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 & 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: 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: 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: 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: 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: 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: 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: 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: 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.