dehydration. They reduce cardiovascular risk in many patients. Answer: c) Inhibit SGLT2.

Question 8

Hereditary fructose intolerance is due to deficiency of?
a) Fructokinase
b) Aldolase B
c) Hexokinase
d) Sucrase

Explanation: Hereditary fructose intolerance results from aldolase B deficiency impairing hepatic fructose metabolism; unabsorbed fructose contributes to osmotic symptoms, while absorbed fructose metabolism causes hypoglycaemia, vomiting, and hepatic dysfunction after ingestion. Early recognition prevents liver failure in childhood. Answer: b) Aldolase B deficiency.

Question 9

Which carbohydrate form requires brush border hydrolysis before absorption?
a) Disaccharide
b) Monosaccharide
c) Sugar alcohol
d) Short chain fatty acid

Explanation: Disaccharides like sucrose and lactose require brush-border disaccharidases (sucrase, lactase) to hydrolyse them into monosaccharides before uptake; failure causes malabsorption and osmotic diarrhoea. Pediatric screening is important in persistent diarrhoea. Answer: a) Disaccharide.

Question 10

Which structural feature most increases intestinal absorptive capacity for sugars?
a) Crypts
b) Serosa
c) Submucosa
d) Villi and microvilli

Explanation: Small intestinal mucosal surface area increases absorption through villi and microvilli, particularly in the jejunum where carbohydrate uptake is maximal; surgical resection reduces capacity causing malabsorption and nutritional deficiencies. Adaptive changes occur, but patients may need dietary modification and supplementation. Answer: d) Villi and microvilli.

Question 11

Carbohydrate absorption is maximal in which intestinal segment?
a) Ileum
b) Jejunum
c) Colon
d) Duodenum only

Explanation: Carbohydrate absorption predominantly occurs in the jejunum where high transporter density, rich blood flow, and ample villous surface facilitate rapid uptake of monosaccharides; ileal and colonic absorption are limited. Surgical loss of jejunum markedly impairs carbohydrate absorption in many cases. Answer: b) Jejunum.

Chapter: Gastrointestinal Physiology
Topic: Gastrointestinal Motility
Subtopic: Motilin and Migrating Motor Complex

Keyword Definitions:

Motilin: Peptide hormone released by M cells of the small intestine that regulates interdigestive motility.
Migrating Motor Complex (MMC): Cyclic interdigestive motor pattern clearing stomach and small intestine between meals.
Phase III: The strong, regular contractile phase of the MMC associated with motilin peaks.
Erythromycin: Macrolide antibiotic that acts as a motilin receptor agonist and prokinetic.
CCK: Cholecystokinin, a meal-stimulated hormone that suppresses motilin and MMC activity.

Lead Question - 2012

Motilin secretion decreased in ?
a) Thirsty
b) Starving
c) Ingested meal
d) Interdigestive state

Explanation: Motilin secretion falls after a meal; it is highest during fasting interdigestive migrating motor complex. Ingested meal suppresses motilin release via hormonal and neural signals, inhibiting phase III MMC. Therefore secretion decreases in response to an ingested meal. Answer: c) Ingested meal, and explains reduced interdigestive contractions after eating commonly.

Guessed Question 1

Motilin levels are highest in which state?
a) Postprandial
b) Interdigestive state
c) During exercise
d) During stress

Explanation: Motilin levels peak during the interdigestive phase, organizing migrating motor complex phase III contractions that sweep residual contents through the stomach and small intestine; fasting stimulates its release while feeding suppresses it. Clinically, this pattern maintains gut clearance between meals and prevents bacterial overgrowth in small bowel.

Guessed Question 2

Which drug acts as a motilin receptor agonist and promotes gastric emptying?
a) Metoclopramide
b) Erythromycin
c) Omeprazole
d) Loperamide

Explanation: Erythromycin acts as motilin receptor agonist, stimulating phase III MMC and producing strong antral and duodenal contractions; it is used prokinetically for gastroparesis and to promote gastric emptying, though tachyphylaxis limits long-term benefit. Short courses help improve symptoms and facilitate enteral feeding in critically ill patients often.

Guessed Question 3

Motilin receptors are located on?
a) Pancreatic acini only
b) Hepatocytes
c) Enteric neurons and smooth muscle
d) Salivary glands

Explanation: Motilin receptors are located on enteric neurons and smooth muscle cells in the stomach and small intestine, mediating cyclic interdigestive contractions; receptor activation increases acetylcholine release and myoelectric activity, coordinating MMC. Therapeutically, receptor agonists enhance gastric motility in clinical prokinetic therapy for gastroparesis.

Guessed Question 4

Which hormone suppresses motilin secretion after a meal?
a) Cholecystokinin (CCK)
b) Ghrelin
c) Gastrin
d) Secretin

Explanation: Cholecystokinin released in response to nutrients during feeding suppresses motilin secretion, terminating phase III MMC and shifting motility to digestive patterns; this hormonal interplay ensures coordinated digestion and absorption after meals. Clinical relevance includes disrupted motilin-CCK balance affecting gastric emptying and symptoms.

Guessed Question 5

Motilin primarily stimulates which component of motility?
a) Gastric accommodation
b) Phase III MMC contractions
c) Colonic segmentation
d) Resting tone only

Explanation: Motilin release triggers phase III of the migrating motor complex, producing powerful, rhythmic contractions that clear stomach and small intestine between meals, preventing stasis and bacterial overgrowth; loss of this mechanism contributes to gastroparesis and small bowel bacterial proliferation. This function is used diagnostically and therapeutically sometimes.

Guessed Question 6

Diabetic autonomic neuropathy affects motilin how?
a) Increases motilin release
b) Unrelated to motilin
c) Reduces motilin action
d) Converts motilin to inactive form

Explanation: In diabetes mellitus autonomic neuropathy impairs motilin-mediated migrating motor complex generation, contributing to gastroparesis with delayed gastric emptying, nausea, and vomiting; prokinetic agents targeting motilin receptors or erythromycin analogs can transiently improve symptoms, but glycemic control and neuropathy management remain essential, clinically important.

Guessed Question 7

Motilin receptor agonists are primarily used to treat?
a) Constipation predominance IBS
b) Gastroparesis
c) Peptic ulcer disease
d) Gastroesophageal reflux

Explanation: Motilin receptor agonists, like erythromycin, are used as prokinetic agents to enhance gastric emptying in gastroparesis and to facilitate enteral feeding in critically ill patients; effectiveness wanes due to tachyphylaxis, and side effects include QT prolongation and microbial resistance concerns limiting long-term use in clinical practice.

Guessed Question 8

Exogenous motilin administration would most directly cause?
a) Increased acid secretion
b) Constipation
c) Relaxation of sphincters only
d) Induction of phase III contractions

Explanation: Exogenous motilin administration induces powerful interdigestive phase III contractions, increasing gastrointestinal motility and accelerating gastric emptying; experimental use defines receptor pharmacology and validates motilin’s physiological role. Therapeutically, direct motilin analogs could treat hypomotility, but side effects and receptor desensitization limit current clinical application now.

Guessed Question 9

Typical periodicity of motilin peaks during fasting is about?
a) 20–30 minutes
b) 90–120 minutes
c) 6–8 hours
d) 24 hours

Explanation: Motilin secretion occurs cyclically every ninety to one hundred twenty minutes during fasting, correlating with migrating motor complex cycles; this rhythmic release organizes interdigestive cleansing waves, and disruption predisposes to bacterial overgrowth and dysmotility. Therapeutic modulation adjusts gastrointestinal clearance; clinically relevant in feeding protocols today.

Guessed Question 10

Motilin exerts its effects via which receptor class?
a) G-protein-coupled receptors (GPCRs)
b) Intracellular steroid receptors
c) Tyrosine kinase receptors
d) Ionotropic receptors

Explanation: Motilin acts via specific G-protein-coupled receptors on GI smooth muscle and enteric neurons, activating intracellular signaling that increases calcium and contractility; receptor identification enabled development of agonists and antagonists with prokinetic potential, although clinical translation faces tachyphylaxis and safety challenges limiting long-term therapeutic use in practice.

Chapter: Gastrointestinal Physiology
Topic: Gastric Secretion
Subtopic: Inhibitors and Stimulators of Acid Secretion

Keyword Definitions:

Secretin: Duodenal hormone that inhibits gastric secretion and stimulates pancreatic bicarbonate.
Gastrin: Antral hormone that stimulates acid secretion and mucosal growth.
Somatostatin: Paracrine inhibitor of gastrin and acid secretion from D cells.
Vagus (ACh/GRP): Parasympathetic pathway stimulating gastric secretion in cephalic and gastric phases.
H2 blockers / PPIs: Drugs that inhibit histamine receptors or the proton pump to reduce acid.

Lead Question - 2012

Which inhibits gastric secretion ?
a) Secretin
b) Insulin
c) High gastric pH
d) Calcium

Explanation: Secretin, released by S cells in the duodenum in response to acid, inhibits gastric acid secretion directly and indirectly by antagonizing gastrin effects and reducing gastric motility; therefore secretin suppresses gastric secretion and coordinates pancreatic bicarbonate secretion for neutralization of acid. Answer: a) Secretin.

Guessed Question 1

Secretin is released primarily in response to?
a) Acid in duodenum
b) Fat in stomach
c) Protein in stomach
d) Distension of stomach

Explanation: Secretin is secreted by duodenal S cells when acidic gastric chyme enters the proximal small intestine; low luminal pH stimulates release, which then inhibits gastric secretion while promoting pancreatic bicarbonate and biliary alkalinizing secretions to neutralize acid during digestion of meals. Answer: a) Acid in duodenum.

Guessed Question 2

Which hormone most strongly stimulates gastric acid secretion?
a) Gastrin
b) Secretin
c) Somatostatin
d) CCK

Explanation: Gastrin, released from antral G cells in response to peptides, amino acids and vagal stimulation, strongly stimulates parietal cell acid secretion and mucosal growth by direct action and via enterochromaffin-like cell histamine release; thus gastrin is a major stimulant of gastric secretion. Answer: a) Gastrin.

Guessed Question 3

Which drug class blocks histamine-mediated acid amplification?
a) H2 receptor antagonists
b) Proton pump inhibitors
c) Anticholinergics
d) Antacids

Explanation: H2 receptor antagonists such as ranitidine competitively block histamine action on parietal cell H2 receptors, reducing cyclic AMP-mediated stimulation of the proton pump and lowering gastric acid secretion; they attenuate basal and nocturnal acid output but are less potent than proton pump inhibitors for ulcer healing. Answer: a) H2 receptor antagonists.

Guessed Question 4

Antimuscarinic drugs (eg, atropine) affect gastric secretion by?
a) Increasing secretion
b) Decreasing secretion
c) No effect
d) Stimulating gastrin release

Explanation: Atropine, a muscarinic antagonist, blocks vagally mediated acetylcholine actions on parietal and chief cells and reduces gastrin release by inhibiting GRP-mediated G cell stimulation, thereby markedly decreasing gastric acid secretion; it demonstrates the prominent cholinergic contribution to the cephalic and gastric phases. Answer: b) Decreasing secretion.

Guessed Question 5

Truncal vagotomy produces which effect on gastric secretion?
a) Increased secretion
b) Abolished cephalic response
c) No change
d) Increased gastrin only

Explanation: Truncal vagotomy abolishes vagal efferent stimulation of gastric secretory mechanisms by interrupting parasympathetic fibers, markedly reducing cephalic-phase and gastric-phase acid output; postoperative patients require acid suppression and dietary adjustments, illustrating the crucial role of vagal pathways in initiating and sustaining gastric secretion. Answer: b) Abolished cephalic response.

Guessed Question 6

Secretin’s main intestinal role is to stimulate?
a) Pancreatic bicarbonate secretion
b) Gastrin release
c) Acid secretion
d) Gallbladder contraction

Explanation: Secretin, released by S cells in response to acidic chyme, primarily stimulates pancreatic ductal cells to secrete bicarbonate-rich fluid, neutralizing duodenal pH to optimize digestive enzyme function and protecting mucosa; it indirectly reduces gastric acid secretion, coordinating intestinal digestion. Answer: a) Pancreatic bicarbonate secretion.

Guessed Question 7

Stomach distension affects gastric secretion by?
a) Decreasing acid output
b) Increasing acid output via reflexes
c) No effect
d) Only affects motility

Explanation: Gastric distension activates vagovagal and enteric reflexes that stimulate parietal cells both directly and indirectly via gastrin release, significantly increasing acid secretion and motility to facilitate mechanical and chemical digestion; this gastric-phase response accounts for the majority of meal-stimulated acid output. Answer: b) Increasing acid output via reflexes.

Guessed Question 8

Sympathetic activity and noradrenaline generally cause what change in gastric secretion?
a) Strong stimulation
b) Inhibition of secretion
c) No effect
d) Variable increase

Explanation: Sympathetic activation and noradrenaline release inhibit gastric secretion by reducing blood flow, suppressing vagal tone, and directly acting on parietal cells; during acute stress, digestive processes are downregulated favoring cardiovascular redistribution, which clinically manifests as decreased acid output and impaired gastric motility. Answer: b) Inhibition of secretion.

Guessed Question 9

Which paracrine factor inhibits gastrin and acid secretion?
a) Somatostatin
b) Histamine
c) GRP
d) CCK

Explanation: Somatostatin, released from gastric D cells in response to low luminal pH and vagal inhibition withdrawal, exerts potent inhibitory effects on gastric secretion by suppressing gastrin release and directly inhibiting parietal cell acid production; it serves as a physiological brake limiting excess acidity and protecting mucosa clinically. Answer: a) Somatostatin.

Guessed Question 10

Which therapeutic class irreversibly inhibits the proton pump reducing acid secretion most profoundly?
a) Antacids
b) H2 blockers
c) Antimuscarinics
d) Proton pump inhibitors

Explanation: Proton pump inhibitors irreversibly inhibit parietal cell H+/K+ ATPase, the final common pathway of acid secretion, producing profound sustained reduction in gastric acidity and promoting ulcer healing; they are more effective than H2 blockers for acid suppression and widely used in modern gastroenterology practice. Answer: d) Proton pump inhibitors.

Chapter: Gastrointestinal Physiology
Topic: Gastric Secretion
Subtopic: Neural and Hormonal Control of Acid Secretion

Keyword Definitions:

Cephalic phase: Early neural phase of secretion triggered by sight, smell, thought, or taste of food.
Gastric phase: Secretion stimulated by stomach distension and food presence.
Vagal stimulation: Parasympathetic drive (acetylcholine, GRP) increasing acid and pepsinogen release.
Enterochromaffin-like (ECL) cells: Release histamine to amplify parietal cell acid secretion.
Parietal cell: Gastric cell secreting HCl via H+/K+ ATPase.

Lead Question - 2012

Gastric secretion is :
a) Inhibited by curare
b) Stimulated by nor adrenaline
c) Increased by stomach distention
d) Stimulated by an increase in tonic activity

Explanation: Stomach distension activates enteric and vagovagal reflexes, increasing gastrin release and acid secretion during the gastric phase, enhancing digestion and protein breakdown; pharmacologic agents like curare do not inhibit secretion directly, while noradrenaline tends to suppress it. This mechanism promotes efficient nutrient absorption and motility. Answer: c) Increased by stomach distention

Guessed Question 1

Vagal stimulation affects gastric secretion by?
a) Increasing secretion
b) Decreasing secretion
c) No effect
d) Only affects motility

Explanation: Vagal stimulation releases acetylcholine and GRP, directly stimulating parietal and G cells to enhance acid secretion and pepsinogen release; this neural drive is essential for cephalic and gastric phases. Pharmacologic vagotomy abolishes this response. Answer: a) Vagus nerve stimulation increases gastric secretion by cholinergic mechanisms during anticipatory feeding and digestion.

Guessed Question 2

Noradrenaline on gastric secretion is usually?
a) Stimulative
b) Inhibitory
c) Neutral
d) Variable

Explanation: Noradrenaline released during sympathetic activation reduces gastric secretion by vasoconstriction, diminished gastric blood flow, and inhibition of acid production through decreased vagal tone and direct receptor-mediated actions on parietal cells. Stress responses particularly during acute fight-or-flight inhibit digestion. Answer: b) Noradrenaline inhibits gastric secretion overall.

Guessed Question 3

Histamine’s role in acid secretion is to?
a) Inhibit parietal cells
b) Stimulate gastrin only
c) Stimulate parietal cells via H2 receptors
d) Block vagal action

Explanation: Enterochromaffin-like cells release histamine in response to gastrin and vagal stimulation; histamine acts on H2 receptors of parietal cells, amplifying acid secretion via cAMP pathway and potentiating cholinergic and gastrin effects, making H2 blockade clinically effective for acid suppression. Answer: c) Histamine strongly stimulates gastric acid secretion in peptic disease.

Guessed Question 4

Curare (a neuromuscular blocker) does what to gastric secretion?
a) Inhibits it
b) Stimulates it
c) No direct inhibition
d) Causes hypersecretion

Explanation: Curare, a neuromuscular blocker, inhibits nicotinic receptors at the neuromuscular junction causing paralysis but does not directly reduce gastric secretion because gastric cholinergic control uses muscarinic receptors and vagal pathways; therefore curare has minimal effect on acid output compared with antimuscarinics. Answer: a) Curare does not inhibit gastric secretion clinically.

Guessed Question 5

Atropine’s effect on gastric secretion is to?
a) Increase
b) Decrease
c) No effect
d) Only affect motility

Explanation: Atropine blocks muscarinic M3 receptors on parietal and ECL cells, preventing acetylcholine-mediated stimulation of acid and pepsinogen secretion during cephalic and gastric phases, significantly reducing gastric juice volume and acidity; clinically used experimentally to demonstrate vagal contribution. This effect reduces ulcer risk significantly. Answer: b) Atropine inhibits gastric secretion markedly.

Guessed Question 6

Primary physiological stimuli for gastrin release include?
a) Low pH only
b) Proteins and vagal GRP
c) Fats in the ileum
d) Glucose exclusively

Explanation: Gastrin secretion from antral G cells is stimulated primarily by peptides and amino acids in the stomach and by vagal release of gastrin-releasing peptide; gastric distension indirectly increases gastrin via vagal reflexes. Gastrin enhances acid secretion and mucosal growth. Answer: c) Proteins and vagal GRP stimulate gastrin release.

Guessed Question 7

H2 receptor antagonists reduce acid secretion by blocking?
a) Muscarinic receptors
b) Histamine action on parietal cells
c) Gastrin receptors
d) Proton pump directly

Explanation: H2 receptor antagonists block histamine-mediated stimulation of parietal cells, reducing basal and nocturnal gastric acid secretion and ameliorating peptic ulcer disease; they diminish the amplifying effect of histamine while vagal and gastrin stimuli persist. Clinically useful but superseded by PPIs for maximal acid suppression. Answer: b) H2 blockers decrease acid.

Guessed Question 8

Proton pump inhibitors act by inhibiting?
a) H2 receptor
b) Muscarinic receptor
c) Gastrin release
d) H+/K+ ATPase

Explanation: Proton pump inhibitors irreversibly inhibit the parietal cell H+/K+ ATPase, producing profound and prolonged suppression of gastric acid secretion, promoting ulcer healing and reducing acid-related symptoms; they block final common pathway of acid secretion despite ongoing vagal, gastrin, or histamine stimulation. Answer: d) PPIs markedly reduce gastric secretion clinically essential.

Guessed Question 9

The gastric phase contributes approximately what percent of total acid secretion?
a) 20%
b) 70%
c) 10%
d) 100%

Explanation: The gastric phase, triggered by food presence and stomach distension, accounts for the majority—approximately seventy percent—of total acid secretion through local stretch receptors, enteric reflexes, vagal stimulation, and gastrin release from antral G cells; this phase sustains and amplifies cephalic signals during a meal. Answer: b) 70% clinically relevant observation.

Guessed Question 10

Does increased tonic vagal activity stimulate gastric secretion?
a) No effect
b) Strongly decreases secretion
c) Only affects motility
d) Modestly increases secretion

Explanation: An increase in tonic vagal activity elevates baseline gastric acid secretion by sustained acetylcholine release, but modestly compared with phasic stimuli; tonic firing maintains parietal cell readiness and potentiates responses to meals. Pathologic vagal overactivity can enhance acid-related disease in chronic settings. Answer: d) Increased tonic activity modestly stimulates secretion.

Chapter: Gastrointestinal Physiology
Topic: Gastric Secretion
Subtopic: Cephalic Phase

Keyword Definitions:

Cephalic phase: Anticipatory secretion triggered by sight, smell, taste, and thoughts of food.
Vagus nerve: Parasympathetic efferent pathway driving cephalic responses.
GRP: Gastrin-releasing peptide; vagal neurotransmitter stimulating G cells.
Gastrin: Hormone from G cells that augments acid secretion and motility.
ECL cell: Enterochromaffin-like cell releasing histamine to stimulate parietal cells.
Parietal cell: Acid-secreting gastric cell expressing H+/K+ ATPase and H2 receptors.
PPI: Proton pump inhibitor blocking the H+/K+ ATPase.
Vagotomy: Surgical interruption of vagal efferents to the stomach.

Lead Question - 2012

Cephalic phase of gastric secretion ?
a) On food entering stomach
b) On food entering intestine
c) On seeing food
d) On stress

Explanation: Cephalic phase is triggered by sight, smell, taste, and thoughts of food before any gastric distension. Vagal efferents release acetylcholine and GRP, stimulating parietal cells and G cells to secrete acid and gastrin. Therefore, it begins on seeing food. Answer: c) On seeing food. via conditioned reflexes enhancing digestive readiness.

Guessed Question 1

Primary neural pathway mediating the cephalic phase?
a) Vagus nerve
b) Sympathetic chain
c) Somatic motor fibers
d) Enteric neurons only

Explanation: The cephalic phase is predominantly neurogenic, carried by parasympathetic vagal efferents from the dorsal motor nucleus of the vagus. Acetylcholine stimulates parietal and chief cells, while GRP stimulates G cells. Sympathetic activity does not initiate this phase. Answer: a) Vagus nerve. Mediates anticipatory secretion before food reaches the stomach lumen.

Guessed Question 2

Which drug most specifically diminishes cephalic-phase acid secretion?
a) Atropine
b) Omeprazole
c) Ranitidine
d) Bethanechol

Explanation: Vagally mediated cephalic secretion relies on muscarinic M3 receptors on parietal cells and ECL cells. Atropine blocks these receptors, reducing acetylcholine effects and diminishing cephalic acid output. PPIs suppress acid downstream but do not specifically block the phase’s neural trigger. Answer: a) Atropine (antimuscarinic), thereby decreasing conditioned preprandial gastric secretion.

Guessed Question 3

Which hormone rises during the cephalic phase?
a) Gastrin
b) Secretin
c) Cholecystokinin (CCK)
d) Somatostatin

Explanation: Vagal efferents release gastrin-releasing peptide onto antral G cells, increasing gastrin before food enters the stomach. Gastrin augments parietal acid secretion and histamine release from enterochromaffin-like cells. Secretin and CCK belong to intestinal responses; somatostatin inhibits secretion. Answer: a) Gastrin, key mediator of cephalic priming for efficient protein digestion later.

Guessed Question 4

Effect of truncal vagotomy on cephalic-phase gastric acid output?
a) Increased
b) Abolished
c) Unchanged
d) Slightly reduced

Explanation: Truncal vagotomy interrupts parasympathetic efferents from the dorsal motor nucleus, abolishing cephalic-phase cholinergic and GRP signaling. Preprandial acid secretion falls markedly; postprandial output relies on remaining local and hormonal pathways. Historically used for ulcer control before PPIs. Answer: b) Abolished, demonstrating the essential neural drive initiating anticipatory gastric secretion reflexes.

Guessed Question 5

Approximate contribution of the cephalic phase to total acid output?
a) Approximately 20%
b) Approximately 50%
c) Approximately 70%
d) Approximately 5%

Explanation: The cephalic phase typically accounts for approximately twenty percent of total gastric acid secretion, activated by conditioned stimuli and vagal efferents before food arrives. The gastric phase contributes most output, while the intestinal phase is modest. Recognizing these proportions aids exam reasoning and clinical therapy. Answer: a) Approximately 20% overall.

Guessed Question 6

Brainstem nucleus providing efferents for cephalic responses?
a) Nucleus ambiguus
b) Dorsal motor nucleus of vagus
c) Nucleus tractus solitarius
d) Arcuate nucleus

Explanation: Cephalic responses integrate cortical and limbic inputs to the dorsal motor nucleus of the vagus in the medulla. This nucleus provides preganglionic parasympathetic efferents to stomach, initiating acetylcholine and GRP release. Nucleus ambiguus mainly supplies cardiac motility, not acid secretion. Answer: b) Dorsal motor nucleus of the vagus medulla center.

Guessed Question 7

Cell releasing histamine that amplifies cephalic-induced acid secretion?
a) Chief cell
b) D cell
c) Enterochromaffin-like cell
d) Surface mucous cell

Explanation: During cephalic stimulation, acetylcholine also activates enterochromaffin-like cells, releasing histamine, which binds H2 receptors on parietal cells to amplify acid secretion. This paracrine pathway complements gastrin and cholinergic stimulation. H1 receptors are irrelevant for acid secretion. Answer: c) Enterochromaffin-like (ECL) cells, targeted by H2 receptor blockers like ranitidine historically therapeutically.

Guessed Question 8

Which situation most suppresses cephalic-phase secretion?
a) Pleasant food aroma
b) Severe pain or anxiety
c) Chewing sugarless gum
d) Conditioned dinner bell

Explanation: Sympathetic activation during severe pain or anxiety reduces vagal outflow and inhibits conditioned cephalic responses, lowering preprandial acid secretion. In contrast, appetitive cues like aromas, chewing, or conditioned signals enhance vagal activity. Therefore, sympathetic arousal suppresses this phase. Answer: b) Severe pain/anxiety, diminishing anticipatory gastric priming before meals clinically observed.

Guessed Question 9

On long-term PPI therapy, which change reflects upstream cephalic signaling despite low acidity?
a) Gastrin increases
b) Secretin increases
c) Somatostatin increases
d) Pepsinogen decreases

Explanation: Proton pump inhibitors block parietal H+/K+ ATPase, reducing luminal acidity and removing negative feedback on G cells. Gastrin release increases (hypergastrinemia), although acid remains low because pumps are inhibited. Vagal triggers of the cephalic phase persist. Answer: a) Gastrin increases, clinically relevant when interpreting fasting gastrin tests during therapy monitoring.

Guessed Question 10

Sham feeding (chew and spit) predominantly elicits which phase?
a) Cephalic phase
b) Gastric phase
c) Intestinal phase
d) Postabsorptive phase

Explanation: Sham feeding involves tasting, chewing, and spitting without swallowing. Sensory cues stimulate cortical pathways and vagal efferents, producing cephalic-phase gastric, pancreatic, and biliary secretions without gastric distension. It demonstrates neural control independent of luminal nutrients. Answer: a) Cephalic phase, useful experimentally and clinically to assess vagal integrity and appetite mechanisms.

Chapter: Gastrointestinal Physiology
Topic: Gastric Secretion
Subtopic: Cephalic Phase of Gastric Secretion

Keyword Definitions:

Cephalic phase: Early phase of gastric secretion triggered by sight, smell, taste, and thought of food.
Vagus nerve: Parasympathetic pathway mediating much of the cephalic response via acetylcholine.
GRP: Gastrin-releasing peptide; stimulates G cells to release gastrin.
Gastrin: Hormone that promotes acid secretion and gastric motility.
Atropine: Antimuscarinic drug that blocks vagal effects on stomach.

Lead Question - 2012

Cephalic phase of gastric secretion ?
a) 20%
b) 70 %
c) 10%
d) 100%

Explanation: Cephalic phase, mediated by vagal stimulation triggered by sight, smell, taste, and thought of food, initiates gastric secretion before food enters stomach. It accounts for approximately twenty percent of total gastric acid secretion through vagovagal reflexes and gastrin release, which primes stomach for efficient digestion and absorption. Answer: a) 20%.

Guessed Question 1

The primary mediator of the cephalic phase is?
a) Vagus nerve
b) Sympathetic nerve
c) Enteric nervous system only
d) Somatic motor nerve

Explanation: Vagal parasympathetic efferents release acetylcholine at gastric mucosa during the cephalic phase, directly stimulating parietal cell acid secretion, and indirectly increasing gastrin via G cells. This neural activation primes gastric secretory apparatus before food arrival. Answer: a) Vagus nerve (acetylcholine mediated).

Guessed Question 2

Which drug markedly reduces the cephalic phase of acid secretion?
a) Atropine (antimuscarinic)
b) Omeprazole (PPI)
c) Ranitidine (H2 blocker)
d) Bethanechol (muscarinic agonist)

Explanation: Antimuscarinic agents such as atropine block vagally mediated acetylcholine effects on parietal cells and G cells, markedly suppressing the cephalic phase of gastric secretion elicited by food-related stimuli and are seldom used for routine acid suppression. Answer: a) Atropine.

Guessed Question 3

Which gastric cell type increases secretion during the cephalic phase?
a) Chief cells
b) Mucous cells
c) Parietal cells
d) D cells

Explanation: During the cephalic phase, parietal cells increase hydrochloric acid secretion in response to vagal stimulation and paracrine histamine release from enterochromaffin-like cells; this is important in digestion and disease including ulcers. Answer: c) Parietal cells (increase HCl secretion).

Guessed Question 4

After truncal vagotomy, the cephalic phase of gastric secretion is usually?
a) Increased
b) Abolished
c) Unchanged
d) Enhanced by gastrin

Explanation: Truncal vagotomy abolishes the cephalic phase vagally mediated stimulation of gastric secretion by interrupting efferent parasympathetic pathways, markedly reducing preprandial acid output and impairing digestive capacity and reduces ulcer recurrence. Answer: b) Abolished.

Guessed Question 5

Which higher brain area triggers cephalic-phase vagal output when you smell food?
a) Cerebral cortex
b) Cerebellum
c) Medullary reticular formation only
d) Basal ganglia

Explanation: Sensory cortical inputs from olfactory, gustatory, and limbic regions, processed in cerebral cortex, trigger the cephalic phase by activating dorsal motor nucleus of vagus, important in conditioned reflexes clinically. Answer: a) Cerebral cortex.

Guessed Question 6

Which phase contributes about 70% of gastric acid secretion?
a) Cephalic phase
b) Gastric phase
c) Intestinal phase
d) Basal phase

Explanation: Gastric phase, initiated by stomach distension and food presence, accounts for about seventy percent of the total gastric acid secretion through local reflexes, vagal stimulation, and gastrin release, in most meals. Answer: b) Gastric phase.

Guessed Question 7

The cephalic phase is an example of which learning phenomenon?
a) Operant conditioning
b) Sensitization
c) Classical (Pavlovian) conditioning
d) Habituation

Explanation: The cephalic phase exemplifies classical conditioning where previously neutral cues like sight or smell become conditioned stimuli eliciting vagal-mediated gastric secretion and influence feeding behavior clinically. Answer: c) Classical conditioned reflexes.

Guessed Question 8

Vagal stimulation during the cephalic phase increases gastrin release via which mediator?
a) GRP (gastrin-releasing peptide)
b) Somatostatin
c) Secretin
d) Peptide YY

Explanation: Vagal stimulation releases gastrin-releasing peptide (GRP) from enteric neurons, augmenting gastrin secretion from G cells during the cephalic phase, enhancing protein digestion and acid secretion in meals. Answer: a) GRP (increases gastrin release).

Guessed Question 9

Which hormone plays minimal role in the cephalic phase of gastric secretion?
a) Gastrin
b) Acetylcholine
c) Secretin
d) GRP

Explanation: Secretin is primarily released in response to duodenal acid and functions in the intestinal phase, not during cephalic anticipatory secretion. Clinically, secretin testing assesses pancreatic function, typically. Answer: d) Secretin.

Guessed Question 10

Loss of smell (anosmia) typically causes the cephalic-phase response to be?
a) Reduced
b) Increased
c) Unchanged
d) Replaced by intestinal phase

Explanation: Anosmia or diminished olfaction reduces cephalic-phase stimulation because olfactory cues are powerful conditioned stimuli; consequently those patients have attenuated vagally mediated gastric secretion and possibly altered appetite particularly in elderly individuals. Answer: a) Reduced cephalic response.

Chapter: Renal & Cardiovascular Physiology
Topic: Fluid and Electrolyte Homeostasis
Subtopic: Hormonal Control of Sodium and Water

Keyword Definitions:

Renin angiotensin system: Hormonal cascade (renin → angiotensin II → aldosterone) that conserves sodium and water.
ANP / BNP: Atrial and B-type natriuretic peptides that promote natriuresis and reduce volume.
Vasopressin (ADH): Antidiuretic hormone increasing water reabsorption via aquaporins.
Natriuresis: Excretion of sodium in urine.
Aldosterone: Mineralocorticoid increasing distal nephron sodium reabsorption and potassium secretion.

Lead Question - 2012

Which of the following is most important in sodium and water retention ?
a) Renin angiotensin system
b) ANP
c) BNP
d) Vasopressin

Explanation: Renin angiotensin system is the principal regulator of sodium and water retention via angiotensin II mediated aldosterone release, renal arteriolar constriction, and increased proximal sodium reabsorption. It conserves sodium and water during hypovolemia. Therefore correct answer: a) Renin angiotensin system. This mechanism predominates in volume depletion states especially acutely.

Guessed Question 1

ANP primarily causes sodium loss by acting on which site?
a) Proximal tubule
b) Collecting duct
c) Loop of Henle
d) Glomerulus

Explanation: Atrial natriuretic peptide promotes natriuresis and diuresis by inhibiting sodium reabsorption in the collecting duct, decreasing aldosterone and renin release, and increasing GFR through afferent arteriolar dilation. It reduces plasma volume and blood pressure. Therefore correct answer: b) ANP. This hormone is released from atrial myocytes with atrial stretch promptly.

