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PY4.1-12 | Gastro-intestinal Physiology — Part 3

Digestion and Absorption of Nutrients (PY4.7)

Digestion is the breakdown of large molecules; absorption is the transfer from lumen to blood or lymph. Most absorption occurs in the jejunum (the first 2 metres of small intestine after the duodenum).

Digestion and Absorption of Nutrients (PY4.7)

Figure: Digestion and Absorption of Nutrients (PY4.7)

Four-panel illustration showing intestinal surface area amplification (folds-villi-microvilli), carbohydrate absorption via SGLT1 and GLUT transporters, protein digestion cascade and absorption, and fat digestion-emulsification-chylomicron pathway.

Structural adaptations that maximise absorption:
Circular folds (plicae circulares) → 3× increase in surface area
Villi (1mm tall) → 10× increase
Microvilli (brush border) → 20× increase
→ Total absorptive area: approximately 200 m² (the size of a tennis court)

Carbohydrate digestion and absorption:
• Salivary amylase (mouth) + pancreatic amylase (duodenum) → oligosaccharides, maltose
• Brush border disaccharidases → monosaccharides (glucose, galactose, fructose)
• Absorption: Glucose and galactose by SGLT-1 (Na⁺-dependent secondary active transport); Fructose by GLUT-5 (facilitated diffusion); all exit via GLUT-2 into portal blood.

Protein digestion and absorption:
• Pepsin (stomach, pH 2) → polypeptides
• Trypsin, chymotrypsin, carboxypeptidase (duodenum) → dipeptides, tripeptides, amino acids
• Brush border peptidases → single amino acids
• Absorption: Active transport (coupled to Na⁺) into enterocytes → portal blood

Fat digestion and absorption (most complex):
• Gastric lipase (stomach) — minor, hydrophilic fats
Bile salts emulsify fat → small droplets (increase surface area for lipase)
Pancreatic lipase (+ co-lipase) → monoglycerides + fatty acids
• Monoglycerides + fatty acids enter micelles (bile salt transport vehicles) → diffuse across brush border
• Inside enterocyte: reassembled into triglycerides → packaged into chylomicrons (lipoproteins)
Chylomicrons exit via lacteals (lymphatic capillaries in villi) → thoracic duct → systemic blood
Long-chain fatty acids go via lymph; short-chain fatty acids (from butter, coconut oil) go directly into portal blood.

Vitamin and mineral absorption:
Iron: As Fe²⁺ in duodenum (HCl from stomach converts Fe³⁺→Fe²⁺). Absorbed by DMT-1 transporter. Vitamin C enhances; phytates inhibit.
Calcium: Active transport in duodenum, facilitated by Vitamin D (calcitriol upregulates calbindin).
Vitamin B12: Bound to intrinsic factor → absorbed in terminal ileum by cubilin receptors.
Fat-soluble vitamins (A, D, E, K): Absorbed with fats via micelles.

SELF-CHECK — : Digestion & Absorption

Chylomicrons formed in enterocytes are transported away from the gut via:

A. Portal vein

B. Hepatic artery

C. Lacteals → thoracic duct

D. Mesenteric veins

Reveal Answer

Answer: C. Lacteals → thoracic duct


Lactase deficiency leads to which set of symptoms after milk consumption?

A. Steatorrhoea and fat-soluble vitamin deficiency

B. Bloating, flatulence, and osmotic diarrhoea

C. Pernicious anaemia

D. Hypoglycaemia

Reveal Answer

Answer: B. Bloating, flatulence, and osmotic diarrhoea

GIT Movements — Regulation and Significance (PY4.8)

Types of GIT Movements

Movement Location Function Neural Control Clinical Relevance
Peristalsis Entire GIT Propulsion of contents Auerbach's plexus; parasympathetic enhances, sympathetic inhibits Absent in adynamic ileus
Segmentation Small intestine Mixing and absorption Auerbach's plexus Dominant during digestion
Mass movement Colon Propels contents toward rectum Gastrocolic reflex (after meals) Absent in Hirschsprung's disease
Migrating motor complex (MMC) Stomach, small intestine Housekeeping between meals Motilin-mediated, every 90 min Prevents bacterial overgrowth

Types of GIT Movements

Movement Location Function Neural Control Clinical Relevance
Peristalsis Entire GIT Propulsion of contents Auerbach's plexus; parasympathetic enhances, sympathetic inhibits Absent in adynamic ileus
Segmentation Small intestine Mixing and absorption Auerbach's plexus Dominant during digestion
Mass movement Colon Propels contents toward rectum Gastrocolic reflex (after meals) Absent in Hirschsprung's disease
Migrating motor complex (MMC) Stomach, small intestine Housekeeping between meals Motilin-mediated, every 90 min Prevents bacterial overgrowth

The gut wall contains smooth muscle that generates different types of movements — each precisely matched to its digestive function.

GIT Movements — Regulation and Significance (PY4.8)

Figure: GIT Movements — Regulation and Significance (PY4.8)

Four-panel illustration showing peristalsis with the law of the intestine, segmentation mixing movements, gastric emptying regulation with duodenal feedback, and the defecation reflex with sphincter control.

Types of GIT movements:

1. Peristalsispropulsive movement
• A wave of contraction preceded by relaxation (receptive relaxation).
• The "law of the intestine" (Bayliss & Starling): contraction above, relaxation below the bolus.
• Mediated by Auerbach's plexus; enhanced by parasympathetic (vagus), inhibited by sympathetic.

