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: 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: 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: 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: 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: Renal Physiology; Subtopic: ENaC – Epithelial Sodium Channels
Keyword Definitions:
• ENaC: Epithelial sodium channel responsible for Na⁺ reabsorption in renal collecting ducts and other epithelia.
• Amiloride: Potassium-sparing diuretic that blocks ENaC activity.
• Subunits: ENaC is composed of α, β, and γ regulatory protein subunits.
• Aldosterone: Hormone increasing ENaC expression and sodium reabsorption.
• Principal cells: Renal collecting duct cells where ENaC channels are located.
• GIT epithelium: ENaC also present in colon for sodium absorption.
Lead Question - 2015
True about ENaC are all except ?
a) Epithelial channel
b) Composed of 2 homologous subunits
c) Present in kidney and GIT
d) Inhibited by amiloride
Explanation (Answer: b) Composed of 2 homologous subunits)
ENaC is an epithelial sodium channel composed of three distinct subunits—α, β, and γ, not two homologous subunits. The channel is located in kidney collecting ducts and gastrointestinal tract. It is a major target of aldosterone and is inhibited effectively by amiloride. Its three-subunit composition ensures proper gating and sodium selectivity.
1. ENaC subunits include:
a) α, β, γ
b) α, β
c) β, γ
d) Only α
Explanation (Answer: a) α, β, γ)
ENaC consists of three separate subunits—alpha, beta, and gamma—each contributing to channel structure and function. The α subunit forms the pore, and β and γ regulate gating and surface expression. Mutation in any of these subunits can lead to disorders of sodium handling, volume imbalance, and conditions like Liddle syndrome.
2. ENaC is regulated mainly by:
a) Vasopressin
b) Aldosterone
c) Parathyroid hormone
d) Prolactin
Explanation (Answer: b) Aldosterone)
Aldosterone strongly regulates ENaC by increasing its synthesis and membrane insertion in the collecting duct, enhancing sodium reabsorption and maintaining extracellular volume. Vasopressin influences water reabsorption, not ENaC. Parathyroid hormone regulates calcium, and prolactin has no renal ENaC-related action.
3. ENaC inhibition causes:
a) Hyperkalemia
b) Hypoglycemia
c) Hypercalcemia
d) Hyperphosphatemia
Explanation (Answer: a) Hyperkalemia)
ENaC inhibition reduces Na⁺ entry into principal cells, decreasing the gradient needed for K⁺ secretion, resulting in hyperkalemia. This is seen in pseudohypoaldosteronism and amiloride therapy. Calcium and phosphate levels are not directly linked to ENaC function, and glucose remains unaffected.
4. ENaC overactivity occurs in:
a) Liddle syndrome
b) Gitelman syndrome
c) Bartter syndrome
d) Addison disease
Explanation (Answer: a) Liddle syndrome)
Liddle syndrome is caused by hyperactive ENaC channels, leading to excessive Na⁺ reabsorption, hypertension, hypokalemia, and metabolic alkalosis. Aldosterone levels are low because channel activation is independent. Amiloride effectively blocks channel activity, reversing symptoms and lowering blood pressure.
5. ENaC blockers are classified as:
a) Loop diuretics
b) Thiazides
c) Potassium-sparing diuretics
d) Osmotic diuretics
Explanation (Answer: c) Potassium-sparing diuretics)
Amiloride and triamterene are potassium-sparing diuretics that block ENaC in the collecting duct. They reduce Na⁺ reabsorption without increasing K⁺ excretion. Loop diuretics and thiazides act on upstream segments, while osmotic diuretics alter tubular osmotic gradient but do not affect ENaC.
6. ENaC is primarily expressed in which nephron segment?
a) Proximal tubule
b) Collecting duct
c) Loop of Henle
d) Distal convoluted tubule
Explanation (Answer: b) Collecting duct)
ENaC channels are located in principal cells of the collecting duct, where they fine-tune sodium handling under aldosterone control. Distal convoluted tubule uses Na⁺/Cl⁻ cotransport. Proximal tubule and loop of Henle absorb sodium differently through other transporters and channels.
