Salivary amylase (ptyalin) begins starch digestion in the mouth at pH 6.8, producing maltose, but its activity is immediately halted when the bolus reaches the stomach's highly acidic environment (pH 1.5–2.0).

The stomach's parietal (oxyntic) cells secrete HCl, which kills ingested bacteria, activates pepsinogen (from chief cells) to pepsin, and maintains the optimal acidic pH for pepsin's proteolytic action on proteins.

Enterokinase — secreted by the duodenal mucosa, NOT the pancreas — converts trypsinogen to trypsin, which then activates chymotrypsinogen, proelastase, and procarboxypeptidase in a cascade within the duodenum.

Bile, produced by the liver and stored in the gallbladder, contains bile SALTS that emulsify large fat globules into smaller droplets; bile contains absolutely no digestive enzymes — this is the single most tested NEET trap.

The small intestine's villi and microvilli (brush border) together amplify the absorptive surface area approximately 600-fold, and membrane-bound brush border enzymes (maltase, sucrase, lactase, aminopeptidase, dipeptidases) complete the final digestion of carbohydrates, proteins, and nucleic acids.

Glucose and amino acids are absorbed by active transport (via sodium co-transporters) into blood capillaries of the villus, draining into the portal vein and first passing through the liver.

Fatty acids and glycerol, reassembled into triglycerides and packaged as chylomicrons within enterocytes, are exported into lacteals (lymph capillaries), travel via the thoracic duct, and enter the left subclavian vein — bypassing the liver entirely.

The large intestine absorbs water (by osmosis) and minerals only; symbiotic bacteria within it synthesize vitamins B and K; it performs no further digestion of nutrients.

Four GI hormones coordinate digestion: gastrin (G-cells, stimulates HCl + pepsinogen), secretin (S-cells, acid → bicarbonate), CCK (I-cells, fats + amino acids → bile + enzymes), and GIP (K-cells, fats + glucose → inhibits gastric acid + stimulates insulin).

Kwashiorkor (protein deficiency → hypoalbuminaemia → oedema) and Marasmus (total calorie deficiency → extreme wasting, no oedema) are the two protein-energy malnutrition disorders, distinguished primarily by the presence or absence of oedema.