E4: GI 3

Review the layers of the small intestine wall.

• Mucosa: epithelium, lamina propria, muscularis mucosae

• Submucosa: Meissner's (submucosal) plexus + glands

• Muscularis externa: circular + longitudinal muscle; Auerbach's (myenteric) plexus between them

• Serosa: outer connective tissue + epithelium

• Villi (finger-like projections) + microvilli (brush border) dramatically increase surface area

• Stem cells in crypts of Lieberkühn → migrate up villus → slough at tip

Explain the countercurrent mechanism in the intestinal villus that promotes epithelial cell turnover.

• Arteriole runs up the center of the villus; venule runs alongside it going back down

• O₂ diffuses from arteriole → venule before reaching the tip (countercurrent exchange)

• Result: O₂ is highest at the base, lowest at the tip → tip is hypoxic

• Hypoxic tip: cells die and slough off, releasing brush border enzymes into the lumen

• Well-oxygenated base: stem cells undergo mitosis → new cells migrate up to replace sloughed cells

• High cell turnover = why chemo drugs (targeting fast-dividing cells) cause GI side effects

Explain the digestion and absorption of carbohydrates in the small intestine.

• Pancreatic amylase breaks carbs into disaccharides

• Brush border enzymes break these into monosaccharides

• Monosaccharides enter the enterocyte via Na⁺ co-transport

• Na⁺/K⁺-ATPase maintains the Na⁺ gradient that drives this

• Monosaccharides exit into the blood via facilitated diffusion

Explain the digestion and absorption of proteins in the small intestine.

• Proteases are released inactive (as zymogens) so they don't digest the pancreas itself — once in the gut, enterokinase activates trypsinogen → trypsin, which then switches on all the other enzymes

• Those enzymes break proteins down into amino acids and small peptides

• Amino acids hitch a ride into the cell with Na⁺ (secondary active transport — Na⁺ gradient does the work)

• Small peptides hitch a ride in with H⁺ instead, then get broken down inside the cell

Explain the digestion and absorption of fats in the small intestine.

• Bile salts (amphipathic, made from cholesterol by the liver) emulsify fat → big globule → tiny droplets → more surface area

• Pancreatic lipase (+ colipase) snips 2 fatty acids off each triglyceride → leaving 1 monoglyceride + 2 free fatty acids, which are small enough to cross the cell membrane

• Micelle: bile salts + digested fat → carries fat to intestinal wall for absorption

• Inside cell (ER/Golgi): resynthesized into triglycerides → packaged into chylomicrons

• Chylomicrons too large for capillaries → exocytosed into lymph lacteals → lymph → thoracic duct → venous blood

Integrate and explain the intrinsic, neural, and hormonal regulators of SI motility.

• Intrinsic: pacemaker cells generate basal electrical rhythm — oscillate below threshold

• Stimulus (stretch, vagus/ACh, hormones) pushes cells to threshold → AP → Ca²⁺ influx → contraction

• ENS coordinates segmentation — mixes chyme, promotes absorption (major motility type in SI)

• Feedback (inhibitory): SI stretch → inhibits gastric emptying; colon stretch → inhibits ileum

• Feedforward (excitatory): stomach stretch → stimulates SI + colon (gastrocolic reflex)

• Motilin (fasting hormone): triggers migrating myoelectric complex (MMC) — peristaltic waves that clean residual material from SI during fasting/sleep