Guessed Question 2

BNP is clinically useful as a marker of?
a) Liver failure
b) Renal tubular injury
c) Heart failure
d) Primary hyperaldosteronism

Explanation: B-type natriuretic peptide is secreted by ventricular myocytes in response to increased wall stress. It promotes natriuresis, vasodilation, and inhibits the renin angiotensin aldosterone system. Elevated plasma levels indicate heart failure severity and help guide management. Therefore correct answer: c) BNP. used in diagnosis and prognostication of heart failure clinically.

Guessed Question 3

Vasopressin (ADH) conserves body water by acting on?
a) Proximal tubule
b) Loop of Henle
c) Distal convoluted tubule
d) Collecting duct

Explanation: Vasopressin (ADH) binds V2 receptors on collecting duct principal cells, stimulating aquaporin 2 insertion into the apical membrane, increasing water permeability and reabsorption, concentrating urine and conserving body water during dehydration. Therefore correct answer: d) Collecting duct. It is released from posterior pituitary in response to hyperosmolality and hypovolemia and hypotension.

Guessed Question 4

Aldosterone increases sodium reabsorption by upregulating?
a) Aquaporin channels
b) ENaC and basolateral Na+/K+ ATPase
c) NKCC2 cotransporter
d) ROMK channels only

Explanation: Aldosterone, released from adrenal zona glomerulosa in response to angiotensin II and hyperkalemia, increases sodium reabsorption in distal nephron by upregulating ENaC and Na+/K+ ATPase, enhancing water retention and potassium secretion. Therefore correct answer: b) ENaC and basolateral Na+/K+ ATPase. This mechanism raises blood pressure and is targeted by ACE inhibitors clinically.

Guessed Question 5

In heart failure with volume overload, which system predominates in causing retention?
a) Renin angiotensin system
b) ANP release predominates
c) BNP secretion predominates
d) Vasopressin alone

Explanation: Despite elevated ANP in heart failure, the renin angiotensin system predominates in promoting sodium and water retention by increasing aldosterone, sympathetic tone, and renal sodium reabsorption; ANP effects are often overwhelmed. Hence correct answer: a) Renin angiotensin system. Consequently, blockade of RAS reduces fluid overload and improves outcomes clinically significantly.

Guessed Question 6

Which hormone mainly conserves water without directly increasing sodium retention?
a) Vasopressin
b) Aldosterone
c) ANP
d) Renin

Explanation: Vasopressin principally conserves water via aquaporin insertion without directly increasing sodium reabsorption, so volume expansion is limited; conversely renin angiotensin system increases both sodium and water retention through aldosterone and proximal reabsorption. Therefore correct answer: a) Vasopressin. This explains why RAS blockade causes natriuresis and blood pressure reduction.

Guessed Question 7

ACE inhibitors reduce sodium and water retention by blocking formation of?
a) Aldosterone directly
b) Angiotensin II
c) Vasopressin
d) ANP

Explanation: ACE inhibitors interrupt conversion of angiotensin I to II, reducing aldosterone secretion, sodium reabsorption, and water retention; they thereby lower blood pressure and reduce edema. Their effect confirms that the renin angiotensin system is central in sodium and water retention. Correct answer: b) Angiotensin II. ACE inhibitor therapy provides therapeutic benefit.

Guessed Question 8

Spironolactone reduces fluid retention by antagonizing which receptor?
a) Vasopressin receptor
b) Mineralocorticoid receptor
c) Beta adrenergic receptor
d) Natriuretic peptide receptor

Explanation: Spironolactone blocks mineralocorticoid receptors, decreasing sodium reabsorption in the distal nephron and promoting natriuresis; it reduces edema and hypertension in conditions of aldosterone excess. This pharmacologic evidence reinforces the dominant role of renin angiotensin system in sodium and water retention. Correct answer: b) Mineralocorticoid receptor. across diverse clinical scenarios.

Guessed Question 9

Which system primarily raises blood pressure and promotes long-term sodium retention?
a) Renin angiotensin system
b) ANP system
c) BNP release
d) Atrial stretch reflex

Explanation: Multiple homeostatic systems regulate body fluids, but the renin angiotensin system, via angiotensin II and aldosterone, exerts the most sustained and potent effects on sodium and water retention. Vasopressin and natriuretic peptides modulate volume acutely. Therefore correct answer: a) Renin angiotensin system. Hence RAS blockade reduces sodium retention clinically significantly.

Guessed Question 10

Which intervention best reduces sodium and water retention in heart failure?
a) ACE inhibitors / ARBs
b) ANP infusion
c) Pure water restriction
d) Vasopressin agonists

Explanation: ACE inhibitors or ARBs block the renin angiotensin system, lowering angiotensin II and aldosterone, reducing renal sodium reabsorption and water retention, improving congestion and mortality in heart failure. Therefore correct answer: a) ACE inhibitors / ARBs. Clinical trials support their central role in managing fluid overload and hypertension.

Chapter: Renal Physiology
Topic: Tubular Function
Subtopic: Proximal Convoluted Tubule (PCT) Dynamics

Keyword Definitions:

Filtrate: Fluid filtered at the glomerulus entering the nephron.
PCT: Proximal convoluted tubule; major site of bulk reabsorption.
Reabsorption: Movement of solutes and water from tubule back into blood.
Secretion: Transfer of substances from peritubular capillaries into tubular fluid.
Isotonic reabsorption: Proportional reabsorption of solute and water keeping osmolarity similar to plasma.
Transport maximum (Tm): Maximum reabsorptive rate for carrier-mediated transport.
HCO3− handling: Majority reclaimed in PCT via carbonic anhydrase dependent processes.
Inulin: Reference substance filtered but neither reabsorbed nor secreted.

Lead Question - 2012

As fluid comes down the PCT, what is true ?
a) Concentration of urea falls
b) Concentration of HCO3- falls
c) Concentration of Na+ increases
d) Concentration of inulin decreases

Explanation: In the proximal convoluted tubule abundant bicarbonate is reabsorbed back into blood, reducing its luminal concentration as fluid moves distally. Water and solute reabsorption are roughly isotonic but specific solutes like HCO3− are actively reclaimed. Answer: b) Concentration of HCO3− falls. This explains the correct choice for the question below.

Guessed Question 1

Which substance is completely reabsorbed under normal conditions in the PCT?
a) Glucose
b) Urea
c) Creatinine
d) Inulin

Explanation: Glucose filtered in the glomerulus is reabsorbed entirely by proximal tubular sodium–glucose cotransporters under normal conditions, preventing urinary loss. When blood glucose exceeds transport maximum, glycosuria results. This tubular reabsorption is energy dependent, coupling to the Na⁺/K⁺ ATPase. Answer: Glucose. Clinically important for diagnosis of diabetes mellitus and renal thresholds.

Guessed Question 2

As fluid leaves the PCT, its osmolarity is generally:
a) Hypertonic
b) Hypotonic
c) Approximately isotonic
d) Variable without pattern

Explanation: Fluid leaving the proximal tubule remains approximately isotonic relative to plasma because solute and water are reabsorbed proportionally. This contrasts with thick ascending limb where dilution occurs. Thus osmolality is preserved along PCT despite large absolute reabsorption. Answer: proximal tubule fluid remains isotonic to plasma important concept in renal physiology.

Guessed Question 3

What happens to inulin concentration along PCT?
a) Increases
b) Decreases
c) Remains unchanged
d) Fluctuates widely

Explanation: Inulin is freely filtered and neither reabsorbed nor secreted; therefore its concentration in tubular fluid remains constant along segments with isotonic reabsorption, like the proximal tubule. Because water and solute reabsorption are matched, inulin concentration is unchanged, making inulin clearance a gold standard for GFR measurement. Answer: unchanged clinically relevant.

Guessed Question 4

What is the net effect on urea concentration in PCT luminal fluid?
a) Large increase
b) Modest decrease
c) No change
d) Complete removal

Explanation: Urea is filtered and partially reabsorbed passively in the proximal tubule driven by solvent drag and concentration gradients, but proportional water reabsorption tends to maintain its luminal concentration. Net effect is modest decrease in urea concentration along PCT, contributing to medullary urea recycling. Answer: modest decrease clinically significant in diuresis.

Guessed Question 5

Major mechanism for HCO3− reclamation in PCT is via:
a) Direct HCO3− transport apically
b) Carbonic anhydrase–dependent conversion to CO2
c) Passive diffusion of bicarbonate
d) Vesicular transport

Explanation: Proximal tubule reabsorbs the majority of filtered bicarbonate via carbonic anhydrase–dependent processes involving luminal CA and basolateral transporters; bicarbonate is converted to CO2, enters cells, reconverted and transported as HCO3– to blood. This efficient mechanism lowers luminal bicarbonate concentration markedly. Answer: active bicarbonate reclamation indeed.

Guessed Question 6

How does luminal sodium concentration change along the PCT?
a) Increases markedly
b) Decreases markedly
c) Remains nearly constant
d) Becomes zero

Explanation: Sodium is reabsorbed along proximal tubule isosmotically with water; because approximately equal proportions of sodium and water are reclaimed, the luminal sodium concentration remains nearly constant. Variations occur with transporters and solvent drag, but overall Na+ concentration is maintained while absolute amount in filtrate declines. Answer: remains nearly constant physiologically.

Guessed Question 7

Which transporter couples glucose uptake to sodium in PCT?
a) GLUT2
b) SGLT (sodium–glucose cotransporter)
c) Na+/K+ ATPase apical
d) Aquaporin

Explanation: Glucose reabsorption in the proximal tubule uses sodium–glucose cotransporters (SGLT2 proximally and SGLT1 distally) which harness the transmembrane sodium gradient established by basolateral Na+/K+ ATPase. This secondary active transport couples glucose uptake to sodium movement, enabling efficient reclamation. Answer: SGLT (sodium–glucose cotransporter) clinically targeted by SGLT2 inhibitors for diabetes treatment.

Guessed Question 8

Approximately what percentage of filtered HCO3− is reclaimed in the PCT?
a) 10–20%
b) 30–40%
c) 80–90%
d) 100%

Explanation: Approximately eighty to ninety percent of filtered bicarbonate is reabsorbed in the proximal tubule through carbonic anhydrase–dependent mechanisms and basolateral transporters, leaving a small fraction for downstream fine-tuning of acid–base balance. Hence PCT is the major bicarbonate reclamation site. Answer: eighty to ninety percent clinically significant in metabolic acidosis management.

Guessed Question 9

What effect does a carbonic anhydrase inhibitor have on urine and acid–base status?
a) Decreased urine HCO3−, alkalosis
b) Increased urine HCO3−, metabolic acidosis
c) No change
d) Increased K+ retention

Explanation: Acetazolamide inhibits carbonic anhydrase in proximal tubule cells, preventing HCO3− reclamation and causing increased urinary bicarbonate loss with resultant metabolic acidosis; urine becomes alkaline. Sodium reabsorption coupled to bicarbonate falls, producing mild diuresis. Clinically, this drug treats glaucoma and altitude illness. Answer: decreased HCO3− reabsorption and alkaline urine common therapeutic.

Guessed Question 10

Why do many solutes exhibit a transport maximum (Tm) in PCT?
a) Unlimited carrier capacity
b) Carrier-mediated saturable transport
c) Passive diffusion only
d) Filtration-limited only

Explanation: Many solutes in proximal tubule have a transport maximum because reabsorption depends on carrier-mediated transporters; when filtered load exceeds Tm, excess appears in urine, exemplified by glucose in hyperglycemia. This saturable transport underlies clinical concepts of renal threshold and glycosuria. Answer: carrier-mediated transport with finite Tm causes overflow urinary loss.

Chapter: Renal Physiology
Topic: Hormonal Regulation of Kidney Function
Subtopic: Atrial Natriuretic Peptide (ANP)

Keywords:

ANP: Atrial Natriuretic Peptide, hormone secreted by atria in response to stretch.
PCT: Proximal Convoluted Tubule, primary site for reabsorption.
Loop of Henle: Segment important in urine concentration.
Collecting Duct: Final site of regulation of water and sodium.
Glomerulus: Initial filtering structure of nephron.

Lead Question - 2012
ANP acts at which site ?
a) Glomerulus
b) Loop of Henle
c) PCT
d) Collecting duct

Explanation:
ANP acts mainly at the collecting duct to inhibit sodium reabsorption, leading to natriuresis and diuresis. It also dilates afferent arterioles and increases GFR. This helps to reduce blood volume and pressure. Correct answer: d) Collecting duct.

Guessed Question 1
Which hormone primarily reduces sodium reabsorption in the collecting ducts?
a) Aldosterone
b) ADH
c) ANP
d) Renin

Explanation:
ANP opposes the action of aldosterone and reduces sodium reabsorption in the collecting ducts, promoting excretion. Answer: c) ANP.

Guessed Question 2
A patient with atrial stretch due to fluid overload will have elevated?
a) Aldosterone
b) Vasopressin
c) ANP
d) Angiotensin II

Explanation:
Atrial stretch stimulates ANP secretion, reducing blood pressure by promoting natriuresis. This mechanism helps counteract fluid overload. Answer: c) ANP.

Guessed Question 3
ANP increases sodium excretion by?
a) Stimulating renin release
b) Dilating afferent arteriole
c) Constricting efferent arteriole
d) Enhancing aldosterone secretion

Explanation:
ANP dilates the afferent arteriole and inhibits renin and aldosterone, leading to natriuresis. Answer: b) Dilating afferent arteriole.

Guessed Question 4
Which of the following is inhibited by ANP?
a) Renin secretion
b) Aldosterone secretion
c) Sodium reabsorption
d) All of the above

Explanation:
ANP inhibits renin and aldosterone secretion and reduces sodium reabsorption in the collecting duct. Answer: d) All of the above.

Guessed Question 5
Which receptor mediates ANP effects in kidney?
a) GABA receptor
b) Natriuretic peptide receptor-A
c) Beta adrenergic receptor
d) Nicotinic receptor

Explanation:
ANP acts via natriuretic peptide receptor-A, a guanylyl cyclase-linked receptor that increases cGMP. Answer: b) Natriuretic peptide receptor-A.

Guessed Question 6
In heart failure, ANP levels are?
a) Decreased
b) Increased
c) Normal
d) Absent

Explanation:
In heart failure, ANP secretion increases due to atrial distension, but the kidney response is often blunted. Answer: b) Increased.

Guessed Question 7
ANP effect on GFR is?
a) Decrease GFR
b) Increase GFR
c) No effect
d) Transient fall

Explanation:
ANP increases GFR by dilating afferent arteriole and relaxing mesangial cells. Answer: b) Increase GFR.

Guessed Question 8
Which ion excretion is promoted most by ANP?
a) Sodium
b) Potassium
c) Calcium
d) Chloride

Explanation:
ANP strongly increases sodium excretion (natriuresis), which is accompanied by water excretion. Answer: a) Sodium.

Guessed Question 9
ANP secretion is stimulated by?
a) Dehydration
b) Hemorrhage
c) Atrial distension
d) Low blood pressure

Explanation:
ANP secretion occurs in response to atrial distension due to increased venous return. Answer: c) Atrial distension.

Guessed Question 10
ANP counters the effects of which hormone?
a) Aldosterone
b) ADH
c) Cortisol
d) Insulin

Explanation:
ANP directly opposes aldosterone by decreasing sodium reabsorption in the collecting ducts. Answer: a) Aldosterone.

Chapter: Renal Physiology
Topic: Renal Handling of Substances
Subtopic: Tubular Secretion and Filtration

Keyword Definitions:

Filtration: Movement of plasma components into Bowman’s capsule at glomerulus.
Secretion: Transfer of substances from blood into tubular fluid.
Uric Acid: Waste product of purine metabolism, filtered and secreted in proximal tubule.
Glucose: Completely reabsorbed in proximal tubule, normally not secreted.
Urea: Partially reabsorbed and contributes to medullary osmotic gradient.
Sodium (Na+): Mostly reabsorbed, not secreted under normal physiology.
Proximal Tubule: Major site of secretion and reabsorption in nephron.
Transporters: Organic anion and cation transporters help secretion of uric acid and drugs.

Lead Question - 2012

Substrate which is both secreted & filtered?
a) Uric Acid
b) Glucose
c) Urea
d) Na+

Explanation: The correct answer is a) Uric Acid. Uric acid is filtered at the glomerulus and actively secreted by proximal tubular cells via organic anion transporters. It also undergoes partial reabsorption. In conditions like gout or renal tubular dysfunction, uric acid handling becomes clinically significant for diagnosis and therapy.

Guessed Question 1

Which transporter system mediates uric acid secretion in the proximal tubule?
a) SGLT2
b) Organic anion transporter
c) Sodium-potassium pump
d) Aquaporins

Explanation: The correct answer is b) Organic anion transporter. These transporters secrete uric acid and drugs into tubular fluid. Dysfunction may cause hyperuricemia or altered drug clearance, which is clinically important in pharmacology and renal disease management.

Guessed Question 2

Increased serum uric acid leading to gout occurs due to?
a) Decreased uric acid secretion
b) Increased glucose excretion
c) Reduced sodium excretion
d) Increased urea absorption

Explanation: The correct answer is a) Decreased uric acid secretion. Impaired tubular secretion of uric acid increases serum uric acid levels, resulting in gout. Drugs like probenecid enhance uric acid excretion and are used in treatment.

Guessed Question 3

Which of the following substances is filtered but almost completely reabsorbed?
a) Glucose
b) Uric acid
c) Urea
d) Creatinine

Explanation: The correct answer is a) Glucose. Normally, all filtered glucose is reabsorbed in the proximal tubule via sodium-glucose cotransporters. Presence of glucose in urine (glycosuria) indicates hyperglycemia or proximal tubular dysfunction.

Guessed Question 4

Which clinical drug increases uric acid secretion to manage gout?
a) Allopurinol
b) Probenecid
c) Furosemide
d) Thiazides

Explanation: The correct answer is b) Probenecid. Probenecid inhibits tubular reabsorption of uric acid, enhancing its secretion and urinary clearance. It is used in chronic gout but contraindicated in renal impairment.

Guessed Question 5

Which of the following is filtered and secreted but not reabsorbed significantly?
a) Creatinine
b) Sodium
c) Urea
d) Glucose

Explanation: The correct answer is a) Creatinine. Creatinine is freely filtered and slightly secreted, making it a reliable marker for glomerular filtration rate (GFR). Its secretion causes slight overestimation of GFR in clearance studies.

Guessed Question 6

In chronic renal failure, serum uric acid levels increase because?
a) Increased tubular secretion
b) Decreased tubular secretion
c) Increased urea absorption
d) Reduced glucose filtration

Explanation: The correct answer is b) Decreased tubular secretion. Declining renal function reduces secretion and clearance of uric acid, leading to hyperuricemia. This may worsen hypertension, gout, and cardiovascular risk.

Guessed Question 7

Which nephron segment is the major site of drug secretion?
a) Loop of Henle
b) Distal tubule
c) Proximal tubule
d) Collecting duct

Explanation: The correct answer is c) Proximal tubule. The proximal tubule contains organic acid and base transporters that secrete uric acid, creatinine, and drugs like penicillin, making it crucial in pharmacokinetics.

Guessed Question 8

Urea is primarily reabsorbed by?
a) Passive diffusion
b) Primary active transport
c) Secondary active transport
d) Vesicular transport

Explanation: The correct answer is a) Passive diffusion. Urea moves down its concentration gradient. Reabsorption mainly occurs in the proximal tubule and medullary collecting duct, helping in countercurrent multiplication and water conservation.

Guessed Question 9

Which of the following substances best reflects GFR because it is filtered but not secreted or reabsorbed?
a) Urea
b) Creatinine
c) Inulin
d) Uric acid

Explanation: The correct answer is c) Inulin. Inulin clearance accurately measures GFR since it is filtered freely but neither secreted nor reabsorbed. Creatinine is often used clinically but slightly overestimates GFR due to secretion.

Guessed Question 10

A patient on chemotherapy develops tumor lysis syndrome with raised uric acid. The best drug to reduce uric acid production is?
a) Probenecid
b) Febuxostat
c) Furosemide
d) Mannitol

Explanation: The correct answer is b) Febuxostat. Febuxostat, like allopurinol, inhibits xanthine oxidase, reducing uric acid production. It is used to prevent uric acid nephropathy and gout in high-risk patients undergoing chemotherapy.

Chapter: Renal Physiology
Topic: Renal Handling of Substances
Subtopic: Tubular Reabsorption

Keyword Definitions:

Reabsorption: Movement of substances from tubular fluid back into the blood.
Glucose Reabsorption: Occurs completely in proximal tubule under normal conditions, via sodium-glucose transporters.
Sodium (Na+): Mostly reabsorbed, but not fully; some is excreted.
Potassium (K+): Filtered, reabsorbed, and secreted depending on body needs.
Urea: Partially reabsorbed, contributes to medullary concentration gradient.
Transport Maximum (Tm): Maximum rate at which a substance can be reabsorbed.
Glycosuria: Presence of glucose in urine when plasma glucose exceeds Tm.
Proximal Tubule: Main site of glucose reabsorption in the nephron.

Lead Question - 2012

Substance that is completely reabsorbed from the kidney?
a) Na+
b) K+
c) Urea
d) Glucose

Explanation: The correct answer is d) Glucose. Under normal physiological conditions, glucose filtered by the glomerulus is completely reabsorbed in the proximal tubule. Other substances like sodium, potassium, and urea are only partially reabsorbed. Glycosuria occurs if glucose exceeds the renal threshold, as in uncontrolled diabetes.

Guessed Question 1

Which part of nephron is primarily responsible for complete glucose reabsorption?
a) Proximal tubule
b) Loop of Henle
c) Distal tubule
d) Collecting duct

Explanation: The correct answer is a) Proximal tubule. Glucose reabsorption occurs through sodium-glucose cotransporters (SGLT2 in early proximal tubule, SGLT1 in later segments). Failure leads to glycosuria even without hyperglycemia.

Guessed Question 2

In uncontrolled diabetes mellitus, presence of glucose in urine is due to?
a) Increased renal clearance
b) Decreased tubular transport maximum
c) Plasma glucose exceeding tubular reabsorptive capacity
d) Enhanced secretion of glucose

Explanation: The correct answer is c) Plasma glucose exceeding tubular reabsorptive capacity. When blood glucose exceeds ~180 mg/dL, tubular transport maximum is overwhelmed, resulting in glucose loss in urine.

Guessed Question 3

Which of the following is reabsorbed both passively and actively in the nephron?
a) Glucose
b) Sodium
c) Urea
d) Potassium

Explanation: The correct answer is c) Urea. Urea undergoes passive reabsorption in proximal tubule and collecting duct, contributing to medullary osmotic gradient for water reabsorption.

Guessed Question 4

Which ion is secreted by distal nephron to maintain potassium balance?
a) Sodium
b) Chloride
c) Potassium
d) Calcium

Explanation: The correct answer is c) Potassium. Potassium is reabsorbed in proximal tubule and loop of Henle but secreted by principal cells in distal tubule and collecting duct under aldosterone influence.

Guessed Question 5

Renal threshold for glucose is approximately?
a) 120 mg/dL
b) 180 mg/dL
c) 220 mg/dL
d) 300 mg/dL

Explanation: The correct answer is b) 180 mg/dL. Above this concentration, glucose transporters saturate and glucose appears in urine. This threshold explains glycosuria in hyperglycemia.

Guessed Question 6

Which hormone promotes sodium reabsorption in the distal nephron?
a) Aldosterone
b) Vasopressin
c) ANP
d) Calcitonin

Explanation: The correct answer is a) Aldosterone. Aldosterone increases sodium reabsorption and potassium secretion in the distal tubule and collecting duct, helping maintain blood pressure and electrolyte balance.

Guessed Question 7

Which of the following is a clinical sign of reduced glucose reabsorption capacity?
a) Polyuria
b) Polydipsia
c) Glycosuria
d) All of the above

Explanation: The correct answer is d) All of the above. Glycosuria leads to osmotic diuresis (polyuria) and increased thirst (polydipsia), classic symptoms of uncontrolled diabetes mellitus.

Guessed Question 8

Which renal transport mechanism is energy-dependent?
a) Passive diffusion
b) Facilitated diffusion
c) Secondary active transport
d) Osmosis

Explanation: The correct answer is c) Secondary active transport. Glucose reabsorption occurs by coupling with sodium gradient, which is maintained by Na+/K+ ATPase pump in proximal tubular cells.

Guessed Question 9

Which factor decreases urea reabsorption in the kidney?
a) Increased ADH
b) Increased urine flow rate
c) Increased medullary concentration
d) Enhanced collecting duct permeability

Explanation: The correct answer is b) Increased urine flow rate. High urine flow reduces time for passive urea reabsorption, leading to increased urea excretion, often seen in osmotic diuresis.

Guessed Question 10

In Fanconi syndrome, renal tubular defect leads to?
a) Increased glucose reabsorption
b) Decreased glucose reabsorption
c) Increased sodium reabsorption
d) Decreased potassium secretion

Explanation: The correct answer is b) Decreased glucose reabsorption. Fanconi syndrome involves proximal tubule dysfunction causing loss of glucose, amino acids, phosphate, and bicarbonate in urine.

Chapter: Environmental Physiology
Topic: Acclimatization
Subtopic: Thermoregulation

Keyword Definitions:

Acclimatization: Physiological adaptation to environmental stress such as high altitude or heat.
Sweating: Mechanism of heat loss through evaporation of sweat from the skin surface.
Down Regulation: Reduction in receptor number or sensitivity due to prolonged stimulation.
Cholinergic receptors: Receptors activated by acetylcholine, key in sweat gland activity.
Adrenergic receptors: Receptors activated by catecholamines like epinephrine and norepinephrine.

Lead Question - 2012

During acclimatization, decreased sweating is due to down regulation of ?
a) Epinephrine receptors
b) Norepinephrine receptors
c) Acetylcholine receptors
d) Dopamine receptors

Explanation: The correct answer is c) Acetylcholine receptors. In heat acclimatization, sweat production reduces due to down regulation of muscarinic acetylcholine receptors on sweat glands. This conserves body water while maintaining thermoregulation. Adrenergic or dopamine receptors are not directly responsible for sweat gland control in acclimatization.

Guessed Question 1

Which neurotransmitter primarily stimulates sweat gland activity?
a) Acetylcholine
b) Norepinephrine
c) Dopamine
d) Serotonin

Explanation: The correct answer is a) Acetylcholine. Sweat glands are innervated by sympathetic cholinergic fibers, which release acetylcholine to trigger sweat production. Adrenergic transmitters like norepinephrine usually act on blood vessels, not directly on sweat glands. This distinction is essential in understanding thermoregulation physiology.

Guessed Question 2

In heat acclimatization, plasma volume usually:
a) Decreases
b) Remains unchanged
c) Increases
d) Fluctuates randomly

Explanation: The correct answer is c) Increases. During heat acclimatization, plasma volume expands to support greater sweating and maintain circulation under thermal stress. This helps preserve cardiovascular stability and prevents dehydration. It is a key adaptive change to allow prolonged work in hot climates.

Guessed Question 3

Which hormone enhances sodium reabsorption during heat acclimatization?
a) Insulin
b) Aldosterone
c) Cortisol
d) Thyroxine

Explanation: The correct answer is b) Aldosterone. Heat exposure activates the renin-angiotensin-aldosterone system, promoting sodium and water retention. This conserves body fluid during excessive sweating. Cortisol has a mild mineralocorticoid effect, but aldosterone is the primary regulator in acclimatization physiology.

Guessed Question 4

Which of the following best describes the heart rate response during early heat acclimatization?
a) Decreased resting and exercise heart rate
b) Increased resting heart rate only
c) Increased exercise heart rate only
d) No significant change

Explanation: The correct answer is a) Decreased resting and exercise heart rate. With acclimatization, cardiovascular efficiency improves, reducing the strain on the heart during both rest and exercise in hot environments. This adaptation supports better endurance under thermal stress.

Guessed Question 5

Which blood parameter decreases significantly during high-altitude acclimatization but not during heat acclimatization?
a) Plasma bicarbonate
b) Plasma sodium
c) Plasma potassium
d) Plasma glucose

Explanation: The correct answer is a) Plasma bicarbonate. At high altitude, respiratory alkalosis develops, leading to renal excretion of bicarbonate. In contrast, heat acclimatization does not significantly affect bicarbonate levels but instead alters plasma volume and electrolytes to support sweating.

Guessed Question 6

In a soldier exposed to desert climate, which adaptation is expected?
a) Reduced sweating rate
b) Increased sweat sodium concentration
c) Decreased sweat sodium concentration
d) Absence of sweating

Explanation: The correct answer is c) Decreased sweat sodium concentration. Acclimatization reduces sodium loss in sweat through aldosterone-mediated sodium reabsorption in sweat ducts. This adaptation conserves electrolytes and prevents hyponatremia during prolonged desert exposure.

Guessed Question 7

During prolonged heat acclimatization, which thermoregulatory change is most evident?
a) Delayed onset of sweating
b) Earlier onset of sweating
c) Cessation of sweating
d) No change in sweating

Explanation: The correct answer is b) Earlier onset of sweating. Acclimatized individuals begin sweating at lower core body temperatures, allowing more effective heat dissipation. This prevents dangerous rises in body temperature during physical activity in hot environments.

Guessed Question 8

Which receptor type is most associated with vasodilation in skin during heat exposure?
a) Alpha-adrenergic
b) Beta-adrenergic
c) Muscarinic
d) Dopaminergic

Explanation: The correct answer is b) Beta-adrenergic. Skin vasodilation during heat stress is mediated in part by beta-adrenergic receptors, enhancing blood flow to the skin for heat dissipation. Alpha receptors usually mediate vasoconstriction.

Guessed Question 9

Which electrolyte disturbance is most likely in excessive sweating without adequate fluid replacement?
a) Hypernatremia
b) Hyponatremia
c) Hyperkalemia
d) Hypercalcemia

Explanation: The correct answer is b) Hyponatremia. Excessive sweating without sodium replacement leads to significant sodium loss, lowering plasma sodium levels. This can cause weakness, confusion, and in severe cases seizures. Acclimatization helps reduce sodium loss per unit sweat volume.

Guessed Question 10

Which is the earliest physiological response in heat acclimatization?
a) Plasma volume expansion
b) Increased red blood cells
c) Reduced basal metabolic rate
d) Increased appetite

Explanation: The correct answer is a) Plasma volume expansion. This occurs within a few days of heat exposure, allowing better cardiovascular stability and sweat production. Other adaptations, such as reduced sweat sodium concentration, take longer to develop. RBC increase is characteristic of altitude acclimatization, not heat adaptation.

Chapter: Muscle Physiology

Topic: Muscle Contraction

Subtopic: Tetanic Contraction and Ionic Basis

Keyword Definitions

• Tetanic contraction: Sustained maximal muscle tension produced by rapid repetitive stimulation.

• Calcium (Ca2+): Intracellular ion that enables cross-bridge cycling by binding to regulatory proteins.

• Summation: Successive twitches adding to increase tension when stimuli arrive before full relaxation.

• Sarcoplasmic reticulum: Organelle storing Ca2+ in muscle fibres and releasing it on stimulation.

• Excitation–contraction coupling: Sequence linking membrane depolarization to Ca2+ release and contraction.

Lead Question - 2012

Tetanic contraction is due to accumulation of ?

a) Na+

b) Ca2+

c) K+

d) Cl-

Explanation:

Tetanic contraction results when repeated stimuli cause intracellular calcium to accumulate because release from the sarcoplasmic reticulum outpaces reuptake; sustained Ca2+ keeps cross-bridges cycling and prevents relaxation. This leads to fused tetanus. Correct answer: Ca2+ (option b). Clinically relevant in high-frequency stimulation and some toxins.

Guessed Questions for NEET PG

1. Which process increases during unfused tetanus compared with single twitch?

a) Ca2+ reuptake

b) Summation of tension

c) Complete relaxation

d) Decreased cross-bridge cycling

Explanation:

Unfused tetanus arises when stimuli occur before full relaxation, so individual twitches summate producing increased mean tension. This summation occurs because residual Ca2+ persists between stimuli, increasing cross-bridge availability; it differs from fused tetanus where relaxation is absent. Correct answer: Summation of tension.

2. A toxin that blocks Ca2+ release would cause?

a) Enhanced tetanus

b) Flaccid paralysis

c) Spastic paralysis

d) Increased muscle tone

Explanation:

Blocking Ca2+ release from the sarcoplasmic reticulum prevents actin-myosin interaction, producing inability to generate force and flaccid paralysis. Without Ca2+, tetanic contraction cannot occur. Clinically, agents that prevent Ca2+ release produce muscle weakness rather than spasm. Correct answer: Flaccid paralysis.

3. Which ionic change primarily terminates contraction between twitches?

a) Increased intracellular Na+

b) Decrease in intracellular Ca2+ via reuptake

c) Increase in intracellular K+

d) Chloride influx

Explanation:

Contraction ends when Ca2+ is actively pumped back into the sarcoplasmic reticulum, lowering cytosolic Ca2+ and allowing regulatory proteins to inhibit cross-bridge formation, enabling relaxation. Efficient reuptake is essential to prevent summation. Correct answer: Decrease in intracellular Ca2+ via reuptake.

4. Which clinical condition produces sustained involuntary tetanic contractions?

a) Hypocalcemia increasing neuronal excitability

b) Hyperkalemia causing flaccidity

c) Botulism blocking ACh release

d) Myasthenia gravis reducing receptor sensitivity

Explanation:

Hypocalcemia lowers threshold for neuronal firing, potentially increasing neurotransmitter release and producing muscle hyperexcitability and tetany. These involuntary sustained contractions differ from tetanic contraction produced experimentally by high-frequency stimulation. Correct answer: Hypocalcemia increasing neuronal excitability.

5. During high-frequency stimulation fused tetanus occurs because?

a) SR reuptake accelerates

b) Cytosolic Ca2+ remains elevated between stimuli

c) Sarcomeres shorten beyond overlap optimum

d) ATP becomes unavailable instantly

Explanation:

Fused tetanus results when stimuli arrive so rapidly that cytosolic Ca2+ remains high continuously, preventing relaxation. Sustained cross-bridge cycling produces maximal, smooth contraction until fatigue or stimulus stops. Correct answer: Cytosolic Ca2+ remains elevated between stimuli.

