Regulation of acid production (parasympathetic system) MCQs With Answer

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Regulation of acid production (parasympathetic system) MCQs With Answer

The parasympathetic regulation of gastric acid is a key topic for B. Pharm students, linking physiology and pharmacology. This introduction reviews how the vagus nerve and acetylcholine acting on M3 muscarinic receptors stimulate parietal cells, enterochromaffin-like (ECL) cells and gastrin release to activate H+/K+ ATPase. Understanding neural pathways, receptor signaling (Gq → IP3/DAG → Ca2+), and pharmacologic modulation by agonists and antagonists is essential for treating peptic ulcer disease and hypersecretory conditions. These Student-friendly keywords include regulation of acid production, parasympathetic system, gastric acid pharmacology, and MCQs for B. Pharm students. Now let’s test your knowledge with 50 MCQs on this topic.

Q1. What is the primary neurotransmitter released by the parasympathetic (vagal) nerves that stimulates gastric acid secretion?

  • Noradrenaline
  • Serotonin
  • Acetylcholine
  • Histamine

Correct Answer: Acetylcholine

Q2. Which muscarinic receptor subtype on parietal cells mediates acetylcholine-induced acid secretion?

  • M1
  • M2
  • M3
  • M4

Correct Answer: M3

Q3. Activation of M3 receptors primarily couples to which G protein and intracellular pathway to increase acid secretion?

  • Gs → increased cAMP
  • Gi → decreased cAMP
  • Gq → IP3/DAG → increased intracellular Ca2+
  • Go → activation of K+ channels

Correct Answer: Gq → IP3/DAG → increased intracellular Ca2+

Q4. The vagal stimulation increases gastric acid secretion directly via parietal cells and indirectly via which cell type that releases histamine?

  • Chief cells
  • Enterochromaffin-like (ECL) cells
  • Mucous neck cells
  • D cells

Correct Answer: Enterochromaffin-like (ECL) cells

Q5. Which peptide hormone is released by G cells and potentiates vagal stimulation of acid secretion?

  • Secretin
  • Gastrin
  • Cholecystokinin
  • Somatostatin

Correct Answer: Gastrin

Q6. How does vagal stimulation promote gastrin release from antral G cells?

  • Direct muscarinic stimulation of G cells by ACh
  • Release of somatostatin which stimulates gastrin
  • Activation of histamine receptors on G cells
  • Inhibition of parietal cells leading to feedback gastrin release

Correct Answer: Direct muscarinic stimulation of G cells by ACh

Q7. Which cell secretes somatostatin that inhibits gastric acid secretion and is modulated by vagal activity?

  • G cells
  • D cells
  • Parietal cells
  • Chief cells

Correct Answer: D cells

Q8. Which enzyme on the apical membrane of parietal cells is the final mediator of acid secretion into the stomach lumen?

  • Na+/K+ ATPase
  • H+/K+ ATPase (proton pump)
  • Carbonic anhydrase
  • Ca2+ ATPase

Correct Answer: H+/K+ ATPase (proton pump)

Q9. Which intracellular messenger rise is most directly responsible for exocytosis of proton pump-containing tubulovesicles in parietal cells?

  • cAMP
  • IP3-mediated Ca2+ increase
  • No change in second messengers is required
  • cGMP elevation

Correct Answer: IP3-mediated Ca2+ increase

Q10. Vagal release of acetylcholine stimulates acid secretion via which combination of effects?

  • Direct parietal cell stimulation only
  • Direct parietal cell stimulation and indirect stimulation via gastrin and histamine release
  • Inhibition of gastrin release only
  • Stimulation of somatostatin release only

Correct Answer: Direct parietal cell stimulation and indirect stimulation via gastrin and histamine release

Q11. Which drug is a muscarinic agonist that can increase gastric acid secretion and is resistant to acetylcholinesterase?

  • Atropine
  • Bethanechol
  • Pirenzepine
  • Neostigmine

Correct Answer: Bethanechol

Q12. Which antimuscarinic drug specifically used to reduce acid secretion was developed to target gastric M1 receptors?

  • Atropine
  • Scopolamine
  • Pirenzepine
  • Bethanechol

Correct Answer: Pirenzepine

Q13. Atropine reduces acid secretion by blocking which receptor on parietal and G cells?

  • M1 muscarinic only
  • M2 muscarinic only
  • Nonselective muscarinic receptors (including M3)
  • Nicotinic receptors in the ganglia

Correct Answer: Nonselective muscarinic receptors (including M3)

Q14. Which statement best explains why vagotomy reduces gastric acid secretion?