7. Activity of ENaC increases in:
a) Hypernatremia
b) Hypovolemia
c) Hyperglycemia
d) Edema
Explanation (Answer: b) Hypovolemia)
In hypovolemia, aldosterone secretion increases, stimulating ENaC expression to enhance Na⁺ retention and restore blood volume. ENaC does not directly respond to hypernatremia or hyperglycemia. Edema formation involves hydrostatic pressure and permeability, not specific ENaC activation in kidney.
8. ENaC dysfunction clinically presents as:
a) Severe salt loss
b) Hypercalcemia
c) Metabolic alkalosis only
d) Hypoglycemia
Explanation (Answer: a) Severe salt loss)
Loss-of-function ENaC defects cause salt-wasting disorders such as pseudohypoaldosteronism type 1. Patients develop dehydration, hypotension, hyperkalemia, metabolic acidosis, and hyponatremia. Calcium and glucose levels remain normal. In contrast, ENaC overactivity results in hypertension with hypokalemia.
9. ENaC function depends on:
a) CFTR regulation
b) ADH activation
c) Renin synthesis
d) Glucagon stimulation
Explanation (Answer: a) CFTR regulation)
CFTR regulates ENaC, particularly in airway and intestinal epithelia. CFTR inhibits ENaC; absence of CFTR in cystic fibrosis causes ENaC hyperactivity, thick mucus, and airway obstruction. ADH regulates water via aquaporins, not ENaC. Renin and glucagon do not directly affect ENaC channels.
10. Drug choice in Liddle syndrome:
a) Spironolactone
b) Amiloride
c) Furosemide
d) Hydrochlorothiazide
Explanation (Answer: b) Amiloride)
Amiloride is effective because it directly blocks ENaC hyperactivity in Liddle syndrome. Spironolactone is ineffective because aldosterone levels are already low. Furosemide and thiazides act on different nephron segments and cannot correct ENaC-driven sodium retention, hypertension, or hypokalemia caused by mutated channels.
Chapter: Physiology; Topic: Body Fluids; Subtopic: Intracellular Fluid – Properties
Keyword Definitions:
• Intracellular fluid (ICF): Fluid inside cells containing high K⁺, Mg²⁺, and proteins.
• Extracellular fluid (ECF): Fluid outside cells including plasma and interstitial fluid.
• pH: Measure of hydrogen ion concentration indicating acidity or alkalinity.
• Buffers: Substances maintaining pH stability by binding or releasing H⁺.
• Acid–base balance: Regulation of pH by lungs, kidneys, and chemical buffers.
• Hydrogen ion concentration: Determines pH and metabolic cell function.
Lead Question - 2015
pH of intracellular fluid is ?
a) Slightly less than ECF
b) Slightly more than ECF
c) Same as ECF
d) Highly alkaline
Explanation (Answer: a) Slightly less than ECF)
The pH of intracellular fluid is slightly less than ECF, typically around 7.0–7.1 due to continuous metabolic production of acids such as CO₂ and lactic acid within cells. ECF maintains a slightly higher pH around 7.35–7.45 because extracellular buffers are more effective and renal or respiratory regulation primarily adjusts extracellular compartments first. This difference is essential for enzyme function, membrane potential, and cellular metabolism.
1. Normal pH of extracellular fluid is:
a) 7.0–7.1
b) 7.35–7.45
c) 6.8–7.0
d) 7.8–8.0
Explanation (Answer: b) 7.35–7.45)
Extracellular fluid maintains a pH of 7.35–7.45, slightly alkaline compared to intracellular fluid. This tight range supports oxygen transport, enzyme function, and neuronal stability. The respiratory system removes CO₂ to regulate acid levels, while kidneys adjust bicarbonate reabsorption and H⁺ secretion. Any deviation below 7.35 is acidosis, and above 7.45 is alkalosis, affecting vital organ function.
2. ICF is more acidic than ECF mainly due to:
a) Low potassium concentration
b) High CO₂ production
c) Less protein buffering
d) Low metabolic activity
Explanation (Answer: b) High CO₂ production)
Cells constantly produce CO₂ during metabolism. CO₂ diffuses into cytoplasm and forms carbonic acid, lowering intracellular pH. Intracellular buffers such as proteins and phosphates help regulate pH, but metabolic processes continually release acids. CO₂ diffuses out to ECF and lungs where it's expelled, keeping extracellular pH slightly higher. Thus, intracellular CO₂ production directly affects ICF acidity.
3. Buffer system predominantly regulating intracellular pH:
a) Bicarbonate buffer
b) Hemoglobin buffer
c) Phosphate buffer
d) Carbonate buffer
Explanation (Answer: c) Phosphate buffer)
The phosphate buffer system is most effective inside cells due to higher phosphate concentration. It resists pH changes by accepting or releasing H⁺. Bicarbonate buffer dominates extracellular fluid. Hemoglobin buffer acts in RBCs but not all cells. Phosphate buffering maintains intracellular enzyme activity and prevents extreme fluctuations in hydrogen ion levels essential for cell integrity.
4. ICF acidosis usually causes movement of K⁺:
a) Into cells
b) Out of cells
c) Into mitochondria only
d) None
Explanation (Answer: b) Out of cells)
In ICF acidosis, H⁺ enters cells in exchange for K⁺ exiting, leading to hyperkalemia. This ion exchange helps preserve intracellular pH but elevates serum potassium. Clinically, metabolic acidosis increases serum K⁺ levels, risking arrhythmias. Thus, potassium shifts are closely linked to acid–base disturbances and must be corrected during management.
5. A patient with diabetic ketoacidosis will show ICF pH that is:
a) Higher than normal
b) Lower than normal
c) Equal to ECF
d) Very alkaline
Explanation (Answer: b) Lower than normal)
In diabetic ketoacidosis, excessive ketone bodies increase hydrogen ion concentration, reducing intracellular pH. ICF pH drops due to acid overload as H⁺ diffuses into cells. Potassium moves out to compensate, leading to hyperkalemia despite total body K⁺ deficit. Both intracellular and extracellular acidosis occur in uncontrolled diabetes.
6. Intracellular pH is mainly maintained by:
a) Bicarbonate ions
b) Cellular proteins
c) Plasma buffers
d) RBC hemoglobin
Explanation (Answer: b) Cellular proteins)
Cellular proteins are major intracellular buffers due to their ability to bind free hydrogen ions. Their negative charges allow stabilization of intracellular pH. Bicarbonate operates extracellularly. RBC hemoglobin acts only within red cells. Plasma buffers influence ECF pH. Protein buffering is essential for maintaining cell homeostasis and enzyme activity.
7. During hypoventilation, ICF pH:
a) Rises
b) Falls
c) Remains unchanged
d) Exceeds 8.0
Explanation (Answer: b) Falls)
Hypoventilation increases CO₂ retention, which diffuses into cells forming carbonic acid. This reduces intracellular and extracellular pH, leading to respiratory acidosis. Compensation begins through renal bicarbonate retention, but immediate effects include decreased ICF pH. Clinical symptoms include confusion, headache, and CO₂ narcosis if untreated.
8. Intracellular pH becomes alkalotic in:
a) Vomiting
b) Severe diarrhea
c) Renal failure
d) Lactic acidosis
Explanation (Answer: a) Vomiting)
Prolonged vomiting results in loss of gastric HCl, causing extracellular alkalosis. H⁺ shifts from ICF to ECF, increasing intracellular alkalinity. Cells compensate by retaining H⁺, but initial effect is intracellular alkalosis. Clinically, muscle cramps, tetany, and hypokalemia may develop due to accompanying potassium shifts.
9. ICF pH is affected by which ion most directly?
a) Sodium
b) Calcium
c) Hydrogen
d) Magnesium
Explanation (Answer: c) Hydrogen)
Hydrogen ions directly determine pH; intracellular concentration changes immediately alter pH. Cellular metabolism produces H⁺ which must be buffered or transported out. Sodium, calcium, and magnesium influence membrane potentials but do not directly set pH. Hydrogen regulation is vital for enzyme reactions and cellular viability.
10. A patient with sepsis and lactic acidosis will have ICF pH that is:
a) Elevated
b) Normal
c) Reduced
d) Unaffected
Explanation (Answer: c) Reduced)
Sepsis increases anaerobic metabolism, producing excess lactic acid and overwhelming buffer systems. Intracellular H⁺ rises as lactate accumulates, reducing pH. Impaired mitochondria worsen acidosis. Clinically, acidosis causes hypotension, organ dysfunction, and arrhythmias. Correcting oxygen delivery and improving perfusion are critical to restoring intracellular and extracellular pH balance.