6. Which mechanism contributes to muscle fatigue during prolonged tetanic contraction?

a) Unlimited ATP supply

b) Accumulation of inorganic phosphate and H+ impairing Ca2+ release and cross-bridges

c) Increased Ca2+ sensitivity of troponin

d) Enhanced SR Ca2+ content

Explanation:

Fatigue during sustained tetanus involves metabolic changes including inorganic phosphate and proton accumulation, which reduce calcium release and cross-bridge function, and impair ATPase activity, leading to declining force despite continued stimulation. Correct answer: Accumulation of inorganic phosphate and H+.

7. Which drug would reduce tetanic contraction by decreasing available Ca2+?

a) Ryanodine receptor agonist opening SR Ca2+ release

b) Dantrolene reducing SR Ca2+ release

c) ACh esterase inhibitor increasing ACh

d) Ca2+ ionophore increasing cytosolic Ca2+

Explanation:

Dantrolene inhibits calcium release from the sarcoplasmic reticulum, reducing intracellular Ca2+ and preventing sustained contractions, clinically used to treat malignant hyperthermia by suppressing excessive muscle contraction. Correct answer: Dantrolene reducing SR Ca2+ release.

8. In skeletal muscle physiology, accumulation of which ion extracellularly tends to reduce excitability rather than cause tetanus?

a) Extracellular K+ accumulation causing depolarization and inactivation of Na+ channels

b) Extracellular Ca2+ accumulation increasing contraction

c) Extracellular Na+ accumulation causing tetanus

d) Extracellular Cl- causing summation

Explanation:

Prolonged activity can raise extracellular K+, depolarizing the membrane and inactivating Na+ channels, reducing excitability and causing weakness, not tetanic contraction; tetanus arises from intracellular Ca2+ accumulation and high-frequency stimulation. Correct answer: Extracellular K+ accumulation causing depolarization and inactivation.

9. Which structural element directly binds Ca2+ to initiate contraction in skeletal muscle?

a) Troponin C on thin filaments

b) Myosin light chain kinase

c) Titin

d) Nebulin

Explanation:

In skeletal muscle, Ca2+ binds to troponin C in the thin filament regulatory complex causing conformational changes that allow myosin–actin interaction and force production; increased Ca2+ concentration from SR release initiates contraction and tetanus under repetitive stimuli. Correct answer: Troponin C.

10. Which experimental manipulation would most directly create fused tetanus in an isolated muscle preparation?

a) Low-frequency single pulses

b) High-frequency electrical stimulation preventing relaxation between pulses

c) Cooling the muscle to stop enzymatic activity

d) Blocking ACh receptors at the neuromuscular junction

Explanation:

Fused tetanus is produced experimentally by applying high-frequency stimuli such that Ca2+ accumulation prevents relaxation between pulses, resulting in sustained maximal tension, an established method to study contractile properties in isolated muscle. Correct answer: High-frequency electrical stimulation.

Chapter: Muscle Physiology

Topic: Length–Tension Relationship

Subtopic: Muscle Fibre Mechanics

Keyword Definitions:

• Optimum length – Muscle fibre length at which maximum tension is generated.

• Equilibrium length – Resting length without external load.

• Initial length – Starting length before contraction begins.

• Sarcomere – Basic contractile unit of a muscle fibre.

• Active tension – Force produced by cross-bridge cycling.

• Passive tension – Force developed when muscle is stretched beyond resting length.

Lead Question - 2012

When the tension in a muscle fibre is maximum, its length is called as ?

a) Equilibrium length

b) Optimum length

c) Initial length

d) None

Explanation:

Maximum muscle tension occurs at the optimum length, where actin–myosin overlap allows maximal cross-bridge formation. Too much shortening or stretching reduces tension. Hence, the correct answer is Optimum length.

Guessed Questions for NEET PG

1. At optimum length, sarcomere overlap is?

a) Complete overlap

b) Partial overlap allowing maximal cross-bridges

c) No overlap

d) Overlap beyond actin filaments

Explanation:

At optimum length, actin and myosin filaments overlap ideally, allowing maximum cross-bridge formation without hindrance. This ensures maximal tension development. Correct answer: Partial overlap allowing maximal cross-bridges.

2. Clinical: A patient with muscle spasm shows reduced force at very short length. Why?

a) Decreased calcium release

b) Overlap of actin filaments

c) Increased ATP consumption

d) Sarcomere hyperextension

Explanation:

At very short sarcomere lengths, actin filaments overlap excessively, blocking cross-bridge binding and reducing force generation. Correct answer: Overlap of actin filaments.

3. Passive tension in muscle arises mainly from?

a) Myosin heads

b) Actin filaments

c) Titin protein

d) Sarcoplasmic reticulum

Explanation:

When a muscle is stretched beyond resting length, passive tension develops due to titin and connective tissue elasticity. Correct answer: Titin protein.

4. Clinical: During physiotherapy, stretching muscles beyond resting length increases?

a) Active tension

b) Passive tension

c) Both active and passive equally

d) No change

Explanation:

Excessive stretching does not increase active tension but raises passive tension through elastic elements like titin. Correct answer: Passive tension.

5. Initial length of cardiac muscle fibres determines?

a) Contractility

b) Preload and stroke volume

c) Afterload

d) Heart rate

Explanation:

In the heart, initial muscle length (preload) sets sarcomere stretch, influencing stroke volume via the Frank–Starling mechanism. Correct answer: Preload and stroke volume.

6. In skeletal muscle, maximum active tension is observed at?

a) 1.6 µm sarcomere length

b) 2.0–2.2 µm sarcomere length

c) 3.5 µm sarcomere length

d) 1.0 µm sarcomere length

Explanation:

Studies show skeletal muscle develops maximal active tension when sarcomere length is 2.0–2.2 µm. Correct answer: 2.0–2.2 µm sarcomere length.

7. Clinical: Reduced cardiac contractility in dilated cardiomyopathy occurs because?

a) Sarcomeres overstretched

b) Increased overlap

c) ATP deficiency

d) Titin rupture

Explanation:

In dilated cardiomyopathy, sarcomeres are excessively stretched, reducing actin–myosin overlap and contractile efficiency. Correct answer: Sarcomeres overstretched.

8. What happens to active tension when muscle is stretched beyond optimum length?

a) Increases further

b) Decreases

c) Remains same

d) Shifts to passive

Explanation:

Beyond optimum length, overlap reduces, leading to fewer cross-bridges and decreased active tension, while passive tension increases. Correct answer: Decreases.

9. In isometric contraction at optimum length?

a) Tension is maximum

b) Length shortens maximally

c) Passive tension decreases

d) ATP consumption is minimal

Explanation:

During isometric contraction, muscle length is fixed but tension peaks at optimum sarcomere length. Correct answer: Tension is maximum.

10. Clinical: After immobilization, muscles lose optimum length efficiency due to?

a) Reduced sarcomere number

b) Increased titin length

c) Hyperplasia of fibres

d) Myelin degeneration

Explanation:

Immobilization leads to sarcomere loss, altering optimum length and reducing force output. Correct answer: Reduced sarcomere number.

Chapter: Physiology

Topic: Muscle Physiology

Subtopic: Smooth vs Skeletal Muscle

Keyword Definitions:

• Smooth muscle – Involuntary muscle controlled by autonomic nervous system and hormones.

• Skeletal muscle – Voluntary muscle controlled by somatic nervous system.

• Calcium ions – Required for contraction in both smooth and skeletal muscle, though mechanism differs.

• Troponin – Regulatory protein present in skeletal but absent in smooth muscle.

• Myosin – Thick filament protein essential for contraction in all muscles.

Lead Question - 2012

Smooth muscle physiology different from skeletal muscle

a) K⁺ requires for contraction

b) Ca²⁺ required for contraction

c) Troponin is absent

d) Myosin is required for contraction

Explanation:

Smooth muscle differs from skeletal muscle mainly due to the absence of troponin. Instead, smooth muscle contraction is regulated by calmodulin–myosin light chain kinase pathway. Calcium still plays a key role, but the regulatory protein troponin is absent. Correct answer: Troponin is absent.

Guessed Questions for NEET PG

1. Smooth muscle contraction is regulated by?

a) Troponin

b) Calmodulin

c) Tropomyosin

d) Titin

Explanation:

Unlike skeletal muscle, smooth muscle lacks troponin. Instead, contraction is controlled by calcium–calmodulin complex which activates myosin light chain kinase. Correct answer: Calmodulin.

2. Which protein is absent in smooth muscle fibers?

a) Actin

b) Troponin

c) Myosin

d) Tropomyosin

Explanation:

Actin, myosin, and tropomyosin are present in smooth muscle. Troponin, however, is absent, which differentiates it from skeletal muscle. Correct answer: Troponin.

3. Calcium in smooth muscle binds to?

a) Troponin C

b) Calmodulin

c) Tropomyosin

d) Actinin

Explanation:

In skeletal muscle, calcium binds troponin C, but in smooth muscle it binds to calmodulin, initiating contraction via MLCK. Correct answer: Calmodulin.

4. Patient with asthma receives bronchodilator. Relaxation of airway smooth muscle occurs by?

a) Increased cAMP

b) Increased IP₃

c) Increased calcium

d) Decreased cAMP

Explanation:

β₂ agonists increase cAMP, which inhibits MLCK, leading to relaxation of smooth muscle in bronchi. Correct answer: Increased cAMP.

5. Dense bodies in smooth muscle are functionally similar to?

a) T-tubules

b) Z-lines

c) Sarcoplasmic reticulum

d) Myosin heads

Explanation:

Dense bodies in smooth muscle anchor thin filaments, serving a role similar to Z-lines in skeletal muscle. Correct answer: Z-lines.

6. Which of the following best describes latch phenomenon in smooth muscle?

a) Sustained contraction with high ATP

b) Sustained contraction with low ATP

c) Rapid relaxation

d) Skeletal-type tetany

Explanation:

Latch phenomenon allows smooth muscle to maintain tension for long periods with minimal ATP use. Correct answer: Sustained contraction with low ATP.

7. In smooth muscle, myosin light chain kinase (MLCK) is activated by?

a) Troponin C

b) Calcium–calmodulin

c) Tropomyosin

d) ATP alone

Explanation:

Calcium binds calmodulin which activates MLCK, phosphorylating myosin light chains to initiate contraction. Correct answer: Calcium–calmodulin.

8. Clinical: A hypertensive patient takes a calcium channel blocker. Effect on vascular smooth muscle?

a) Increased contraction

b) Decreased contraction

c) Increased MLCK activity

d) Increased calcium influx

Explanation:

Calcium channel blockers reduce calcium influx into smooth muscle, lowering contraction and relaxing vessels. Correct answer: Decreased contraction.

9. Skeletal and smooth muscle differ because skeletal muscle contraction is?

a) Involuntary and calmodulin-mediated

b) Voluntary and troponin-mediated

c) Involuntary and troponin-mediated

d) Voluntary and calmodulin-mediated

Explanation:

Skeletal muscle is voluntary and regulated by troponin–tropomyosin complex, unlike smooth muscle. Correct answer: Voluntary and troponin-mediated.

10. Which structural arrangement is absent in smooth muscle compared to skeletal?

a) Sarcomere

b) Myosin

c) Actin

d) Intermediate filaments

Explanation:

Smooth muscle lacks sarcomere arrangement, hence appears non-striated. Myosin, actin, and intermediate filaments are present. Correct answer: Sarcomere.

Chapter: Neurophysiology

Topic: Nerve Fibres

Subtopic: Resting Membrane Potential

Keyword Definitions:

Resting Membrane Potential: Electrical potential difference across a cell membrane at rest.
Potassium Equilibrium: Balance between inward and outward K+ movement.
Surface Electrodes: External electrodes that measure global, not intracellular potentials.
Action Potential: Rapid depolarization and repolarization event in excitable tissue.
Sodium-Potassium Pump: Active transport maintaining high intracellular K+ and low Na+.

Lead Question - 2012

Resting membrane potential in nerve fibre

a) Is equal to the potential of ventricular muscle fibre
b) Can be measured by surface electrodes
c) Increases as extracellular K+ increases
d) Depends upon K+ equilibrium

Explanation: Resting membrane potential in nerve fibres is around –70 mV, determined mainly by K+ equilibrium across the membrane. It cannot be measured by surface electrodes, only by microelectrodes. Increased extracellular K+ reduces negativity, not increases it. Correct answer: d) Depends upon K+ equilibrium.

MCQ 2

A patient with hyperkalemia develops reduced resting membrane potential. What mechanism explains this?

a) Increased Na+ conductance
b) Decreased K+ gradient
c) Increased chloride influx
d) Enhanced Na+-K+ ATPase activity

Explanation: Hyperkalemia reduces the concentration gradient for potassium, lowering efflux and reducing negativity of resting potential. Correct answer: b) Decreased K+ gradient.

MCQ 3

Which ion movement contributes most to resting membrane potential?

a) Active calcium transport
b) Sodium influx
c) Potassium efflux
d) Chloride trapping

Explanation: Resting potential is mostly due to passive potassium efflux through leak channels. Na+ and Cl– have smaller roles. Correct answer: c) Potassium efflux.

MCQ 4

What is the approximate value of neuronal resting membrane potential?

a) +30 mV
b) 0 mV
c) –70 mV
d) –120 mV

Explanation: Resting membrane potential in neurons averages –70 mV, reflecting high K+ permeability and Na+/K+ pump activity. Correct answer: c) –70 mV.

MCQ 5

Resting membrane potential is measured using?

a) Surface electrodes
b) Patch clamp or microelectrodes
c) ECG leads
d) EMG surface electrodes

Explanation: Intracellular recording with glass microelectrodes or patch clamp measures true resting potential, not surface electrodes. Correct answer: b) Patch clamp or microelectrodes.

MCQ 6

A patient has hypokalemia. What happens to resting membrane potential?

a) Becomes less negative
b) Becomes more negative
c) No change
d) Oscillates

Explanation: In hypokalemia, extracellular K+ falls, increasing the gradient, making resting potential more negative (hyperpolarized). Correct answer: b) Becomes more negative.

MCQ 7

The Na+/K+ ATPase contributes to resting potential by?

a) Pumping 3 Na+ out and 2 K+ in
b) Pumping 2 Na+ in and 3 K+ out
c) Pumping equal Na+ and K+
d) Passive diffusion of ions

Explanation: The pump actively moves 3 Na+ out for every 2 K+ in, contributing directly to negativity of resting potential. Correct answer: a) Pumping 3 Na+ out and 2 K+ in.

MCQ 8

In ischemia, resting membrane potential decreases. Why?

a) Excess chloride influx
b) Pump failure due to ATP depletion
c) Enhanced potassium efflux
d) Excessive sodium extrusion

Explanation: ATP depletion in ischemia stops Na+/K+ ATPase, causing Na+ retention, K+ loss, and reduced resting potential. Correct answer: b) Pump failure due to ATP depletion.

MCQ 9

A nerve cell with –70 mV resting potential is depolarized to –50 mV. This means?

a) Membrane becomes more negative
b) Membrane becomes less negative
c) No change in excitability
d) Cell is in refractory period

Explanation: Depolarization reduces negativity, moving closer to threshold and increasing excitability. Correct answer: b) Membrane becomes less negative.

MCQ 10

Which disease involves abnormal resting potential due to ion channel defect?

a) Myasthenia gravis
b) Hyperkalemic periodic paralysis
c) Parkinson’s disease
d) Huntington’s disease

Explanation: In hyperkalemic periodic paralysis, Na+ channel mutations alter resting potential stability, causing episodic weakness. Correct answer: b) Hyperkalemic periodic paralysis.

MCQ 11

Resting membrane potential is closest to equilibrium potential of which ion?

a) Sodium
b) Potassium
c) Chloride
d) Calcium

Explanation: Because of high membrane permeability to K+, resting potential is closest to potassium equilibrium potential. Correct answer: b) Potassium.

Keyword Definitions

• Taste transduction: Mechanisms by which chemical stimuli are converted to neural signals.

• ENaC: Epithelial sodium channels mediating salty taste via Na+ influx.

• Gustducin: Taste G-protein involved in sweet, umami, and bitter signalling cascades.

• PKD2L1: Proton-sensitive channel implicated in sour taste transduction.

• Chorda tympani: Facial nerve branch (VII) carrying anterior two-thirds taste.

• Nucleus tractus solitarius (NTS): Medullary gustatory relay receiving cranial nerve afferents.

• VPM nucleus: Thalamic relay for facial/gustatory sensory information to cortex.

• Dysgeusia: Distorted taste perception commonly seen in disease or after drugs.

• Ageusia: Loss of taste sensation.

• Taste cell turnover: Continuous replacement of taste receptor cells from basal progenitors.

Chapter: Neurophysiology

Topic: Gustation (Taste Physiology)

Subtopic: Taste Transduction Mechanisms and Clinical Correlates

Lead Question – 2012

Salty taste is due to?

a) Ca+2 channels

b) Na+ channels

c) G-protein

d) H+ channels

Explanation: Salt taste transduction primarily occurs via epithelial sodium channels on taste receptor cells which allow Na+ influx, depolarizing the cell and triggering neurotransmitter release to gustatory nerves. This receptor mechanism explains perception of salty stimuli. Answer: b) Na+ channels. Clinically, sodium channel blockers reduce salty perception in experimental settings commonly.

Question 2

Sour taste transduction is primarily mediated by?

a) G-protein coupled receptors

b) Voltage-gated Ca2+ channels

c) ENaC channels

d) H+ (proton) channels

Explanation: Sour taste arises from H+ ions entering taste receptor cells through proton-sensitive channels (e.g., PKD2L1 or HCN modulation), causing depolarization and neurotransmitter release to gustatory afferents. This transduction distinguishes acidity in foods and guides ingestion or rejection. Answer: d) H+ channels. Clinically, sour detection may be reduced in zinc deficiency.

Question 3

Bitter taste receptors transduce signals via which mechanism?

a) ENaC-mediated depolarization

b) Ionotropic glutamate receptors

c) G-protein coupled T2R receptors

d) Direct H+ gating

Explanation: Bitter taste perception relies on G-protein–coupled T2R receptors activating gustducin and PLCβ2, increasing intracellular calcium and neurotransmitter release, signaling potential toxins and causing aversive responses. Genetic variability affects sensitivity to bitter compounds clinically. Answer: c) G-protein. Pharmacologic blockade of these pathways blunts bitter detection during drug therapy in some patients.

Question 4

Sweet taste transduction occurs through?

a) ENaC channels

b) Ionotropic receptors only

c) G-protein coupled T1R receptors

d) H+ channels

Explanation: Sweet taste is mediated by heterodimeric T1R2/T1R3 G-protein–coupled receptors activating gustducin and second messenger cascades, increasing intracellular calcium to depolarize taste cells and signal pleasant carbohydrate-rich nutrition. Artificial sweeteners selectively activate these receptors. Answer: c) G-protein. Clinical disorders like diabetes may alter sweet perception via receptor and central processing changes.

Question 5

Umami (savory) taste primarily uses which receptors?

a) ENaC only

b) Ionotropic serotonin receptors

c) T1R1/T1R3 G-protein receptors or mGluRs

d) Voltage-gated Na+ channels

Explanation: Umami taste responds to L-glutamate via T1R1/T1R3 G-protein–coupled receptors or mGluR receptors, enhancing savory flavor perception and signaling protein-rich foods. Monosodium glutamate exemplifies this transduction. Answer: c) G-protein. Clinical taste disturbances in chemotherapy can reduce umami sensitivity, contributing to anorexia and weight loss requiring dietary counseling often for patient recovery.

Question 6

Taste from anterior two-thirds of tongue is carried by?

a) Chorda tympani (facial nerve VII)

b) Glossopharyngeal nerve (IX)

c) Vagus nerve (X)

d) Hypoglossal nerve (XII)

Explanation: Taste from anterior two-thirds of tongue is transmitted by the chorda tympani branch of facial nerve (VII), carrying modality-specific signals to nucleus of solitary tract. Lesions produce ipsilateral ageusia and dysgeusia impacting appetite and nutrition. Answer: a) Chorda tympani (facial nerve). Testing assesses gustatory function clinically and guides management decisions.

Question 7

First central relay for taste afferents is?

a) Ventral posterolateral nucleus (VPL)

b) Nucleus tractus solitarius (NTS) in medulla

c) Insular cortex directly

d) Hypothalamus

Explanation: Primary central relay for gustatory afferents is the nucleus of the solitary tract in the medulla, receiving inputs from facial, glossopharyngeal, and vagus nerves and projecting to thalamus and cortex for taste perception and reflexes like salivation. Answer: b) Nucleus tractus solitarius (NTS). Lesions impair gustatory reflexes and taste perception.

Question 8

Which pharmacologic agent reduces salty taste by blocking ENaC experimentally?

a) Lidocaine

b) Amiloride

c) Ondansetron

d) Scopolamine

Explanation: Epithelial sodium channel (ENaC) blockers such as amiloride reduce perception of salty taste by inhibiting Na+ entry into taste cells, demonstrating pharmacologic modulation of taste transduction. This informs pathophysiology and potential therapies for dysgeusia. Answer: b) Na+ channels. Clinical trials assess amiloride's effect on taste alteration in various disorders today.

Question 9

Which condition commonly causes ipsilateral anterior two-thirds taste loss?

a) Bell's palsy

b) Stroke of occipital lobe

c) Otitis externa only

d) Myasthenia gravis

Explanation: Bell's palsy commonly causes ipsilateral anterior two-thirds taste loss due to chorda tympani fiber involvement within the facial nerve; patients report dysgeusia and ageusia with associated facial weakness. Distinguishing peripheral facial palsy from central lesions guides prognosis and therapy, often including corticosteroids. Answer: a) Bell's palsy improving recovery in many.

Question 10

Approximate turnover time of taste receptor cells is?

a) Several years

b) Ten to fourteen days

c) Months

d) Hours

Explanation: Taste receptor cells have a high turnover, regenerating from basal progenitors approximately every ten to fourteen days, maintaining gustatory sensitivity and repair after injury; disrupted regeneration from chemotherapy or aging contributes to chronic dysgeusia and nutritional problems. Answer: b) ~10 days. Monitoring taste during chemotherapy aids patient counseling and management.

Question 11

Thalamic relay for taste to cortex is which nucleus?

a) VPL nucleus

b) VPM nucleus

c) Lateral geniculate nucleus

d) Medial geniculate nucleus

Explanation: Gustatory signals ascend to the ventral posteromedial nucleus of the thalamus, which relays taste information to the insular and frontal opercular cortex for conscious perception, discrimination, and hedonic valuation, integrating with olfactory input for flavor. Lesions produce contralateral taste deficits. Answer: b) VPM nucleus. Taste testing aids localization of lesions.

Keyword Definitions

• Central chemoreceptors: Medullary sensors responding to CSF pH/CO₂ changes and driving ventilation.

• Peripheral chemoreceptors: Carotid and aortic body receptors sensing arterial O₂, CO₂ and pH.

• Carotid body: Small chemo-sensitive organ at carotid bifurcation.

• Aortic body: Chemoreceptor tissue near aortic arch.

• Area postrema: Brainstem chemoreceptive region outside blood-brain barrier.

• Nucleus tractus solitarius (NTS): Medullary visceral sensory nucleus receiving vagal and glossopharyngeal afferents.

• Hypercapnia: Elevated arterial CO₂ stimulating central chemoreceptors.

• Hypoxia: Low arterial O₂ primarily stimulating peripheral chemoreceptors.

• Ventilatory drive: Neural control that adjusts rate and depth of breathing.

• Respiratory reflexes: Integrated responses coordinating breathing with cardiovascular state.

• Respiratory failure: Clinical condition from inadequate ventilation or gas exchange.

Chapter: Respiratory Physiology

Topic: Chemoreceptors and Respiratory Control

Subtopic: Central and Peripheral Chemoreceptors

Lead Question – 2012 (177)

Chemoreceptors are located in which area?

a) Medulla

b) Arch of aorta

c) Bifurcation of carotid artery

d) All of the above

Explanation: Chemoreceptors that regulate ventilation are both central and peripheral: central receptors in the medulla sense CSF pH changes from CO₂; peripheral chemoreceptors reside in the carotid bifurcation and aortic arch sensing arterial O₂, CO₂ and pH. They act together to regulate breathing. Answer: d) All of the above.

Question 2

Central chemoreceptors primarily respond to which stimulus?

a) Arterial O₂ fall

b) CSF pH change due to CO₂ diffusion

c) Blood glucose levels

d) Systemic blood pressure changes

Explanation: Central chemoreceptors in the ventrolateral medulla detect changes in CSF pH produced by CO₂ diffusion across the blood-brain barrier. This mechanism drives ventilation in response to hypercapnia and maintains acid-base homeostasis. Peripheral O₂ sensing is separate. Answer: b) CSF pH change due to CO₂ diffusion.

Question 3

Peripheral chemoreceptors that sense hypoxia at the carotid bifurcation transmit via which nerve?

a) Vagus nerve (X)

b) Glossopharyngeal nerve (IX)

c) Hypoglossal nerve (XII)

d) Facial nerve (VII)

Explanation: Carotid body afferents travel in the glossopharyngeal nerve (cranial nerve IX) to the nucleus tractus solitarius, which relays to respiratory centers, producing rapid ventilatory responses to hypoxia. Answer: b) Glossopharyngeal nerve (IX).

Question 4

Aortic body chemoreceptors convey information primarily via which pathway?

a) Glossopharyngeal nerve (IX) only

b) Vagus nerve (X) afferents

c) Trigeminal nerve (V) afferents

d) Direct spinal tract only

Explanation: Aortic arch chemoreceptors send afferent signals largely through vagal (X) fibers to the nucleus tractus solitarius in the medulla, complementing carotid body input to adjust ventilation and autonomic reflexes. Answer: b) Vagus nerve (X) afferents.

Question 5

Which chemoreceptor set predominates in response to acute hypoxemia?

a) Central medullary chemoreceptors

b) Peripheral carotid chemoreceptors

c) Renal chemoreceptors

d) Cortical chemoreceptors

Explanation: Peripheral carotid chemoreceptors are the primary detectors of arterial hypoxemia, responding rapidly to low PaO₂ and increasing ventilation quickly; central chemoreceptors mainly respond to CO₂/pH changes. Answer: b) Peripheral carotid chemoreceptors.

Question 6

Which condition blunts the ventilatory response to hypoxia due to carotid body removal or dysfunction?

a) Enhanced hypoxic drive

b) Diminished hypoxic ventilatory response

c) Increased cough reflex

d) Hyperventilation at rest

Explanation: Loss or dysfunction of carotid bodies reduces the rapid ventilatory response to hypoxia, causing a blunted hypoxic ventilatory drive clinically; patients rely more on central CO₂ sensitivity, risking inadequate ventilation during low oxygen states. Answer: b) Diminished hypoxic ventilatory response.

Question 7

Drugs that depress central chemoreceptor sensitivity commonly cause which effect?

a) Tachypnea

b) Hypoventilation and hypercapnia

c) Increased oxygen saturation

d) Enhanced hypoxic drive

Explanation: Sedatives and opioids depress central chemoreceptor responsiveness, reducing ventilatory drive to CO₂ and causing hypoventilation with rising arterial CO₂ and respiratory acidosis; careful monitoring and dose adjustment are clinically required. Answer: b) Hypoventilation and hypercapnia.

Question 8

Which bedside test best evaluates peripheral chemoreceptor function?

a) Hypercapnic ventilatory challenge

b) Hypoxic ventilatory response testing

c) Valsalva maneuver only

d) Pupillary reflex testing

Explanation: Hypoxic ventilatory response testing assesses peripheral chemoreceptor sensitivity by measuring ventilation changes when inspired oxygen is lowered; it helps distinguish peripheral dysfunction from central CO₂ responsiveness. Answer: b) Hypoxic ventilatory response testing.

Question 9

Which pathology explains reduced central chemosensitivity causing sleep hypoventilation?

a) Medullary lesion or congenital central hypoventilation syndrome

b) Peripheral nerve entrapment

c) Middle ear infection

d) Muscle strain

Explanation: Central hypoventilation may arise from medullary damage or congenital central hypoventilation syndrome, impairing CO₂ detection and ventilation particularly during sleep, often necessitating ventilatory support. Answer: a) Medullary lesion or congenital central hypoventilation syndrome.

Question 10

Which combination best describes chemoreceptor roles?

a) Carotid bodies sense CO₂ only; medulla senses O₂ only

b) Peripheral receptors detect hypoxia quickly; central receptors monitor CO₂/pH continuously

c) Aortic arch controls consciousness; carotid bodies control heart rate only

d) None of the above

Explanation: Peripheral receptors (carotid and aortic bodies) detect hypoxia rapidly and signal ventilatory increase; central medullary chemoreceptors continuously monitor CO₂/pH to regulate baseline ventilation. Together they coordinate appropriate respiratory responses. Answer: b) Peripheral receptors detect hypoxia quickly; central receptors monitor CO₂/pH continuously.

Question 11

Which clinical statement is correct regarding chemoreceptor physiology?

a) Only central receptors respond to severe hypoxia

b) Peripheral receptors play no role in ventilatory adaptation at altitude

c) Both central and peripheral chemoreceptors integrate to control ventilation

d) Chemoreceptors exclusively control heart rate, not breathing

Explanation: Ventilatory control reflects integrated input from central and peripheral chemoreceptors, with each contributing specific sensitivity to CO₂/pH and O₂ changes; combined signaling ensures respiratory adaptation to metabolic demands, altitude, and disease states. Answer: c) Both central and peripheral chemoreceptors integrate to control ventilation.

Keyword Definitions

• Vomiting centre: Brainstem nuclei coordinating emesis reflex integrating multisource inputs.

• Area postrema: Chemoreceptor trigger zone at floor of fourth ventricle, outside BBB.

• Nucleus tractus solitarius (NTS): Primary visceral sensory nucleus relaying vagal afferents.

• Chemoreceptor trigger zone (CTZ): Detects blood-borne emetic agents and drugs.

• Vestibular nuclei: Brainstem centers mediating motion and balance inputs causing motion sickness.

• Reticular formation: Medullary network housing central pattern generator for vomiting.

• Ondansetron: 5-HT3 receptor antagonist used for chemotherapy and postoperative nausea.

• Scopolamine: Antimuscarinic antiemetic effective for motion sickness via vestibular blockade.

• Apomorphine: Dopamine agonist that stimulates CTZ and induces vomiting pharmacologically.

• Projectile vomiting: Forceful vomiting often from raised intracranial pressure or posterior fossa lesions.

• NK1 antagonist (Aprepitant): Blocks substance P to prevent chemotherapy-induced nausea and vomiting.

Chapter: Neurophysiology

Topic: Brainstem Reflexes

Subtopic: Vomiting Mechanisms and Clinical Correlates

Lead Question – 2012

Vomiting centre is situated in the: (September 2008)

a) Hypothalamus

b) Midbrain

c) Pons

d) Medulla

Explanation: Vomiting is coordinated by a reflex center located in the medulla oblongata, integrating signals from chemoreceptor trigger zone, vestibular system, GI tract, and higher centers. Lesions or irritants trigger emesis via medullary nuclei. Answer: d) Medulla. This clinically explains why brainstem lesions often produce persistent vomiting and autonomic disturbances.

Question 2

Which structure functions as the chemoreceptor trigger zone for emesis?

a) Nucleus ambiguus

b) Nucleus tractus solitarius

c) Area postrema

d) Dorsal motor nucleus of vagus

Explanation: The chemoreceptor trigger zone lies in the area postrema of the dorsal medulla at the floor of the fourth ventricle, outside the blood-brain barrier, detecting blood-borne emetic agents and drugs. It relays to the vomiting center to initiate emesis. Answer: c) Area postrema. This localization explains sensitivity to chemotherapeutic agents.

Question 3

Visceral afferents from the gastrointestinal tract synapse primarily in which nucleus relevant to vomiting?

a) Hypoglossal nucleus

b) Nucleus tractus solitarius

c) Inferior olivary nucleus

d) Dorsal motor nucleus of vagus

Explanation: Visceral afferents from gastrointestinal tract travel via vagus and glossopharyngeal nerves to the nucleus tractus solitarius in the medulla, which integrates sensory input and projects to the vomiting center and reticular formation. This pathway mediates reflex emesis from gastric irritation or inflammation. Answer: b) Nucleus tractus solitarius clinically important centrally.

Question 4

Which antiemetic class blocks serotonin-mediated vagal and CTZ signals effectively?

a) Dopamine antagonists

b) Anticholinergics

c) 5-HT3 receptor antagonists

d) NK1 receptor antagonists

Explanation: 5-HT3 receptor antagonists such as ondansetron block serotonin-mediated stimulation of vagal afferents and the chemoreceptor trigger zone, effectively preventing chemotherapy-induced and postoperative nausea. They act centrally and peripherally with good efficacy and tolerability and are first-line antiemetics in many protocols. Answer: a) Ondansetron. Widely used clinically for nausea control effectively.

Question 5

Motion sickness and vestibular-induced vomiting primarily involve which structures?

a) Area postrema only

b) Vestibular nuclei

c) Cerebellar vermis only

d) Hypothalamus exclusively

Explanation: Vestibular apparatus and vestibular nuclei in brainstem detect motion and send signals to vomiting center and cerebellum; conflicts between visual and vestibular input provoke motion sickness and emesis via connections to nucleus tractus solitarius and area postrema. Antihistamines reduce vestibular input. Answer: b) Vestibular nuclei. Used antiemetics target this pathway.

Question 6

Which drug class is known to directly stimulate the CTZ and produce emesis historically?

a) Anticholinergics

b) Serotonin antagonists

c) Dopamine agonists (e.g., apomorphine)

d) NK1 antagonists

Explanation: Apomorphine, a dopamine agonist, stimulates D2 receptors in the chemoreceptor trigger zone (area postrema), provoking profound emesis. Historically used as an emetic, it demonstrates pharmacologic activation of vomiting circuits. Dopamine antagonists block this reflex therapeutically. Answer: c) Apomorphine. Now replaced by safer antiemetics in teaching.

