Memory tricks for digestion, absorption, and GI physiology

Mouth: mechanical and chemical digestion begins — teeth, tongue, salivary amylase (starch → maltose). Pharynx/Esophagus: transport only — peristalsis moves bolus to stomach. Lower esophageal sphincter (LES) prevents reflux. Stomach: mechanical churning + HCl + pepsin (protein digestion). Produces chyme. Small intestine: 6 meters — duodenum (most digestion), jejunum and ileum (absorption). Largest surface area (villi + microvilli = 250 m²). Large intestine: 1.5 meters — water and electrolyte absorption, bacterial fermentation (vitamin K + B vitamins), feces formation. Rectum/anus: storage and elimination. Four layers of GI wall: mucosa (innermost), submucosa, muscularis externa (inner circular + outer longitudinal), serosa (outermost).

Peristalsis: wave of contraction behind bolus + relaxation ahead → propels contents forward. Occurs throughout GI tract. Controlled by myenteric (Auerbach's) plexus. Segmentation: rhythmic contractions that mix contents without propulsion — dominant in small intestine, maximizes contact with absorptive surface. Mass movements: powerful peristaltic waves in colon — 1-3 times/day — propel feces toward rectum. Triggered by gastrocolic reflex (eating → colon contracts). Enteric nervous system: 500 million neurons — "second brain." Operates independently of CNS. Submucosal plexus controls secretion. Myenteric plexus controls motility. Sympathetic input suppresses GI activity (fight or flight). Parasympathetic (vagus) stimulates GI activity (rest and digest).

Cephalic phase (30%): sight/smell/taste/thought of food → vagus nerve (CN X) → ACh → parietal cells (HCl) and chief cells (pepsinogen). Before food reaches stomach — Pavlovian. Gastric phase (60%): food in stomach → distension + protein → gastrin from G cells (antrum) → parietal cells → HCl. Largest phase. Intestinal phase (10%): chyme in duodenum → initially small gastrin → then secretin and CCK inhibit gastric secretion. Parietal cells secrete HCl: stimulated by gastrin, ACh, histamine (H2). Blocked by PPIs (omeprazole — block H+/K+ ATPase) and H2 blockers (ranitidine). Chief cells secrete pepsinogen → activated to pepsin by HCl (pH <2). Intrinsic factor from parietal cells → essential for vitamin B12 absorption.

Gastrin: from G cells (stomach antrum). Trigger: protein + distension + vagal stimulation. Action: stimulates HCl secretion, gastric motility, mucosal growth. Secretin: from S cells (duodenum). Trigger: acid (low pH chyme) entering duodenum. Action: pancreatic bicarbonate secretion (neutralizes acid), inhibits gastric acid and motility. CCK (cholecystokinin): from I cells (duodenum). Trigger: fat and protein in duodenum. Action: gallbladder contraction (releases bile), pancreatic enzyme secretion, inhibits gastric emptying. GIP (glucose-dependent insulinotropic peptide) from K cells: glucose + fat → stimulates insulin release (incretin effect — basis of GLP-1 agonist drugs). VIP (vasoactive intestinal peptide): promotes intestinal secretion and relaxes smooth muscle.

Carbohydrates: salivary amylase (mouth) + pancreatic amylase (duodenum) → maltose + dextrins. Brush border enzymes complete digestion: maltase, sucrase, lactase → monosaccharides. Glucose + galactose absorbed via SGLT1 (Na+ cotransport). Fructose via GLUT5 (facilitated). All exit via GLUT2. Proteins: pepsin (stomach, pH<2) begins. Pancreatic proteases secreted as INACTIVE zymogens → enterokinase (duodenal brush border) activates trypsinogen → trypsin → activates chymotrypsinogen, proelastase, procarboxypeptidase. Brush border peptidases + cytoplasmic peptidases → free amino acids → absorbed via Na+ cotransport → portal blood. Lactase deficiency: undigested lactose → osmotic + fermentation diarrhea.

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.

Metabolism: carbohydrates (glycogenesis, glycogenolysis, gluconeogenesis — maintains blood glucose), lipids (fatty acid oxidation, ketogenesis, cholesterol synthesis), proteins (deamination, transamination, urea cycle — converts NH₃ → urea). Detoxification: cytochrome P450 enzymes metabolize drugs, alcohol, toxins. First-pass effect. Bile production: bile salts + cholesterol + bilirubin (from Hb breakdown) + lecithin. Bile stored in gallbladder (CCK triggers release). Blood protein synthesis: albumin (oncotic pressure, drug transport), clotting factors (I, II, VII, IX, X — vitamin K dependent), transport proteins. Storage: glycogen, fat-soluble vitamins (A, D, E, K), iron (ferritin). Liver failure: jaundice, coagulopathy, hypoalbuminemia → edema, hepatic encephalopathy (NH₃ accumulation).

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.

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.