2. Segmentationmixing movement
• Alternating rings of contraction and relaxation — churns chyme, mixes it with digestive juices, increases contact with mucosa.
• Most active in the duodenum and jejunum.
• No net propulsion — purely local mixing.

3. Mass peristalsis — occurs in the colon, 1–3 times/day, propels faecal matter into rectum. Triggered by the gastrocolic reflex (food in stomach → strong colonic contractions — which is why you often feel the urge to defecate after a meal).

4. Migrating Myoelectric Complex (MMC) — "housekeeper" contractions during fasting, every 90 minutes, sweep food residue and bacteria from the small intestine into the colon. Regulated by motilin. Disruption → small intestinal bacterial overgrowth (SIBO).

Swallowing (deglutition): Three phases:
1. Oral phase (voluntary): Tongue pushes bolus to posterior pharynx.
2. Pharyngeal phase (reflex): Soft palate closes nasopharynx; larynx elevates, epiglottis covers glottis; upper oesophageal sphincter opens. Breathing pauses.
3. Oesophageal phase (reflex): Primary peristalsis propels bolus; lower oesophageal sphincter (LOS) relaxes.

Defecation reflex:
• Faeces in rectum → rectal wall distension → stretch receptors → afferent signals to sacral spinal cord (S2–S4) → parasympathetic efferents → contraction of sigmoid colon and rectum + internal anal sphincter relaxes (involuntary, smooth muscle).
External anal sphincter (voluntary, striated muscle — under conscious control via pudendal nerve) → when socially appropriate: relax → defecation.
• Valsalva manoeuvre (raised intra-abdominal pressure) assists.

Role of dietary fibre:
• Insoluble fibre (cellulose, wheat bran): Adds bulk to stool, speeds transit, reduces constipation and colon cancer risk.
• Soluble fibre (pectin, guar gum, oats): Forms a gel, slows glucose absorption (lowers GI index), binds bile acids (lowers LDL cholesterol).
• WHO recommendation: ≥25g/day. Typical Indian rural diet: adequate (traditional whole grains, vegetables). Urban Indian diet: increasingly deficient.

Liver and Gallbladder — Structure, Functions, Secretion (PY4.9)

The liver (weighing ~1.5 kg in adults) is the largest gland in the body and performs >500 metabolic functions. Its digestive role is the secretion of bile.

Liver and Gallbladder — Structure, Functions, Secretion (PY4.9)

Figure: Liver and Gallbladder — Structure, Functions, Secretion (PY4.9)

Four-panel illustration showing the hepatic lobule structure with blood and bile flow directions, bile composition and enterohepatic circulation, gallbladder function with CCK regulation, and the major metabolic functions of the liver.

Functional unit: the hepatic lobule — hexagonal structure with a central vein and portal triads (hepatic artery, portal vein, bile duct) at the corners. Blood flows from portal triads → hepatic sinusoids → central vein. Bile flows in the opposite direction: hepatocytes → bile canaliculi → bile ducts → hepatic duct.

Composition of bile:
• Water (97%)
Bile salts (primary: cholic and chenodeoxycholic acid, secondary: deoxycholic and lithocholic acid) — essential for fat emulsification
Bilirubin — breakdown product of haem; conjugated in liver (water-soluble) → excreted in bile
• Cholesterol, phospholipids, mucus
• Bile is not an enzyme — it is an emulsifier. It does not digest fats chemically; it increases the surface area for pancreatic lipase.

Enterohepatic circulation: Bile salts are reabsorbed in the terminal ileum (95%), returned to liver via portal blood, and re-secreted. Total bile salt pool recycles 6–10 times per day. Bile acid sequestrants (cholestyramine) interrupt this cycle → lower LDL.

Gallbladder: Stores and concentrates bile (10×) between meals. Cholecystokinin (CCK) → contracts gallbladder + relaxes sphincter of Oddi → bile released into duodenum. The gallbladder cannot synthesise bile — it only stores it.

Functions of the liver (beyond bile):
• Metabolism: glycogen synthesis/breakdown, gluconeogenesis, lipid synthesis, protein synthesis (albumin, clotting factors, CRP)
• Detoxification: drug metabolism (CYP450 enzymes), ammonia → urea (urea cycle)
• Storage: glycogen, fat-soluble vitamins (A, D, B12), iron (as ferritin)
• Immunological: Kupffer cells (macrophages lining sinusoids) phagocytose gut bacteria from portal blood

Liver Function Tests (LFTs):

TestMeasuresElevated in
Serum bilirubinBilirubin conjugation and secretionHepatitis, obstruction
ALT (SGPT)Hepatocellular damageHepatitis (most specific)
AST (SGOT)Hepatocellular + muscle damageHepatitis, MI
ALPBiliary obstruction, boneCholestasis, bone disease
GGTBiliary/alcoholAlcohol abuse, biliary disease
Serum albuminSynthetic functionChronic liver disease
PT/INRClotting factor synthesisLiver failure

SELF-CHECK — : GIT Movements & Liver

Which reflex causes the urge to defecate after a meal by triggering mass peristalsis in the colon?

A. Enterogastric reflex

B. Gastrocolic reflex

C. Defecation reflex

D. Ileocaecal reflex

Reveal Answer

Answer: B. Gastrocolic reflex


Which liver function test is MOST specific for hepatocellular damage (hepatitis)?

A. ALP

B. GGT

C. ALT (SGPT)

D. Serum albumin

Reveal Answer

Answer: C. ALT (SGPT)