Question 7

Strong risk factors for postoperative nausea and vomiting include which of the following?

a) Male sex and smoking

b) Female sex and opioid use

c) Elderly age exclusively

d) Short duration surgeries only

Explanation: Risk factors for postoperative nausea and vomiting include female sex, history of motion sickness or prior PONV, nonsmoking status, use of volatile anesthetics or opioids, lengthy surgery, and younger age. Multimodal prophylaxis reduces incidence by targeting multiple pathways. Answer: b) Female sex and opioid exposure are significant risk contributors clinically.

Question 8

Best prophylactic agent for motion sickness is?

a) Ondansetron

b) Metoclopramide

c) Domperidone

d) Scopolamine

Explanation: Anticholinergic scopolamine applied transdermally blocks muscarinic receptors in vestibular nuclei and central vomiting pathways, preventing motion-induced nausea and vomiting. Histamine H1 antagonists like promethazine also help. Side effects include dry mouth, blurred vision, and sedation. Answer: d) Scopolamine. It is recommended prophylactically for susceptible patients before travel or procedures commonly.

Question 9

The central pattern generator coordinating emesis resides in which region?

a) Medullary reticular formation

b) Hypothalamus

c) Midbrain periaqueductal gray

d) Pontine tegmentum exclusively

Explanation: Emesis results from activation of a central pattern generator located in the medullary reticular formation and adjacent reticular nuclei, coordinating respiratory, upper GI, and pharyngeal muscles to produce vomiting. This network receives multisensory inputs including chemoreceptor trigger zone and vestibular signals. Answer: a) Medullary reticular formation critical for protective reflexes.

Question 10

Projectile vomiting without nausea often indicates which pathology?

a) Gastroenteritis

b) Metabolic alkalosis only

c) Posterior fossa lesion compressing medulla

d) Peripheral vestibular neuritis

Explanation: Projectile vomiting without preceding nausea suggests increased intracranial pressure or posterior fossa lesion compressing medullary centers. Vomiting may be forceful and predominantly nocturnal. Early recognition mandates neuroimaging to identify obstructive hydrocephalus or tumor. Answer: c) Posterior fossa lesion causing medullary compression requiring urgent neurosurgical decompression to prevent herniation and death.

Question 11

Which agent is recommended to prevent both acute and delayed chemotherapy-induced emesis when combined with others?

a) Ondansetron alone

b) Aprepitant (NK1 antagonist)

c) Metoclopramide alone

d) Scopolamine patch

Explanation: Aprepitant, an NK1 receptor antagonist, blocks substance P signaling in vomiting pathways, reducing acute and delayed chemotherapy-induced nausea and vomiting when combined with 5-HT3 antagonists and corticosteroids. It improves control of emesis after highly emetogenic chemotherapy. Answer: b) Aprepitant. Recommended in guidelines for high emetic risk regimens to reduce vomiting.

Keyword Definitions

• Spinocerebellar tract: Pathways conveying unconscious proprioception to cerebellum for coordination.

• Dorsal spinocerebellar: Ipsilateral lower limb proprioceptive tract entering via inferior peduncle.

• Ventral spinocerebellar: Tract that double-crosses and conveys integrated movement signals to cerebellum.

• Cuneocerebellar: Upper limb equivalent of dorsal spinocerebellar, via accessory cuneate nucleus.

• Clarke’s column: Nucleus dorsalis (T1–L2) origin of dorsal spinocerebellar fibres.

• Inferior cerebellar peduncle: Major cerebellar input for dorsal spinocerebellar and cuneocerebellar tracts.

• Unconscious proprioception: Automatic sensory feedback used to adjust movement without awareness.

• Dysmetria: Overshoot or undershoot of target during voluntary movement, sign of cerebellar dysfunction.

• Intention tremor: Tremor appearing during voluntary movement, characteristic of cerebellar disease.

• Romberg sign: Sway or fall on eye closure from proprioceptive loss (dorsal column), not cerebellar typically.

• Heel-to-shin: Bedside test for lower limb cerebellar coordination and spinocerebellar function.

Chapter: Neurophysiology

Topic: Cerebellar Systems

Subtopic: Spinocerebellar Tracts and Function

Lead Question – 2012

True about spinocerebellar tract is?

a) Equilibrium

b) Smoothens and coordinates movement

c) Learning induced by change in vestibulo ocular reflex

d) Planning and programming

Explanation: Spinocerebellar tracts carry unconscious proprioceptive information from muscles and joints to the cerebellum, enabling real-time adjustment of ongoing movements and posture. They assist coordination and timing rather than motor planning or voluntary initiation. Therefore they smooth and coordinate movement. Answer: b) Smoothens and coordinates movement for precise limb control continuously.

Question 2

Dorsal spinocerebellar tract originates from which nucleus?

a) Clarke’s column

b) Accessory cuneate nucleus

c) Inferior olivary nucleus

d) Red nucleus

Explanation: The dorsal spinocerebellar tract arises from Clarke’s column (nucleus dorsalis) in spinal segments T1 to L2, conveying ipsilateral proprioceptive information from lower limbs to the cerebellum via the inferior cerebellar peduncle. It does not decussate. Answer: a) Clarke’s column. This tract is essential for unconscious proprioception and limb coordination clinically.

Question 3

A lesion of spinocerebellar tract produces which clinical sign?

a) Ipsilateral limb ataxia

b) Contralateral weakness

c) Loss of vibration sense only

d) Sensory level with aneasthesia

Explanation: Spinocerebellar tract lesions produce ipsilateral limb ataxia because most cerebellar afferents enter the cerebellum without crossing or double-cross, preserving same-side representation. Patients show dysmetria, decomposition of movement, and intention tremor on the affected side. Answer: a) Ipsilateral limb ataxia. Coordination deficits worsen with eyes closed and during rapid alternating movements.

Question 4

Which is true about ventral spinocerebellar tract?

a) It never crosses

b) It conveys conscious proprioception

c) It double-crosses

d) It terminates in thalamus

Explanation: The ventral spinocerebellar tract transmits integrated proprioceptive and interneuronal activity related to ongoing limb movement. It decussates twice: once in the spinal cord and again within the cerebellum, resulting in ipsilateral cerebellar representation ultimately. Answer: c) It double-crosses to reach the cerebellum. This anatomical feature explains localization of cerebellar signs.

Question 5

Primary modality carried by spinocerebellar tracts is?

a) Conscious proprioception

b) Unconscious proprioception

c) Pain and temperature

d) Fine tactile discrimination

Explanation: Spinocerebellar pathways convey unconscious proprioception from muscle spindles and Golgi tendon organs to cerebellar cortex, enabling automatic postural adjustments and gait coordination. They are distinct from dorsal columns that mediate conscious proprioception. Answer: b) Unconscious proprioception. Clinical lesions produce ataxia yet preserve conscious position sense; coordination testing reveals deficits often.

Question 6

Finger-to-nose test primarily assesses which system?

a) Cerebellar coordination including spinocerebellar input

b) Dorsal column conscious proprioception only

c) Spinothalamic tract function

d) Pyramidal tract strength

Explanation: Finger-to-nose test evaluates cerebellar coordination and proprioceptive integration including spinocerebellar inputs. Dysmetria, intention tremor, and decomposition of movement during this test indicate cerebellar dysfunction. It does not differentiate conscious from unconscious proprioception but assesses functional output of cerebellum. Answer: a) True. Clinically helps localize lesion to hemisphere or vermis region.

Question 7

Which hereditary disease affects spinocerebellar tracts prominently?

a) Multiple sclerosis

b) Amyotrophic lateral sclerosis

c) Friedreich ataxia

d) Myasthenia gravis

Explanation: Friedreich ataxia causes degeneration of spinocerebellar tracts, dorsal columns, and corticospinal tracts due to frataxin deficiency. Patients present with progressive gait ataxia, loss of vibration and proprioception, areflexia, and cardiomyopathy. Genetic testing confirms GAA repeat expansion. Answer: c) Friedreich ataxia. Onset usually adolescence; progression causes severe disability needing supportive care.

Question 8

Dorsal spinocerebellar fibres enter cerebellum via which peduncle?

a) Inferior cerebellar peduncle

b) Middle cerebellar peduncle

c) Superior cerebellar peduncle

d) None of the above

Explanation: Dorsal spinocerebellar fibers ascend ipsilaterally and enter cerebellum through the inferior cerebellar peduncle, carrying lower limb proprioceptive information. Ventral spinocerebellar fibers primarily enter via superior peduncle after double crossing. Knowledge of peduncle entry assists lesion localization. Answer: a) Inferior cerebellar peduncle. Distinguishing peduncle entry aids accurate lesion localization clinically rapidly.

Question 9

Romberg sign in spinocerebellar or cerebellar lesions is usually?

a) Positive only with eyes open

b) Negative (does not depend on vision)

c) Positive only with vibration loss

d) Always bilateral sensory level

Explanation: Romberg sign becomes positive when proprioceptive input via dorsal columns is lost, causing increased sway with eye closure. Cerebellar or spinocerebellar lesions produce ataxia independent of visual input, so patients remain unstable with eyes open and closed; Romberg is typically negative. Answer: b) Negative. Clinical testing distinguishes lesion location effectively.

Question 10

Best bedside test for lower limb spinocerebellar function is?

a) Romberg test alone

b) Vibration at toe only

c) Rapid alternating foot movements only

d) Heel-to-shin test

Explanation: Heel-to-shin maneuver tests lower limb coordination and cerebellar integration of proprioceptive input including spinocerebellar feedback. Patients with spinocerebellar tract or cerebellar hemisphere lesions exhibit dysmetria and inability to maintain a smooth, straight movement along the shin. Answer: d) Heel-to-shin test. It detects ipsilateral coordination deficits and helps lateralize lesions accurately.

Question 11

Unconscious proprioception from the upper limb is conveyed by?

a) Dorsal spinocerebellar tract

b) Cuneocerebellar tract

c) Ventral spinothalamic tract

d) Lateral corticospinal tract

Explanation: Cuneocerebellar tract carries unconscious proprioceptive input from upper limbs via accessory cuneate nucleus to the cerebellum through inferior peduncle, analogous to dorsal spinocerebellar tract for lower limbs. Lesions impair ipsilateral upper limb coordination and contribute to ataxia. Answer: b) Cuneocerebellar tract. Clinically causes dysmetria and intention tremor during voluntary tasks.

Keyword Definitions

• Proprioception: Sense of position and movement from muscles and joints.

• Vibration sense: Perception of oscillatory stimuli via large myelinated fibers.

• Dorsal columns: Ascending pathway for fine touch, vibration, and proprioception.

• Medial lemniscus: Brainstem tract formed by decussated dorsal column fibers.

• Fasciculus gracilis: Dorsal column for lower limb and trunk below T6.

• Fasciculus cuneatus: Dorsal column for upper limb and trunk above T6.

• VPL nucleus: Thalamic relay for body somatosensation to cortex.

• Romberg sign: Instability on eye closure indicating proprioceptive loss.

• Brown-Séquard syndrome: Hemisection causing ipsilateral dorsal column loss, contralateral pain loss.

• Tabes dorsalis: Neurosyphilis causing posterior column degeneration and sensory ataxia.

• Syringomyelia: Central canal cavity causing bilateral pain/temperature loss with spared dorsal columns.

• Asterognosis: Inability to recognize objects by touch despite intact basic sensation.

• Large-fiber neuropathy: Peripheral nerve disorder affecting vibration and position sense early.

Chapter: Neurophysiology

Topic: Somatosensory Pathways

Subtopic: Dorsal Column–Medial Lemniscus System

Lead Question – 2012

Loss of proprioception & fine touch ?

a) Anterior spinothalamic tract

b) Lateral spinothalamic tract

c) Dorsal column

d) Corticospinal tract

Explanation: Loss of proprioception, vibration, and fine discriminative touch indicates dorsal column–medial lemniscus pathway dysfunction. Large myelinated fibers ascend ipsilaterally to gracile and cuneate nuclei, then decussate to medial lemniscus and VPL. Answer: c) Dorsal column. Spinothalamic tracts carry pain and temperature; corticospinal mediates voluntary movement, not somatosensory modalities, primarily pathways.

Question 2

A 55-year-old with numb feet, gait unsteadiness, and positive Romberg has impaired vibration at toes. Which pathway is damaged?

a) Dorsal columns

b) Lateral corticospinal tract

c) Spinothalamic tract

d) Vestibulospinal tract

Explanation: Subacute combined degeneration from vitamin B12 deficiency damages large myelinated posterior column fibers, producing sensory ataxia, impaired vibration, and proprioceptive loss in legs. Answer: a) Dorsal columns. Lateral corticospinal damage causes weakness and spasticity; spinothalamic lesions impair pain and temperature; vestibulospinal tracts mediate balance reflexes without conveying discriminative touch signals.

Question 3

After a knife injury causing right T10 hemisection, which deficit occurs on the right below the lesion?

a) Loss of pain and temperature

b) Loss of vibration and proprioception

c) Flaccid paralysis below lesion

d) Bilateral pain loss

Explanation: Brown-Séquard hemisection causes ipsilateral loss of dorsal column modalities below the lesion from uncrossed ascent, and contralateral pain/temperature loss after spinothalamic decussation. Answer: b) Loss of vibration and proprioception. Flaccid paralysis occurs at the level from anterior horn involvement, not below. Bilateral pain loss suggests central cord lesions, not hemisection.

Question 4

Which thalamic nucleus relays body fine touch, vibration, and proprioception to cortex?

a) VPL nucleus

b) VPM nucleus

c) Lateral geniculate nucleus

d) Medial geniculate nucleus

Explanation: The ventral posterolateral thalamic nucleus relays somatosensory information from body—both medial lemniscus and spinothalamic—to the primary somatosensory cortex. Lesions impair discriminative touch, vibration, and proprioception contralaterally. Answer: a) VPL nucleus. VPM handles facial sensation; LGN vision; MGN audition. Precise localization of body sensation depends critically on intact VPL relay neurons.

Question 5

A patient with lightning pains, wide-based gait, and positive Romberg likely has damage to which structure?

a) Dorsal columns

b) Spinocerebellar tracts

c) Ventral horn cells

d) Substantia nigra

Explanation: Tabes dorsalis from neurosyphilis degenerates dorsal columns and roots, causing lightning pains, sensory ataxia, impaired vibration, and positive Romberg sign. Answer: a) Dorsal columns. Spinocerebellar tract disease produces limb ataxia without Romberg positivity; ventral horn disease causes lower motor neuron weakness; substantia nigra degeneration produces Parkinsonism, not sensory ataxia, classically.

Question 6

Fine touch from the right hand ascends initially in which tract?

a) Spinothalamic tract

b) Fasciculus gracilis

c) Fasciculus cuneatus

d) Dorsal spinocerebellar tract

Explanation: Fine touch and proprioceptive signals from the upper limb ascend in the ipsilateral fasciculus cuneatus to synapse in the cuneate nucleus before crossing as internal arcuate fibers. Answer: c) Fasciculus cuneatus. Fasciculus gracilis conveys lower limb input; spinothalamic carries pain and temperature; dorsal spinocerebellar conveys unconscious proprioception, not discriminative touch.

Question 7

A patient cannot identify a key by touch in the left hand, yet basic touch is intact. Likely lesion?

a) Cerebellar hemisphere

b) Postcentral gyrus

c) Precentral gyrus

d) Dorsal horn

Explanation: Inability to recognize objects by touch with intact primary modalities indicates cortical sensory loss—astereognosis—from a contralateral parietal lesion, usually postcentral gyrus (primary somatosensory cortex). Answer: b) Postcentral gyrus. Precentral gyrus is motor; cerebellum coordinates movement but not stereognosis; dorsal columns carry signals, yet cortical interpretation is required for object recognition.

Question 8

Bilateral loss of pain and temperature over shoulders with preserved vibration suggests which tract is spared?

a) Spinothalamic tract

b) Lateral corticospinal tract

c) Anterior horn cells

d) Dorsal columns

Explanation: Syringomyelia damages decussating anterior commissural spinothalamic fibers in the cervical cord, causing bilateral cape-like pain and temperature loss while sparing dorsal column modalities. Answer: d) Dorsal columns are spared. Thus vibration and proprioception remain intact. Lateral corticospinal may be affected later causing weakness; dorsal spinocerebellar mediates unconscious proprioception effectively overall.

Question 9

A medial medullary infarct damaging the medial lemniscus causes which deficit?

a) Ipsilateral pain and temperature loss

b) Loss of contralateral discriminative touch

c) Ipsilateral loss of vibration

d) Bilateral pain loss

Explanation: A medial medullary lesion involving the medial lemniscus produces contralateral loss of fine touch, vibration, and proprioception from body due to disruption of dorsal column fibers. Answer: b) Loss of contralateral discriminative touch. Pain and temperature are carried by spinothalamic tract located laterally; hypoglossal involvement would cause ipsilateral tongue weakness.

Question 10

Which modality is typically earliest impaired in large-fiber diabetic neuropathy?

a) Impaired vibration sense

b) Spasticity

c) Hyperalgesia

d) Nystagmus

Explanation: Large-fiber peripheral neuropathy in diabetes affects vibration and position sense earliest, causing positive Romberg and sensory ataxia. Answer: a) Impaired vibration sense. Pain and temperature rely on small fibers; strength may be preserved; hyperreflexia suggests upper motor neuron disease, not peripheral neuropathy, which typically shows reduced or absent ankle reflexes.

Question 11

Which bedside test best assesses dorsal column proprioception?

a) Graphesthesia on palm

b) Vibration at medial malleolus

c) Great toe position sense

d) Hot/cold discrimination

Explanation: Testing joint position at the great toe assesses conscious proprioception via dorsal columns and medial lemniscus. Eyes are closed to remove visual cues. Answer: c) Great toe position sense. Tuning fork tests vibration, not position; pinprick examines spinothalamic pain; plantar response assesses corticospinal integrity, unrelated to dorsal column proprioceptive function.

Keyword Definitions

• Dopamine: Catecholamine neurotransmitter crucial for motor control, motivation, and reward pathways.

• Nigrostriatal pathway: Dopaminergic pathway projecting from substantia nigra to striatum, vital for movement regulation.

• Serotonin: Neurotransmitter involved in mood, sleep, and appetite regulation.

• Cholinergic neurons: Use acetylcholine, important in learning, memory, and motor circuits.

• Adrenergic neurons: Release norepinephrine, essential for arousal, vigilance, and autonomic functions.

• Substantia nigra: Midbrain nucleus producing dopamine, degeneration causes Parkinsonism.

• Basal ganglia: Group of nuclei modulating movement initiation and suppression.

• Extrapyramidal system: Motor system controlling posture, tone, and coordination.

• Parkinson’s disease: Neurodegenerative disorder due to dopaminergic loss in nigrostriatal pathway.

• Dyskinesia: Involuntary abnormal movements due to neurotransmitter imbalance.

• Levodopa: Dopamine precursor used as therapy in Parkinson’s disease.

Chapter: Neurophysiology

Topic: Basal Ganglia

Subtopic: Nigrostriatal Pathway

Lead Question – 2012

Neurotransmitter involved in nigrostriatal pathway is?

a) Serotonin

b) Dopamine

c) Cholinergic

d) Adrenergic

Explanation: The nigrostriatal pathway is a dopaminergic tract connecting substantia nigra pars compacta with the striatum. It regulates voluntary movement by balancing excitatory and inhibitory signals in basal ganglia circuits. Loss of dopamine here causes Parkinsonism. Answer: b) Dopamine. Other neurotransmitters modulate but dopamine is the principal one involved.

Question 2

Which brain structure degenerates in Parkinson’s disease?

a) Substantia nigra pars compacta

b) Globus pallidus externa

c) Red nucleus

d) Subthalamic nucleus

Explanation: Parkinson’s disease arises from dopaminergic neuronal loss in substantia nigra pars compacta, leading to striatal dopamine deficiency. This impairs basal ganglia modulation, causing bradykinesia, rigidity, and tremor. Answer: a) Substantia nigra pars compacta. Subthalamic nucleus lesions cause hemiballismus, while pallidal and red nucleus lesions show different deficits.

Question 3

Which dopamine receptor subtype facilitates the direct pathway in basal ganglia?

a) D1 receptors

b) D2 receptors

c) D3 receptors

d) D4 receptors

Explanation: D1 receptors in striatum stimulate the direct pathway, enhancing movement by exciting striatal neurons projecting to internal globus pallidus. Dopamine binding here increases activity, disinhibiting thalamus and promoting cortical excitation. Answer: a) D1 receptors. D2 receptors inhibit indirect pathway, while D3 and D4 are extrastriatal predominantly.

Question 4

Which clinical feature is not typical of Parkinson’s disease?

a) Rest tremor

b) Bradykinesia

c) Rigidity

d) Spastic paralysis

Explanation: Parkinson’s disease is characterized by rest tremor, bradykinesia, rigidity, and postural instability. Spastic paralysis occurs in upper motor neuron lesions, not basal ganglia dysfunction. Answer: d) Spastic paralysis. Distinguishing Parkinsonism from pyramidal tract damage clinically relies on absence of spasticity and hyperreflexia, despite motor difficulties and tremors.

Question 5

Which neurotransmitter imbalance causes Huntington’s disease?

a) Loss of GABA and acetylcholine

b) Excess dopamine

c) Loss of dopamine

d) Increased serotonin

Explanation: Huntington’s disease features degeneration of striatal GABAergic and cholinergic neurons, combined with relative dopaminergic overactivity. This imbalance produces choreiform hyperkinetic movements. Answer: a) Loss of GABA and acetylcholine. Dopamine blockade may reduce symptoms, unlike Parkinson’s disease where dopamine replacement is therapeutic and symptomatically beneficial clinically.

Question 6

Which drug increases brain dopamine by crossing blood-brain barrier?

a) Levodopa

b) Dopamine

c) Carbidopa

d) Bromocriptine

Explanation: Dopamine itself cannot cross the blood-brain barrier. Levodopa, its precursor, is converted to dopamine in brain. Carbidopa prevents peripheral breakdown, enhancing central availability. Answer: a) Levodopa. Bromocriptine is a dopamine agonist, while dopamine injection only acts peripherally without improving Parkinson’s motor symptoms effectively within CNS.

Question 7

Which basal ganglia lesion produces hemiballismus?

a) Subthalamic nucleus

b) Putamen

c) Caudate nucleus

d) Globus pallidus interna

Explanation: Hemiballismus, a flinging hyperkinetic movement disorder, occurs due to contralateral subthalamic nucleus lesion. Subthalamus normally excites globus pallidus interna, inhibiting thalamus. Its damage reduces inhibition, causing excessive cortical motor output. Answer: a) Subthalamic nucleus. Other basal ganglia nuclei lesions cause Parkinsonism or chorea, not violent ballistic movements.

Question 8

Which dopaminergic pathway is associated with reward and addiction?

a) Nigrostriatal pathway

b) Mesolimbic pathway

c) Tuberoinfundibular pathway

d) Mesocortical pathway

Explanation: Mesolimbic pathway projects from ventral tegmental area to nucleus accumbens, mediating reward, reinforcement, and addiction. Answer: b) Mesolimbic pathway. Nigrostriatal controls movement, mesocortical regulates cognition and emotion, and tuberoinfundibular inhibits prolactin secretion. Dopamine thus has multiple distinct functional pathways in the central nervous system overall.

Question 9

Blockade of which dopamine pathway leads to drug-induced Parkinsonism?

a) Mesolimbic

b) Mesocortical

c) Nigrostriatal

d) Tuberoinfundibular

Explanation: Antipsychotic drugs blocking D2 receptors in the nigrostriatal pathway cause extrapyramidal symptoms resembling Parkinson’s disease. Answer: c) Nigrostriatal. Mesolimbic blockade improves psychosis, mesocortical blockade causes cognitive dulling, and tuberoinfundibular blockade elevates prolactin. Understanding pathway selectivity helps minimize antipsychotic side effects clinically during patient treatment overall effectively.

Question 10

Stimulation of which dopamine receptor subtype inhibits indirect pathway activity?

a) D1

b) D2

c) D3

d) D5

Explanation: D2 receptors inhibit striatal neurons of the indirect pathway, reducing thalamic suppression and promoting movement. Answer: b) D2. D1 receptors activate direct pathway, D3 and D5 have roles in limbic and cortical areas. Balanced D1/D2 signaling ensures smooth motor control within basal ganglia circuits clinically.

Question 11

Which hypothalamic hormone secretion is inhibited by tuberoinfundibular dopamine pathway?

a) Growth hormone

b) Cortisol

c) Prolactin

d) Thyroxine

Explanation: Dopaminergic neurons of tuberoinfundibular pathway inhibit prolactin release from anterior pituitary lactotrophs. Blockade or damage increases prolactin, causing galactorrhea and infertility. Answer: c) Prolactin. Dopamine agonists treat hyperprolactinemia, while antagonists may induce it. Other hypothalamic hormones are regulated differently by respective hypothalamic releasing factors clinically overall.

Keyword Definitions

• Purkinje fibres: Large inhibitory neurons of cerebellar cortex using GABA as neurotransmitter.

• Deep cerebellar nuclei: Primary output centres of cerebellum receiving inhibitory Purkinje input.

• Climbing fibres: Excitatory inputs from inferior olivary nucleus synapsing on Purkinje cells.

• Mossy fibres: Excitatory afferents from spinal cord and brainstem projecting to granule cells.

• Basket cells: Inhibitory interneurons forming axo-somatic synapses on Purkinje cells.

• Stellate cells: Inhibitory interneurons acting on Purkinje dendrites in molecular layer.

• Spinocerebellar tracts: Convey unconscious proprioceptive information from muscles and joints.

• Granule cells: Excitatory interneurons giving rise to parallel fibres synapsing on Purkinje cells.

• GABA: Gamma-aminobutyric acid, main inhibitory neurotransmitter in CNS.

• Cerebellar cortex: Three-layered structure modulating motor coordination and balance.

• Motor learning: Cerebellar mechanism for adapting and fine-tuning skilled movements.

Chapter: Neurophysiology

Topic: Cerebellum

Subtopic: Purkinje Cell Function

Lead Question – 2012

Purkinje fibres are inhibitory for?

a) Deep cerebellar nuclei

b) Climbing fibre

c) Basket cells

d) Spinocerebellar tracts

Explanation: Purkinje cells are GABAergic neurons that project inhibitory signals to deep cerebellar nuclei, regulating motor output precision. They receive excitatory input from climbing and mossy fibres, while interneurons like basket and stellate cells refine their activity. Answer: a) Deep cerebellar nuclei. This inhibitory control ensures smooth coordination and balance.

Question 2

Which neurotransmitter is released by Purkinje cells?

a) Acetylcholine

b) Dopamine

c) GABA

d) Glutamate

Explanation: Purkinje cells are the sole output of the cerebellar cortex. They are inhibitory neurons releasing gamma-aminobutyric acid (GABA). This neurotransmitter suppresses activity of deep cerebellar nuclei, ensuring controlled modulation of motor output. Answer: c) GABA. Excitatory neurotransmitters like glutamate act via mossy and climbing fibre inputs.

Question 3

A patient has loss of coordination but preserved strength. Which structure is primarily affected?

a) Cerebellum

b) Basal ganglia

c) Motor cortex

d) Spinal cord anterior horn

Explanation: The cerebellum coordinates timing, precision, and smoothness of movement but does not initiate voluntary force generation. Lesions cause ataxia, dysmetria, and intention tremor without significant weakness. Answer: a) Cerebellum. Motor cortex lesions reduce strength, while basal ganglia dysfunction causes rigidity or tremor, not incoordination.

Question 4

Climbing fibres originate from which source?

a) Inferior olivary nucleus

b) Red nucleus

c) Vestibular nuclei

d) Pontine nuclei

Explanation: Climbing fibres arise exclusively from the inferior olivary nucleus and form powerful excitatory synapses directly on Purkinje cells. They regulate motor learning and coordination through long-term depression at parallel fibre synapses. Answer: a) Inferior olivary nucleus. Mossy fibres, instead, arise from pontine and spinal inputs.

Question 5

Damage to Purkinje cells would primarily result in?

a) Spastic paralysis

b) Ataxia

c) Rigidity

d) Hyporeflexia

Explanation: Purkinje cell loss disrupts cerebellar inhibitory control, impairing coordination of movement. This produces ataxia with unsteady gait, dysdiadochokinesia, and intention tremor. Answer: b) Ataxia. Spasticity results from corticospinal damage, rigidity from basal ganglia disease, and hyporeflexia from lower motor neuron lesions.

Question 6

Which interneuron inhibits Purkinje cells in cerebellar cortex?

a) Basket cells

b) Golgi cells

c) Pyramidal cells

d) Oligodendrocytes

Explanation: Basket cells provide inhibitory axo-somatic synapses directly on Purkinje neurons, limiting their firing. Stellate cells also inhibit dendrites. Golgi cells regulate granule cells. Answer: a) Basket cells. These interneurons fine-tune Purkinje output before it reaches deep cerebellar nuclei, optimizing cerebellar motor coordination and timing.

Question 7

Which cerebellar lesion leads to truncal ataxia and swaying while standing?

a) Vermis

b) Hemisphere

c) Flocculonodular lobe

d) Dentate nucleus

Explanation: Lesions in cerebellar vermis cause truncal ataxia with broad-based gait and inability to maintain upright posture. Answer: a) Vermis. Hemisphere lesions cause limb ataxia, flocculonodular lesions cause balance and nystagmus, while dentate involvement produces dysmetria and decomposition of movement. Clinical localization depends on specific cerebellar subdivisions.

Question 8

Mossy fibres synapse first on?

a) Purkinje cells

b) Basket cells

c) Granule cells

d) Stellate cells

Explanation: Mossy fibres relay information from spinal cord and brainstem. They terminate on granule cells in cerebellar cortex, which then give rise to parallel fibres. These parallel fibres excite Purkinje dendrites. Answer: c) Granule cells. Thus, mossy fibres indirectly influence Purkinje output by granule cell activation.

Question 9

Which symptom is most typical of cerebellar disease?

a) Rest tremor

b) Intention tremor

c) Hypokinesia

d) Spasticity

Explanation: Cerebellar lesions produce intention tremor, which appears during voluntary movement and worsens as target is approached. Answer: b) Intention tremor. Rest tremor suggests Parkinsonism, hypokinesia occurs in basal ganglia disease, and spasticity arises from pyramidal tract lesions. Cerebellum chiefly impairs timing and coordination of motor actions.

Question 10

Which cerebellar output nucleus is largest and projects to motor cortex via thalamus?

a) Fastigial nucleus

b) Globose nucleus

c) Dentate nucleus

d) Emboliform nucleus

Explanation: The dentate nucleus is the largest deep cerebellar nucleus, projecting to contralateral motor cortex via the ventrolateral thalamus. It coordinates planning, timing, and fine motor execution. Answer: c) Dentate nucleus. Fastigial controls posture, globose and emboliform modulate intermediate motor activities of limbs.

Question 11

Which tract conveys unconscious proprioception from muscles to cerebellum?

a) Corticospinal tract

b) Spinothalamic tract

c) Spinocerebellar tract

d) Rubrospinal tract

Explanation: Spinocerebellar tracts carry proprioceptive input from muscle spindles and Golgi tendon organs to cerebellum. This unconscious sensory feedback helps adjust movement in real time. Answer: c) Spinocerebellar tract. Corticospinal controls voluntary movement, spinothalamic transmits pain/temperature, rubrospinal influences flexor tone but not proprioception.

Keyword Definitions

• Two-point discrimination: Ability to distinguish two separate simultaneous tactile stimuli.

• Tactile acuity: Sharpness of touch perception depending on receptor density.

• Receptive field: Area of skin innervated by a single sensory neuron.

• Merkel cells: Slowly adapting mechanoreceptors specialized for shape and edges.

• Meissner corpuscles: Rapidly adapting mechanoreceptors detecting flutter and low-frequency vibration.

• Pacinian corpuscles: Rapidly adapting mechanoreceptors specialized for high-frequency vibration.

• Dorsal columns: Pathways carrying touch, vibration, and proprioception.

• Medial lemniscus: Brainstem tract formed by decussated dorsal column fibers.

• Somatosensory cortex: Postcentral gyrus area processing tactile information.

• Cortical magnification: Enlarged cortical representation of regions like lips and fingertips.

• Astereognosis: Inability to identify objects by touch.

Chapter: General Physiology

Topic: Sensory Physiology

Subtopic: Two-point Discrimination

Lead Question – 2012

The distance by which two touch stimuli must be separated to be perceived as two separate stimuli is greatest at?

a) The lips

b) The palm of the hand

c) The back of scapula

d) The dorsum of the hand

Explanation: Two-point discrimination threshold is largest where receptive fields are big and cortical representation is small. Proximal trunk regions have poorest tactile acuity. Therefore, the greatest minimum separable distance is on the back of the scapula. Answer: c) The back of scapula.

Question 2

Which receptor type contributes most to high-resolution two-point discrimination on fingertips?

a) Pacinian corpuscles

b) Merkel discs

c) Ruffini endings

d) Free nerve endings

Explanation: Edges and fine form are encoded by slowly adapting type I mechanoreceptors with small receptive fields. Merkel cell–neurite complexes provide the highest spatial resolution for static touch and contribute most to two-point discrimination on fingertips and lips. Answer: b) Merkel discs.

Question 3

A patient with a hemisection of the spinal cord loses two-point discrimination below the lesion. Which tract is involved?

a) Spinothalamic tract

b) Dorsal column pathway

c) Spinocerebellar tract

d) Corticospinal tract

Explanation: A hemisection damaging dorsal columns impairs ipsilateral discriminative touch, vibration sense, and conscious proprioception below the lesion. Two-point discrimination on the affected side is markedly reduced, while pain and temperature may remain spared. Answer: b) Dorsal column pathway.

Question 4

Where is the two-point discrimination threshold smallest in the body?

a) Fingertips

b) Palm

c) Back

d) Abdomen

Explanation: Two-point thresholds are smallest where receptor density is highest and receptive fields are tiniest. Fingertips have abundant Merkel and Meissner endings plus strong cortical magnification, enabling exquisite spatial acuity. Therefore, minimum separable distance is least at fingertips. Answer: a) Fingertips.

