Practice 7 structured short- and long-answer medical questions on Weekly Year 2: GIT Physiology Exam - April 21, 2026 (Sections B & C). Review model answers...
Answer: The cephalic phase occurs before food enters the stomach, triggered by sight, smell, or thought of food. Sensory stimuli activate the cerebral cortex and appetite centers in the hypothalamus, which send signals to the dorsal motor nucleus of the vagus nerve. Vagal stimulation leads to: 1. Direct stimulation of parietal cells via Ach to secrete HCl. 2. Stimulation of G-cells via Gastrin-Releasing Peptide (GRP) to release gastrin. 3. Inhibition of D-cells to reduce somatostatin. This accounts for approximately 30% of total acid secretion.
Answer: The gastric mucosal barrier is a physiological and structural defense mechanism that prevents autodigestion of the stomach lining by HCl and pepsin. Key factors include: 1. Impermeable apical membranes of surface epithelial cells (tight junctions). 2. A thick mucus layer primarily composed of mucins. 3. Bicarbonate secretion by epithelial cells creating a pH gradient. 4. High mucosal blood flow which removes excess H+ ions and provides nutrients for cell repair. 5. Prostaglandins (PGE2) which stimulate mucus/bicarbonate production.
Answer: Lipid digestion begins with emulsification by bile salts to increase surface area. Pancreatic lipase breaks down triglycerides into monoglycerides and free fatty acids. These products associate with bile salts and phospholipids to form micelles (water-soluble cylindrical aggregates). Micelles transport the lipids to the brush border of enterocytes. Lipids diffuse across the membrane, are re-esterified into triglycerides in the smooth ER, packaged into chylomicrons, and released into the lacteals via exocytosis.
Answer: CCK is secreted by I-cells in the duodenum and jejunum in response to the presence of fatty acids and amino acids in the chyme. Its primary functions are: 1. Stimulation of pancreatic enzyme secretion (acinar cells). 2. Contraction of the gallbladder to release bile. 3. Relaxation of the Sphincter of Oddi. 4. Inhibition of gastric emptying to ensure adequate time for digestion. 5. Induction of satiety via the hypothalamus.
Answer: The MMC is a pattern of electromechanical activity observed in the GI smooth muscle during the interdigestive state (fasting). It consists of three phases: Phase I (quiescence), Phase II (irregular contractions), and Phase III (regular, high-amplitude 'housekeeping' contractions). It is regulated by the hormone motilin. Its significance is to clear the stomach and small intestine of undigested debris, excess mucus, and bacteria, preventing small intestinal bacterial overgrowth (SIBO).
Answer: The enterogastric reflex is a neural reflex initiated by the presence of acid, distension, or hypertonic chyme in the duodenum. It involves the enteric nervous system, sympathetic nerves, and the vagus nerve. When triggered, it inhibits gastric motility and constricts the pyloric sphincter. This serves to slow down gastric emptying, preventing the duodenum from being overwhelmed by acid or osmotic pressure, ensuring efficient neutralization and digestion.
Answer: (a) Production/Ion Transporters: Inside the parietal cell, CO2 and H2O react via carbonic anhydrase to form H+ and HCO3-. H+ is actively pumped into the gastric lumen by the H+/K+ ATPase (proton pump) in exchange for K+. K+ recycles back to the lumen via K+ channels. HCO3- is transported out of the cell into the blood via a Cl-/HCO3- exchanger (alkaline tide). Cl- then follows its electrochemical gradient through chloride channels into the lumen to combine with H+ to form HCl. (b) Secretagogues: 1. Histamine: Released by ECL cells, binds H2 receptors, acts via cAMP/Gs pathway. 2. Gastrin: Released by G-cells, binds CCK2 receptors, acts via PLC/IP3/Ca2+ pathway. 3. Acetylcholine: Released by vagal endings, binds M3 receptors, acts via PLC/IP3/Ca2+ pathway. (c) Inhibition: Somatostatin is released by D-cells in response to low luminal pH. It binds to Gi-coupled receptors on parietal cells to directly inhibit adenylate cyclase, reducing cAMP. It also indirectly inhibits HCl by suppressing the release of gastrin and histamine.