11. Which compartment exhibits the fastest pH change in acute acidosis?
a) Intracellular fluid
b) Plasma
c) Bone
d) Synovial fluid
Explanation (Answer: b) Plasma)
Plasma pH changes rapidly in acute acidosis because respiratory compensation and bicarbonate buffering occur primarily in the extracellular compartment. Intracellular buffers respond later as hydrogen ions equilibrate across membranes. Bone buffering is slow and synovial fluid remains largely stable initially. Plasma changes guide early diagnosis and acute management.
Chapter: Physiology; Topic: Blood Physiology; Subtopic: Plasma Proteins and Viscosity
Keyword Definitions:
• Plasma viscosity: Thickness/resistance of plasma to flow influenced by protein content.
• Fibrinogen: Clotting protein increasing viscosity significantly due to large molecular size.
• Albumin: Most abundant plasma protein responsible for oncotic pressure, not major viscosity contributor.
• Globulins: Immune-related proteins with moderate effect on viscosity.
• Oncotic pressure: Pressure exerted by plasma proteins regulating fluid balance.
• Erythrocyte aggregation: Rouleaux formation influenced by fibrinogen increasing viscosity.
Lead Question - 2015
Increased in plasma viscosity is maximally caused by which plasma protein?
a) Fibrinogen
b) Albumin
c) Globulin
d) All have equal effect
Explanation (Answer: a) Fibrinogen)
Fibrinogen contributes most significantly to plasma viscosity due to its large molecular size and strong ability to promote erythrocyte aggregation. Albumin, though abundant, has minimal effect on viscosity because of its smaller size. Globulins increase viscosity moderately but not as much as fibrinogen. Plasma viscosity influences blood flow resistance, microcirculation, and clotting tendencies in pathological states.
1. Which plasma protein maintains oncotic pressure most effectively?
a) Albumin
b) Fibrinogen
c) α-globulin
d) β-globulin
Explanation (Answer: a) Albumin)
Albumin is responsible for nearly 80% of plasma oncotic pressure due to its abundance and small size, allowing efficient osmotic control. It prevents fluid leakage into tissues, maintaining blood volume. Fibrinogen and globulins contribute slightly. Low albumin causes edema, ascites, and decreased plasma oncotic pressure, common in malnutrition and liver failure.
2. Rouleaux formation increases mainly due to:
a) Albumin
b) Fibrinogen
c) IgG
d) Transferrin
Explanation (Answer: b) Fibrinogen)
Fibrinogen promotes rouleaux formation by increasing erythrocyte aggregation. Elevated fibrinogen levels slow blood flow and increase ESR. It is involved in inflammation, tissue injury, and chronic infections. Globulins may also contribute but less significantly. Albumin reduces aggregation due to its negative charge and smaller molecular size.
3. ESR increases primarily due to elevated:
a) Albumin
b) Fibrinogen
c) Sodium
d) Potassium
Explanation (Answer: b) Fibrinogen)
An increased fibrinogen level accelerates ESR by enhancing erythrocyte aggregation. The rouleaux settle faster in a vertical column. ESR is a nonspecific marker of inflammation and infection. Albumin opposes rouleaux formation; electrolytes do not directly affect ESR. Elevated ESR indicates inflammatory processes including rheumatoid arthritis and malignancy.
4. Plasma viscosity is decreased in:
a) Hypoproteinemia
b) Hyperglobulinemia
c) Hyperfibrinogenemia
d) Dehydration
Explanation (Answer: a) Hypoproteinemia)
Hypoproteinemia lowers plasma viscosity due to reduced protein concentration, especially albumin. Conditions like liver disease and nephrotic syndrome reduce proteins, lowering viscosity and impairing oncotic pressure. Hyperglobulinemia and hyperfibrinogenemia increase viscosity, while dehydration concentrates proteins, raising viscosity, not lowering it.
5. Plasma viscosity is highest in:
a) Acute hemorrhage
b) Multiple myeloma
c) Hypoalbuminemia
d) Renal tubular acidosis
Explanation (Answer: b) Multiple myeloma)
Multiple myeloma causes marked hyperglobulinemia due to excessive monoclonal proteins, sharply increasing plasma viscosity. Patients exhibit headaches, blurred vision, neurological deficits, and thrombosis. Hypoalbuminemia reduces viscosity, hemorrhage dilutes plasma, and renal tubular acidosis affects ions, not viscosity directly. Viscosity crisis requires immediate therapeutic plasmapheresis.