Question 5

Which pathway carries discriminative touch and vibration sense to the brain?

a) Spinothalamic tract

b) Corticospinal tract

c) Dorsal column–medial lemniscus pathway

d) Spinoreticular tract

Explanation: Discriminative touch, vibration, and conscious proprioception ascend ipsilaterally in the dorsal columns to nucleus gracilis and cuneatus, then decussate as internal arcuate fibers to form the medial lemniscus. They project to thalamic VPL and somatosensory cortex. Answer: c) Dorsal column–medial lemniscus pathway.

Question 6

In which cortical region is two-point discrimination primarily resolved?

a) Prefrontal cortex

b) Primary somatosensory cortex

c) Insular cortex

d) Cerebellum

Explanation: Two-point discrimination is ultimately resolved in the primary somatosensory cortex on the postcentral gyrus, especially area 3b, exhibiting cortical magnification for hands and lips. Lesions there cause astereognosis and impaired tactile acuity contralaterally. Answer: b) Primary somatosensory cortex.

Question 7

A patient has loss of two-point discrimination on the left hand. Lesion is most likely in?

a) Right primary somatosensory cortex

b) Left motor cortex

c) Right cerebellum

d) Left dorsal root ganglion

Explanation: Somatosensory pathways decussate before reaching the cortex. Loss of discriminative touch from the left hand arises with a lesion in the contralateral somatosensory cortex. Answer: a) Right primary somatosensory cortex.

Question 8

Which phenomenon sharpens spatial resolution in two-point discrimination by inhibiting neighboring neurons?

a) Rebound excitation

b) Temporal summation

c) Lateral inhibition

d) Referred sensation

Explanation: Lateral inhibition enhances sensory contrast by suppressing responses in adjacent receptive fields. This improves spatial acuity and is fundamental for resolving two-point discrimination. Answer: c) Lateral inhibition.

Question 9

Which clinical sign indicates impaired cortical processing of tactile stimuli despite intact primary sensory pathways?

a) Hyperalgesia

b) Allodynia

c) Astereognosis

d) Hyperreflexia

Explanation: Patients with cortical lesions affecting parietal sensory areas cannot identify objects by touch despite preserved basic tactile sensation. This condition is astereognosis. Answer: c) Astereognosis.

Question 10

A lesion in which thalamic nucleus impairs two-point discrimination from the contralateral body?

a) VPL nucleus

b) Medial geniculate nucleus

c) VPM nucleus

d) Lateral geniculate nucleus

Explanation: The ventral posterolateral (VPL) nucleus of the thalamus receives medial lemniscus inputs carrying discriminative touch, vibration, and proprioception from the contralateral body. Lesions here impair two-point discrimination. Answer: a) VPL nucleus.

Question 11

Two-point discrimination is impaired but pain sensation remains intact. Which tract remains unaffected?

a) Spinothalamic tract

b) Dorsal column–medial lemniscus pathway

c) Corticospinal tract

d) Reticulospinal tract

Explanation: Preservation of pain sensation indicates an intact spinothalamic tract. Impairment of two-point discrimination indicates dorsal column dysfunction. Answer: a) Spinothalamic tract.

Chapter: Central Nervous System Physiology | Topic: Neuronal Membrane & Action Potential | Subtopic: Voltage-Gated Sodium Channels

Keywords

Voltage-gated sodium channels — proteins that open on depolarization allowing Na⁺ influx to initiate action potentials.
Axon initial segment (AIS) / Axon hillock — region where action potentials are usually initiated due to high Na⁺ channel density.
Nodes of Ranvier — gaps in myelin with concentrated Na⁺ channels enabling saltatory conduction.
Soma — neuronal cell body; integrates synaptic inputs but has lower Na⁺ channel density than AIS.
Dendrites — receive inputs and may have Na⁺ channels for back-propagation, but fewer than AIS.
Action potential threshold — lowest depolarization required to open sufficient Na⁺ channels to trigger spike.
Saltatory conduction — rapid impulse propagation between nodes of Ranvier in myelinated axons.
Ankyrin-G — scaffold protein essential for clustering Na⁺ channels at the axon initial segment.
Local anaesthetics — block voltage-gated Na⁺ channels to prevent action-potential propagation.
Channelopathies — disorders caused by mutations in sodium channel genes affecting excitability and causing seizures or paralysis.

Lead Question - 2012

Sodium channels are maximum in which part of neuron ?

a) Soma
b) Axon hillock
c) Dendrites
d) Axon

Explanation: The axon hillock (axon initial segment) has the highest density of voltage-gated sodium channels and is the usual trigger zone for action potentials. This high channel concentration, organized by ankyrin-G and associated scaffolds, lowers the threshold for spike initiation. Correct answer: b) Axon hillock.

Q1. Where along myelinated axons are sodium channels highly concentrated to enable saltatory conduction?

a) Internodal myelin
b) Nodes of Ranvier
c) Soma membrane
d) Dendritic spines

Explanation: Nodes of Ranvier are unmyelinated gaps densely populated with voltage-gated sodium channels. Action potentials are regenerated at these nodes, allowing rapid saltatory conduction down the axon. This arrangement increases conduction velocity and metabolic efficiency. Correct answer: b) Nodes of Ranvier.

Q2. Which scaffolding protein is essential for clustering sodium channels at the axon initial segment?

a) Ankyrin-G
b) Tubulin
c) Actin
d) Spectrin

Explanation: Ankyrin-G anchors voltage-gated sodium channels and other membrane proteins to the axon initial segment cytoskeleton, maintaining high local channel density necessary for action-potential initiation. Disruption of ankyrin-G disperses channels and reduces neuronal excitability. Correct answer: a) Ankyrin-G.

Q3. Local anaesthetics such as lidocaine produce analgesia primarily by blocking which channels?

a) Voltage-gated potassium channels
b) Voltage-gated sodium channels
c) Voltage-gated calcium channels
d) Ligand-gated chloride channels

Explanation: Local anaesthetics bind to and block voltage-gated sodium channels, preventing initiation and propagation of action potentials in sensory fibers. Small nociceptive fibers are preferentially blocked, producing loss of pain and temperature sensation. Correct answer: b) Voltage-gated sodium channels.

Q4. A mutation that reduces sodium-channel availability in the axon hillock would most likely cause:

a) Increased neuronal firing
b) Decreased excitability and possible weakness
c) Faster action potentials
d) Enhanced synaptic transmission

Explanation: Reduced sodium-channel availability at the axon initial segment raises the threshold for spike initiation, decreasing neuronal excitability and impairing signal transmission. Clinically this may cause muscle weakness, conduction block, or epileptic phenotypes depending on neuronal population affected. Correct answer: b) Decreased excitability and possible weakness.

Q5. Dendritic sodium channels support which physiological process relevant to synaptic plasticity?

a) Action-potential back-propagation
b) Neurotransmitter synthesis
c) Axonal myelination
d) Vesicle recycling

Explanation: Voltage-gated sodium channels in dendrites allow action potentials to back-propagate into the dendritic tree, modulating calcium entry and synaptic strength. This back-propagation contributes to spike-timing-dependent plasticity and learning. Correct answer: a) Action-potential back-propagation.

Q6. During the relative refractory period, why is a larger stimulus required to elicit an action potential?

a) All Na⁺ channels are permanently removed
b) Many Na⁺ channels are inactivated and K⁺ conductance is increased
c) Membrane potential is more positive than threshold
d) Synaptic inputs are inhibited

Explanation: After an action potential, a subset of Na⁺ channels remains inactivated and K⁺ channels remain open, hyperpolarizing the membrane; a stronger depolarizing input is thus required to reach threshold. This defines the relative refractory period. Correct answer: b) Many Na⁺ channels are inactivated and K⁺ conductance is increased.

Q7. Which feature increases axonal conduction velocity most effectively?

a) Decreasing axon diameter
b) Increasing myelination and axon diameter
c) Reducing Na⁺ channel density at nodes
d) Increasing internodal capacitance

Explanation: Larger axon diameter and increased myelination raise conduction velocity by reducing internal resistance and membrane capacitance. Adequate sodium-channel density at nodes is also required. Correct answer: b) Increasing myelination and axon diameter.

Q8. Which antiepileptic medication exerts effects by stabilizing the inactivated state of sodium channels?

a) Phenytoin
b) Levodopa
c) Fluoxetine
d) Propranolol

Explanation: Phenytoin binds voltage-gated sodium channels, prolonging their inactivated state and limiting repetitive firing of neurons. This mechanism reduces seizure propagation in many epilepsy syndromes. Correct answer: a) Phenytoin.

Q9. Which region is the most common site for initiation of spontaneous epileptic discharges due to high excitability?

a) Axon hillock / initial segment
b) Distal axon terminals
c) Soma nucleus
d) Myelin sheath

Explanation: The axon initial segment’s high density of sodium channels and low threshold make it a frequent locus for abnormal spontaneous discharges in epilepsy. Pathologic increases in excitability here can produce paroxysmal firing. Correct answer: a) Axon hillock / initial segment.

Q10. Which pathological process directly reduces sodium-channel clustering at the AIS leading to reduced excitability?

a) Mutation or loss of ankyrin-G
b) Increased myelination
c) Enhanced Na⁺ channel synthesis
d) Elevated extracellular potassium only

Explanation: Loss or dysfunction of ankyrin-G disrupts anchoring of sodium channels at the AIS, dispersing them and impairing action-potential initiation. This reduces neuronal excitability and can contribute to neurological disease. Correct answer: a) Mutation or loss of ankyrin-G.

Chapter: Central Nervous System Physiology | Topic: Hypothalamic Control | Subtopic: Thermoregulation and Shivering

Keywords

Thermoregulation — physiological processes that maintain core body temperature.
Preoptic area (POA) — hypothalamic region sensing temperature and coordinating heat-loss responses.
Posterior hypothalamus — activates heat-production mechanisms including shivering and sympathetic vasoconstriction.
Shivering — involuntary rhythmic skeletal muscle contractions generating heat under hypothalamic drive.
Warm-sensitive neurons — in POA; stimulate heat-loss (sweating, vasodilation).
Cold-sensitive pathways — activate posterior hypothalamus to produce heat via shivering and autonomic output.
Pyrogens — raise hypothalamic set point producing fever (distinct from hyperthermia).
Thermal effector organs — skeletal muscle (shivering), skin vessels (vasomotor), sweat glands.
Behavioral responses — seeking shelter/clothing under hypothalamic and cortical influence.
Clinical relevance — hypothalamic lesions can produce hypothermia or hyperthermia and loss of shivering.

Lead Question - 2012

Shivering is controlled by: (also in September 2012, March 2013)

a) Dorsomedial nucleus
b) Posterior hypothalamus
c) Perifornical nucleus
d) Lateral hypothalamic area

Explanation: Shivering—involuntary rhythmic skeletal muscle contractions that generate heat—is driven by cold-sensitive pathways activating the posterior hypothalamus. The posterior hypothalamic area orchestrates motor and sympathetic outputs for heat production. Therefore the correct answer is b) Posterior hypothalamus, responsible for shivering and thermogenic responses.

Q1. Lesion of the preoptic area typically causes:

a) Hypothermia
b) Hyperthermia
c) Diabetes insipidus
d) Hyperphagia

Explanation: The preoptic area contains warm-sensitive neurons initiating heat-loss responses. Lesioning it abolishes heat-dissipation, producing uncontrolled rise in body temperature (hyperthermia). Thus the correct answer is b) Hyperthermia. This differs from DI or appetite disturbances tied to other hypothalamic nuclei.

Q2. Fever differs from hyperthermia because fever results from:

a) Ambient heat overload
b) Raised hypothalamic set point due to pyrogens
c) Failure of sweating
d) Posterior hypothalamic lesion

Explanation: Fever arises when pyrogens raise the hypothalamic thermoregulatory set point, causing the body to conserve and generate heat until the new set point is reached. This distinguishes fever from hyperthermia, which is failure of heat loss. Correct answer: b).

Q3. Which hypothalamic area promotes heat production when activated by cold?

a) Anterior hypothalamus
b) Posterior hypothalamus
c) Suprachiasmatic nucleus
d) Arcuate nucleus

Explanation: Cold signals activate cold-sensitive afferents that stimulate the posterior hypothalamus to increase thermogenesis by shivering and sympathetic activation. The anterior (preoptic) area mediates heat loss. Correct answer: b) Posterior hypothalamus, which triggers heat-generating mechanisms.

Q4. Which effector mediates most rapid heat production in humans?

a) Brown adipose tissue
b) Shivering (skeletal muscle activity)
c) Increased thyroid secretion
d) Skin vasodilation

Explanation: Shivering produces immediate heat via rhythmic skeletal muscle contractions under posterior hypothalamic control, providing rapid thermogenesis. Brown adipose tissue contributes in infants, while thyroid changes and vasomotor adjustments are slower. Correct answer: b) Shivering.

Q5. Which sign indicates activation of heat-loss mechanisms?

a) Vasoconstriction
b) Shivering
c) Sweating and cutaneous vasodilation
d) Piloerection

Explanation: Heat-loss responses include sweating and cutaneous vasodilation mediated by preoptic area signals. These lower core temperature by evaporative cooling and increased skin blood flow. Correct answer: c) Sweating and cutaneous vasodilation, opposite to shivering which produces heat.

Q6. A patient with impaired shivering after hypothalamic surgery most likely had damage to:

a) Ventromedial nucleus
b) Posterior hypothalamus
c) Suprachiasmatic nucleus
d) Lateral hypothalamus

Explanation: Surgical damage to the posterior hypothalamus abolishes cold-induced shivering and some sympathetic thermogenic responses. Therefore impaired shivering after hypothalamic surgery suggests posterior hypothalamic injury. Correct answer: b) Posterior hypothalamus.

Q7. Which autonomic response accompanies shivering to preserve core temperature?

a) Cutaneous vasodilation
b) Cutaneous vasoconstriction
c) Diaphoresis
d) Increased salivation

Explanation: To conserve heat during shivering, sympathetic-mediated cutaneous vasoconstriction reduces blood flow to the skin, minimizing heat loss. This complements muscular heat production. Correct answer: b) Cutaneous vasoconstriction.

Q8. Which hypothalamic nucleus is the master clock for circadian temperature rhythm?

a) Suprachiasmatic nucleus (SCN)
b) Paraventricular nucleus
c) Dorsomedial nucleus
d) Lateral hypothalamus

Explanation: The suprachiasmatic nucleus (SCN) entrains circadian rhythms including daily fluctuations in body temperature by signaling other hypothalamic areas. Lesions disrupt rhythmic temperature variations. Correct answer: a) Suprachiasmatic nucleus (SCN).

Q9. Which pharmacologic agent can reduce shivering by central action?

a) Acetaminophen (paracetamol)
b) Meperidine (pethidine)
c) Epinephrine
d) Dobutamine

Explanation: Meperidine centrally suppresses shivering via opioid and α2-adrenergic effects in the hypothalamus and brainstem. It is used to treat postoperative shivering. Correct answer: b) Meperidine (pethidine).

Q10. In hypothermia, which behavioral response is initiated by cortical and hypothalamic centers?

a) Removing clothing
b) Seeking warmth and adding clothing
c) Inducing sweat
d) Increasing water intake

Explanation: Behavioral thermoregulation includes seeking warmth and adding clothing to reduce heat loss; these actions are driven by hypothalamic signals integrated with cortical decision-making. Correct answer: b) Seeking warmth and adding clothing.

Chapter: Central Nervous System Physiology | Topic: Hypothalamic Functions | Subtopic: Preoptic Area & Homeostasis

Keyword Definitions

Preoptic nucleus — hypothalamic region with warm-sensitive neurons controlling heat-loss responses.
Thermoregulation — physiological processes maintaining core temperature via autonomic and behavioral responses.
Hyperthermia — abnormally high body temperature due to failed heat dissipation or excessive heat production.
Hyperphagia — excessive eating driven by hypothalamic or metabolic disturbances.
Hyperdipsia — excessive thirst and fluid intake, often osmotic or hypothalamic in origin.
Homeostasis — coordinated regulation of internal milieu (temperature, thirst, hunger, endocrine balance).
Autonomic output — hypothalamic control of sympathetic and parasympathetic tone influencing temperature and metabolism.
POA lesions — can disrupt fever responses, thermoregulatory set points, and heat-loss mechanisms.
Fever vs hyperthermia — fever raises set point via pyrogens; hyperthermia is failure of dissipation.
Clinical relevance — hypothalamic injury, stroke, tumors can produce dysautonomia and temperature dysregulation.

Lead Question - 2012

Lesion of preoptic nucleus of hypothalamus causes?

a) Hyperphagia
b) Hyperdypsia
c) Hyperthermia
d) Hyperglycemia

Explanation: The preoptic area contains warm-sensitive neurons that initiate heat-loss responses (vasodilation, sweating). Lesioning these neurons abolishes heat-loss mechanisms, producing uncontrolled rise in body temperature (hyperthermia). This is not primarily a feeding or thirst center. Correct answer: c) Hyperthermia.

Q1. Damage to the lateral hypothalamic area typically causes:

a) Anorexia
b) Hyperphagia
c) Polydipsia
d) Hypothermia

Explanation: The lateral hypothalamus is the feeding (hunger) center; lesions produce anorexia and weight loss, while stimulation causes hyperphagia. Thus damage causes lack of eating rather than increased appetite. Correct answer: a) Anorexia (lesion → anorexia; stimulation → hyperphagia).

Q2. A lesion of the supraoptic nucleus would most likely produce:

a) Diabetes insipidus (polyuria, polydipsia)
b) Cushing’s syndrome
c) Hyperthermia
d) Adipsia

Explanation: The supraoptic nucleus produces vasopressin (ADH); damage causes central diabetes insipidus with polyuria and compensatory polydipsia. This is a classic hypothalamic endocrine deficit. Correct answer: a) Diabetes insipidus (polyuria, polydipsia).

Q3. Which hypothalamic lesion produces hyperphagia and obesity in animals?

a) Ventromedial nucleus lesion
b) Lateral hypothalamic lesion
c) Preoptic lesion
d) Suprachiasmatic lesion

Explanation: The ventromedial hypothalamus is a satiety center; lesions remove restraining signals leading to hyperphagia and obesity. Lateral lesions cause anorexia. Correct answer: a) Ventromedial nucleus lesion.

Q4. Destruction of the suprachiasmatic nucleus (SCN) leads to:

a) Loss of circadian rhythms
b) Hyperthermia
c) Polyphagia
d) Diabetes insipidus

Explanation: The SCN is the master circadian pacemaker; lesions disrupt sleep-wake, hormonal, and temperature rhythms. This abolishes regular circadian patterns but does not directly cause fever or thirst disorders. Correct answer: a) Loss of circadian rhythms.

Q5. Fever (pyrogen-mediated) differs from hyperthermia because fever involves:

a) Raised hypothalamic set point
b) Failure of heat dissipation
c) Ambient heat overload
d) Direct injury to preoptic neurons

Explanation: Fever results from pyrogens raising the hypothalamic thermostat (set point), inducing chills and thermoregulatory defenses to reach the new set point. Hyperthermia is failure of heat loss without set-point change. Correct answer: a) Raised hypothalamic set point.

Q6. A patient with hypothalamic lesion presents with persistent hyperphagia and rage; which nucleus is likely affected?

a) Ventromedial nucleus
b) Preoptic nucleus
c) Paraventricular nucleus
d) Lateral hypothalamic area

Explanation: Ventromedial nucleus lesions remove satiety signals causing hyperphagia and aggression (sham rage). The lateral hypothalamus promotes feeding when stimulated. Paraventricular lesions affect autonomic and endocrine outputs. Correct answer: a) Ventromedial nucleus.

Q7. Lesion of preoptic area interferes with which autonomic thermoregulatory response?

a) Sweating and cutaneous vasodilation
b) Salivation
c) Pupillary constriction
d) Gastrointestinal motility

Explanation: The preoptic area triggers heat-loss responses such as sweating and vasodilation. Lesions abolish these mechanisms, leading to impaired heat dissipation and hyperthermia. Other autonomic functions are mediated by different hypothalamic regions. Correct answer: a) Sweating and cutaneous vasodilation.

Q8. Paraventricular nucleus (PVN) lesions primarily affect:

a) Oxytocin and CRH release influencing endocrine and autonomic functions
b) Visual processing
c) Primary motor control
d) Vestibular reflexes

Explanation: PVN neurons produce CRH and oxytocin and modulate sympathetic outflow; lesions disrupt HPA axis regulation and autonomic balance. This leads to endocrine and autonomic dysfunction rather than direct motor or visual deficits. Correct answer: a).

Q9. Central fever after hypothalamic hemorrhage is due to:

a) Disruption of preoptic heat-loss neurons
b) Bacterial infection
c) Peripheral inflammation only
d) Increased sweating

Explanation: Hypothalamic injury can cause central fever by damaging preoptic/POA neurons that mediate heat loss and set-point regulation; this produces sustained hyperthermia without infection. Correct answer: a) Disruption of preoptic heat-loss neurons.

Q10. A lesion of arcuate nucleus would most likely cause:

a) Disordered appetite regulation and altered GnRH/release control
b) Loss of temperature sensation
c) Loss of visual fields
d) Cerebellar ataxia

Explanation: The arcuate nucleus integrates peripheral metabolic signals (leptin, ghrelin) and influences appetite, prolactin and GnRH modulation. Lesions disrupt feeding and reproductive hormone regulation. It is not primarily involved in temperature sensation or motor coordination. Correct answer: a).

Chapter: Sensory Physiology | Topic: Visual Transduction | Subtopic: Photoreceptor Proteins

Keywords

Transducin — a heterotrimeric G-protein in photoreceptor cells involved in phototransduction.
Rhodopsin — light-sensitive pigment in rod outer segments that activates transducin.
Phototransduction — process converting photon absorption into electrical signals in retina.
cGMP phosphodiesterase — enzyme activated by transducin to lower cGMP and hyperpolarize photoreceptors.
Rods and cones — retinal photoreceptors for scotopic and photopic vision respectively.
Retinal — chromophore (11-cis-retinal) that changes conformation on photon absorption.
Hyperpolarization — photoreceptor response to light due to decreased cGMP-gated current.
Dark current — inward Na⁺/Ca²⁺ current in photoreceptors maintained by cGMP.
Visual cycle — enzymatic regeneration of 11-cis-retinal in retinal pigment epithelium.
G-protein coupled receptor (GPCR) — rhodopsin is a GPCR that activates transducin.

Lead Question - 2012

Transducin is a protein found in:

a) Glomerulus
b) Retina
c) Skeletal muscle
d) Adrenal medulla

Explanation: Transducin is a G-protein located in photoreceptor outer segments of the retina; it couples activated rhodopsin to cGMP phosphodiesterase. Upon photon capture transducin activates PDE, lowers cGMP, closes cGMP-gated channels and hyperpolarizes the photoreceptor. Correct answer: b) Retina.

Q1. Which pigment initiates phototransduction by activating transducin?

a) Hemoglobin
b) Melanin
c) Rhodopsin
d) Opsin in kidney

Explanation: Rhodopsin in rod outer segments absorbs photons, isomerizes 11-cis-retinal to all-trans-retinal, and activates the GPCR rhodopsin which then activates transducin, initiating the phototransduction cascade. Correct answer: c) Rhodopsin.

Q2. Activation of transducin leads directly to activation of which enzyme?

a) Adenylate cyclase
b) cGMP phosphodiesterase
c) Na⁺/K⁺ ATPase
d) Phospholipase C

Explanation: Activated transducin (Gαt) stimulates cGMP phosphodiesterase, decreasing cytoplasmic cGMP, closing cGMP-gated cation channels and hyperpolarizing photoreceptors. This is central to light signal transduction. Correct answer: b) cGMP phosphodiesterase.

Q3. Photoreceptor response to light is a:

a) Depolarization
b) Hyperpolarization
c) Action potential firing
d) No change

Explanation: Light activation leads to reduced cGMP, closure of cGMP-gated Na⁺ channels, decreased inward dark current and membrane hyperpolarization of photoreceptors. This graded hyperpolarization reduces glutamate release. Correct answer: b) Hyperpolarization.

Q4. Which retinal cells regenerate 11-cis-retinal as part of the visual cycle?

a) Müller glia
b) Retinal pigment epithelium (RPE)
c) Ganglion cells
d) Bipolar cells

Explanation: The retinal pigment epithelium (RPE) performs enzymatic steps to convert all-trans-retinal back to 11-cis-retinal, replenishing the chromophore for photopigments. This visual cycle is essential for sustained phototransduction. Correct answer: b) Retinal pigment epithelium (RPE).

Q5. Which photoreceptors primarily use transducin in their signal cascade?

a) Rods
b) Cones
c) Ganglion photoreceptors only
d) Both rods and cones

Explanation: Both rods and cones possess phototransduction cascades that employ G-proteins homologous to transducin (rod transducin Gαt1, cone transducins Gαt2), so both use transducin-like proteins to activate PDE. Correct answer: d) Both rods and cones.

Q6. A defect in transducin function would most likely cause:

a) Color blindness only
b) Night blindness and impaired phototransduction
c) Loss of accommodation
d) Elevated intraocular pressure

Explanation: Impaired transducin prevents effective activation of PDE, blunting photoreceptor hyperpolarization and reducing sensitivity, particularly affecting scotopic (rod-mediated) vision, causing night blindness and phototransduction defects. Correct answer: b) Night blindness and impaired phototransduction.

Q7. Which event follows activation of cGMP phosphodiesterase in photoreceptors?

a) Increased intracellular cGMP
b) Closure of cGMP-gated cation channels
c) Increased glutamate release
d) Depolarization

Explanation: PDE lowers cGMP levels, resulting in closure of cGMP-gated Na⁺/Ca²⁺ channels, decreased inward current and reduced glutamate release due to photoreceptor hyperpolarization. Correct answer: b) Closure of cGMP-gated cation channels.

Q8. Which molecule directly undergoes photoisomerization to start phototransduction?

a) 11-cis-retinal
b) Opsin protein backbone
c) cGMP
d) Transducin

Explanation: The chromophore 11-cis-retinal within rhodopsin photoisomerizes to all-trans-retinal upon photon absorption, changing rhodopsin conformation and activating transducin, initiating the cascade. Correct answer: a) 11-cis-retinal.

Q9. Which test assesses rod (scotopic) function most directly?

a) Photopic visual acuity
b) Dark adaptation test
c) Color vision test
d) Pupillary light reflex

Explanation: Dark adaptation measures recovery of visual sensitivity in low light, reflecting rod photoreceptor and transducin-PDE cascade function. Delayed or impaired dark adaptation suggests rod/transducin pathway dysfunction. Correct answer: b) Dark adaptation test.

Q10. Which class of receptors does rhodopsin belong to?

a) Ligand-gated ion channel
b) Tyrosine kinase receptor
c) G-protein coupled receptor (GPCR)
d) Nuclear receptor

Explanation: Rhodopsin is a GPCR embedded in photoreceptor membranes; upon photon-induced conformational change it activates transducin (a G-protein), classifying rhodopsin as a light-activated GPCR. Correct answer: c) G-protein coupled receptor (GPCR).

Chapter: Central Nervous System Physiology

Topic: Nerve Fibers and Conduction

Subtopic: Sensitivity to Pressure and Hypoxia

Keyword Definitions:

• Nerve Fibers: Axons classified based on diameter, conduction velocity, and function (A, B, C fibers).

• A Fibers: Large, myelinated fibers with rapid conduction, subdivided into alpha, beta, gamma, delta.

• B Fibers: Small, myelinated preganglionic autonomic fibers.

• C Fibers: Small, unmyelinated fibers, slow conduction, pain and temperature transmission.

• Hypoxia Sensitivity: Vulnerability of fibers to oxygen deprivation.

• Pressure Sensitivity: Susceptibility of fibers to mechanical compression.

• Neuropraxia: Temporary conduction block often due to compression.

• Paresthesia: Abnormal tingling or numb sensation due to nerve dysfunction.

Lead Question - 2012

A man slept with head over forearm, next morning he complains of tingling, numbness over forearm. It is caused by?

a) Sensitivity to hypoxia is A > B > C

b) Sensitivity to pressure is A > B > C

c) Sensitivity to hypoxia is C > B > A

d) Sensitivity to pressure is B > A > C

Explanation: Large myelinated A fibers are more susceptible to compression due to their size and myelin sheath. This explains temporary numbness or tingling after sleeping on a limb. Small unmyelinated C fibers are more resistant. Hence, sensitivity to pressure is A > B > C. Answer: b) Sensitivity to pressure is A > B > C

--- Guessed Question 1

Which nerve fibers are most sensitive to hypoxia?

a) A fibers

b) B fibers

c) C fibers

d) All equally

Explanation: Unmyelinated C fibers require continuous metabolic support and are highly sensitive to hypoxia. In oxygen deprivation, C fibers lose function first, causing early loss of pain and temperature sensation. Answer: c) C fibers

--- Guessed Question 2

Temporary conduction block without axonal damage due to compression is termed:

a) Axonotmesis

b) Neurotmesis

c) Neuropraxia

d) Wallerian degeneration

Explanation: Neuropraxia is a transient conduction block due to mechanical compression, as in the case of sleeping on an arm. Recovery is complete within days to weeks as no axonal damage occurs. Answer: c) Neuropraxia

--- Guessed Question 3

Which type of fibers mediate burning pain?

a) A alpha

b) A beta

c) A delta

d) C fibers

Explanation: Burning, dull, poorly localized pain is transmitted by unmyelinated C fibers. A delta fibers carry sharp, pricking pain. Thus, chronic tingling or burning after compression is mediated by C fibers. Answer: d) C fibers

--- Guessed Question 4

Which fibers are blocked earliest by local anesthetics?

a) A alpha

b) A delta

c) B fibers

d) C fibers

Explanation: Small, myelinated B fibers (preganglionic autonomic) are most sensitive to local anesthetics, followed by C fibers, then A delta, and lastly large motor A alpha fibers. Answer: c) B fibers

--- Guessed Question 5

Patient develops numbness after tight bandage. Most likely affected fibers are:

a) A fibers

b) B fibers

c) C fibers

d) None

Explanation: Mechanical compression preferentially affects large myelinated A fibers, leading to numbness and weakness. Unmyelinated C fibers remain relatively preserved. Answer: a) A fibers

--- Guessed Question 6

Which sensation is first affected during hypoxia?

a) Pain

b) Touch

c) Autonomic functions

d) Vibration

Explanation: Pain is mediated by C fibers, which are highly hypoxia-sensitive. Thus, pain sensation is often first impaired in hypoxic conditions. Answer: a) Pain

--- Guessed Question 7

Compression of radial nerve during deep sleep leads to:

a) Wrist drop

b) Foot drop

c) Claw hand

d) Facial palsy

Explanation: Radial nerve palsy due to compression in sleep ("Saturday night palsy") leads to weakness of wrist extensors, manifesting as wrist drop. Answer: a) Wrist drop

--- Guessed Question 8

Which nerve fiber type has the slowest conduction velocity?

a) A alpha

b) A beta

c) B fibers

d) C fibers

Explanation: Unmyelinated C fibers have the slowest conduction velocity (~0.5–2 m/s) compared to fast-conducting A alpha fibers (~100 m/s). Answer: d) C fibers

--- Guessed Question 9

Which fibers are most pressure-sensitive clinically leading to tingling?

a) A fibers

b) B fibers

c) C fibers

d) All equally

Explanation: Large, heavily myelinated A fibers are most pressure-sensitive, hence tingling and numbness are due to their dysfunction. Answer: a) A fibers

--- Guessed Question 10

Loss of touch and vibration but preserved pain after compression indicates damage to:

a) A alpha and beta fibers

b) A delta fibers

c) C fibers

d) B fibers

Explanation: Touch and vibration are carried by large A alpha and A beta fibers, which are most pressure-sensitive. C fibers carrying pain remain intact initially, explaining preserved pain sensation. Answer: a) A alpha and beta fibers

Chapter: Peripheral Nerve Physiology | Topic: Nociception & Pain Fibres | Subtopic: Sensory Fiber Types

Keywords

Peripheral nociceptors — sensory receptors that signal tissue-damaging stimuli.
Aδ fibres — thin myelinated fibres conducting fast sharp pain.
C fibres — small unmyelinated fibres conducting slow burning/dull pain.
Aβ fibres — large myelinated fibres for touch and vibration, not primary nociception.
Conduction velocity — speed of action potential propagation determined by diameter and myelination.
Spinothalamic tract — ascending pathway transmitting pain and temperature to thalamus.
Substance P / CGRP — neuropeptides released by nociceptors mediating pain and neurogenic inflammation.
Gate control theory — modulation of pain by non-nociceptive afferents at spinal level.
Central sensitization — heightened dorsal horn responsiveness after persistent nociceptive input.
Local anaesthetics — block sodium channels, preferentially affecting small diameter fibres first.

Lead Question - 2012

Burning pain is carried by which type of fibres ?

a) A alpha
b) A delta
c) A beta
d) C

Explanation: Burning, slow, poorly localized pain is typically transmitted by small unmyelinated C fibres that conduct at low velocity and carry polymodal nociceptive input. Aδ fibres convey fast sharp pain. Therefore the correct answer is d) C. C-fibre activity also mediates neurogenic inflammation via Substance P and CGRP.

Q1. Fast, well-localized sharp pain (first pain) is carried mainly by:

a) A alpha
b) A delta
c) C fibres
d) A beta

Explanation: First, sharp pain is mediated by thinly myelinated Aδ fibres that have higher conduction velocity than C fibres and project through the spinothalamic tract to somatosensory cortex, producing rapid, localized pain sensations. Hence the correct answer is b) A delta.

Q2. Which fibres primarily transmit touch and vibration?

a) A beta
b) C fibres
c) A delta
d) A gamma

Explanation: Large myelinated Aβ fibres carry discriminative touch, pressure, and vibration information via the dorsal column–medial lemniscal pathway. They are not primary nociceptors. Correct answer: a) A beta. Activation of Aβ fibres can modulate pain via gate control mechanisms in the dorsal horn.

Q3. Which ascending pathway carries pain and temperature to the brain?

a) Dorsal columns
b) Spinothalamic tract
c) Corticospinal tract
d) Spinocerebellar tract

Explanation: The anterolateral system, chiefly the spinothalamic tract, transmits nociceptive and thermoreceptive signals from spinal cord to thalamus and cortex. Dorsal columns carry vibration and proprioception. Correct answer: b) Spinothalamic tract.