  • Vagotomy increases somatostatin release enhancing acid secretion
  • Vagotomy eliminates parasympathetic stimulation of parietal and G cells
  • Vagotomy directly inhibits H+/K+ ATPase activity enzymatically
  • Vagotomy increases gastric blood flow thereby diluting acid

Correct Answer: Vagotomy eliminates parasympathetic stimulation of parietal and G cells

Q15. Which receptor antagonist would most directly block histamine-mediated potentiation of acid secretion?

  • H1 antagonist
  • H2 antagonist
  • M3 antagonist
  • P2Y receptor antagonist

Correct Answer: H2 antagonist

Q16. Combined blockade of which two pathways would most effectively reduce basal and stimulated acid secretion?

  • Beta-adrenergic and nicotinic pathways
  • Muscarinic and H2 histamine receptors
  • Somatostatin and CCK receptors
  • Prostaglandin and nitric oxide synthase

Correct Answer: Muscarinic and H2 histamine receptors

Q17. Which experimental stimulus mimics vagal activation to increase acid secretion in clinical testing?

  • Pentagastrin injection
  • Histamine infusion
  • Physostigmine infusion or insulin hypoglycemia
  • Prostaglandin E2 administration

Correct Answer: Physostigmine infusion or insulin hypoglycemia

Q18. How does acetylcholine potentiate histamine release from ECL cells?

  • By activating nicotinic receptors on ECL cells
  • By stimulating M3 receptors and increasing intracellular Ca2+
  • By increasing cAMP via Gs coupling
  • By blocking somatostatin receptors

Correct Answer: By stimulating M3 receptors and increasing intracellular Ca2+

Q19. Which of the following is least involved in parasympathetic stimulation of acid secretion?

  • Vagus nerve activity
  • Acetylcholine acting on M3 receptors
  • NE acting on beta receptors
  • Gastrin release from G cells

Correct Answer: NE acting on beta receptors

Q20. In parietal cells, carbonic anhydrase contributes to acid secretion by producing which ions?

  • Sodium and chloride
  • Hydrogen and bicarbonate
  • Potassium and bicarbonate
  • Calcium and phosphate

Correct Answer: Hydrogen and bicarbonate

Q21. Which pharmacologic class directly inhibits the H+/K+ ATPase and is the most potent antisecretory therapy?

  • H2 receptor antagonists
  • Proton pump inhibitors (PPIs)
  • Antacids
  • Muscarinic agonists

Correct Answer: Proton pump inhibitors (PPIs)

Q22. How do PPIs indirectly affect vagal-stimulated acid secretion pharmacodynamically?

  • They antagonize muscarinic receptors
  • They irreversibly inhibit the final proton pump, blocking acid regardless of vagal drive
  • They block histamine receptors on ECL cells
  • They increase somatostatin release to counteract vagal effects

Correct Answer: They irreversibly inhibit the final proton pump, blocking acid regardless of vagal drive

Q23. Which clinical condition is characterized by excessive gastrin secretion and markedly increased acid production that can overwhelm vagal regulation?

  • Peptic ulcer disease secondary to H. pylori
  • Zollinger-Ellison syndrome
  • Gastric atrophy due to autoimmune gastritis
  • Gastroesophageal reflux disease without hypersecretion

Correct Answer: Zollinger-Ellison syndrome

Q24. Which diagnostic test assesses maximal acid secretory capacity often after vagal stimulation or pentagastrin administration?

  • Basal acid output (BAO) only
  • 24-hour pH monitoring
  • Maximal acid output (MAO) after pentagastrin
  • Urea breath test

Correct Answer: Maximal acid output (MAO) after pentagastrin

Q25. Which of the following best describes the role of somatostatin in regulating vagal-induced acid secretion?

  • Somatostatin from D cells is stimulated by vagal activity and enhances acid secretion
  • Somatostatin inhibits gastrin and directly inhibits parietal cell secretion, attenuating vagal effects
  • Somatostatin has no effect on acid secretion
  • Somatostatin directly stimulates ECL cells to release histamine

Correct Answer: Somatostatin inhibits gastrin and directly inhibits parietal cell secretion, attenuating vagal effects

Q26. Which neurotransmitter acts at nicotinic receptors to convey preganglionic parasympathetic signals to postganglionic neurons?

  • Acetylcholine acting at nicotinic receptors
  • Norepinephrine acting at alpha receptors
  • Dopamine acting at D2 receptors
  • Serotonin acting at 5-HT3 receptors

Correct Answer: Acetylcholine acting at nicotinic receptors

Q27. In the context of parasympathetic regulation of acid, the term “vagovagal reflex” refers to:

  • Reflexes entirely within the vagus nerve regulating gastric secretion and motility
  • A reflex mediated solely by sympathetic fibers
  • Local enteric reflexes independent of vagus
  • Reflex inhibition of vagus by somatostatin

Correct Answer: Reflexes entirely within the vagus nerve regulating gastric secretion and motility

Q28. Which adverse effect is most likely with systemic antimuscarinic therapy used to reduce gastric acid?