6. Most abundant plasma protein is:
a) Albumin
b) Fibrinogen
c) Globulin
d) Prothrombin
Explanation (Answer: a) Albumin)
Albumin accounts for 60% of total plasma proteins. Synthesized in the liver, it plays key roles in oncotic pressure, transport of drugs, hormones, and fatty acids. Despite being abundant, it does not contribute majorly to viscosity due to small molecular size. Fibrinogen contributes to viscosity and clotting but constitutes less proportion.
7. Which protein shows maximum rise during acute-phase reaction?
a) Albumin
b) Globulin
c) Fibrinogen
d) Prealbumin
Explanation (Answer: c) Fibrinogen)
Fibrinogen increases in acute inflammation due to cytokine stimulation (IL-6). Elevated fibrinogen improves clotting stability and increases plasma viscosity. Albumin is a negative acute-phase reactant and decreases. Globulins increase moderately during inflammation but fibrinogen rise is most prominent and directly measurable via elevated ESR.
8. Hyperviscosity syndrome commonly presents with:
a) Muscle paralysis
b) Visual disturbances
c) Constipation
d) Hypothermia
Explanation (Answer: b) Visual disturbances)
Hyperviscosity syndrome leads to sluggish blood flow causing blurred vision, headaches, mucosal bleeding, and neurological symptoms. Increased plasma proteins and RBC aggregation impair microcirculation. Common in multiple myeloma, Waldenström macroglobulinemia, and high fibrinogen states. Management includes plasmapheresis and treating underlying cause.
9. Which protein primarily contributes to clot formation?
a) Albumin
b) Fibrinogen
c) Transferrin
d) Ceruloplasmin
Explanation (Answer: b) Fibrinogen)
Fibrinogen is converted to fibrin during coagulation, forming a stable clot. It stabilizes platelet plug and ensures hemostasis. Deficiency causes prolonged bleeding and poor clot formation. Albumin transports molecules; transferrin carries iron; ceruloplasmin transports copper but none are involved directly in clot structure.
10. Increased fibrinogen levels are expected in:
a) Severe malnutrition
b) Pregnancy
c) Chronic liver failure
d) Dehydration
Explanation (Answer: b) Pregnancy)
Pregnancy increases fibrinogen levels as part of physiological hypercoagulable state preparing for potential blood loss during delivery. Elevated fibrinogen raises ESR and slightly increases plasma viscosity. Malnutrition lowers fibrinogen; liver failure reduces synthesis; dehydration concentrates proteins but does not increase fibrinogen synthesis.
11. Severe inflammation causes increased viscosity due to elevation of:
a) Bilirubin
b) Fibrinogen
c) Potassium
d) Chloride
Explanation (Answer: b) Fibrinogen)
Fibrinogen rises significantly during inflammation due to cytokine stimulation. The increased fibrinogen promotes erythrocyte aggregation, slowing blood flow and increasing viscosity. This is reflected as elevated ESR. Electrolytes and bilirubin play no major role in viscosity changes. Inflammatory viscosity changes improve clotting but may impair microcirculation.
Chapter: Physiology; Topic: Body Fluids & Plasma Proteins; Subtopic: Oncotic Pressure – Determinants
Keyword Definitions:
• Oncotic pressure: Osmotic pressure generated by plasma proteins that retain water in blood vessels.
• Albumin: Major plasma protein responsible for maintaining oncotic pressure.
• Electrolytes: Ions like sodium and chloride that influence osmolarity, not oncotic pressure.
• Plasma proteins: Proteins in blood involved in transport, coagulation, and oncotic regulation.
• Colloid osmotic pressure: Pressure exerted by proteins preventing capillary fluid loss.
• Hypoalbuminemia: Low albumin causing edema due to reduced oncotic pressure.
Lead Question - 2015
Oncotic pressure is contributed by?
a) Sodium
b) Chloride
c) Chloride
d) Albumin
Explanation (Answer: d) Albumin)
Albumin contributes the maximum oncotic pressure, accounting for nearly 80% of total colloid osmotic pressure. Its small size and high plasma concentration allow it to exert strong osmotic pull, retaining water within blood vessels. Sodium and chloride determine osmolarity but not oncotic pressure. Reduced albumin causes edema due to fluid shift into interstitial tissues, highlighting its physiologic importance.