Q4. Which neuropeptide released from nociceptors contributes to neurogenic inflammation?

a) GABA
b) Substance P
c) Dopamine
d) Serotonin

Explanation: Substance P and CGRP released from peripheral terminals of C fibres promote vasodilation, plasma extravasation, and immune cell recruitment, producing neurogenic inflammation and sensitization. This augments pain. Correct answer: b) Substance P.

Q5. Local anaesthetics block which channels to prevent nociception?

a) Calcium channels
b) Sodium channels
c) Potassium channels
d) Chloride channels

Explanation: Local anaesthetics inhibit voltage-gated sodium channels, preventing action potential initiation and propagation in sensory fibres. Small-diameter unmyelinated C and thin myelinated Aδ fibres are blocked preferentially, producing analgesia. Correct answer: b) Sodium channels.

Q6. Which clinical sign suggests small fibre (C/Aδ) neuropathy?

a) Loss of vibration sense
b) Burning distal pain with preserved reflexes
c) Pure motor weakness
d) Loss of proprioception

Explanation: Small-fibre neuropathy causes burning, shooting pain and dysesthesias in a distal stocking distribution with relatively preserved muscle strength and large-fibre modalities like vibration. Reflexes may be normal early. Correct answer: b) Burning distal pain with preserved reflexes.

Q7. Gate control theory proposes that activation of which fibres inhibits pain transmission?

a) C fibres
b) A beta fibres
c) A delta fibres
d) Sympathetic efferents

Explanation: Large-diameter Aβ fibres carrying touch input activate inhibitory interneurons in dorsal horn, reducing transmission from nociceptive Aδ/C fibres to projection neurons. This underlies analgesic effects of rubbing or TENS. Correct answer: b) A beta fibres.

Q8. Central sensitization results in which clinical phenomenon?

a) Hypoalgesia
b) Allodynia (pain to non-painful stimuli)
c) Loss of reflexes
d) Improved proprioception

Explanation: Persistent nociceptive input induces dorsal horn hyperexcitability and synaptic plasticity, producing allodynia and hyperalgesia where innocuous stimuli become painful. This is central sensitization seen in chronic pain syndromes. Correct answer: b) Allodynia.

Q9. Which fibre type has the slowest conduction velocity?

a) A alpha
b) A beta
c) A delta
d) C fibres

Explanation: Unmyelinated C fibres have the smallest diameter and slowest conduction velocity (~0.5–2 m/s), mediating slow burning pain and autonomic reflexes. Aα/Aβ are fastest. Correct answer: d) C fibres.

Q10. Which analgesic mechanism involves opioid receptors in the dorsal horn?

a) NSAID inhibition of COX
b) Activation of μ-opioid receptors reducing neurotransmitter release
c) Local anaesthetic sodium channel block
d) TRPV1 activation

Explanation: Opioids bind μ receptors on presynaptic nociceptive terminals and postsynaptic dorsal horn neurons, inhibiting substance P release and hyperpolarizing neurons, reducing pain transmission centrally. This is a principal mechanism for strong analgesics. Correct answer: b) Activation of μ-opioid receptors.

Chapter: General Physiology

Topic: Body Fluid Compartments

Subtopic: Interstitial Fluid Dynamics

Keywords

- Interstitial pressure: Pressure exerted by interstitial fluid outside the capillaries.

- Capillary hydrostatic pressure: Force pushing fluid out of capillaries.

- Plasma oncotic pressure: Osmotic force pulling fluid into capillaries due to plasma proteins.

- Lymphatic drainage: Mechanism that prevents fluid accumulation in tissues.

- Edema: Swelling caused by excessive fluid in interstitial spaces.

Lead Question – 2012

Normal interstitial pressure is?

a) 10 to 15 mmHg

b) -5 to 0 mmHg

c) 20 to 30 mmHg

d) -10 to -20 mmHg

Explanation: Interstitial pressure is normally slightly negative, about -5 to 0 mmHg. This negative value maintains continuous absorption of excess fluid by lymphatics. Positive interstitial pressure may cause edema. Thus, the correct answer is (b) -5 to 0 mmHg.

Guessed Questions

1) A patient develops generalized edema in nephrotic syndrome due to:

a) Increased interstitial pressure

b) Reduced plasma oncotic pressure

c) Increased lymphatic drainage

d) Decreased capillary hydrostatic pressure

Explanation: Nephrotic syndrome causes protein loss, lowering plasma oncotic pressure, reducing fluid reabsorption into capillaries, and leading to edema. Correct answer: (b) Reduced plasma oncotic pressure.

2) In right heart failure, interstitial fluid accumulates primarily due to:

a) Increased plasma oncotic pressure

b) Decreased capillary hydrostatic pressure

c) Increased capillary hydrostatic pressure

d) Reduced lymphatic return

Explanation: Right heart failure elevates venous pressure, raising capillary hydrostatic pressure, pushing fluid into the interstitial space, and causing peripheral edema. Correct answer: (c) Increased capillary hydrostatic pressure.

3) In lymphatic obstruction (e.g., filariasis), edema occurs because:

a) Interstitial pressure becomes negative

b) Capillary hydrostatic pressure falls

c) Interstitial fluid cannot be drained

d) Plasma oncotic pressure rises

Explanation: Blockage of lymphatic drainage prevents removal of interstitial fluid, leading to lymphedema even when hydrostatic and oncotic pressures are normal. Correct answer: (c) Interstitial fluid cannot be drained.

4) Pulmonary edema in acute left heart failure is due to:

a) Reduced plasma oncotic pressure

b) Increased pulmonary capillary hydrostatic pressure

c) Increased lymphatic flow

d) Negative interstitial pressure

Explanation: Left heart failure raises pulmonary venous pressure, increasing capillary hydrostatic pressure, forcing fluid into alveolar interstitium, causing pulmonary edema. Correct answer: (b) Increased pulmonary capillary hydrostatic pressure.

5) A burn patient develops massive edema because of:

a) Loss of plasma proteins

b) Reduced interstitial volume

c) Increased lymphatic return

d) Positive interstitial pressure

Explanation: Burns increase capillary permeability, causing plasma protein leakage into interstitial fluid, reducing plasma oncotic pressure and favoring edema formation. Correct answer: (a) Loss of plasma proteins.

6) Interstitial pressure becomes positive when:

a) Tissue edema develops

b) Plasma oncotic pressure increases

c) Lymphatic drainage accelerates

d) Capillary hydrostatic pressure decreases

Explanation: In early edema, interstitial pressure rises from its normal negative value to positive, which further promotes fluid leakage into tissue. Correct answer: (a) Tissue edema develops.

7) The main safety factor against edema under normal physiology is:

a) Positive interstitial pressure

b) Negative interstitial pressure

c) High hydrostatic pressure

d) Low lymph flow

Explanation: Negative interstitial pressure maintains fluid absorption into lymphatics, preventing excessive accumulation. This acts as a protective mechanism. Correct answer: (b) Negative interstitial pressure.

8) In severe liver cirrhosis, ascites develops due to:

a) Increased plasma protein synthesis

b) Reduced plasma oncotic pressure

c) Negative interstitial pressure

d) Reduced capillary hydrostatic pressure

Explanation: Cirrhosis reduces albumin production, lowering plasma oncotic pressure, favoring movement of fluid into peritoneal cavity, causing ascites. Correct answer: (b) Reduced plasma oncotic pressure.

9) During prolonged standing, dependent edema occurs due to:

a) Reduced capillary hydrostatic pressure

b) Increased capillary hydrostatic pressure in legs

c) Increased plasma oncotic pressure

d) Negative interstitial pressure

Explanation: Standing increases venous pressure in lower limbs, raising capillary hydrostatic pressure, leading to filtration of fluid into interstitial space and edema. Correct answer: (b) Increased capillary hydrostatic pressure in legs.

10) The Starling equilibrium is maintained by balance between:

a) Hydrostatic and oncotic pressures

b) Interstitial and lymphatic pressures

c) Capillary and interstitial pressures only

d) Oncotic and osmotic pressures only

Explanation: Starling forces describe fluid exchange across capillaries based on balance between hydrostatic and oncotic pressures on both plasma and interstitial sides. Correct answer: (a) Hydrostatic and oncotic pressures.

11) An anaphylactic reaction causes edema mainly by:

a) Increased capillary permeability

b) Reduced plasma oncotic pressure

c) Negative interstitial pressure

d) Increased lymphatic drainage

Explanation: Histamine release in anaphylaxis increases capillary permeability, allowing plasma proteins and fluid to leak into interstitial space, causing angioedema. Correct answer: (a) Increased capillary permeability.

Chapter: Cardiovascular Physiology

Topic: Autonomic Regulation of Blood Vessels

Subtopic: Cutaneous Circulation

Keywords

- Vasoconstriction: Narrowing of blood vessels reducing blood flow.

- Sympathetic system: Autonomic nervous system division controlling vasoconstriction.

- Parasympathetic system: Autonomic division with minimal role in skin vessels.

- Wheal and flare: Triple response due to histamine release.

- Thermoregulation: Adjustments in blood flow to skin for heat balance.

Lead Question – 2012

Vasoconstriction in skin?

a) Sympathetic

b) Parasympathetic

c) Wheal and flare

d) Warm climate

Explanation: Skin vasoconstriction is mediated by sympathetic adrenergic activity via norepinephrine acting on α1-receptors. Parasympathetic innervation is negligible in skin. Vasoconstriction conserves heat in cold climates. Thus, the correct answer is (a) Sympathetic.

Guessed Questions

1) A patient with spinal cord injury at T1 loses vasoconstrictor tone in skin below the lesion. This occurs because:

a) Parasympathetic denervation

b) Sympathetic denervation

c) Histamine release

d) Loss of local autoregulation

Explanation: Sympathetic fibers originate from thoracolumbar segments; interruption leads to loss of vasoconstriction below the lesion. The answer is (b) Sympathetic denervation.

2) During hemorrhage, cutaneous vasoconstriction helps by:

a) Increasing blood flow to skin

b) Redirecting blood to vital organs

c) Activating parasympathetic tone

d) Preventing sweating

Explanation: In shock, sympathetic vasoconstriction reduces skin perfusion, shunting blood to heart and brain. This is a protective response. The answer is (b) Redirecting blood to vital organs.

3) Administration of α-blocker (e.g., phentolamine) would cause skin vessels to:

a) Constrict

b) Dilate

c) Show no change

d) Collapse

Explanation: Blocking α1-receptors prevents sympathetic vasoconstriction, leading to vasodilation and flushing of skin. The correct answer is (b) Dilate.

4) In cold exposure, skin appears pale due to:

a) Parasympathetic constriction

b) Sympathetic vasoconstriction

c) Histamine effect

d) Increased nitric oxide

Explanation: Cold triggers sympathetic adrenergic vasoconstriction, decreasing skin blood flow and causing pallor. This conserves heat. Answer: (b) Sympathetic vasoconstriction.

5) A burn patient develops erythema around the wound due to:

a) Sympathetic tone

b) Histamine-mediated vasodilation

c) Parasympathetic reflex

d) Loss of autoregulation

Explanation: Burn injury releases histamine and other mediators causing local vasodilation and erythema (flare response). Correct answer is (b) Histamine-mediated vasodilation.

6) Vasoconstrictor fibers to the skin mainly release:

a) Acetylcholine

b) Norepinephrine

c) Dopamine

d) Serotonin

Explanation: Sympathetic adrenergic fibers release norepinephrine, activating α1-receptors to constrict vessels. The correct answer is (b) Norepinephrine.

7) Emotional stress causing pallor in face is due to:

a) Parasympathetic cholinergic activity

b) Sympathetic adrenergic vasoconstriction

c) Histamine release

d) Serotonin effect

Explanation: Stress triggers sympathetic activation, leading to facial skin vasoconstriction and pallor. The answer is (b) Sympathetic adrenergic vasoconstriction.

8) In Raynaud’s phenomenon, exaggerated vasoconstriction of fingers is triggered by:

a) Heat

b) Cold or stress

c) Infection

d) Exercise

Explanation: Raynaud’s is a disorder with excessive sympathetic-mediated vasoconstriction in response to cold or stress, causing pallor, cyanosis, and pain. Answer is (b) Cold or stress.

9) Which of the following drugs causes cutaneous vasodilation?

a) Phenylephrine

b) Atropine

c) Nitroprusside

d) Norepinephrine

Explanation: Sodium nitroprusside releases nitric oxide, causing potent vasodilation including cutaneous vessels. The answer is (c) Nitroprusside.

10) A soldier in desert heat collapses with flushed, dilated skin vessels. The mechanism is:

a) Sympathetic cholinergic vasodilation

b) Parasympathetic activation

c) Histamine response

d) α-receptor stimulation

Explanation: Heat stress activates sympathetic cholinergic fibers in skin, causing vasodilation and sweating for thermoregulation. Correct answer: (a) Sympathetic cholinergic vasodilation.

11) A patient with pheochromocytoma often has cold extremities due to:

a) Increased sympathetic vasoconstriction

b) Increased parasympathetic tone

c) Reduced adrenergic activity

d) Loss of histamine response

Explanation: Excess catecholamines in pheochromocytoma overstimulate α1-receptors, causing persistent vasoconstriction and cold extremities. Answer: (a) Increased sympathetic vasoconstriction.

Chapter: Cardiovascular Physiology

Topic: Cardiac Action Potential

Subtopic: Plateau Phase Mechanism

Keywords

- Plateau phase: Sustained depolarization of cardiac action potential.

- Calcium channels: L-type Ca2+ channels allowing inward current.

- Potassium permeability: Decreased during plateau maintaining depolarization.

- Sodium influx: Occurs early, not during plateau.

- Excitation-contraction coupling: Calcium influx triggers muscle contraction.

Lead Question – 2012

The plateau phase of this graph is due to:

a) The movement of fewer sodium ions across the cell membrane

b) The calcium channels remaining open longer than the sodium channels

c) The increased membrane permeability to potassium ion

d) A decrease in the amount of calcium diffusing across the membrane

Explanation: The plateau phase of the cardiac action potential is primarily maintained by the prolonged opening of L-type calcium channels, while potassium efflux is reduced. This sustained calcium influx prolongs depolarization, essential for contraction. Hence, the correct answer is (b) The calcium channels remaining open longer than the sodium channels.

Guessed Questions

1) Which ion influx is most critical for triggering myocardial contraction?

a) Sodium

b) Calcium

c) Potassium

d) Chloride

Explanation: Myocardial contraction is dependent on calcium influx during the plateau phase, which binds to troponin to initiate contraction. Thus, calcium is the essential ion. Answer: (b) Calcium.

2) A patient receiving verapamil therapy would show reduced:

a) Sodium influx

b) Calcium influx

c) Potassium efflux

d) Chloride influx

Explanation: Verapamil blocks L-type calcium channels, reducing calcium influx, shortening plateau, and decreasing contractility. The answer is (b) Calcium influx.

3) Which phase of the cardiac action potential is most affected by calcium channel blockers?

a) Phase 0

b) Phase 1

c) Phase 2

d) Phase 3

Explanation: Calcium channel blockers reduce calcium entry during phase 2 (plateau phase), altering contraction strength. The correct answer is (c) Phase 2.

4) The refractory period of cardiac muscle is prolonged due to:

a) Rapid sodium influx

b) Calcium influx during plateau

c) Potassium efflux

d) Chloride movement

Explanation: The plateau phase extends depolarization and refractory period, preventing tetany. This is mediated by calcium influx. Answer: (b) Calcium influx during plateau.

5) A drug that increases potassium efflux during phase 2 will:

a) Prolong plateau phase

b) Shorten plateau phase

c) Increase calcium entry

d) Increase refractory period

Explanation: Increased potassium efflux would counter depolarization, leading to early repolarization and shortening of the plateau. The answer is (b) Shorten plateau phase.

6) In pacemaker cells, the plateau phase is:

a) Prominent

b) Absent

c) Longer than in ventricular cells

d) Stronger than atrial cells

Explanation: Pacemaker cells (SA node) do not have a distinct plateau phase; instead, they exhibit gradual depolarization. Thus, the answer is (b) Absent.

7) The plateau phase in ventricular myocytes ensures:

a) Summation of contractions

b) Sustained contraction for effective ejection

c) Prevention of depolarization

d) Immediate relaxation

Explanation: Plateau phase sustains depolarization, allowing sufficient contraction for ejection of blood and preventing rapid re-excitation. The answer is (b) Sustained contraction for effective ejection.

8) Which ion is mainly responsible for repolarization following the plateau?

a) Sodium influx

b) Calcium influx

c) Potassium efflux

d) Chloride efflux

Explanation: Repolarization after the plateau is mediated by increased potassium efflux, which restores resting membrane potential. The answer is (c) Potassium efflux.

9) Digitalis toxicity prolongs plateau by increasing:

a) Calcium influx

b) Sodium influx

c) Potassium efflux

d) Chloride entry

Explanation: Digitalis increases intracellular calcium by inhibiting Na+/K+ ATPase, prolonging the plateau and contraction. The answer is (a) Calcium influx.

10) A mutation causing prolonged opening of calcium channels may lead to:

a) Tachyarrhythmia

b) Short QT syndrome

c) Long QT syndrome

d) Increased potassium clearance

Explanation: Prolonged calcium entry prolongs action potential duration, predisposing to long QT syndrome. Answer: (c) Long QT syndrome.

11) During exercise, sympathetic stimulation increases calcium influx, which results in:

a) Decreased stroke volume

b) Increased contractility

c) Shortened plateau phase

d) Reduced cardiac output

Explanation: Sympathetic activity increases calcium influx, strengthening contraction and raising stroke volume. Answer: (b) Increased contractility.

Chapter: Cardiovascular Physiology | Topic: Cardiac Output and Stroke Volume | Subtopic: Determinants of Stroke Volume

Keywords

Stroke volume — volume of blood ejected by left ventricle per beat.
End-diastolic volume (EDV) — ventricular volume at end of filling.
End-systolic volume (ESV) — ventricular volume at end of contraction.
Ejection fraction (EF) — fraction of EDV ejected, SV/EDV × 100.
Preload — ventricular stretch at end of diastole, approximated by EDV.
Afterload — resistance the ventricle must overcome to eject blood.
Contractility — intrinsic ability of myocardium to contract independent of preload/afterload.
Frank-Starling law — stroke volume rises with increased venous return (EDV) up to a point.
Cardiac output — stroke volume × heart rate.
Clinical relevance — heart failure alters preload, afterload, and contractility, reducing stroke volume.

Lead Question - 2012

Stroke volume is increased by ?

a) Increased end-diastolic and end-systolic volumes
b) Decreased end-diastolic and end-systolic volumes
c) Increased end-diastolic volume and decreased end-systolic volume
d) Decreased end-diastolic volume and increased end-systolic volume

Explanation: Stroke volume depends on preload (EDV), afterload, and contractility. An increased EDV (greater filling) combined with a decreased ESV (stronger ejection) yields maximum stroke volume. Thus the correct answer is c. This mechanism reflects both the Frank-Starling effect and improved myocardial contractility.

Q2. A patient with severe mitral regurgitation typically has increased stroke volume because of:

a) Increased preload
b) Increased afterload
c) Decreased contractility
d) Reduced ejection fraction

Explanation: In mitral regurgitation, left ventricular volume overload increases EDV (preload). The Frank-Starling mechanism initially augments stroke volume despite regurgitation. Correct answer is a. Over time, chronic overload reduces contractility and ejection fraction.

Q3. Stroke volume decreases in which of the following clinical states?

a) Hemorrhagic shock
b) Athlete’s heart
c) Sympathetic stimulation
d) Increased venous return

Explanation: Hemorrhage reduces preload (EDV) due to hypovolemia, leading to reduced stroke volume despite compensatory tachycardia. Correct answer is a. In contrast, exercise, sympathetic drive, and increased venous return augment stroke volume.

Q4. A hypertensive patient with high afterload will most likely have:

a) Increased stroke volume
b) Decreased stroke volume
c) No effect on stroke volume
d) Increased preload

Explanation: Increased afterload (arterial resistance) makes ejection more difficult, raising ESV and lowering stroke volume. Correct answer is b. Chronic high afterload may also lead to concentric LV hypertrophy.

Q5. In septic shock, stroke volume is often:

a) Increased due to reduced afterload
b) Decreased due to low preload
c) Unchanged
d) Increased due to sympathetic stimulation

Explanation: Septic shock features vasodilation and capillary leak. Although afterload decreases, low preload and impaired myocardial contractility often lower stroke volume. Correct answer is b. Fluids and vasopressors are used to restore volume and perfusion.

Q6. Which of the following increases stroke volume physiologically?

a) Beta-adrenergic stimulation
b) Beta-blocker therapy
c) Acidosis
d) Myocardial ischemia

Explanation: Beta-adrenergic stimulation enhances myocardial contractility, reducing ESV and increasing stroke volume. Correct answer is a. Beta-blockers, ischemia, and acidosis depress contractility, reducing stroke volume.

Q7. Stroke volume is most reduced in which of the following?

a) Acute myocardial infarction
b) Athlete’s bradycardia
c) Moderate exercise
d) Positive inotrope infusion

Explanation: In acute myocardial infarction, contractility falls acutely, causing a rise in ESV and a fall in stroke volume. Correct answer is a. In athletes, stroke volume is preserved or enhanced despite slower heart rates.

Q8. Stroke volume increases during exercise due to:

a) Increased EDV and sympathetic stimulation
b) Decreased EDV and afterload
c) Decreased contractility
d) Increased ESV

Explanation: Exercise boosts venous return (increasing preload) and sympathetic activity (enhancing contractility), lowering ESV and raising stroke volume. Correct answer is a. This adaptation supports higher cardiac output during physical activity.

Q9. Which condition decreases stroke volume most significantly?

a) Cardiac tamponade
b) Exercise
c) Sympathetic stimulation
d) Early pregnancy

Explanation: Cardiac tamponade impairs diastolic filling by external compression of the heart, reducing preload and stroke volume. Correct answer is a. Exercise, sympathetic drive, and pregnancy normally increase stroke volume.

Q10. Stroke volume is increased by which pharmacological agent?

a) Dobutamine
b) Beta-blockers
c) Calcium channel blockers (verapamil)
d) Digoxin toxicity

Explanation: Dobutamine, a beta-1 agonist, enhances myocardial contractility and reduces ESV, increasing stroke volume. Correct answer is a. Other listed agents impair contractility or conduction and reduce stroke volume.

Q11. Which of the following is used clinically as a surrogate measure of stroke volume?

a) Pulse pressure
b) Diastolic pressure
c) Heart rate
d) Central venous pressure

Explanation: Pulse pressure (SBP–DBP) is proportional to stroke volume when arterial compliance is constant. Thus it serves as a surrogate measure. Correct answer is a. Diastolic pressure, HR, or CVP do not directly reflect stroke volume.

Chapter: Cardiovascular Physiology | Topic: Cardiac Function | Subtopic: Ejection Fraction

Keywords

Ejection fraction (EF) — fraction of end-diastolic volume ejected during systole.
Stroke volume (SV) — difference between end-diastolic and end-systolic volumes.
Preload — ventricular end-diastolic volume or pressure.
Afterload — resistance against which the ventricle ejects blood.
Contractility — intrinsic myocardial ability to contract independently of preload and afterload.
Frank-Starling mechanism — relationship between preload and stroke volume.
Cardiac output (CO) — product of stroke volume and heart rate.
End-diastolic volume (EDV) — volume in ventricle before systole.
End-systolic volume (ESV) — volume remaining after contraction.
Heart failure — clinical syndrome with reduced EF in systolic type.

Lead Question - 2012

Calculate the ejection fraction from the given volume pressure curve:

a) 40%
b) 50%
c) 55%
d) 60%

Explanation: Ejection fraction = (EDV – ESV) / EDV × 100. A normal EF ranges from 55%–70%. On the curve, the calculated value is about 55%, making option c correct. EF is a key marker of left ventricular systolic function and important in diagnosing heart failure and cardiomyopathies.

Q1. A 60-year-old man with ischemic heart disease has EF of 35%. What type of heart failure is most likely?

a) Heart failure with preserved EF
b) Systolic heart failure
c) Diastolic heart failure
d) High-output failure

Explanation: An EF below 40% indicates systolic dysfunction where the ventricle fails to contract effectively. This is termed systolic heart failure. Diastolic failure occurs when EF is preserved but relaxation is impaired. Thus, option b is correct. Low EF is a major prognostic marker in ischemic cardiomyopathy.

Q2. Which factor directly increases stroke volume and ejection fraction?

a) Increased afterload
b) Increased preload
c) Decreased contractility
d) Increased heart rate

Explanation: Increasing preload within physiological limits enhances stroke volume by the Frank-Starling mechanism, thereby raising ejection fraction. Increased afterload reduces EF, while reduced contractility decreases EF. Tachycardia shortens filling time, lowering stroke volume. Correct answer is b. Preload optimization is key in volume-responsive patients.

Q3. In which condition is ejection fraction usually preserved?

a) Dilated cardiomyopathy
b) Hypertrophic cardiomyopathy
c) Systolic heart failure
d) Post-myocardial infarction scar

Explanation: Hypertrophic cardiomyopathy primarily causes impaired diastolic filling but systolic contraction is preserved or even hyperdynamic, so EF remains normal or high. Dilated cardiomyopathy and post-MI cause systolic dysfunction and reduced EF. Thus, correct answer is b. Clinical diagnosis relies on echocardiography.

Q4. A patient’s EDV is 120 mL and ESV is 60 mL. What is his EF?

a) 40%
b) 45%
c) 50%
d) 60%

Explanation: EF = (120 – 60) / 120 × 100 = 60 / 120 × 100 = 50%. This is at the lower end of normal. EF quantifies contractile function and is easily measured by echocardiography. Option c is correct. Values under 50% suggest borderline systolic impairment.

Q5. Which investigation most commonly measures ejection fraction in clinical practice?

a) ECG
b) Echocardiography
c) Chest X-ray
d) Coronary angiography

Explanation: Echocardiography is the most widely used, non-invasive, bedside method to estimate EF through Simpson’s biplane method or M-mode. ECG shows rhythm, chest X-ray shows size, and angiography evaluates coronaries but not EF directly. Correct answer is b. Cardiac MRI is gold standard but less available.

Q6. A patient on dobutamine infusion shows increased EF. The drug acts by:

a) Decreasing preload
b) Increasing contractility
c) Reducing afterload
d) Increasing heart rate only

Explanation: Dobutamine is a β1 agonist that increases myocardial contractility, thereby enhancing stroke volume and EF. It also slightly increases heart rate but the primary effect is inotropy. Correct answer is b. Used in acute decompensated heart failure and diagnostic stress echocardiography.

Q7. Which condition classically presents with reduced EF?

a) Restrictive cardiomyopathy
b) Aortic stenosis (chronic)
c) Dilated cardiomyopathy
d) Hypertrophic cardiomyopathy

Explanation: Dilated cardiomyopathy features stretched, weakened ventricles with impaired systolic contraction, leading to low EF. Restrictive and hypertrophic cardiomyopathy often show preserved EF but impaired filling. Aortic stenosis may reduce EF late but not initially. Correct answer is c. EF monitoring is key in prognosis and therapy.

Q8. Which of the following decreases ejection fraction?

a) Increased sympathetic activity
b) Positive inotropic drugs
c) Acute myocardial infarction
d) Exercise

Explanation: Acute myocardial infarction causes loss of functional myocardium, reducing contractility and EF. Sympathetic activation, inotropes, and exercise generally increase EF by enhancing contractility. Correct answer is c. Serial EF assessment post-MI helps guide therapy and detect ventricular remodeling.

Q9. A 70-year-old hypertensive diabetic patient has EF 60% but shows signs of heart failure. What is the likely diagnosis?

a) Heart failure with reduced EF
b) Right-sided failure
c) Heart failure with preserved EF
d) High-output failure

Explanation: HF with preserved EF (HFpEF) occurs when diastolic relaxation is impaired, as in elderly hypertensive diabetics with stiff ventricles. EF remains ≥50% but symptoms occur due to poor filling. Correct answer is c. Diagnosis requires echo showing preserved EF but diastolic dysfunction features.

Q10. Chemotherapy drug doxorubicin can cause cardiotoxicity. What EF change would you expect?

a) Increased EF
b) No effect on EF
c) Reduced EF
d) Transient rise in EF

Explanation: Doxorubicin-induced cardiomyopathy is a well-known cause of systolic dysfunction with reduced EF. Monitoring EF before and during therapy is standard. A significant fall necessitates discontinuation. Correct answer is c. EF decline reflects irreversible myocardial damage from oxidative stress caused by anthracycline therapy.

Chapter: Cardiovascular Physiology | Topic: Blood Pressure Regulation | Subtopic: Mean Arterial Pressure (MAP) and Determinants

Keywords

Mean arterial pressure (MAP) — average arterial pressure during one cardiac cycle.
Systolic blood pressure (SBP) — peak arterial pressure during ventricular systole.
Diastolic blood pressure (DBP) — lowest arterial pressure during diastole.
Pulse pressure — SBP minus DBP; reflects stroke volume and arterial compliance.
Total peripheral resistance (TPR) — resistance to blood flow in systemic circulation.
Cardiac output (CO) — stroke volume × heart rate; determines MAP with SVR.
Autoregulation — intrinsic tissue control of blood flow within a pressure range.
Arterial compliance — arterial elasticity influencing pressure changes.
Hypertensive emergency — sudden BP rise with organ damage.
Vasopressors/vasodilators — drugs altering vascular tone and MAP.

Lead Question - 2012

Mean arterial pressure is calculated as:

a) (SBP + 2DBP) / 3
b) (DBP + 2SBP) / 3
c) (SBP + 3DBP) / 2
d) (DBP + 3SBP) / 2

Explanation: The approximate formula is (SBP + 2×DBP)/3 because diastole occupies two-thirds of the cardiac cycle. This method is valid at normal heart rates and rhythms, making option a correct. MAP reflects tissue perfusion pressure, critical for organ blood supply and often targeted in critical care settings.

Q2. A 45-year-old hypertensive patient suddenly stands and feels dizzy. Which receptor mediates rapid correction?

a) Chemoreceptors
b) Baroreceptors
c) Osmoreceptors
d) Mechanoreceptors in joints

Explanation: Baroreceptors in carotid sinus and aortic arch sense stretch changes, activating reflexes to stabilize MAP. Upon standing, reduced venous return decreases stretch, leading to sympathetic activation and BP restoration. Correct answer is b. Dysfunction causes orthostatic hypotension, often seen in autonomic neuropathies or elderly patients.

Q3. During septic shock, which factor primarily lowers MAP?

a) Increased TPR
b) Decreased TPR
c) Increased cardiac contractility
d) Elevated SBP

Explanation: In septic shock, vasodilation due to inflammatory mediators decreases systemic vascular resistance (TPR), which in turn lowers MAP despite preserved or even elevated cardiac output. Thus, the correct answer is b. Management includes vasopressors to restore vascular tone and adequate tissue perfusion.

Q4. Which parameter has the greatest direct effect on mean arterial pressure?

a) Stroke volume
b) Cardiac output
c) Venous return
d) Systemic vascular resistance

Explanation: Mean arterial pressure is primarily determined by cardiac output × systemic vascular resistance. Both cardiac output and resistance contribute, but b (cardiac output) is the immediate determinant of blood flow and pressure, especially in clinical measurements. Drugs targeting either component affect MAP significantly in critical settings.

Q5. In a patient with chronic renal failure, MAP is often elevated due to:

a) Reduced stroke volume
b) Increased sympathetic tone
c) Decreased vascular resistance
d) Loss of baroreceptor reflex

Explanation: Chronic renal failure leads to sodium and water retention, activating renin-angiotensin and sympathetic pathways, elevating systemic vascular resistance. The result is higher MAP. Correct answer is b. This mechanism explains why antihypertensives targeting the RAAS system are especially effective in renal disease–related hypertension.

Q6. Which organ maintains constant blood flow across a wide MAP range due to autoregulation?

a) Kidney
b) Skin
c) Spleen
d) Muscle

Explanation: The kidney autoregulates blood flow across MAP of 80–180 mmHg, preserving GFR despite systemic fluctuations. This is critical for excretory function. Correct answer is a. Breakdown of autoregulation in shock or severe hypotension leads to acute kidney injury, making MAP support crucial in ICU settings.

Q7. In hypertensive emergencies, lowering MAP too rapidly may cause:

a) Stroke
b) Reflex tachycardia
c) Organ hypoperfusion
d) Increased cerebral perfusion

Explanation: In chronic hypertension, autoregulation shifts to higher MAP levels. Abrupt reduction can reduce perfusion below critical threshold, causing ischemia. The correct answer is c. Guidelines recommend gradual BP lowering by 20–25% within the first hour to prevent hypoperfusion of brain, heart, and kidneys.

Q8. A patient with tachycardia will have MAP estimation error because:

a) Systolic occupies longer cycle time
b) Diastolic shortens disproportionately
c) Formula is independent of HR
d) Stroke volume decreases

Explanation: MAP formula assumes diastole is two-thirds of cardiac cycle. In tachycardia, diastole shortens disproportionately, reducing accuracy of (SBP + 2×DBP)/3. The correct answer is b. In such cases, direct invasive arterial monitoring provides more accurate MAP estimation in intensive care.

Q9. Which drug increases MAP mainly by elevating systemic vascular resistance?

a) Dobutamine
b) Noradrenaline
c) Nitroglycerin
d) Milrinone

Explanation: Noradrenaline (norepinephrine) is a potent α-adrenergic agonist that increases vascular tone, raising systemic vascular resistance and MAP. Thus, the correct answer is b. It is first-line vasopressor in septic shock. Dobutamine and milrinone act more on cardiac contractility and vasodilation, while nitroglycerin reduces MAP.

Q10. MAP is best maintained in shock resuscitation above:

a) 50 mmHg
b) 60 mmHg
c) 65 mmHg
d) 75 mmHg

Explanation: Guidelines recommend maintaining MAP ≥65 mmHg to ensure vital organ perfusion during shock resuscitation. This target balances risks of underperfusion and excessive vasopressor use. Thus, the correct answer is c. Individualization may be required for patients with chronic hypertension or intracranial pathology.

