Gut Physiology ABSITE Killer Review

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Gut Physiology

L vagus n (anterior) gives hepatic branch, R (posterior) gives celiac brance and the ‘criminal nerve of Grassi’ which if undivided can keep elevated acid levels post vagotomy

Chief cells produce pepsinogen (converted to pepsin) which initiates proteolysis

Parietal cells produce H+ and intrinsic factor which binds B12, and is absorbed in terminal ileum

Acetylcholine (ACh), gastrin and histamine are main stimuli for H+ production

ACh (vagus) and gastrin activate PIP, DAG to incr Ca, activate protein kinase C which incr HCl production

Histamine acts on parietal cells via cAMP (H for Happy cAMPer) to incr HCl production

Gastrin produced by antral G cells (why antrectomy helpful); inhibited by H+ in duodenum. Stimulated by amino acids, Ach

Omeprazole blocks H/K ATPase of parietal cell (Every Year)

Somatostatin inhibits gastrin, insulin, secretin, ACh; decreases pancreatic and biliary output. Stimulated by acid in duodenum

Proximal vagotomy abolishes receptive relaxation which incr liquid emptying; no change for solids

Truncal vagotomy also incr emptying of solids when pyloroplasty done. Decreases basal acid by 80%

Most common symptom post-vagotomy is diarrhea (35%). Dumping syndrom in 10%; early due to hyperosmotic load, fluid shift; late due to increased insulin with decr glucose. Very rare (1%) that dumping is unresponsive to dietary measures (Every Year)

Enterokinase activates trypsinogen to trypsin which then activates other enzymes of digestion

CCK: from intestinal mucosa 1) contract gallbladder 2) relax Sphincter of Oddi 3) incr pancreatic enzyme secretion (Every Year)

Secretin: primary stimulus of pancreatic bicarb secretion. High flow rate = high bicarb, low Cl. Slow flow allows HCO3/Cl exchange so low HCO3, high Cl concentration

Enterglucagon: increased in small bowel mucosal hypertrophy, adaptation after small bowel resection

Peptide YY: released from terminal ileum with mixed meal, inhibits acid secretion “ileal brake”

Bile: 80% bile salts, 15% lecithin, 5% cholesterol. Stones form if incr chol or decr salts or decr lecithin. Gallbladder concentrates bile by active resorptiono of NaCl, H2O then follows. Bile pool 5g, recirculated q4h, lose 0.5g daily (10%) (Every Year)

Primary bile acids: cholic acid, chenodeoxycholic acid
Secondary (formed by intestinal bacteria): deoxycholic acid and lithocholic acid

MMC: interdigestive motility; 90 minute cycles, starts in stomach, goes to TI;
Phase I quiescence
Phase II gallbladder contraction
Phase III peristalsis
Phase IV subsiding electric activity
Motilin is key stimulatory hormone (erythromycin is prokinetic by stimulating motilin receptor)

Jejunum absorbs most Na and H2O (paracellular), more permeable than ileum