1. Primary function of oncotic pressure is:
a) Maintain blood viscosity
b) Retain fluid in vasculature
c) Increase RBC count
d) Enhance oxygen binding
Explanation (Answer: b) Retain fluid in vasculature)
Oncotic pressure generated by plasma proteins like albumin retains fluid in the intravascular compartment, counteracting hydrostatic pressure that pushes fluid out of capillaries. This balance prevents edema formation. Loss of proteins decreases oncotic pressure, leading to fluid leakage into tissues. Thus, it maintains circulatory volume and prevents interstitial fluid overload.
2. Hypoalbuminemia leads to:
a) Increased blood viscosity
b) Peripheral edema
c) Hypertension
d) Hypernatremia
Explanation (Answer: b) Peripheral edema)
Reduced albumin lowers oncotic pressure, allowing fluid to shift from plasma into interstitial tissues, producing edema. Conditions such as malnutrition, liver disease, nephrotic syndrome, and burns decrease albumin. Blood viscosity decreases instead of increasing. Electrolytes remain unaffected initially, and hypertension is not typical unless fluid retention occurs secondarily.
3. Which compartment exerts oncotic pressure?
a) Plasma
b) Interstitial fluid
c) Intracellular fluid
d) Transcellular fluid
Explanation (Answer: a) Plasma)
Plasma proteins, especially albumin, generate oncotic pressure. Interstitial fluid has few proteins, producing low oncotic pressure. Intracellular fluid contains proteins but not accessible for vascular oncotic regulation. Plasma oncotic pressure opposes hydrostatic forces across capillaries, maintaining fluid balance crucial for circulatory stability.
4. A child with kwashiorkor develops edema due to:
a) Hypernatremia
b) Reduced oncotic pressure
c) Hyperkalemia
d) Hyperviscosity
Explanation (Answer: b) Reduced oncotic pressure)
Kwashiorkor causes severe protein malnutrition, resulting in decreased albumin synthesis. This dramatically reduces oncotic pressure, leading to fluid accumulation in tissues and generalized edema. Electrolyte changes occur later, but the primary mechanism is albumin deficiency impairing plasma fluid retention. Hyperviscosity is not associated with malnutrition.
5. Albumin level decreases in:
a) Nephrotic syndrome
b) Dehydration
c) Multiple myeloma
d) Polycythemia
Explanation (Answer: a) Nephrotic syndrome)
In nephrotic syndrome, albumin is lost excessively through damaged glomeruli, leading to hypoalbuminemia and decreased oncotic pressure, causing edema. Dehydration increases albumin concentration. Myeloma increases globulins but not albumin. Polycythemia affects RBC count, not albumin. The resultant low oncotic pressure explains swelling, frothy urine, and fluid retention.
6. Major factor opposing oncotic pressure in capillaries:
a) Osmotic pressure
b) Hydrostatic pressure
c) Filtration pressure
d) Diastolic pressure
Explanation (Answer: b) Hydrostatic pressure)
Capillary hydrostatic pressure pushes fluid out of vessels, opposing oncotic pressure. Oncotic pressure pulls fluid inward. The balance between these determines net filtration. Increased hydrostatic pressure in heart failure leads to edema, while strong oncotic pressure prevents excessive fluid leakage.
7. Liver disease causes edema due to:
a) Increased albumin synthesis
b) Decreased albumin synthesis
c) Excess RBC destruction
d) Increased lymph flow
Explanation (Answer: b) Decreased albumin synthesis)
The liver synthesizes albumin. Hepatocellular failure reduces production, lowering oncotic pressure. Fluid shifts into interstitial spaces, producing ascites and edema. RBC destruction and lymph flow changes cannot compensate. Chronic liver disease commonly shows low serum albumin with swelling and fluid accumulation.
8. Oncotic pressure decreases significantly in:
a) Severe burns
b) Hyperaldosteronism
c) Diabetes insipidus
d) Hyperlipidemia
Explanation (Answer: a) Severe burns)
Burns cause massive protein loss from plasma due to capillary damage and exudation, decreasing albumin levels and oncotic pressure. This leads to shock and fluid imbalance. Hyperaldosteronism affects sodium but not protein. Diabetes insipidus alters water, not oncotic pressure. Hyperlipidemia increases viscosity but does not affect oncotic pressure directly.
