PY4.1-12 | Gastro-intestinal Physiology — Gate Quiz

Correct! Parietal (oxyntic) cells of the gastric glands secrete HCl (via H⁺/K⁺-ATPase, the proton pump) and intrinsic factor. Chief cells secrete pepsinogen; G cells secrete gastrin; mucous cells secrete protective mucus.

Key concept: Gastric secretory cells — Parietal: HCl + intrinsic factor; Chief: pepsinogen (activated to pepsin by HCl); G cells (antrum): gastrin; Mucous cells: mucus + bicarbonate (protection). PPI (omeprazole) irreversibly blocks H⁺/K⁺-ATPase. Intrinsic factor deficiency → vitamin B12 malabsorption → pernicious anaemia.

Incorrect. HCl is secreted by parietal (oxyntic) cells via the H⁺/K⁺-ATPase (proton pump). Chief cells secrete pepsinogen; G cells secrete gastrin.

Correct! The cephalic phase is initiated before food reaches the stomach, mediated entirely by the vagus nerve (parasympathetic). Stimuli include sight, smell, taste, and thought of food. It accounts for ~20–30% of total gastric acid response to a meal.

Key concept: Phases of gastric secretion — Cephalic (20–30%): vagal, mediated by ACh and gastrin; Gastric (60–70%): distension → mechanoreceptors → gastrin + histamine → acid; Intestinal (<5%): chyme in duodenum, initially stimulates then inhibits. Vagotomy reduces acid secretion (treats peptic ulcers).

Incorrect. The cephalic phase (before food enters the stomach) is triggered by sensory stimuli and mediated by the vagus nerve. Gastric phase = food in stomach; Intestinal phase = food in duodenum.

Correct! Enterokinase (enteropeptidase) on the duodenal brush border cleaves a hexapeptide from trypsinogen, converting it to active trypsin. Trypsin then auto-activates more trypsinogen and activates other pancreatic pro-enzymes (chymotrypsinogen, proelastase, procarboxypeptidase).

Key concept: Pancreatic enzymes are secreted as inactive zymogens (except amylase and lipase) to prevent auto-digestion. Enterokinase activates trypsinogen → trypsin → activates chymotrypsinogen, proelastase, procarboxypeptidase. Pancreatic trypsin inhibitor protects against premature activation. In acute pancreatitis, premature activation causes gland auto-digestion.

Incorrect. Trypsinogen is activated by enterokinase (enteropeptidase) on the duodenal mucosa → trypsin, which then activates all other pancreatic zymogens.

Correct! 95% of bile salts are actively reabsorbed by Na⁺-coupled co-transporters (ASBT) in the terminal ileum and recirculate to the liver via the portal blood (enterohepatic circulation). The remaining 5% are lost in faeces, constituting the only route of cholesterol elimination.

Key concept: Enterohepatic circulation of bile — 95% of bile salts reabsorbed from terminal ileum → portal blood → liver. Total pool recycled 6–10 times/day. Interrupted by terminal ileal disease (Crohn's) or resection → fat malabsorption, steatorrhoea, fat-soluble vitamin deficiency (ADEK), gallstone formation. Bile acid sequestrants (cholestyramine) interrupt EHC → lower cholesterol.

Incorrect. Bile salts are reabsorbed in the terminal ileum (95%) via Na⁺-coupled transporters. This enterohepatic circulation allows each bile salt molecule to be recycled 6–10 times per day.

Correct! Secretin is released from S cells of the duodenum when acidic chyme (pH <4.5) enters from the stomach. It stimulates pancreatic ductal cells to secrete large volumes of bicarbonate-rich juice, neutralising the acid and creating the optimal pH for pancreatic enzyme activity.

Key concept: GI hormones — Secretin (S cells, duodenum): stimulus = acid → ↑pancreatic HCO₃⁻ secretion, ↓gastric acid; CCK (I cells, duodenum/jejunum): stimulus = fat + protein → ↑pancreatic enzymes, ↑bile flow, gallbladder contraction; Gastrin (G cells, antrum): stimulus = protein → ↑HCl; GIP: glucose + fat → ↑insulin (incretin).

Incorrect. Secretin is released by acid (low pH, <4.5) entering the duodenum. It stimulates pancreatic bicarbonate secretion to neutralise the acid. (CCK is stimulated by fat and protein.)

