Memory tricks for digestion, absorption, and GI physiology
GI tract anatomy, motility, digestive enzymes, GI hormones, carbohydrate/protein/fat digestion, absorption mechanisms, and the liver and pancreas — these memory tricks tie together the anatomy of the digestive system with exactly how it processes and absorbs nutrients.
Fat bypasses portal blood — absorbed via lymphatic lacteals as chylomicrons
How fats are digested and absorbed — the unique lymphatic pathway
Fat digestion is unique because fats are water-insoluble. Bile salts (from liver, stored in gallbladder, released by CCK) emulsify fat globules → tiny droplets → enormous surface area for lipase. Pancreatic lipase cleaves triglycerides → fatty acids + monoglycerides. These combine with bile salts to form micelles — tiny soluble packages that ferry fatty acids to enterocyte brush border. Fatty acids + monoglycerides diffuse into enterocyte → reassembled into triglycerides in smooth ER → packaged with cholesterol and apoprotein B-48 into chylomicrons → enter lacteals (lymphatic capillaries in villi) → thoracic duct → blood. Bypass the portal system entirely. Short-chain fatty acids are exception — go directly to portal blood.
Bile salts
Made in liver from cholesterol. Stored in gallbladder. Released by CCK. Emulsify fat.
Micelles
Bile salts + fatty acids + monoglycerides → soluble packages → ferry to brush border.
Two components of pancreatic juice — aqueous bicarbonate and digestive enzymes
What the pancreas secretes and what controls it — anatomy and physiology together
The exocrine pancreas secretes 1-2 L/day of pancreatic juice into the duodenum via the pancreatic duct (joins common bile duct at ampulla of Vater). Two components: Aqueous (ductal cells): water + bicarbonate → stimulated by secretin → neutralizes acid chyme from stomach (raises pH from ~2 to ~7 in duodenum — essential for enzyme function). Enzymatic (acinar cells): amylase (starch), lipase (fats — needs bile for emulsification), proteases as inactive zymogens — stimulated by CCK + vagal input. Acute pancreatitis: premature activation of proteases inside pancreas → autodigestion → severe epigastric pain radiating to back, elevated amylase/lipase. Causes: gallstones (most common), alcohol. Cystic fibrosis: CFTR mutation → thick secretions block ducts → malabsorption.
Absorb water · Bacteria make Vitamin K · No digestion — just concentration
Water and Na+ absorption · Bacterial fermentation · Defecation reflex
What the large intestine does — four functions beyond waste storage
The colon receives ~1.5 L of liquid chyme from the ileum daily and reduces it to ~150 mL of stool. Water absorption: Na+ absorbed actively → water follows osmotically — colon absorbs 90% of water it receives. Bacterial fermentation: colonic bacteria ferment undigested carbohydrates → short-chain fatty acids (main fuel for colonocytes) + gas (H₂, CO₂, methane). Bacterial synthesis: vitamin K (essential for clotting) and some B vitamins — clinically significant when antibiotics disrupt flora. Defecation reflex: stool in rectum → stretch → parasympathetic → internal anal sphincter relaxes (involuntary) → external sphincter voluntary. Diarrhea: too little water absorption (secretory) or too much solute (osmotic). Constipation: too much water absorbed, slow transit.
Water absorption
1.5 L in → 0.15 L out. Colon absorbs Na+ → water follows. Diarrhea = lost water + electrolytes.
Vitamin K synthesis
Gut bacteria → vitamin K2. Antibiotics deplete → bleeding risk. Warfarin antagonizes vitamin K.
Q: What are the four major GI hormones and what do each do?
A: Gastrin (G cells, antrum): released by protein, distension, vagus → stimulates HCl secretion from parietal cells, promotes gastric motility, stimulates chief cells (pepsinogen). Secretin (S cells, duodenum): released by acid (low pH) → stimulates pancreatic HCO3- secretion, inhibits gastric acid/motility, stimulates bile secretion. CCK (I cells, duodenum): released by fat and protein → stimulates pancreatic enzyme secretion, gallbladder contraction, sphincter of Oddi relaxation, inhibits gastric emptying, satiety signal. GIP (K cells, duodenum): released by fat/glucose → stimulates insulin release (incretin effect), inhibits gastric acid.
Q: Describe the digestion and absorption of fats.
A: Emulsification: bile salts break large fat globules into small droplets (increase surface area). Pancreatic lipase: digests triglycerides → monoglycerides + fatty acids. Micelles: bile salts surround digestion products → soluble complex that can reach brush border. Absorption: monoglycerides and fatty acids enter enterocyte by diffusion. Inside enterocyte: reassembled into triglycerides → packaged with cholesterol, phospholipids, and apolipoproteins into chylomicrons. Chylomicrons exit via lacteals (lymphatic) → thoracic duct → bloodstream. Short-chain fatty acids (<12C) absorbed directly into portal blood. Fat-soluble vitamins (ADEK) absorbed with fats — malabsorption in fat malabsorption syndromes.
Q: What are the functions of the liver?
A: Metabolism: glucose (glycogenesis, glycogenolysis, gluconeogenesis), fatty acid oxidation, amino acid deamination (ammonia → urea), ketone body synthesis. Synthesis: albumin (oncotic pressure), clotting factors (I, II, V, VII, IX, X, XI — not VIII), VLDL, cholesterol. Detoxification: cytochrome P450 enzymes metabolize drugs and toxins; conjugates bilirubin (unconjugated → conjugated) → excreted in bile. Bile production: 600-1000 mL/day; bile salts emulsify fats. Storage: glycogen, fat-soluble vitamins (A, D, B12), iron, copper. Liver disease: elevated AST, ALT (hepatocellular damage), elevated ALP, GGT (cholestasis), low albumin, elevated PT/INR (synthetic dysfunction).
Q: How does the stomach produce and regulate hydrochloric acid?
A: Parietal cells secrete HCl via H+/K+ ATPase (proton pump) — target of PPIs (omeprazole). Three phases of stimulation: Cephalic (before food reaches stomach): vagus nerve (ACh) → stimulates parietal cells directly and via ECL cells (histamine) and G cells (gastrin). Gastric: protein and distension → gastrin from G cells → stimulates parietal cells; histamine from ECL cells amplifies response. Intestinal: inhibitory — secretin and GIP inhibit acid when acid/fat enters duodenum. Regulation: somatostatin from D cells inhibits gastrin and parietal cells. H2 blockers (ranitidine) block histamine receptor on parietal cells. Achlorhydria (no HCl): risk of B12 deficiency (intrinsic factor still made but less effective), bacterial overgrowth.
Q: What is the difference between osmotic and secretory diarrhea?
A: Secretory diarrhea: intestinal cells actively secrete fluid — persists with fasting. Caused by: cholera toxin (activates adenylate cyclase → cAMP → Cl- secretion), E. coli heat-labile toxin, VIPoma. Large volume, watery, osmotic gap normal (<50). Osmotic diarrhea: unabsorbed solutes pull water into lumen — stops with fasting. Caused by: lactose intolerance (lactase deficiency → undigested lactose fermented by bacteria), lactulose, celiac disease (malabsorption), sorbitol. Osmotic gap elevated (>125). Stool osmotic gap = 290 - 2(Na+ + K+). Inflammatory diarrhea (dysentery): bloody diarrhea + fever = invasion of mucosa. Caused by: Shigella, Salmonella, Campylobacter, E. coli O157:H7, Entamoeba histolytica.