Physiology

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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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