9. Albumin contributes more to oncotic pressure because of:
a) Large molecular weight
b) High plasma concentration
c) High sodium content
d) Rapid synthesis
Explanation (Answer: b) High plasma concentration)
Albumin contributes most to oncotic pressure primarily due to its high concentration in plasma. Though smaller in size than globulins, its abundance makes it osmotically dominant. Its negative charge also attracts water. Molecular weight alone would not explain its effect; concentration is key.
10. Fluid shift in hypoalbuminemia occurs from:
a) Tissues to blood
b) Blood to tissues
c) Lymph to blood
d) CSF to plasma
Explanation (Answer: b) Blood to tissues)
Low albumin reduces vascular oncotic pressure, causing fluid to leave blood and accumulate in tissues, resulting in edema, ascites, and pleural effusions. This pattern is typical in liver failure, malnutrition, or nephrotic syndrome. Opposite shift occurs when oncotic pressure is high, such as dehydration or albumin infusion.
11. Maximum protein loss causing reduced oncotic pressure occurs in:
a) Acute diarrhea
b) Nephrotic syndrome
c) Hyperuricemia
d) Thyroid disorders
Explanation (Answer: b) Nephrotic syndrome)
Nephrotic syndrome causes massive protein loss in urine due to glomerular damage, especially albumin, drastically lowering oncotic pressure. This results in edema, frothy urine, and hyperlipidemia. Diarrhea causes fluid loss but not significant protein loss. Thyroid problems alter metabolism, not protein loss. Hyperuricemia is unrelated.
Chapter: Physiology; Topic: Special Senses – Taste Physiology; Subtopic: Taste Sensations and Receptors
Keyword Definitions:
• Taste sensation: Chemical perception of dissolved substances via taste buds.
• Umami: Recent taste sensation responsive to amino acids like glutamate.
• Taste buds: Chemoreceptors located on tongue papillae and oropharynx.
• Gustatory pathway: Neural pathway transmitting taste signals to brainstem.
• Lingual papillae: Structures containing taste buds, including fungiform and circumvallate.
• Glutamate receptor: Umami receptor sensitive to monosodium glutamate (MSG).
Lead Question - 2015
Most recent taste sensation is?
a) Sweet
b) Sour
c) Bitter
d) Umami
Explanation (Answer: d) Umami)
Umami is the most recently identified taste sensation, recognized scientifically in the early 20th century but widely accepted only in recent decades. It detects glutamate and nucleotides and is associated with savory or meaty flavors. Sweet, sour, and bitter have long been established. Umami receptors are present in taste buds and contribute to protein recognition and appetite regulation, highlighting their nutritional importance.
1. Receptor responsible for umami taste is:
a) T1R1 + T1R3
b) T2R
c) ENaC
d) TRPV1
Explanation (Answer: a) T1R1 + T1R3)
Umami sensation is mediated by a heterodimer of T1R1 and T1R3 receptors. These receptors detect amino acids, especially glutamate. T2R receptors are involved in bitter taste, ENaC mediates salty taste, and TRPV1 responds to pain/heat. The umami receptor helps detect protein-rich foods, aiding nutritional preference and metabolic regulation.
2. Taste buds responsible for bitter taste are mainly located on:
a) Tip of tongue
b) Lateral margins
c) Circumvallate papillae
d) Filiform papillae
Explanation (Answer: c) Circumvallate papillae)
Circumvallate papillae contain numerous taste buds and are primarily responsible for bitter taste detection. Bitter taste has a protective role by detecting toxins. Filiform papillae lack taste buds. Sour and salty tastes are located on lateral surfaces and sweet at tip. Circumvallate papillae are innervated by glossopharyngeal nerve and highly sensitive to bitter stimuli.
3. Loss of umami sensation may occur in deficiency of:
a) Glutamate receptors
b) Vitamin C
c) Iron
d) Sodium
Explanation (Answer: a) Glutamate receptors)
Umami detection depends on glutamate-sensitive receptors (T1R1 + T1R3). Damage or dysfunction reduces savory taste perception. Conditions affecting receptor expression include aging, neurodegenerative diseases, and certain medications. Vitamin C and iron deficiency affect other taste perceptions but not specifically umami. Sodium affects salty taste, not umami recognition.