Correct! Fat digestion: emulsification by bile salts → pancreatic lipase (+ colipase) cleaves TG to 2-monoglyceride + 2 FFAs → mixed micelles → enter enterocytes → re-esterified to TG → packaged as chylomicrons → secreted into lacteals (lymphatics) → thoracic duct → bloodstream.

Key concept: Fat absorption requires bile (emulsification, micelle formation) and pancreatic lipase. Absorbed fat enters lymphatics as chylomicrons (bypasses portal circulation — allows absorption of fat-soluble vitamins ADEK). In cholestasis or pancreatic insufficiency → steatorrhoea. Medium-chain TGs absorbed directly into portal blood — used in malabsorption syndromes.

Incorrect. The complete sequence: bile salt emulsification → pancreatic lipase hydrolysis → micelle formation → enterocyte absorption → TG re-synthesis → chylomicron → lacteals → lymphatics.

Correct! The colon receives approximately 1.5–2 L of fluid from the ileum daily and absorbs ~1.3–1.8 L, leaving ~100–150 mL in faeces. Maximum absorptive capacity is ~5–6 L/day; exceeding this causes diarrhoea.

Key concept: Daily fluid handling in GI tract — Oral intake: 2 L + secretions (saliva 1.5L, gastric 2L, bile 0.5L, pancreatic 1.5L, intestinal 1.5L) = ~9 L total. Small intestine absorbs ~7.5 L; colon absorbs 1.3–1.8 L; faeces contains only ~100–150 mL. Secretory diarrhoea: excess fluid secretion overwhelms colonic capacity.

Incorrect. The colon absorbs approximately 1.3–1.8 L/day from the ~1.5 L entering from the ileum, leaving 100–150 mL in faeces.

Correct! H. pylori produces urease, converting urea to ammonia and CO₂. Ammonia disrupts the mucous bicarbonate protective barrier, and bacterial virulence factors (CagA, VacA) trigger inflammation, reduce somatostatin (normally inhibits gastrin), increasing acid secretion — all leading to mucosal injury.

Key concept: H. pylori virulence — urease (ammonia), CagA (oncogenic, disrupts cell junctions), VacA (vacuolating cytotoxin). Diagnosis: urea breath test (gold standard non-invasive), rapid urease test (biopsy), serology. Eradication: triple therapy (PPI + amoxicillin + clarithromycin) for 14 days reduces ulcer recurrence from 80% to <5%.

Incorrect. H. pylori produces urease (used in the urea breath test) → ammonia → disrupts the gastric mucous barrier. It also reduces somatostatin → ↑gastrin → ↑acid. Dual mucosal injury and acid hypersecretion lead to ulceration.

Correct! The MMC (migrating motor complex) occurs during fasting (interdigestive period) in 90–120 minute cycles. It sweeps debris, bacteria, and undigested material from the stomach through to the distal ileum, earning its nickname "intestinal housekeeper." It is inhibited by eating.

Key concept: MMC phases — Phase I (quiet, 45 min), Phase II (irregular contractions, 30 min), Phase III (intense regular contractions, the "activity front," 5–10 min). Motilin initiates MMC. SIBO (small intestinal bacterial overgrowth) is more common when MMC is impaired (e.g., diabetes, opioids). Eating suppresses MMC and initiates fed-state motility patterns.

Incorrect. The MMC occurs during FASTING (not during digestion), in 90–120 min cycles, sweeping the intestine clean. It is suppressed when a meal is consumed.

Correct! After total gastrectomy, all parietal cells are removed — no intrinsic factor (IF) is produced. IF is essential for B12 absorption in the terminal ileum via cubilin receptors. Without IF, B12 deficiency develops over 2–3 years (body stores last 3–5 years), causing megaloblastic anaemia and subacute combined degeneration (demyelination of posterior and lateral spinal columns).

Key concept: Intrinsic factor (IF) produced by parietal cells is essential for ileal B12 absorption. IF deficiency causes: post-gastrectomy, pernicious anaemia (autoimmune), atrophic gastritis. B12 deficiency: megaloblastic anaemia + SACD (posterior column + lateral corticospinal tract demyelination). Treat post-gastrectomy with IM cyanocobalamin monthly.

Incorrect. Total gastrectomy removes all parietal cells → no intrinsic factor → B12 cannot be absorbed in terminal ileum → B12 deficiency → megaloblastic anaemia + neurological complications (SACD).