Memory tricks for digestion and absorption

Peristalsis is coordinated by the enteric nervous system (the "second brain") — 500 million neurons in the gut wall that function independently of the CNS. The myenteric (Auerbach's) plexus controls motility. The submucosal (Meissner's) plexus controls secretion. Peristaltic reflex: bolus detected → contraction behind (ascending excitation via ACh) + relaxation ahead (descending inhibition via VIP/NO). Segmentation: rhythmic contractions that mix contents without propulsion — dominant in small intestine. Mass movements: in colon, 1-3 times/day, propel contents to rectum — triggered by gastrocolic reflex after eating.

Cephalic phase (30%): sight, smell, taste, thought of food → vagus nerve (CN X) → stimulates gastrin release and direct ACh stimulation of parietal cells → HCl secretion. Occurs BEFORE food reaches stomach. Gastric phase (60%): food in stomach → stomach distension → protein stimulates gastrin from G cells → more HCl. Largest phase. Intestinal phase (10%): chyme in duodenum → initially stimulates gastrin → then inhibited by secretin and CCK as acid/fat detected → reduces gastric secretion. Net effect: acid production is maximized when food is present and reduced when acid moves into duodenum.

Gastrin: G cells in stomach antrum. Trigger: protein + distension + vagus. Action: HCl secretion, gastric motility, mucosal growth. Secretin: S cells in duodenum. Trigger: acid (low pH) entering duodenum. Action: pancreatic bicarbonate secretion (neutralizes acid), inhibits gastric acid and motility. CCK (cholecystokinin): I cells in duodenum. Trigger: fat and protein entering duodenum. Action: gallbladder contraction, pancreatic enzyme secretion, inhibits gastric emptying (buys time for digestion). GIP (glucose-dependent insulinotropic peptide): K cells. Trigger: glucose and fat. Action: stimulates insulin release — the incretin effect.

Fat digestion is unique because fats are insoluble in water. Bile salts emulsify fat globules → large surface area for lipase. Pancreatic lipase breaks triglycerides → fatty acids + monoglycerides. These combine with bile salts to form micelles — tiny soluble packages. Micelles deliver fatty acids to enterocyte surface → diffuse into enterocyte. Inside enterocyte: reassembled into triglycerides → packaged with cholesterol and protein into chylomicrons. Chylomicrons enter lacteals (lymphatic capillaries) → thoracic duct → left subclavian vein → bloodstream. This bypasses the portal system — dietary fat goes to lymph, not portal blood.

Salivary amylase begins starch digestion in mouth → pancreatic amylase continues in duodenum → both produce maltose, maltotriose, and dextrins. Brush border enzymes complete digestion: maltase (maltose → glucose + glucose), sucrase (sucrose → glucose + fructose), lactase (lactose → glucose + galactose). Glucose and galactose absorbed via SGLT1 (Na+ cotransport, active). Fructose via GLUT5 (facilitated diffusion). All exit enterocyte via GLUT2 into portal blood. Lactase deficiency → lactose intolerance — undigested lactose fermented by bacteria → bloating, diarrhea, gas.

Protein digestion requires multiple enzymes to break peptide bonds. Pepsin: activated from pepsinogen by HCl in stomach → begins protein digestion. Pancreatic proteases: secreted as INACTIVE zymogens to prevent self-digestion. Enterokinase (on duodenal brush border) activates trypsinogen → trypsin → trypsin then activates all other proteases (chymotrypsin, elastase, carboxypeptidase). Brush border peptidases and cytoplasmic peptidases complete digestion → free amino acids and small peptides absorbed via secondary active transport (Na+ cotransport) → portal blood. Acute pancreatitis: premature activation of proteases inside pancreas → autodigestion.

Gastric emptying rate: liquids (fastest) > carbohydrates > proteins > fats (slowest). Fat slows emptying most because CCK and other enterogastrones released when fat enters duodenum inhibit gastric motility — allowing time for fat digestion. Hyperosmolar solutions empty slower than isotonic. The pyloric sphincter regulates emptying — opens to let small boluses through. Rapid gastric emptying (dumping syndrome): post-surgical, large amounts of hyperosmolar food reach small intestine quickly → water pulled in → osmotic diarrhea + hypoglycemia. Delayed emptying (gastroparesis): common in diabetes — vagal neuropathy impairs motility.

The exocrine pancreas secretes 1-2 L/day of pancreatic juice. Two components: Aqueous component: ductal cells produce water + bicarbonate (HCO3-) in response to secretin — neutralizes acid chyme entering duodenum. Enzymatic component: acinar cells produce digestive enzymes in response to CCK and vagal stimulation — proteases (zymogens), lipase, amylase, nucleases. The pH in the duodenum rises from ~2 (gastric) to ~7 after bicarbonate buffering — essential because pancreatic enzymes work best at neutral pH. Cystic fibrosis: thick mucus blocks pancreatic ducts → enzymes can't reach duodenum → malabsorption.

The colon receives ~1.5 L of liquid chyme from the ileum and reduces it to ~150 mL of stool. Primary function: water and electrolyte absorption (Na+ absorbed, K+ secreted). Colonic bacteria ferment undigested carbohydrates → short-chain fatty acids (colonocyte fuel) + gas (H2, CO2, methane). Bacteria synthesize vitamin K and some B vitamins — clinically important. Defecation reflex: stool enters rectum → rectal wall stretches → parasympathetic signals → internal anal sphincter relaxes (involuntary) → external sphincter under voluntary control. Diarrhea: too little water absorption or too much secretion. Constipation: too much water absorbed, slow transit.