  • Excessive salivation
  • Bronchospasm
  • Dry mouth and blurred vision
  • Bradycardia exclusively

Correct Answer: Dry mouth and blurred vision

Q29. When comparing the roles of cAMP and Ca2+ in parietal cell activation, which is correct for parasympathetic stimulation?

  • Parasympathetic (ACh) acts mainly via cAMP
  • Parasympathetic (ACh) acts mainly via increased intracellular Ca2+
  • Parasympathetic (ACh) decreases both cAMP and Ca2+
  • Parasympathetic (ACh) acts via nitric oxide production

Correct Answer: Parasympathetic (ACh) acts mainly via increased intracellular Ca2+

Q30. Which therapeutic approach targets neural input to reduce acid secretion in refractory peptic ulcer disease?

  • High-dose PPIs only
  • Truncal or highly selective vagotomy
  • Long-term H2 agonists
  • Prokinetic agents exclusively

Correct Answer: Truncal or highly selective vagotomy

Q31. Pirenzepine reduces acid secretion primarily by blocking which component of vagal-stimulated acid release?

  • Ganglionic transmission at nicotinic receptors
  • M1 muscarinic receptors on enteric neurons that mediate vagal stimulation
  • H+/K+ ATPase directly
  • Histamine H2 receptors on parietal cells

Correct Answer: M1 muscarinic receptors on enteric neurons that mediate vagal stimulation

Q32. Which statement about pentagastrin and vagal stimulation is correct in clinical testing?

  • Pentagastrin acts via muscarinic receptors to mimic vagal effects
  • Pentagastrin directly stimulates parietal cells via CCK-B (gastrin) receptors to measure maximal secretory capacity
  • Pentagastrin is an H2 antagonist used to measure basal acid output
  • Pentagastrin inhibits gastrin receptors to assess vagal tone

Correct Answer: Pentagastrin directly stimulates parietal cells via CCK-B (gastrin) receptors to measure maximal secretory capacity

Q33. Which cellular event links gastrin receptor activation to increased histamine release from ECL cells?

  • Increase in intracellular cAMP in ECL cells exclusively
  • Activation of CCK-B receptors on ECL cells, increasing intracellular Ca2+ and histamine release
  • Decreased ATP production in ECL cells
  • Activation of nicotinic receptors on ECL cells

Correct Answer: Activation of CCK-B receptors on ECL cells, increasing intracellular Ca2+ and histamine release

Q34. Which pharmacokinetic property of proton pump inhibitors is important for their antisecretory effect?

  • They require activation in the acidic canaliculus of parietal cells and have irreversible binding to the pump
  • They are active orally without need of absorption
  • They are competitive reversible inhibitors of H2 receptors
  • They act as antacids to neutralize acid immediately

Correct Answer: They require activation in the acidic canaliculus of parietal cells and have irreversible binding to the pump

Q35. Which mechanism explains why anticholinesterases can sometimes increase gastric acid secretion?

  • They block muscarinic receptors preventing ACh action
  • They increase synaptic ACh levels, enhancing vagal effects on parietal cells
  • They inhibit H+/K+ ATPase directly
  • They stimulate somatostatin release to increase acid

Correct Answer: They increase synaptic ACh levels, enhancing vagal effects on parietal cells

Q36. Which is true about the interplay between prostaglandins and vagal-mediated acid secretion?

  • Prostaglandins stimulate parietal cells and enhance vagal acid secretion
  • Prostaglandins inhibit acid secretion and protect mucosa, opposing vagal stimulation
  • Prostaglandins have no effect on acid secretion
  • Prostaglandins convert gastrin into an inactive form

Correct Answer: Prostaglandins inhibit acid secretion and protect mucosa, opposing vagal stimulation

Q37. Which receptor blockade would blunt both vagal-induced and gastrin-mediated acid secretion by reducing histamine release?

  • H1 receptor blockade
  • H2 receptor blockade
  • CCK-B receptor blockade on ECL cells
  • Muscarinic M3 receptor blockade on parietal cells

Correct Answer: CCK-B receptor blockade on ECL cells

Q38. Which clinical scenario would most likely reduce vagal stimulation of gastric acid?

  • Sympathetic arousal with stress-induced vagal activation
  • Vagal nerve injury after thoracic surgery
  • Administration of bethanechol
  • High carbohydrate meal increasing gastrin

Correct Answer: Vagal nerve injury after thoracic surgery

Q39. Which molecular change occurs in parietal cells following sustained vagal stimulation leading to increased acid secretion?

  • Decrease in mitochondria number
  • Fusion of tubulovesicles with apical canalicular membrane increasing proton pump density
  • Internalization of H+/K+ ATPase reducing acid output
  • Conversion of H+/K+ ATPase to Na+/K+ ATPase

Correct Answer: Fusion of tubulovesicles with apical canalicular membrane increasing proton pump density

Q40. Which effect is expected following administration of a selective M3 antagonist?

