Gut Physiology

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

 

Chief Cells produce pepsinogen (-> 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 increase Ca, activate protein Kinase C which increases HCL production

 

Histamine acts on parietal cell via cAMP (H for Happy cAMPer) to increase HCL production

 

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

 

Omeprazole blocks H/K ATPase of parietal cell

 

Somatostatin inhibits gastrin, insulin, secretin, Ach; decreases pancreatic/biliary output

    -stimulated by acid in duodenum

 

Proximal vagotomy abolishes receptive relaxation which increases liquid emptying; no chance for solids

 

Truncal vagotomy also increases emptying of solids when pyloroplasty done.  TV decreases basal acid by 80%

 

Most common symptom post vagotomy is diarrhea (35%)

    -dumping syndrome is 10%, early due to hyperosmotic load, fluid shift; late due to increased

    insulin, decreased glucose

    -very rare (1%) that dumping unresponsive to dietary measures

 

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

 

CCK: from intestinal mucosa

    -contracts gallbladder

    -relaxes sphincter of Oddi

    -increases pancreatic enzyme secretion

 

Secretin: primary stimulus of pancreatic bicarb secretion, high flow rate=high bicarb, low Cl

    -slow flow allows HCO3/Cl exchange so low bicarb, high Cl concentration

 

Enteroglucagon: increases 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 increased cholesterol or decreased salts or lecithin

    -gallbladder concentrates bile by active reabsorption of Na, Cl; H2O then follows

    -bile pool 5g, recirculated q4 hours, lose .5g daily (10%)

 

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 1 quiescence, II gallbladder contraction, III peristalsis, 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

 

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