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PY4.1-12 | Gastro-intestinal Physiology — Part 4

Gut-Brain Axis (PY4.10)

The Gut-Brain Axis is a bidirectional communication network between the gastrointestinal tract and the central nervous system. It involves three interacting systems:

Figure: Gut-Brain Axis (PY4.10)

1. Enteric Nervous System (ENS) — 500 million neurons; functions autonomously; the "gut brain"
2. Autonomic Nervous System — vagal (parasympathetic) and splanchnic (sympathetic) pathways
3. Neuroendocrine pathways — gut hormones (CCK, GLP-1, serotonin) that signal to the hypothalamus

Key pathways:
• Vagus nerve carries ~80% afferent (gut → brain) and ~20% efferent (brain → gut) signals. Most of what the brain "knows" about the gut is from afferent vagal fibres — not pain fibres (gut pain travels via sympathetic routes).
• Gut serotonin (5-HT): 95% of the body's serotonin is in the gut (enterochromaffin cells). It regulates gut motility and sends satiety signals to the brain. Low gut serotonin → constipation; high → diarrhoea. This is why SSRIs (e.g., fluoxetine) cause GI side effects.
• Gut microbiome (the "microbiota-gut-brain axis"): Gut bacteria produce short-chain fatty acids, neurotransmitter precursors (GABA, serotonin), and modulate vagal afferents. Dysbiosis (disrupted microbiome) is linked to depression, anxiety, autism spectrum disorders, and IBS.

Physiological significance:
• Explains Irritable Bowel Syndrome (IBS) — a disorder of gut-brain communication with no structural pathology: stress → altered gut motility, visceral hypersensitivity.
• Explains stress-induced gastric ulcers (Cushing's ulcer — raised ICP; Curling's ulcer — burns): stress → sympathetic dominance → mucosal ischaemia + Brunner's gland suppression.
• Hunger and satiety regulation: GLP-1 (from L cells of ileum), PYY, and CCK signal satiety to hypothalamus. GLP-1 receptor agonists (semaglutide — Ozempic) exploit this axis for obesity and type 2 diabetes management — one of the most significant drug developments of the 2020s.

Applied Physiology of GIT (PY4.11)

Peptic Ulcer Disease (PUD):
Imbalance between aggressive factors (HCl, pepsin, H. pylori toxins, NSAIDs) and defensive factors (mucus-bicarbonate barrier, prostaglandins, mucosal blood flow). H. pylori infection is present in ~70% of Indian patients with PUD (vs 30–40% in high-income countries). Treatment: PPI + antibiotics (triple/quadruple therapy).

Figure: Applied Physiology of GIT (PY4.11)

Gastro-oesophageal Reflux Disease (GERD):
Reflux of gastric contents into oesophagus due to: lower oesophageal sphincter (LOS) incompetence, hiatus hernia, increased intra-abdominal pressure (obesity, pregnancy). Symptoms: heartburn, acid regurgitation, chronic cough. Complications: oesophagitis → Barrett's oesophagus → adenocarcinoma. Treatment: lifestyle (avoid lying down after meals, elevate head end of bed) + PPIs.

Vomiting:
Protective reflex coordinated by the vomiting centre (dorsal vagal complex in medulla). Afferent triggers: chemoreceptor trigger zone (CTZ — on floor of 4th ventricle, outside blood-brain barrier, senses drugs/toxins), vestibular system, GIT distension, psychological stimuli. Efferent: reverse peristalsis, pyloric spasm, lower oesophageal sphincter relaxation, diaphragm and abdominal muscle contraction, deep inspiration, glottis closure. Complications: aspiration, dehydration, Mallory-Weiss tears, hypokalemia and alkalosis.

Diarrhoea:
>3 loose stools/day or >200g stool/day.
• Secretory: toxins stimulate active Cl⁻ secretion (cholera, ETEC) → persists with fasting
• Osmotic: unabsorbed solutes retain water (lactase deficiency, magnesium laxatives) → stops with fasting
• Inflammatory (exudative): mucosal damage, pus and blood in stool (dysentery — Shigella, amoeba)
• Malabsorptive: fat malabsorption → steatorrhoea (chronic pancreatitis, coeliac disease)

Constipation:
<3 bowel movements/week. Causes: low fibre diet, dehydration, hypothyroidism, diabetes (autonomic neuropathy), drugs (opioids, anticholinergics), colonic motility disorders.

Adynamic Ileus (Paralytic Ileus):
Absence of peristalsis without mechanical obstruction. Causes: post-operative (especially abdominal surgery), peritonitis, severe electrolyte disturbances (hypokalaemia — K⁺ is required for smooth muscle repolarisation), uraemia. Clinical: absent bowel sounds, abdominal distension, no flatus/stool. Treatment: NPO, nasogastric decompression, correct electrolytes.

Hirschsprung's Disease (Congenital Aganglionic Megacolon):
Congenital absence of ganglion cells (Auerbach's plexus) in a segment of colon (usually rectosigmoid). Due to failure of neural crest cells to migrate into the colon during development (weeks 5–12). The aganglionic segment remains in permanent spasm → functional obstruction → proximal colon dilates. Presents in neonates: failure to pass meconium within 48h, abdominal distension. Diagnosis: rectal biopsy (absent ganglion cells), barium enema (transition zone). Treatment: surgical resection of aganglionic segment.

Abdominal Examination — History and Clinical Skills (PY4.12)

PY4.12 is a skill competency (shows_how). This page provides the cognitive framework; the hands-on practice occurs in Physiology practicals with a standardised patient or mannequin.

Figure: Abdominal Examination — History and Clinical Skills (PY4.12)

Relevant History — GI System:

Chief complaint: Pain (location, onset, character, radiation, aggravating/relieving factors, severity), nausea/vomiting, bowel habits, appetite and weight changes, jaundice, dysphagia, haematemesis, melaena, haematochezia.

Pain patterns to recognise:
• Epigastric + burning + 2h post-meal, relieved by food → peptic ulcer
• Right hypochondrial colic radiating to right shoulder after fatty meal → biliary colic
• Central colicky pain → small bowel obstruction
• Left iliac fossa pain with altered bowel habits → colonic pathology

Dietary history: NSAID use (ulcers), alcohol (pancreatitis, cirrhosis), spicy food (GERD).
Drug history: Antibiotics, proton pump inhibitors, laxatives, opioids.

Clinical Examination — Abdominal:

Position: Patient supine, arms by sides, legs extended, abdomen fully exposed from xiphisternum to groin. Examiner stands on right side of patient.

Inspection (look):
• Shape: scaphoid (concave — malnutrition), distended (gas, fluid, obesity, mass)
• Umbilicus: everted (ascites), Sister Mary Joseph nodule (peritoneal metastasis)
• Skin: visible veins (caput medusae — portal hypertension; lateral → IVC obstruction), striae, scars
• Visible peristalsis (gastric outlet obstruction), pulsation

Palpation (feel):
• Light palpation first (tenderness, guarding, rigidity) — all 9 regions
• Deep palpation — organ enlargement
• Liver: palpate from right iliac fossa upward. Normal: not palpable (or <2 cm below RCM). Measure hepatomegaly in cm below right costal margin.
• Spleen: palpate from right iliac fossa toward left hypochondrium. Spleen must be 3× normal size to be palpable. Cannot get above it (unlike kidney). Moves with respiration.
• Kidneys: bimanual ballottement. Can get above and below (unlike spleen).

Percussion (tap):
• Liver dullness: right 5th intercostal space → right iliac fossa
• Splenic dullness: left 9th–11th ICS, midaxillary line
• Ascites: shifting dullness + fluid thrill (both needed for diagnosis)
• Tympanic (gas) vs dull (solid/fluid)

Auscultation (listen):
• Bowel sounds: normal (every 2–5 sec), increased (early obstruction, diarrhoea), absent (paralytic ileus, peritonitis)
• Bruits: renal artery stenosis (para-umbilical), aortic aneurysm (midline)

Special tests: Murphy's sign (cholecystitis), Rovsing's sign (appendicitis), McBurney's point tenderness, Carnett's sign (abdominal wall vs intraperitoneal pain).