Q11. A 60-year-old with head injury requires MAP support. Adequate MAP is essential primarily to maintain:

a) Cerebral perfusion pressure
b) Pulmonary artery pressure
c) Right atrial pressure
d) Venous return

Explanation: Cerebral perfusion pressure = MAP − intracranial pressure. Adequate MAP is critical to prevent secondary brain ischemia in head injury. Therefore, the correct answer is a. Critical care guidelines recommend maintaining CPP >60 mmHg, which depends on sustaining sufficient MAP alongside reducing raised intracranial pressure.

Chapter: Cardiovascular Physiology

Topic: Cardiac Electrophysiology

Subtopic: Parasympathetic Regulation of Heart Rate

Keywords:

• Acetylcholine – parasympathetic neurotransmitter acting on muscarinic receptors

• SA Node – pacemaker of the heart controlling heart rate

• Diastolic Depolarization – slow rise of membrane potential in pacemaker cells

• Vagal Stimulation – reduces firing rate of SA node

• Chronotropy – effect on heart rate

Lead Question - 2012

Mechanism by which Ach decreases heart rate is by:

a) Delayed diastolic depolarization

b) Increase in plateau

c) Decrease preload

d) Increase afterload

Explanation: Acetylcholine (ACh) released by vagus nerve activates M2 muscarinic receptors in the SA node, increasing K⁺ efflux and reducing slope of diastolic depolarization. This slows pacemaker activity, lowering heart rate. Correct answer: (a).

Guessed Question 1

A 25-year-old athlete presents with episodes of dizziness and bradycardia. Increased vagal tone is suspected. What is the direct ionic mechanism?

a) Increased Ca²⁺ influx

b) Increased K⁺ efflux

c) Decreased Na⁺ influx

d) Increased Cl⁻ influx

Explanation: Vagal stimulation releases ACh, which increases K⁺ efflux via muscarinic K⁺ channels, hyperpolarizing SA node cells and slowing pacemaker firing. Correct answer: (b).

Guessed Question 2

Parasympathetic stimulation primarily affects which cardiac region?

a) Ventricular myocardium

b) SA node and AV node

c) Purkinje fibers

d) Papillary muscles

Explanation: Parasympathetic fibers mainly innervate the SA and AV nodes, altering conduction and rate. Ventricles have minimal vagal innervation. Correct answer: (b).

Guessed Question 3

Increased vagal activity during sleep results in:

a) Tachycardia

b) Bradycardia

c) Increased stroke volume

d) Hypertension

Explanation: During sleep, parasympathetic tone predominates, reducing heart rate and producing physiologic bradycardia without compromising cardiac output. Correct answer: (b).

Guessed Question 4

A patient receives atropine. Which of the following changes is expected?

a) Decreased heart rate

b) Increased heart rate

c) AV nodal delay

d) Enhanced vagal tone

Explanation: Atropine blocks muscarinic receptors, thereby inhibiting vagal effects and increasing heart rate. Correct answer: (b).

Guessed Question 5

Carotid sinus massage produces reflex bradycardia primarily by:

a) Increased vagal discharge

b) Increased sympathetic discharge

c) Reduced baroreceptor firing

d) Decreased preload

Explanation: Carotid massage stretches baroreceptors, enhancing vagal discharge and slowing SA node activity, producing bradycardia. Correct answer: (a).

Guessed Question 6

A 40-year-old man develops AV block due to excessive vagal stimulation. Which interval is prolonged on ECG?

a) PR interval

b) QRS duration

c) QT interval

d) ST segment

Explanation: Excessive vagal stimulation slows AV nodal conduction, prolonging the PR interval. Correct answer: (a).

Guessed Question 7

Which neurotransmitter is responsible for parasympathetic slowing of heart rate?

a) Noradrenaline

b) Dopamine

c) Acetylcholine

d) Adrenaline

Explanation: Acetylcholine released by vagal nerve endings binds muscarinic receptors, slowing the SA node pacemaker. Correct answer: (c).

Guessed Question 8

During vasovagal syncope, the patient faints due to:

a) Sympathetic overactivity

b) Combined bradycardia and vasodilation

c) Hypertension and tachycardia

d) Coronary spasm

Explanation: Vasovagal syncope results from sudden vagal discharge causing bradycardia and systemic vasodilation, leading to transient cerebral hypoperfusion. Correct answer: (b).

Guessed Question 9

Which drug enhances vagal effect on the heart and is contraindicated in bradyarrhythmias?

a) Digoxin

b) Atropine

c) Dobutamine

d) Isoprenaline

Explanation: Digoxin enhances vagal tone, slowing AV nodal conduction, beneficial in supraventricular tachyarrhythmias but contraindicated in bradycardia. Correct answer: (a).

Guessed Question 10

A 32-year-old patient with acute inferior wall MI develops sinus bradycardia. This is most likely due to:

a) Increased sympathetic tone

b) Vagal hyperactivity

c) AV node ischemia

d) Loss of pacemaker cells

Explanation: Inferior wall MI often involves the right coronary artery supplying SA node, leading to vagal hyperactivity and sinus bradycardia. Correct answer: (b).

Chapter: Cardiovascular Physiology

Topic: Electrocardiography

Subtopic: Einthoven’s Law

Keywords:

• Einthoven’s Triangle – imaginary equilateral triangle around the heart formed by limb leads

• Bipolar Limb Leads – leads I, II, III measuring potential difference between limb electrodes

• Augmented Leads – unipolar limb leads (aVR, aVL, aVF)

• Vector – direction and magnitude of electrical activity of the heart

• Lead Axis – orientation of a lead in the frontal plane

Lead Question - 2012

Einthoven’s law -

a) I + III = II

b) I - III = II

c) I + II + III = 0

d) I + III = avL

Explanation: Einthoven’s law states that in a standard ECG, the potential of lead II is equal to the sum of the potentials of leads I and III (II = I + III). This relationship helps in verifying lead placement and ECG recording accuracy. Correct answer: (a).

Guessed Question 1

A 60-year-old male presents with chest pain. His ECG shows ST elevation in leads II, III, and aVF. Which coronary artery is most likely involved?

a) Left anterior descending artery

b) Left circumflex artery

c) Right coronary artery

d) Left main coronary artery

Explanation: ST elevation in leads II, III, and aVF indicates inferior wall myocardial infarction, most commonly due to right coronary artery occlusion. Correct answer: (c).

Guessed Question 2

Lead aVR normally shows:

a) Upright P wave and QRS

b) Negative deflection of P, QRS, and T waves

c) Positive ST segment

d) No consistent wave pattern

Explanation: Lead aVR usually records negative deflections for P, QRS, and T waves because it views the heart from the right shoulder, opposite to the main vector. Correct answer: (b).

Guessed Question 3

PR interval on ECG represents:

a) Atrial depolarization

b) Conduction time from atria to ventricles

c) Ventricular depolarization

d) Atrial repolarization

Explanation: The PR interval corresponds to the time taken for impulse conduction from atria through AV node to ventricles, normally 0.12–0.20 seconds. Correct answer: (b).

Guessed Question 4

In complete heart block, the ECG shows:

a) Prolonged PR interval

b) Progressive PR prolongation

c) Dissociation between P waves and QRS complexes

d) Absent P waves

Explanation: In complete heart block, atrial and ventricular activities are independent, with P waves not related to QRS complexes. Correct answer: (c).

Guessed Question 5

QT interval on ECG corresponds to:

a) Ventricular depolarization

b) Atrial depolarization

c) Ventricular depolarization and repolarization

d) Atrial repolarization

Explanation: The QT interval represents the total duration of ventricular depolarization and repolarization. It is rate-dependent and prolongation predisposes to arrhythmias. Correct answer: (c).

Guessed Question 6

In a patient with hyperkalemia, which ECG change is most characteristic?

a) Flattened T waves

b) Tall peaked T waves

c) Short PR interval

d) Prolonged QT interval

Explanation: Hyperkalemia classically produces tall, peaked T waves due to accelerated repolarization. Severe hyperkalemia can lead to conduction block and cardiac arrest. Correct answer: (b).

Guessed Question 7

Which ECG lead best represents atrial activity?

a) Lead I

b) Lead II

c) Lead III

d) Lead aVL

Explanation: Lead II best shows atrial activity (P waves) because its axis is parallel to the atrial depolarization vector. Correct answer: (b).

Guessed Question 8

A 25-year-old male experiences sudden syncope during exercise. His ECG shows prolonged QT interval. The likely diagnosis is:

a) Brugada syndrome

b) Long QT syndrome

c) WPW syndrome

d) AV nodal reentrant tachycardia

Explanation: Long QT syndrome, congenital or acquired, predisposes to torsades de pointes and sudden death during exertion. Correct answer: (b).

Guessed Question 9

Which component of the ECG corresponds to ventricular depolarization?

a) P wave

b) QRS complex

c) T wave

d) U wave

Explanation: The QRS complex corresponds to ventricular depolarization. Normally < 120 ms, its widening indicates conduction delay or bundle branch block. Correct answer: (b).

Guessed Question 10

A 50-year-old hypertensive patient has left ventricular hypertrophy. Which ECG finding is most consistent?

a) Tall R waves in V1

b) Tall R waves in left chest leads (V5, V6)

c) Deep S waves in V5, V6

d) Low voltage QRS

Explanation: Left ventricular hypertrophy produces tall R waves in left-sided chest leads (V5, V6) and deep S waves in V1, V2 due to increased left ventricular mass. Correct answer: (b).

Chapter: Cardiovascular Physiology

Topic: Coronary Circulation

Subtopic: Regulation of Coronary Blood Flow

Keywords:

• Coronary Blood Flow – blood supply to myocardium through coronary arteries

• Perfusion Pressure – pressure gradient driving blood flow through tissues

• Vascular Resistance – opposition offered by vessels to blood flow

• Autoregulation – intrinsic ability of tissue to maintain constant flow despite pressure changes

• Oxygen Demand – myocardial requirement driving blood flow regulation

Lead Question - 2012

Which one of the following is the CORRECT statement regarding coronary blood flow?

a) Coronary blood flow is directly related to perfusion pressure and inversely related to resistance

b) Coronary blood flow is inversely related to perfusion pressure and directly related to resistance

c) Coronary blood flow is directly related to perfusion pressure and also to resistance

d) Coronary blood flow is inversely related to both pressure and resistance

Explanation: Coronary blood flow is directly proportional to perfusion pressure and inversely proportional to coronary vascular resistance. The myocardium relies on autoregulation and oxygen demand to control flow. Hence, option (a) is correct.

Guessed Question 1

In coronary circulation, maximum blood flow occurs during:

a) Systole

b) Early diastole

c) Mid-diastole

d) Late systole

Explanation: Coronary perfusion predominantly occurs during diastole due to compression of intramyocardial vessels in systole. Peak flow is in early diastole. Correct answer: (b).

Guessed Question 2

Which factor is the most important regulator of coronary blood flow?

a) Perfusion pressure

b) Myocardial oxygen demand

c) Autonomic nervous system

d) Endothelial factors

Explanation: The primary determinant of coronary blood flow is myocardial oxygen demand. Metabolites like adenosine mediate vasodilation. Hence, option (b) is correct.

Guessed Question 3

In left ventricular coronary circulation, systolic flow is reduced because:

a) Aortic valve closure

b) High intramyocardial pressure

c) Reduced perfusion pressure

d) Increased venous return

Explanation: High intramyocardial pressure during systole compresses coronary vessels, especially in the left ventricle, reducing flow. Correct answer: (b).

Guessed Question 4

Coronary flow reserve is:

a) The difference between basal and maximal coronary blood flow

b) Maximum coronary blood flow

c) Flow at rest

d) Myocardial venous return

Explanation: Coronary flow reserve is the ability of coronary circulation to increase flow above basal level in response to demand. Correct answer: (a).

Guessed Question 5

Coronary steal phenomenon occurs due to:

a) Vasodilation in stenosed vessels

b) Preferential blood flow to non-stenosed vessels

c) Coronary spasm

d) Increased venous drainage

Explanation: In stenosed vessels, distal arterioles are already maximally dilated. Vasodilators divert blood to normal vessels, reducing flow to ischemic zones—coronary steal. Correct answer: (b).

Guessed Question 6

Which substance is the most potent coronary vasodilator?

a) Adenosine

b) Nitric oxide

c) Carbon dioxide

d) Prostacyclin

Explanation: Adenosine, generated during hypoxia, is the most powerful coronary vasodilator, matching supply to oxygen demand. Correct answer: (a).

Guessed Question 7

In coronary circulation, autoregulation maintains flow between pressures of:

a) 30–60 mmHg

b) 60–140 mmHg

c) 80–180 mmHg

d) 40–100 mmHg

Explanation: Coronary autoregulation works effectively between mean arterial pressures of 60–140 mmHg, maintaining constant flow despite fluctuations. Correct answer: (b).

Guessed Question 8

Which vessel supplies blood to the sinoatrial (SA) node in most individuals?

a) Right coronary artery

b) Left coronary artery

c) Circumflex artery

d) Anterior interventricular artery

Explanation: In ~60% of cases, the SA node is supplied by the right coronary artery; in others, the circumflex. Correct answer: (a).

Guessed Question 9

A patient develops chest pain at rest due to coronary vasospasm. This condition is termed:

a) Stable angina

b) Unstable angina

c) Prinzmetal’s angina

d) Silent ischemia

Explanation: Prinzmetal’s (variant) angina occurs due to transient coronary vasospasm at rest, often with ST elevation. Correct answer: (c).

Guessed Question 10

The major site of resistance in coronary circulation is:

a) Epicardial arteries

b) Arterioles

c) Capillaries

d) Venules

Explanation: Coronary arterioles are the main resistance vessels controlling coronary flow. Correct answer: (b).

Keywords (for all questions)

Diffusion: Movement of gas down partial pressure gradients across thin membranes.
Partial pressure (P): Driving force for gas transfer; P_O₂ and P_CO₂ determine direction and rate.
Capillary: Thin-walled microvessel providing maximal surface area for gas exchange.
Transit time: Time blood spends in capillary; affects equilibration of gases.
Fick’s law: Rate ∝ (diffusion coefficient × area × ΔP) / thickness.
Diffusion coefficient: Depends on gas solubility and molecular weight (CO₂ diffuses faster than O₂).
Diffusion distance: Separation between blood and tissue; increased by edema or fibrosis.
Capillary recruitment: More capillaries perfused increases exchange surface area (important in exercise).
Oxygen content vs PO₂: Content depends on hemoglobin concentration and saturation; PO₂ measures dissolved gas.
Diffusion limitation vs perfusion limitation: Diffusion-limited when membrane thickening limits equilibration; perfusion-limited when transit time limits uptake.
Clinical examples: Pulmonary fibrosis → diffusion limitation; anemia → low O₂ content; pulmonary edema → increased diffusion distance.

Chapter: Respiratory Physiology | Topic: Gas Exchange | Subtopic: Tissue Gas Exchange

Lead Question – 2012

Gas exchange in tissues takes place at ?

a) Artery

b) Capillary

c) Vein

d) Venules

Explanation: Gas exchange in tissues occurs across capillary walls where oxygen diffuses from blood to cells and carbon dioxide diffuses back into plasma. Capillaries provide thin endothelium and large surface area for diffusion; arterioles/venules serve as conduits. Thus exchange primarily occurs in capillaries. Answer: b) Capillary.

1) Which law best describes the rate of gas transfer across the capillary membrane?

a) Fick's law

b) Boyle's law

c) Henry's law

d) Charles's law

Explanation: Fick’s law quantifies net gas transfer across membranes: rate = (diffusion coefficient × area × partial pressure difference)/thickness. Increasing surface area or partial pressure gradient or diffusion coefficient, or decreasing membrane thickness, augments exchange. Clinically, emphysema reduces area, pulmonary fibrosis increases thickness, reducing oxygen transfer markedly. Answer: a) Fick’s law.

2) During strenuous exercise capillary transit time falls. What is the usual effect on O₂ uptake?

a) O₂ uptake falls drastically

b) Minimal effect due to compensation

c) Equilibration impossible

d) O₂ uptake becomes zero

Explanation: During exercise capillary transit time shortens due to increased cardiac output; despite reduced transit, elevated perfusion and larger partial pressure gradients maintain oxygen uptake by increased diffusion and recruitment of capillaries. In severe pathology, very short transit may limit saturation. Answer: b) Minimal effect due to compensation in healthy individuals.

3) Interstitial edema increases diffusion distance. What happens to tissue oxygenation?

a) No change

b) Increased oxygenation

c) Decreased tissue oxygenation

d) Only CO₂ affected

Explanation: Interstitial edema increases diffusion distance between capillary and cells, reducing oxygen delivery and impairing CO₂ removal; tissues may become hypoxic despite normal arterial oxygen content. Severe edema in lungs causes impaired gas exchange and hypoxemia. Clinically, pulmonary edema reduces arterial PO₂. Answer: c) Decreased tissue oxygenation, especially during exertion episodes.

4) Which gas diffuses faster across biological membranes?

a) Carbon dioxide

b) Oxygen

c) Nitrogen

d) Helium

Explanation: Carbon dioxide diffuses approximately 20 times faster than oxygen across biological membranes because of higher solubility despite lower gradient; CO₂'s greater diffusion coefficient allows rapid removal from tissues though O₂ transport remains diffusion-limited. Clinically, CO₂ clearance often preserved when oxygenation fails. Answer: a) Carbon dioxide in many disease states too.

5) Typical systemic arterial PO₂ that provides driving force for tissue diffusion is approximately?

a) 40 mmHg

b) 100 mmHg

c) 250 mmHg

d) 760 mmHg

Explanation: Normal systemic arterial PO₂ is about 100 mmHg, creating a substantial gradient versus tissue PO₂ (~40 mmHg) that drives diffusion. Lowered arterial PO₂ reduces this gradient and compromises oxygen delivery, leading to tissue hypoxia if severe. Answer: b) Arterial PO₂ ≈ 100 mmHg, commonly measured by arterial blood gas analysis.

6) In anemia, how is tissue oxygen delivery affected despite normal PaO₂?

a) Unchanged oxygen content

b) Increased oxygen content

c) Reduced oxygen content despite normal PaO₂

d) PaO₂ falls dramatically

Explanation: In anemia arterial oxygen content falls due to reduced hemoglobin concentration despite normal saturation and PO₂; tissues compensate by increasing cardiac output and extracting more oxygen, but severe anemia produces tissue hypoxia even with normal gas exchange. Transfusion raises oxygen content. Answer: c) Reduced oxygen content despite normal PaO₂ levels.

7) Which pathology is classically diffusion-limited for O₂ transfer?

a) Pulmonary fibrosis

b) Right-to-left shunt

c) Hypoventilation

d) Anemia

Explanation: Pulmonary fibrosis thickens alveolar-capillary membrane, increasing diffusion distance and causing diffusion limitation especially during exercise when transit time shortens; oxygen uptake is impaired causing hypoxemia and widened A–a gradient. Right-to-left shunt causes hypoxemia but not diffusion limitation mechanism. Answer: a) Pulmonary fibrosis treatment may include oxygen therapy and antifibrotic agents.

8) Exercise increases oxygen exchange by which microvascular change?

a) Decreased diffusion capacity

b) Increased diffusion capacity due to recruitment

c) Reduced capillary surface area

d) Increased diffusion distance

Explanation: During exercise pulmonary and systemic capillary recruitment and increased perfusion elevate overall diffusion capacity for oxygen (DL_O₂), shortening transit time but increasing surface area and partial pressure gradients, thereby enhancing gas exchange. Diffusion capacity measurements rise with workload. Answer: b) Increased diffusion capacity due to recruitment and higher cardiac output.

9) Diffusion hypoxia is a clinical phenomenon seen when?

a) Nitrous oxide is discontinued

b) Patient breathes 100% oxygen for prolonged period

c) During carbon monoxide poisoning

d) With severe anemia only

Explanation: Diffusion hypoxia occurs when nitrous oxide is discontinued; rapid efflux of N₂O from blood into alveoli dilutes alveolar oxygen and may transiently lower its partial pressure, causing hypoxia if supplemental oxygen not provided. This is a clinical example of diffusion phenomenon. Answer: a) After nitrous oxide discontinuation during emergence recovery.

10) Why are venules not primary sites for gas exchange?

a) They have maximal exchange

b) They have thin walls like capillaries

c) They are upstream of capillaries

d) Venules are not primary exchange sites

Explanation: Venules and veins have thicker walls, lower surface area, and are located downstream where diffusion gradients are reduced; primary gas exchange occurs across capillary endothelium with minimal exchange at venules. Venules specialize in fluid and leukocyte trafficking rather than gas diffusion. Answer: d) Venules are not primary exchange sites clinically.

Keywords (for all questions)

Microcirculation: Network of arterioles, capillaries, venules (± metarterioles, thoroughfare channels) where exchange occurs.
Precapillary sphincter: Smooth muscle collar regulating capillary perfusion/recruitment.
Starling forces (revised): Filtration depends on hydrostatic/oncotic pressures and endothelial glycocalyx.
Glycocalyx: Endothelial surface layer modulating permeability and oncotic gradient; degraded in sepsis.
Functional hyperemia: ↑Flow to active tissues via metabolites (adenosine, CO₂, H⁺, K⁺).
Reactive hyperemia: Transient ↑Flow after occlusion due to vasodilator washout and myogenic response.
Autoregulation: Local maintenance of flow vs pressure via myogenic/metabolic mechanisms.
Poiseuille’s law: Resistance ∝ viscosity × length / radius⁴; small radius changes drastically alter flow.
Fåhræus–Lindqvist effect: Apparent blood viscosity falls in small vessels (down to ~10–300 μm).
Diffusion distance: Capillaries keep cells within ~100 μm for adequate O₂ exchange.
Capillary types: Continuous (muscle, brain), fenestrated (kidney, intestine), sinusoidal (liver, spleen).
NO/Endothelin: Endothelial vasodilator (NO) and vasoconstrictor (endothelin-1) balancing tone.
Capillary hydrostatic pressure (Pc): ~15–35 mmHg; higher at arteriolar end.
Lymphatics: Return filtered fluid/proteins; failure → edema.
Sepsis microvascular dysfunction: Glycocalyx loss, shunting, ↑permeability → lactate rise.

Chapter: Cardiovascular Physiology | Topic: Microcirculation | Subtopic: Structure and Function

Lead Question – 2012

Microcirculation consists of ?

a) Capillaries

b) Capillaries venules and arterioles

c) Aorta

d) Arteries and veins

Explanation: Microcirculation refers to the smallest vessels involved in exchange and resistance control—terminal arterioles, capillaries, and venules (often including metarterioles/thoroughfare channels). Large arteries, veins, and the aorta are macrocirculatory. Exchange and Starling flux occur at this level. Answer: b) Capillaries venules and arterioles.

1) A runner’s active skeletal muscle shows increased flow. The predominant cause at the microvascular level is:

a) Sympathetic α1 vasoconstriction

b) Local metabolic vasodilation

c) Increased venous pressure

d) Baroreceptor unloading

Explanation: Functional hyperemia is driven by local metabolites (adenosine, CO₂, K⁺, H⁺) opening precapillary sphincters and dilating arterioles, recruiting capillaries and boosting exchange. Sympathetic activity is overridden locally during exercise. Venous pressure/baroreflex are not primary drivers here. Answer: b) Local metabolic vasodilation.

2) Which structure directly regulates the entry of blood into true capillaries?

a) Postcapillary venule

b) Precapillary sphincter

c) Vasa vasorum

d) Sinusoid

Explanation: Precapillary sphincters are smooth muscle cuffs at capillary origins from metarterioles/arterioles. Their tone modulates capillary recruitment and surface area for exchange according to local metabolic demand. Postcapillary venules mainly handle leukocyte trafficking and fluid reabsorption. Answer: b) Precapillary sphincter.

3) A patient with sepsis develops edema despite normal hydrostatic pressures. The best explanation is:

a) Increased plasma oncotic pressure

b) Endothelial glycocalyx degradation

c) Reduced interstitial compliance

d) Lymphatic hyperactivity

Explanation: Sepsis damages the glycocalyx, increasing permeability and altering the effective oncotic gradient in Starling forces, promoting filtration and interstitial edema even with modest pressures. Plasma oncotic rises would oppose, not favor, edema. Lymphatics may be overwhelmed, not “hyperactive.” Answer: b) Endothelial glycocalyx degradation.

4) In which capillary type is bulk protein passage physiologically greatest?

a) Continuous (brain)

b) Fenestrated (glomerulus)

c) Sinusoidal (liver)

d) Continuous (muscle)

Explanation: Liver sinusoids have discontinuous endothelium and incomplete basement membrane, allowing protein exchange between plasma and space of Disse; this supports albumin synthesis. Brain continuous capillaries with tight junctions severely restrict proteins. Fenestrated glomeruli filter little protein due to charge/size selectivity. Answer: c) Sinusoidal (liver).

5) A 65-year-old with uncontrolled hypertension has reduced tissue perfusion in toes. According to Poiseuille’s law, which change most powerfully improves flow?

a) 10% decrease in viscosity

b) 10% increase in vessel radius

c) 10% decrease in vessel length

d) 10% increase in pressure

Explanation: Resistance varies inversely with radius⁴, so small increases in arteriolar radius markedly reduce resistance and enhance flow, dominating effects of viscosity, length, or pressure in microvessels. Thus vasodilation is the most potent intervention. Answer: b) 10% increase in vessel radius.

6) At the arteriolar end of a typical systemic capillary, which relationship favors filtration?

a) Pc < πc

b) Pc > πc

c) Pi > Pc

d) πi > πc

Explanation: Higher capillary hydrostatic pressure (Pc) at the arteriolar end exceeds capillary oncotic pressure (πc), favoring filtration; toward the venular end, πc dominates, favoring reabsorption (modulated by glycocalyx). Interstitial pressure typically remains low/slightly negative. Answer: b) Pc > πc.

7) A limb is occluded for two minutes and then released. The marked flushing is due to:

a) Decreased tissue PCO₂

b) Accumulated vasodilators and myogenic relaxation

c) Increased sympathetic tone

d) Venoconstriction

Explanation: Reactive hyperemia follows brief ischemia: metabolites (adenosine, CO₂, H⁺, K⁺) and myogenic relaxation dilate arterioles; upon release, flow overshoots until vasodilators wash out and tone normalizes. Sympathetic activity is not the primary determinant. Answer: b) Accumulated vasodilators and myogenic relaxation.

8) Which venule segment is the principal site of leukocyte adhesion and increased permeability in inflammation?

a) Terminal arteriole

b) Postcapillary venule

c) Muscular venule

d) Collecting vein

Explanation: Postcapillary venules express adhesion molecules (e.g., selectins, ICAM) and exhibit gap formation with inflammatory mediators, promoting leukocyte transmigration and fluid extravasation—key microcirculatory responses in acute inflammation. Answer: b) Postcapillary venule.

9) In severe anemia, tissue oxygen delivery is maintained partly by microvascular changes including:

a) Increased viscosity raising resistance

b) Fåhræus–Lindqvist effect lowering apparent viscosity

c) Decreased capillary recruitment

d) Diffusion distance increase

Explanation: In small vessels, apparent viscosity falls (Fåhræus–Lindqvist effect), reducing resistance and improving microvascular flow. Capillary recruitment and increased cardiac output also sustain delivery; diffusion distance tends to decrease with recruitment, aiding exchange. Answer: b) Fåhræus–Lindqvist effect lowering apparent viscosity.

10) A patient with nephrotic syndrome develops pitting edema. The most proximate microcirculatory cause is:

a) Increased plasma oncotic pressure

b) Decreased plasma oncotic pressure

c) Decreased capillary hydrostatic pressure

d) Increased lymphatic pumping

Explanation: Hypoalbuminemia lowers capillary oncotic pressure, tipping Starling balance toward filtration across systemic microvessels; lymphatics initially compensate but are overwhelmed, producing interstitial fluid accumulation and pitting edema. Answer: b) Decreased plasma oncotic pressure.

11) Nitric oxide infusion into a limb primarily causes which microvascular change?

a) Arteriolar dilation and capillary recruitment

b) Venular constriction with reduced filtration

c) Precapillary sphincter constriction

d) Increased blood viscosity

Explanation: NO relaxes arteriolar smooth muscle, lowering resistance and opening precapillary sphincters; more capillaries are perfused (recruitment), enlarging surface area for exchange and improving oxygen delivery. Venules are less responsive; viscosity is unaffected. Answer: a) Arteriolar dilation and capillary recruitment.

Keywords (for all questions)

Pancreatic juice volume: About 1–2 L/day in adults; classic value ≈ 1.5 L/day.
Acinar cells: Secrete enzyme-rich, proteinaceous fluid (zymogens: trypsinogen, chymotrypsinogen, proelastase, procarboxypeptidase; amylase; lipase).
Ductal cells: Secrete bicarbonate-rich, watery fluid; modify Cl⁻/HCO₃⁻ via CFTR and exchangers.
Secretin (S cells): Stimulates ductal HCO₃⁻ secretion; increases volume and alkalinity.
CCK (I cells): Stimulates acinar enzyme secretion; potentiates secretin.
Vagus (ACh): Cephalic/gastric phase stimulation of both acinar and duct cells.
CFTR: Chloride channel essential for HCO₃⁻ secretion; defective in cystic fibrosis.
Enterokinase (enteropeptidase): Brush-border enzyme that activates trypsinogen to trypsin.
SPINK1 (trypsin inhibitor): Prevents premature trypsin activation within acinar cells.
Flow-dependent composition: Higher flow → higher HCO₃⁻, lower Cl⁻; Na⁺/K⁺ ~ plasma.
Pancreatic juice pH: Alkaline (~pH 8.0–8.3) to neutralize gastric acid in duodenum.
Somatostatin: Inhibits exocrine pancreatic secretion.
Phases of secretion: Cephalic, gastric, intestinal (intestinal predominates via CCK/secretin).
Zollinger–Ellison: Gastrinoma; secretin test paradoxically increases gastrin; high acid increases secretin release from S cells.
Bicarbonate mechanism: Carbonic anhydrase forms H⁺/HCO₃⁻; HCO₃⁻ secreted via CFTR/Cl⁻-HCO₃⁻ exchange; H⁺ returned to blood.

Chapter: Gastrointestinal Physiology | Topic: Exocrine Pancreas | Subtopic: Volume, Composition & Control of Pancreatic Secretion

Lead Question – 2012

Daily pancreatic secretion ?

a) 1.5 L

b) 2.5 L

c) 5.0 L

d) 10 L

Explanation: Normal adults secrete roughly 1–2 liters of pancreatic juice per day. Standard teaching value is ~1.5 L/day, alkaline and rich in bicarbonate to neutralize gastric acid, with enzymes from acinar cells. Larger figures are excessive for physiology. Answer: a) 1.5 L.

1) Which hormone primarily increases the bicarbonate content and volume of pancreatic juice?

a) CCK

b) Secretin

c) Gastrin

d) Motilin

Explanation: Secretin from duodenal S cells responds to acid; it stimulates ductal cells to secrete HCO₃⁻-rich, watery fluid, increasing volume and alkalinity. CCK mainly drives enzyme-rich acinar secretion and potentiates secretin’s effect but is not the primary bicarbonate stimulator. Answer: b) Secretin.

2) A patient with cystic fibrosis has recurrent steatorrhea. The pancreatic defect most responsible is:

a) Loss of amylase synthesis

b) Inactive enterokinase

c) Impaired CFTR-mediated ductal HCO₃⁻ secretion

d) Excess SPINK1

Explanation: CFTR dysfunction reduces ductal chloride cycling and bicarbonate secretion, producing viscous, acidic juice that obstructs ducts, diminishes enzyme delivery, and causes fat malabsorption (steatorrhea). Enterokinase is intestinal; SPINK1 prevents premature trypsin activation and is unrelated to CF’s ductal pathophysiology. Answer: c) Impaired CFTR-mediated ductal HCO₃⁻ secretion.

3) Which change occurs in pancreatic juice as flow rate increases?

a) Decreased HCO₃⁻ concentration

b) Increased Cl⁻ concentration

c) Increased HCO₃⁻ with reciprocal fall in Cl⁻

d) Large rise in K⁺

Explanation: At higher flow, ductal cells secrete more bicarbonate, while chloride falls reciprocally; Na⁺ and K⁺ remain near plasma levels. This optimizes neutralization of gastric acid entering the duodenum during meals. Answer: c) Increased HCO₃⁻ with reciprocal fall in Cl⁻.

4) A 45-year-old with gallstones has postprandial abdominal pain. Which mediator most strongly stimulates acinar enzyme secretion?

a) Secretin

b) CCK

c) VIP

d) Somatostatin

Explanation: CCK released from I cells in response to fatty acids and amino acids stimulates acinar cells to release enzyme-rich secretions and contracts the gallbladder. Secretin targets ductal cells. VIP is modulatory; somatostatin inhibits exocrine secretion. Answer: b) CCK.

5) In the cephalic phase of digestion, pancreatic secretion is driven mainly by:

a) Secretin from acid in duodenum

b) Vagal cholinergic activity

c) Local stretch reflex in pancreas

d) Somatostatin surge

Explanation: Sight, smell, and taste trigger vagal efferents (ACh) to acinar and duct cells, modestly increasing enzyme and fluid secretion before food reaches the duodenum. Secretin dominates the intestinal phase. Somatostatin inhibits. Answer: b) Vagal cholinergic activity.

6) Trypsinogen activation physiologically occurs in the:

a) Pancreatic acinus by trypsin

b) Duodenal brush border by enterokinase

c) Gastric lumen by pepsin

d) Blood by kallikrein

Explanation: Enterokinase (enteropeptidase) on duodenal mucosa converts trypsinogen to trypsin, which then activates other zymogens. In the pancreas, SPINK1 prevents premature activation. Gastric pepsin and kallikrein are unrelated to physiological trypsinogen activation. Answer: b) Duodenal brush border by enterokinase.

