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Digestion transforms macronutrients into absorbable molecules by secreted enzymes (saliva, gastric pepsin, pancreatic enzymes, brush border enzymes) and peristalsis moves chyme along the digestive tract. The transit speed determines the contact time with the mucosa and therefore absorption.

Intestinal absorption follows Fick's Law for fat-soluble solutes (passive diffusion through the lipid bilayer: J = P_mem·A·C, where P_mem depends on the partition coefficient K_part and the diffusivity D). Hydrophilic solutes such as glucose and amino acids are absorbed by secondary active transport (Na-glucose cotransporters SGLT1, SGLT2) with Michaelis-Menten kinetics.

Gastric emptying follows first-order kinetics for liquids (t½ 1520 min) and zero-order kinetics for solids up to an inflection point, then exponential (t½ 14 h depending on particle size and caloric content). Metformin delays gastric emptying and modifies postprandial glucose absorption. GLP-1 analogs also delay emptying.

The oral bioavailability (F) of a drug is the product of intestinal absorption, escape from enteric metabolism, and escape from the hepatic first-pass effect: F = F_abs × (1-E_H). Drugs with high hepatic extraction (E_H > 0.7: nitroglycerin, morphine, lidocaine) have very low F orally but high interpersonal variability according to hepatic flow Q_H and CYP450 activity.

Osmotic diarrhea occurs when non-absorbable or poorly absorbed solutes retain water in the lumen by osmosis (lactulose, mannitol, magnesium): the difference in osmolality creates an osmotic pressure (van't Hoff: = RT·C) that retains water in the lumen. Secretory diarrhea (cholera, enterotoxigenic E. coli) is different: the toxin activates adenylate cyclase cAMP Cl hypersecretion water follows passively.

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ID:('ky', 43)

Description

ID:(0, 43)