  • Increased gastric acid secretion
  • Decreased salivary secretion and decreased acid secretion
  • Increased gastric motility
  • Stimulation of nicotinic ganglia

Correct Answer: Decreased salivary secretion and decreased acid secretion

Q41. Which combination best explains synergy in acid secretion between vagal activity and histamine?

  • Vagal stimulation raises cAMP while histamine increases Ca2+
  • Vagal stimulation increases intracellular Ca2+ while histamine increases cAMP; both potentiate proton pump activation
  • Both vagal stimulation and histamine use identical second messengers and thus cancel out
  • Histamine inhibits vagal action on parietal cells

Correct Answer: Vagal stimulation increases intracellular Ca2+ while histamine increases cAMP; both potentiate proton pump activation

Q42. In pharmacology, why might a nonselective muscarinic blocker cause more side effects than a selective M1 antagonist like pirenzepine?

  • Nonselective blockers do not cross the blood-brain barrier
  • Nonselective blockers inhibit multiple muscarinic subtypes throughout the body causing widespread anticholinergic effects
  • Selective M1 antagonists are more potent at cardiac muscarinic receptors
  • Nonselective blockers enhance nicotinic transmission causing autonomic storms

Correct Answer: Nonselective blockers inhibit multiple muscarinic subtypes throughout the body causing widespread anticholinergic effects

Q43. Which physiological stimulus potentiates vagal-mediated acid secretion in anticipation of a meal?

  • Postprandial increase in somatostatin only
  • Cephalic phase mediated by sight, smell and taste through vagal pathways
  • Fasting state mediated by sympathetic tone
  • Supine position alone

Correct Answer: Cephalic phase mediated by sight, smell and taste through vagal pathways

Q44. Which drug interaction could increase vagal-driven acid secretion indirectly by increasing gastrin levels?

  • Long-term PPI therapy leading to hypergastrinemia
  • H2 receptor antagonists decreasing gastrin release
  • Prostaglandin analogues increasing somatostatin
  • Anticholinergics causing increased D cell activity

Correct Answer: Long-term PPI therapy leading to hypergastrinemia

Q45. In an experiment, blocking which enzyme in parietal cells would most directly prevent generation of H+ for secretion?

  • ATP synthase
  • Carbonic anhydrase
  • H+/K+ ATPase
  • Na+/K+ ATPase

Correct Answer: Carbonic anhydrase

Q46. Which is a correct pharmacodynamic reason that H2 antagonists reduce vagally potentiated acid secretion?

  • They block histamine-mediated cAMP rise in parietal cells, removing one potentiating signal
  • They block muscarinic receptors directly
  • They irreversibly inhibit proton pumps
  • They stimulate somatostatin release to increase gastric acid

Correct Answer: They block histamine-mediated cAMP rise in parietal cells, removing one potentiating signal

Q47. Which experimental observation would indicate a dominant role of vagal stimulation in acid secretion?

  • Acid secretion unchanged after vagotomy
  • Marked reduction in acid secretion after vagotomy despite normal gastrin and histamine levels
  • No change in acid secretion after antimuscarinic drugs
  • Increase in acid secretion with somatostatin infusion

Correct Answer: Marked reduction in acid secretion after vagotomy despite normal gastrin and histamine levels

Q48. Which choice best describes the role of enteric nervous system in mediating vagal effects on acid secretion?

  • Vagal preganglionic fibers synapse on enteric neurons which then regulate parietal, G and D cells
  • Enteric neurons are not involved in acid regulation
  • Enteric nervous system only mediates intestinal secretion, not gastric
  • Vagal fibers bypass enteric neurons and act directly on parietal cells without synapse

Correct Answer: Vagal preganglionic fibers synapse on enteric neurons which then regulate parietal, G and D cells

Q49. Which laboratory finding would be consistent with increased parasympathetic drive to the stomach?

  • Decreased basal acid output
  • Elevated basal acid output and increased response to cephalic stimuli
  • Markedly reduced gastrin levels
  • Increased somatostatin and decreased acid

Correct Answer: Elevated basal acid output and increased response to cephalic stimuli

Q50. For B. Pharm students, which integrated pharmacologic strategy best reduces acid from parasympathetic, histaminergic and gastrin-mediated pathways?

  • Monotherapy with a low-dose prokinetic agent
  • Combination therapy: muscarinic antagonist or vagotomy + H2 antagonist or PPI to block histamine and proton pump
  • Only dietary modification without drugs
  • Administration of acetylcholinesterase inhibitors

Correct Answer: Combination therapy: muscarinic antagonist or vagotomy + H2 antagonist or PPI to block histamine and proton pump

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