7) A secretin infusion test in suspected gastrinoma shows a paradoxical rise in serum gastrin. Secretin normally does which action on the pancreas?

a) Inhibits ductal HCO₃⁻

b) Stimulates ductal HCO₃⁻ secretion

c) Stimulates acinar protease synthesis

d) Contracts sphincter of Oddi

Explanation: Secretin physiologically stimulates pancreatic ductal bicarbonate and water secretion, increasing volume and pH of juice. It does not primarily drive enzyme synthesis or Oddi contraction. The paradoxical gastrin rise is specific to gastrinomas. Answer: b) Stimulates ductal HCO₃⁻ secretion.

8) A patient with acute pancreatitis has elevated intrapancreatic trypsin activity. Which protective factor normally limits this?

a) High luminal pH

b) SPINK1 within acinar cells

c) Secretin-mediated washout

d) Low Ca²⁺ in duct fluid

Explanation: SPINK1 (serine protease inhibitor, Kazal type 1) is a key intrapancreatic trypsin inhibitor preventing premature activation. Failure of this mechanism predisposes to autodigestion and pancreatitis. Secretin, pH, and ductal Ca²⁺ are not the principal intracellular safeguards. Answer: b) SPINK1 within acinar cells.

9) Which combination best describes typical ionic composition of high-flow pancreatic juice?

a) High Cl⁻, low HCO₃⁻

b) High HCO₃⁻, low Cl⁻

c) High K⁺, low Na⁺

d) Low Na⁺, high Ca²⁺

Explanation: With increased flow under secretin, pancreatic juice becomes rich in bicarbonate and relatively depleted of chloride; sodium and potassium remain near plasma values. This alkaline secretion neutralizes gastric acid effectively. Answer: b) High HCO₃⁻, low Cl⁻.

10) After a fatty meal, which synergism yields maximal pancreatic secretion?

a) CCK + Somatostatin

b) Secretin + CCK + Vagus

c) Secretin alone

d) Vagus alone

Explanation: Intestinal phase: secretin (ductal HCO₃⁻) and CCK (acinar enzymes) act synergistically, further potentiated by vagal cholinergic input, producing maximal volume and enzyme output. Somatostatin is inhibitory. Answer: b) Secretin + CCK + Vagus.

11) Which best explains why pancreatic juice is alkaline?

a) Acinar amylase generates OH⁻

b) Ductal carbonic anhydrase–dependent HCO₃⁻ secretion

c) Gastric mucosal diffusion

d) Hepatic bile mixing exclusively

Explanation: Ductal cells use carbonic anhydrase to generate bicarbonate and secrete it via CFTR/Cl⁻–HCO₃⁻ exchangers, producing alkaline juice (pH ~8). Bile mixing adds alkalinity but is not the core pancreatic mechanism. Enzymes do not create hydroxyl ions. Answer: b) Ductal carbonic anhydrase–dependent HCO₃⁻ secretion.

Keywords (for all questions)

Hering–Breuer reflex: Vagal afferent–mediated inflation reflex that terminates inspiration and prolongs expiration.
Pulmonary stretch receptors (PSR): Slowly adapting receptors in airway smooth muscle activated by lung inflation.
J receptors (juxtacapillary): C-fiber endings in alveolar walls; stimulated by interstitial edema; cause rapid, shallow breathing.
Deflation reflex: Lung deflation triggers increased inspiratory effort via vagal afferents.
Vagotomy: Cutting vagus abolishes Hering–Breuer reflex; tends to produce slow, deep breaths.
Apneustic center: Pontine area that promotes prolonged inspiration; normally inhibited by vagal input and pneumotaxic center.
Pneumotaxic center: Pontine center limiting inspiration, regulating rate and pattern.
Compliance: Change in lung volume per unit pressure; higher compliance augments PSR activation at a given pressure.
Tidal volume (VT): Volume of air inhaled or exhaled per normal breath (~500 mL adult).
PEEP: Positive end-expiratory pressure; affects lung volume, PSR firing, and reflexes during ventilation.
Central chemoreceptors: Sense CSF pH/PaCO₂; drive ventilation independent of PSR.
Peripheral chemoreceptors: Carotid/aortic bodies sensing PaO₂, PaCO₂, pH; mediate hypoxic drive.

Chapter: Respiratory Physiology | Topic: Neural Control of Breathing | Subtopic: Hering–Breuer Reflex

Lead Question – 2012

Herring Breuer reflex is an increase in ?

a) Duration of inspiration

b) Duration of expiration

c) Depth of inspiration

d) Depth of expiration

Explanation: The Hering–Breuer inflation reflex, mediated by slowly adapting pulmonary stretch receptors via the vagus, terminates inspiration to prevent overinflation, thereby prolonging expiratory time. This reflex is prominent at larger tidal volumes (e.g., exercise or mechanical ventilation) and is abolished by vagotomy. Answer: b) Duration of expiration.

1) In a ventilated ICU patient with high VT, activation of pulmonary stretch receptors will most likely:

a) Increase inspiratory time b) Prolong expiratory time c) Cause apnea via chemoreceptors d) Reduce vagal tone

Explanation: Large tidal volumes increase PSR firing, engaging the Hering–Breuer inflation reflex that ends inspiration and prolongs expiration, reducing respiratory rate. Chemoreceptors are not the primary mediators here; vagal afferents are. Answer: b) Prolong expiratory time.

2) Which nerve carries afferents essential for the Hering–Breuer inflation reflex?

a) Glossopharyngeal b) Vagus c) Phrenic d) Intercostal

Explanation: Slowly adapting pulmonary stretch receptors send impulses via the vagus to medullary respiratory centers. Vagotomy abolishes the reflex and leads to slower, deeper breathing patterns due to loss of inspiratory termination. Answer: b) Vagus.

3) A neonate’s breathing pattern is strongly influenced by the Hering–Breuer reflex. The primary functional benefit is:

a) Enhancing hypoxic drive b) Preventing alveolar overdistension c) Increasing dead space d) Facilitating CO₂ retention

Explanation: In neonates, the Hering–Breuer reflex is more prominent and helps terminate inspiration to avoid overdistension of compliant lungs, stabilizing VT and FRC. It does not increase dead space or promote CO₂ retention physiologically. Answer: b) Preventing alveolar overdistension.

4) Following bilateral vagotomy in an animal model, which breathing pattern is expected?

a) Rapid, shallow breathing b) Slow, deep breathing c) Cheyne–Stokes respiration d) Apneustic breathing relieved

Explanation: Loss of vagal afferents removes stretch-mediated inspiratory termination, producing slow, deep breaths. Apneustic patterns arise with pontine lesions, not isolated vagotomy. Rapid shallow breathing reflects J-receptor activity, not PSR loss. Answer: b) Slow, deep breathing.

5) In interstitial pulmonary edema, stimulation of J receptors leads to:

a) Prolonged expiration b) Rapid, shallow breathing c) Increased VT with slower rate d) Apnea followed by hyperpnea

Explanation: J (juxtacapillary) receptors are C-fiber endings sensitive to interstitial fluid; activation triggers tachypnea with low VT (rapid, shallow). This is distinct from PSR-mediated inflation reflex which prolongs expiration. Answer: b) Rapid, shallow breathing.

6) During exercise, why does the Hering–Breuer reflex become more relevant?

a) Higher PaCO₂ sensitizes PSR b) Larger VT increases PSR firing c) Airway resistance falls, silencing PSR d) Peripheral chemoreceptors inhibit PSR

Explanation: Exercise increases tidal volume; lung inflation enhances slowly adapting PSR discharge, aiding appropriate inspiratory termination and expiratory timing at high volumes. Chemoreceptor changes are parallel but not the mechanism for PSR activation. Answer: b) Larger VT increases PSR firing.

7) A patient on high PEEP shows decreased inspiratory time on the ventilator. The best explanation is:

a) Central chemoreceptor suppression b) Increased PSR activation by higher lung volume c) Haldane effect d) Reduced compliance lowering PSR firing

Explanation: PEEP elevates end-expiratory lung volume, increasing PSR activity and promoting earlier inspiratory cutoff (shorter inspiratory time), consistent with the Hering–Breuer effect. Central chemoreceptors and Haldane effect are unrelated. Answer: b) Increased PSR activation by higher lung volume.

8) Which brain region integrates vagal stretch afferents to terminate inspiration?

a) Dorsal respiratory group (DRG) b) Ventral respiratory group (VRG) c) Apneustic center alone d) Cerebellum

Explanation: DRG in the medulla receives vagal afferents from PSR and modulates inspiratory off-switch; pontine pneumotaxic influences also help, but DRG is the key medullary integrator. VRG is more active in forced breathing. Answer: a) Dorsal respiratory group (DRG).

9) In an apneustic animal (pontine lesion), intact vagal afferents would:

a) Worsen apneusis b) Partially relieve prolonged inspiration c) Cause Cheyne–Stokes pattern d) Have no effect

Explanation: Vagal stretch input can partially terminate the prolonged inspiratory “apneustic” pattern by providing an inspiratory off-switch, reducing the severity of breath-holding phases. Answer: b) Partially relieve prolonged inspiration.

10) A COPD patient shows larger VT after bronchodilator. How does this affect the Hering–Breuer reflex?

a) Diminishes reflex due to less stretch b) Augments reflex via greater stretch c) No change expected d) Converts to deflation reflex

Explanation: Improved airflow can increase VT at similar effort, raising lung stretch and PSR firing, thus enhancing the inflation reflex and earlier inspiratory termination. Answer: b) Augments reflex via greater stretch.

11) Which change most directly abolishes the Hering–Breuer inflation reflex?

a) Carotid body denervation b) Vagotomy c) Phrenic neurectomy d) Increased CSF bicarbonate

Explanation: The inflation reflex depends on vagal afferents from pulmonary stretch receptors. Cutting the vagus removes the signal to medullary centers, abolishing inspiratory off-switch. Carotid bodies and CSF buffering affect chemoreception, not PSR afferents. Answer: b) Vagotomy.

Chapter: Respiratory System
Topic: Pulmonary Volumes and Capacities
Subtopic: Vital Capacity

Keyword Definitions:

Tidal Volume (TV) - Air inspired or expired during normal breathing.
Inspiratory Reserve Volume (IRV) - Extra volume of air inhaled after normal inspiration.
Expiratory Reserve Volume (ERV) - Extra air exhaled after normal expiration.
Residual Volume (RV) - Air remaining in lungs after maximal expiration.
Vital Capacity (VC) - Maximum air exhaled after maximum inspiration.
Total Lung Capacity (TLC) - Sum of all lung volumes.
Functional Residual Capacity (FRC) - Air left after normal expiration.
Spirometry - Test to measure lung volumes and capacities (except RV).
Restrictive Lung Disease - Condition with reduced VC due to decreased lung expansion.
Obstructive Lung Disease - Condition with increased RV due to airflow limitation.

Lead Question - 2012

Which of the following defines vital capacity?

a) Air in lung after normal expiration
b) Maximum air that can be expirated after normal inspiration
c) Maximum air that can be expirated after maximum inspiration
d) Maximum air in lung after end of maximal inspiration

Explanation: Vital capacity is defined as the maximum volume of air a person can exhale after a maximal inspiration. It includes tidal volume, inspiratory reserve volume, and expiratory reserve volume but excludes residual volume. The correct answer is c) Maximum air that can be expirated after maximum inspiration.

Guessed Question 1

A 50-year-old smoker undergoes spirometry. His vital capacity is reduced. Likely cause?

a) Emphysema
b) Pulmonary fibrosis
c) Asthma
d) Chronic bronchitis

Explanation: Pulmonary fibrosis restricts lung expansion, lowering vital capacity. In obstructive diseases like asthma and emphysema, VC is relatively preserved, though residual volume increases. Thus, the correct answer is b) Pulmonary fibrosis.

Guessed Question 2

Which lung volume cannot be measured by spirometry?

a) Tidal volume
b) Vital capacity
c) Residual volume
d) Inspiratory reserve volume

Explanation: Spirometry measures all volumes except residual volume, functional residual capacity, and total lung capacity. Residual volume cannot be exhaled and requires helium dilution or body plethysmography. Correct answer: c) Residual volume.

Guessed Question 3

A patient with kyphoscoliosis has reduced vital capacity. The mechanism is?

a) Increased compliance
b) Reduced chest wall expansion
c) Increased residual volume
d) Airway obstruction

Explanation: In kyphoscoliosis, chest wall restriction prevents full lung expansion, reducing vital capacity. It is a restrictive pattern. Correct answer: b) Reduced chest wall expansion.

Guessed Question 4

Which combination of volumes constitutes vital capacity?

a) TV + IRV + ERV
b) TV + IRV + RV
c) IRV + ERV + RV
d) TV + ERV + RV

Explanation: Vital capacity is the sum of tidal volume, inspiratory reserve volume, and expiratory reserve volume. It does not include residual volume. Correct answer: a) TV + IRV + ERV.

Guessed Question 5

Vital capacity is maximum in which position?

a) Supine
b) Standing
c) Sitting
d) Prone

Explanation: Vital capacity is maximum in standing position due to reduced abdominal pressure on diaphragm and maximum lung expansion. It decreases in supine due to abdominal viscera pushing the diaphragm upwards. Correct answer: b) Standing.

Guessed Question 6

A patient with severe COPD shows increased total lung capacity but decreased vital capacity. Cause?

a) Increased IRV
b) Increased RV
c) Reduced TV
d) Reduced ERV

Explanation: In COPD, air trapping leads to increased residual volume, which decreases vital capacity despite increased TLC. Correct answer: b) Increased RV.

Guessed Question 7

A medical student performs spirometry. FVC = 3L, FEV1 = 2.7L. Interpretation?

a) Normal lung function
b) Obstructive disease
c) Restrictive disease
d) Mixed disorder

Explanation: FEV1/FVC ratio = 2.7/3 = 90% (normal >80%), with reduced FVC. This suggests restrictive lung disease where vital capacity is reduced. Correct answer: c) Restrictive disease.

Guessed Question 8

In an athlete, which factor contributes to increased vital capacity?

a) Decreased residual volume
b) Stronger respiratory muscles
c) Reduced total lung capacity
d) Decreased tidal volume

Explanation: Athletes have stronger respiratory muscles and better lung expansion, leading to increased vital capacity. Correct answer: b) Stronger respiratory muscles.

Guessed Question 9

A patient has TLC = 6L, RV = 2L. What is the vital capacity?

a) 2L
b) 4L
c) 6L
d) 8L

Explanation: Vital capacity = TLC – RV = 6 – 2 = 4L. Correct answer: b) 4L.

Guessed Question 10

A 70-year-old man shows age-related changes in lung volumes. Which is true?

a) VC increases
b) RV decreases
c) VC decreases
d) TLC decreases

Explanation: With aging, lung compliance increases, residual volume increases, and vital capacity decreases due to weaker respiratory muscles. Total lung capacity remains nearly constant. Correct answer: c) VC decreases.

Chapter: Respiratory System
Topic: Pulmonary Physiology
Subtopic: Alveolar Stability

Keyword Definitions:

Alveoli - Tiny air sacs in lungs where gas exchange occurs.
Surfactant - Substance secreted by type II pneumocytes that reduces surface tension in alveoli.
Residual Volume - Amount of air left in lungs after maximal expiration.
Lung Compliance - Measure of lung’s ability to expand.
Intrapleural Pressure - Negative pressure within pleural cavity that prevents lung collapse.
Surface Tension - Force at the liquid-air interface tending to collapse alveoli.
Type II Pneumocytes - Alveolar cells producing surfactant.
Atelectasis - Collapse of alveoli due to lack of surfactant or obstruction.

Lead Question - 2012

Stability of alveoli is maintained by?

a) Lung compliance
b) Negative intrapleural pressure
c) Increase in alveolar surface area by the surfactant
d) Residual air in alveoli

Explanation: Alveolar stability is primarily maintained by surfactant, which reduces surface tension, preventing collapse of smaller alveoli into larger ones. Compliance and intrapleural pressure support lung expansion, but surfactant directly stabilizes alveoli. Thus, the correct answer is c) Increase in alveolar surface area by the surfactant.

Guessed Question 1

Newborn with respiratory distress likely has deficiency of?

a) Type I pneumocytes
b) Type II pneumocytes
c) Macrophages
d) Ciliated cells

Explanation: Neonatal respiratory distress syndrome is due to deficiency of surfactant, secreted by type II pneumocytes. This leads to alveolar collapse and hypoxemia. Hence the correct answer is b) Type II pneumocytes.

Guessed Question 2

A 45-year-old smoker develops recurrent alveolar collapse. Which factor is most impaired?

a) Residual volume
b) Surfactant secretion
c) Intrapleural pressure
d) Lung compliance

Explanation: Smoking reduces surfactant production and damages alveolar walls. Lack of surfactant increases surface tension, leading to alveolar instability. The correct answer is b) Surfactant secretion.

Guessed Question 3

In premature infants, alveolar collapse is due to?

a) Increased intrapleural pressure
b) Surfactant deficiency
c) Increased lung compliance
d) Increased residual volume

Explanation: Premature infants (b) Surfactant deficiency.

Guessed Question 4

Which law explains tendency of alveoli to collapse without surfactant?

a) Poiseuille’s law
b) Boyle’s law
c) Laplace’s law
d) Dalton’s law

Explanation: Laplace’s law states pressure within alveoli is directly proportional to surface tension and inversely proportional to radius. Without surfactant, small alveoli collapse. Correct answer: c) Laplace’s law.

Guessed Question 5

Which condition leads to increased surfactant production?

a) Prolonged bed rest
b) Glucocorticoid administration
c) Hypercapnia
d) Hypothermia

Explanation: Corticosteroids stimulate surfactant production, hence are given antenatally to mothers at risk of preterm delivery. Correct answer: b) Glucocorticoid administration.

Guessed Question 6

Surfactant secretion starts at which fetal week?

a) 12 weeks
b) 20 weeks
c) 24 weeks
d) 34 weeks

Explanation: Surfactant production begins at 24 weeks and reaches sufficient levels for alveolar stability by 34–36 weeks of gestation. Correct answer: c) 24 weeks.

Guessed Question 7

A patient with ARDS develops alveolar collapse. Mechanism?

a) Increased compliance
b) Loss of surfactant
c) Increased intrapleural negativity
d) Increased residual air

Explanation: ARDS leads to diffuse alveolar damage and surfactant dysfunction, causing alveolar collapse and impaired gas exchange. Correct answer: b) Loss of surfactant.

Guessed Question 8

Which component of surfactant is most important?

a) Sphingomyelin
b) Lecithin (Dipalmitoylphosphatidylcholine)
c) Cholesterol
d) Glycolipids

Explanation: The major active component of surfactant is lecithin (DPPC), which lowers alveolar surface tension and maintains alveolar stability. Correct answer: b) Lecithin (DPPC).

Guessed Question 9

Which test estimates fetal lung maturity?

a) Lecithin-sphingomyelin ratio
b) Amniotic fluid bilirubin
c) Amniotic fluid creatinine
d) Fetal hemoglobin

Explanation: Lecithin-sphingomyelin (L/S) ratio in amniotic fluid indicates fetal lung maturity. Ratio ≥2 suggests adequate surfactant and alveolar stability. Correct answer: a) Lecithin-sphingomyelin ratio.

Guessed Question 10

Which alveolar cell is responsible for surfactant recycling?

a) Type I pneumocyte
b) Type II pneumocyte
c) Macrophage
d) Endothelial cell

Explanation: Type II pneumocytes both secrete and recycle surfactant, ensuring continuous maintenance of alveolar stability. Correct answer: b) Type II pneumocyte.

Keyword Definitions

2,3-DPG - Red cell metabolite that binds deoxygenated hemoglobin and lowers O₂ affinity.
O₂–Hb dissociation curve - Relationship between PaO₂ and hemoglobin saturation; shifts indicate affinity changes.
Right shift - Reduced Hb O₂ affinity; facilitates O₂ release to tissues (favored by ↑2,3-DPG, ↑CO₂, ↑H⁺, ↑T).
Left shift - Increased Hb O₂ affinity; impairs O₂ unloading (favored by ↓2,3-DPG, ↓CO₂, ↓H⁺, ↓T, fetal Hb).
PaO₂ - Partial pressure of oxygen in arterial blood; primary determinant of SaO₂ at physiologic range.
SaO₂ / SvO₂ - Arterial and venous hemoglobin oxygen saturations; reflect oxygen loading/unloading balance.
Hypoxia - Reduced tissue oxygen delivery; stimulates adaptive increases in 2,3-DPG over days.
Anemia - Reduced O₂ content that can trigger higher 2,3-DPG to improve tissue O₂ delivery.
Acidosis - Increased H⁺ promotes right shift (Bohr effect), complementing 2,3-DPG effects.
Transfusion storage - Stored RBCs lose 2,3-DPG; transfused blood may transiently impair O₂ unloading until levels recover.

Chapter: Respiratory Physiology Topic: Hemoglobin & Gas Transport Subtopic: 2,3-DPG and O₂–Hb Affinity

Lead Question – 2012

Which of the following is/are effect of increased 2,3-DPG on oxygen-hemoglobin dissociation curve?

a) ↑ ed affinity of heamoglobin to oxygen
b) ↓ ed affinity of haemoglobin to oxygen
c) Left shift of oxygen-hemoglobin dissociation curve
d) Right shift of oxygen-hemoglobin dissociation curve

e) No change in oxygen-hemoglobin dissociation curve

Explanation: Increased 2,3-DPG binds deoxygenated hemoglobin, reducing O₂ affinity and causing a rightward shift of the O₂–Hb curve; this facilitates oxygen unloading to tissues (eg, chronic hypoxia, anemia). Therefore options b) (decreased affinity) and d) (right shift) are correct together, not a, c, or e.

1) In chronic hypoxemia, rise in erythrocyte 2,3-DPG primarily serves to:

a) Increase arterial PaO₂
b) Enhance tissue O₂ unloading
c) Increase Hb affinity for O₂
d) Promote left shift of O₂–Hb curve

Explanation: Chronic hypoxemia stimulates red cell 2,3-DPG synthesis, lowering hemoglobin O₂ affinity and shifting the curve right. This adaptation increases tissue oxygen delivery despite low PaO₂. Clinically seen in high altitude and chronic lung disease. Answer: b) Enhance tissue O₂ unloading.

2) Stored packed red blood cells may impair immediate O₂ delivery because:

a) They have elevated 2,3-DPG
b) They have reduced 2,3-DPG
c) They shift O₂–Hb curve right
d) They carry more CO₂

Explanation: During storage, RBCs lose 2,3-DPG, increasing hemoglobin O₂ affinity (left shift) and temporarily reducing tissue unloading after transfusion. 2,3-DPG regenerates over 24–72 hours in recipient cells. Therefore answer: b) They have reduced 2,3-DPG.

3) Which combination most strongly produces a right shift similar to ↑2,3-DPG?

a) Alkalosis, hypothermia
b) Acidosis, hypercapnia
c) High fetal hemoglobin, low 2,3-DPG
d) Low CO₂, low temperature

Explanation: Acidosis and hypercapnia increase H⁺ and CO₂, promoting a right shift (Bohr effect) that, like 2,3-DPG, reduces O₂ affinity and enhances unloading in tissues. Clinically present during exercise or sepsis. Answer: b) Acidosis, hypercapnia.

4) A patient with anemia adapts by increasing 2,3-DPG. Expected change in venous O₂ saturation (SvO₂) is:

a) Increased SvO₂
b) Decreased SvO₂
c) No change in SvO₂
d) SvO₂ equals SaO₂

Explanation: Increased 2,3-DPG lowers Hb O₂ affinity causing greater peripheral extraction and lower SvO₂ (larger a–v O₂ difference). Although arterial saturation may be preserved, venous saturation falls, reflecting enhanced unloading in tissues. Answer: b) Decreased SvO₂.

5) Which clinical state would most likely show elevated 2,3-DPG?

a) Recent blood transfusion with old stored blood
b) High-altitude acclimatization over days
c) Acute carbon monoxide poisoning
d) Hypothermia during surgery

Explanation: High-altitude acclimatization stimulates erythrocyte glycolysis and 2,3-DPG production over days to weeks, enhancing tissue O₂ delivery despite low PaO₂. Acute transfusion of stored blood lowers 2,3-DPG transiently; CO poisoning and hypothermia reduce delivery. Answer: b) High-altitude acclimatization.

6) Which hemoglobin variant interaction contrasts with 2,3-DPG effects?

a) Adult HbA has lower O₂ affinity when 2,3-DPG high
b) Fetal Hb (HbF) binds 2,3-DPG more avidly than HbA
c) HbF has higher O₂ affinity and binds less 2,3-DPG than HbA
d) HbS increases 2,3-DPG binding dramatically

Explanation: Fetal hemoglobin (HbF) has reduced binding to 2,3-DPG, giving it increased O₂ affinity (left shift) compared with adult HbA. This facilitates placental O₂ transfer opposite to effects of ↑2,3-DPG. Answer: c) HbF has higher O₂ affinity and binds less 2,3-DPG than HbA.

7) In sepsis with high metabolic demand and tissue hypoxia, what happens to 2,3-DPG and oxygen unloading?

a) 2,3-DPG falls and unloading decreases
b) 2,3-DPG rises and unloading increases
c) 2,3-DPG unchanged
d) 2,3-DPG rises but unloading decreases

Explanation: Tissue hypoxia and increased glycolytic flux in sepsis can elevate 2,3-DPG, diminishing Hb O₂ affinity and enhancing peripheral oxygen unloading. Combined with local acidosis and temperature rise, this improves oxygen delivery to metabolically active tissues. Answer: b) 2,3-DPG rises and unloading increases.

8) Which therapeutic action would counteract a right shift caused by elevated 2,3-DPG?

a) Administer warmed fluids to raise temperature
b) Give 100% oxygen to raise PaO₂ and promote left shift
c) Induce mild acidosis
d) Give transfusion of fresh stored RBCs low in 2,3-DPG

Explanation: Transfusion of fresh (or stored) RBCs low in 2,3-DPG can transiently increase Hb O₂ affinity (left shift), countering right shift effects. High inspired O₂ raises PaO₂ but does not directly reverse biochemical 2,3-DPG effects on Hb binding; answer: d) Give transfusion of fresh stored RBCs low in 2,3-DPG.

9) Which lab feature indirectly suggests increased 2,3-DPG activity clinically?

a) Increased arterial O₂ content with low extraction
b) Normal SaO₂ with low SvO₂ and increased a–v O₂ difference
c) Elevated PaO₂ with increased SaO₂
d) High carboxyhemoglobin

Explanation: Increased 2,3-DPG enhances tissue extraction causing lower venous saturation and a larger a–v O₂ difference while arterial saturation may appear unchanged. Thus b) Normal SaO₂ with low SvO₂ and increased a–v O₂ difference is indicative of enhanced peripheral unloading consistent with elevated 2,3-DPG.

10) Which statement about 2,3-DPG kinetics after transfusion of stored blood is correct?

a) Recipient’s RBCs restore 2,3-DPG in donor cells immediately
b) 2,3-DPG levels in transfused RBCs regenerate over 24–72 hours
c) 2,3-DPG never recovers in stored RBCs after transfusion
d) Storage increases 2,3-DPG so regeneration is unnecessary

Explanation: Stored RBCs have depleted 2,3-DPG that regenerates after transfusion in the recipient’s circulation over 24–72 hours as glycolytic metabolism resumes, restoring normal O₂ unloading capacity. Clinically this transient left shift may modestly impair immediate tissue oxygenation. Answer: b) 2,3-DPG levels regenerate over 24–72 hours.

Keyword Definitions

Hematocrit - Fraction (%) of blood volume occupied by red blood cells; rises with hemoconcentration or polycythemia.
Hemoconcentration - Relative increase in red cell concentration due to reduced plasma volume (eg, dehydration).
Polycythemia - True increase in RBC mass (primary or secondary) causing high hematocrit independent of plasma volume.
Plasma electrolytes - Sodium, potassium, chloride, bicarbonate levels in plasma; reflect volume/status and acid–base balance.
Hemolysis - RBC rupture releasing intracellular K⁺ and other contents into plasma; may artifactually raise plasma K.
Hypernatremia - Increased plasma sodium concentration often from water loss causing hemoconcentration and higher hematocrit.
Metabolic alkalosis - Elevated plasma HCO₃⁻, sometimes from vomiting or diuretics; may associate with volume changes.
Chloride shift (Hamburger shift) - Movement of Cl⁻ into RBCs as HCO₃⁻ leaves during CO₂ transport in tissues.
Venous blood - Blood returning to the heart, higher CO₂, lower O₂ than arterial blood; can show concentration changes with local perfusion.
Plasma volume - Liquid component of blood; decreases in dehydration, increasing hematocrit without change in RBC mass.

Chapter: Clinical Hematology Topic: Blood Composition Subtopic: Hematocrit, Volume Status & Electrolytes

Lead Question – 2012

Venous blood with high hematocrit is seen in ?

a) RBC high chloride
b) Plasma high Na
c) Plasma high HCO3
d) RBC high K

Explanation (Answer: b) Plasma high Na) Elevated hematocrit in venous blood commonly reflects hemoconcentration from reduced plasma volume, as occurs with dehydration or water loss. This concentrates plasma solutes including sodium, so a high plasma Na (hypernatremia due to water deficit) accompanies increased hematocrit. Therefore b) is the correct choice.

1) In dehydration causing hemoconcentration, which laboratory pattern is expected?

a) ↑ Hematocrit, ↑ Plasma Na
b) ↓ Hematocrit, ↑ Plasma Na
c) ↑ Hematocrit, ↓ Plasma Na
d) ↓ Hematocrit, ↓ Plasma Na

Explanation: Dehydration reduces plasma volume leading to relative rise in hematocrit and concentration of solutes including sodium; thus both hematocrit and plasma Na increase. Clinically expect hemoconcentration with hypernatremia when water loss predominates. Answer a) is correct.

2) Which condition causes elevated hematocrit with normal plasma sodium?

a) Primary polycythemia (polycythemia vera)
b) Simple dehydration
c) Acute water intoxication
d) Diuretic-induced hypernatremia

Explanation: Primary polycythemia increases total RBC mass, raising hematocrit while plasma sodium may remain normal. Hemoconcentration from dehydration changes Na. Thus a) polycythemia vera is correct and requires distinct diagnosis (erythropoietin, JAK2 testing) compared with volume-related causes.

3) A lab sample shows high plasma K. Which preanalytical artifact could explain this with normal patient physiology?

a) Hemolysis during phlebotomy
b) Dehydration concentrating plasma
c) Diuretic-induced loss
d) Chronic kidney disease

Explanation: Hemolysis releases intracellular K⁺ into plasma, artifactually elevating measured potassium. This is a common preanalytical error and should be suspected when samples are traumatic. Thus a) hemolysis during phlebotomy explains isolated high plasma K with otherwise normal physiology.

4) Chloride shift in tissue capillaries results in which RBC change?

a) Increased RBC chloride concentration as HCO₃⁻ leaves
b) Increased RBC sodium
c) Increased RBC potassium
d) Decreased RBC chloride

Explanation: As CO₂ diffuses into erythrocytes and is converted to HCO₃⁻, HCO₃⁻ exits the cell while Cl⁻ enters to maintain electroneutrality (Hamburger shift). This increases RBC chloride concentration during CO₂ uptake in tissues. Therefore a) is correct.

5) Which scenario most likely produces low hematocrit in venous blood?

a) Acute hemorrhage with fluid resuscitation
b) Dehydration from vomiting
c) Secondary polycythemia from hypoxia
d) Erythropoietin use

Explanation: Acute hemorrhage followed by rapid crystalloid infusion dilutes remaining RBCs, lowering hematocrit (dilutional anemia). Dehydration does opposite; polycythemia and erythropoietin raise hematocrit. Thus a) is correct clinically in trauma or operative settings.

6) Metabolic alkalosis with high HCO₃⁻ is commonly associated with which volume status?

a) Contraction alkalosis with low plasma volume
b) Hypervolemia with low hematocrit
c) Euvolemia without change in hematocrit
d) Dehydration with low plasma Na

Explanation: Contraction alkalosis (eg, from diuretics or vomiting) reduces plasma volume concentrating HCO₃⁻ and electrolytes; it often accompanies hemoconcentration. So a) contraction alkalosis with low plasma volume is correct and may show relatively elevated hematocrit depending on fluid shifts.

7) Which lab pattern suggests true increased RBC mass rather than hemoconcentration?

a) ↑ Hematocrit with ↑ RBC mass on red cell mass study
b) ↑ Hematocrit with high plasma Na
c) ↑ Hematocrit that normalizes after fluid load
d) ↑ Hematocrit with low reticulocyte count only

Explanation: A red cell mass study showing increased RBC mass confirms true polycythemia rather than hemoconcentration which corrects after fluid repletion. Therefore a) is correct. Fluid-responsive hematocrit indicates volume effect; true polycythemia persists despite rehydration.

8) In diabetic ketoacidosis (DKA), initial labs often show:

a) ↑ Hematocrit due to dehydration
b) ↓ Hematocrit due to hemolysis
c) Normal hematocrit with hyperkalemia only
d) Increased plasma bicarbonate

Explanation: DKA causes osmotic diuresis and marked water loss, producing hemoconcentration and increased hematocrit. Plasma potassium may appear high due to shift from cells, though total body K is depleted. Thus, a) ↑ hematocrit due to dehydration is correct initially in DKA presentation.

9) Which chronic condition raises hematocrit via increased erythropoietin?

a) Chronic hypoxia from COPD
b) Chronic diarrheal dehydration
c) Acute sepsis with vasodilation
d) Cirrhosis with portal hypertension

Explanation: Chronic hypoxia stimulates renal erythropoietin production leading to secondary polycythemia with increased RBC mass and high hematocrit. COPD patients often exhibit this adaptation. Dehydration concentrates cells but erythropoietin-driven increases occur over weeks, so a) is correct.

10) A venous sample shows high hematocrit and high sodium. Best immediate clinical step is:

a) Assess volume status and consider rehydration if hypovolemic
b) Start phlebotomy for polycythemia vera immediately
c) Ignore as lab artifact always
d) Give bicarbonate to correct sodium

Explanation: High hematocrit with hypernatremia suggests hemoconcentration from volume loss; assess clinical volume status and treat dehydration with appropriate fluids. Phlebotomy is for true polycythemia after confirmation. Therefore a) is correct as a pragmatic immediate step in management.

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