4. A patient with glossopharyngeal nerve injury loses taste from:
a) Anterior 2/3 of tongue
b) Posterior 1/3 of tongue
c) Palate only
d) Epiglottis only
Explanation (Answer: b) Posterior 1/3 of tongue)
The glossopharyngeal nerve (IX) supplies taste sensation to the posterior one-third of the tongue, especially from circumvallate papillae responsible for bitter taste. Injury causes loss of bitter and some umami sensation. Anterior two-thirds are supplied by chorda tympani (VII). Palate and epiglottis receive innervation from vagus nerve (X).
5. MSG enhances which taste?
a) Sweet
b) Bitter
c) Sour
d) Umami
Explanation (Answer: d) Umami)
Monosodium glutamate directly stimulates umami receptors and enhances savory taste. It binds to T1R1 + T1R3 receptors improving flavor depth in protein-rich foods. Excessive use may cause headaches in sensitive individuals, known as "Chinese restaurant syndrome." Sweet, bitter, and sour tastes do not respond to glutamate activation.
6. Sour taste is mediated by movement of:
a) Na⁺ ions
b) H⁺ ions
c) K⁺ ions
d) Cl⁻ ions
Explanation (Answer: b) H⁺ ions)
Sour taste is mediated by hydrogen ions from acidic substances. These ions directly affect taste cell membranes, depolarizing them. Na⁺ mediates salty taste, bitter involves G-protein pathways, and Cl⁻ is not directly linked. High H⁺ concentration in foods like lemons enhances sour intensity and helps regulate food intake and pH sensitivity.
7. A patient undergoing chemotherapy develops taste loss. The earliest taste lost is:
a) Sweet
b) Bitter
c) Umami
d) Salty
Explanation (Answer: b) Bitter)
Chemotherapy damages rapidly dividing taste bud cells causing dysgeusia. Bitter taste is often lost first due to the sensitivity of circumvallate papillae. Drugs also cause metallic taste. Sweet and salty may be preserved initially. Umami detection also declines but bitter loss is most prominent early in chemotherapy-induced taste dysfunction.
8. Sweet taste receptors are located mainly on:
a) Posterior tongue
b) Anterior tongue
c) Lateral tongue
d) Epiglottis
Explanation (Answer: b) Anterior tongue)
Sweet taste is sensed predominantly at the tip of the tongue where fungiform papillae are abundant. These papillae house taste buds sensitive to sugars and sweet compounds. Posterior tongue senses bitter. Lateral margins detect salty and sour. Sweet taste contributes to carbohydrate recognition and energy intake regulation.
9. Taste adaptation occurs fastest for:
a) Sweet
b) Sour
c) Bitter
d) Umami
Explanation (Answer: a) Sweet)
Sweet taste adapts rapidly because receptors undergo quick desensitization after continuous stimulation. This prevents overstimulation when consuming sugary foods. Bitter adapts slowly due to protective evolutionary role. Sour and umami have intermediate adaptation. Rapid adaptation helps control caloric intake and enhances sensory balance during prolonged eating.
10. A patient with zinc deficiency presents with impaired taste. Zinc deficiency most affects:
a) Sweet taste
b) Bitter taste
c) Umami taste
d) All taste modalities
Explanation (Answer: d) All taste modalities)
Zinc deficiency impairs all taste modalities due to its role in taste bud regeneration and enzyme carbonic anhydrase VI. Loss of zinc reduces cell turnover, causing hypogeusia. Clinical conditions include malnutrition, chronic diarrhea, and liver diseases. Supplementation restores taste gradually. Bitter and umami loss are early signs in zinc deficiency-mediated taste dysfunction.
11. Taste sensation of umami is important for detection of:
a) Carbohydrates
b) Fats
c) Amino acids
d) Minerals
Explanation (Answer: c) Amino acids)
Umami receptors detect amino acids, particularly glutamate and aspartate, signaling protein-rich foods. This mechanism evolved to promote intake of nutritious foods essential for tissue repair and growth. Sweet detects carbs, fats have separate receptors, and minerals relate to salty taste. Umami contributes to appetite regulation and enhances flavor complexity.