Regulation of Gastric Secretion MCQ Quiz | Gastrointestinal System

Welcome to this specialized quiz on the Regulation of Gastric Secretion, designed for MBBS students. This module is a cornerstone of gastrointestinal physiology, covering the intricate neural, hormonal, and paracrine mechanisms that control stomach acid production. This quiz features 25 multiple-choice questions to test your understanding of the cephalic, gastric, and intestinal phases, the roles of key mediators like gastrin, histamine, and somatostatin, and their clinical relevance. After submitting your answers, you’ll receive your score and see a detailed breakdown of correct and incorrect responses. For your revision, you can also download a PDF copy of all questions with their correct answers. Good luck, and deepen your knowledge of this vital physiological process!

1. The cephalic phase of gastric secretion is primarily mediated by which of the following?

2. Which hormone, secreted by G-cells in the stomach antrum, is the most potent stimulant of gastric acid secretion?

3. Somatostatin, released from D-cells, exerts its inhibitory effect on acid secretion primarily by:

4. Zollinger-Ellison syndrome is characterized by hypersecretion of gastric acid due to a tumor secreting which hormone?

5. Histamine stimulates HCl secretion from parietal cells by binding to which type of receptor?

6. During the intestinal phase, the presence of acid in the duodenum triggers the release of which hormone that inhibits gastric acid secretion?

7. A surgical vagotomy would most significantly reduce gastric acid secretion during which phase?

8. Proton Pump Inhibitors (PPIs) like omeprazole reduce gastric acid by directly blocking which of the following?

9. G-cells, responsible for gastrin secretion, are most concentrated in which region of the stomach?

10. Pepsinogen, the inactive precursor of pepsin, is secreted by which cells in the gastric glands?

11. Intrinsic factor, secreted by parietal cells, is essential for the absorption of which vitamin in the terminal ileum?

12. Enterochromaffin-like (ECL) cells are stimulated by gastrin to release which paracrine substance that acts on parietal cells?

13. The most powerful stimulus for the release of secretin from duodenal S-cells is:

14. Which substance demonstrates a synergistic (potentiating) effect with acetylcholine and gastrin to maximally stimulate acid secretion from parietal cells?

15. The gastric phase of acid secretion, which accounts for the majority of the response to a meal, is primarily initiated by:

16. Atropine, a muscarinic antagonist, reduces gastric acid secretion by blocking the action of which neurotransmitter on parietal cells?

17. Which hormone is often referred to as “nature’s antacid” due to its potent, widespread inhibitory effects on gastrointestinal secretion and motility?

18. Cholecystokinin (CCK), released in response to fats and proteins in the duodenum, primarily inhibits which gastric function?

19. Chronic infection with Helicobacter pylori can lead to peptic ulcers by disrupting the mucosal barrier and causing hypergastrinemia, which is a result of:

20. The majority of HCl-secreting parietal cells are located in which part of the stomach?

21. Gastric Inhibitory Peptide (GIP), now also known as glucose-dependent insulinotropic polypeptide, is released from the duodenum in response to:

22. The direct pathway of vagal stimulation of acid secretion involves the release of acetylcholine, which acts on which receptors on the parietal cell?

23. The indirect pathway of vagal stimulation involves the release of Gastrin-Releasing Peptide (GRP) from vagal efferents, which stimulates:

24. Which of the following substances is NOT a direct stimulant of the parietal cell’s H+/K+ ATPase pump?

25. The enterogastric reflex, triggered by duodenal distension and irritation, is a: