Gastrointestinal Physiology

Question 1

Describe the role of the mouth, saliva, oesophagus, stomach, small and large intestines in digestion and the absorption of food.

Answer 1

Mouth

Mechanical digestion: Chewing increases surface area.
Saliva:
Contains amylase (starch breakdown), lipase (minor role), mucins for lubrication, and lysozyme for antimicrobial defense.
pH ~6.8; begins carbohydrate digestion.

Oesophagus

Transports food from mouth to stomach via peristalsis.
No digestive enzymes secreted.

Stomach

Mechanical churning mixes food with gastric secretions → chyme.
Parietal cells secrete HCl (kills microbes, denatures proteins).
Chief cells release pepsinogen → pepsin (protein digestion).
Mucous cells secrete protective mucus.
Minimal absorption (except alcohol, aspirin).

Small Intestine

Main site of digestion and absorption.
Duodenum: Receives chyme, bile, and pancreatic enzymes.
Jejunum: Absorbs nutrients (carbs, proteins, lipids).
Ileum: Absorbs bile salts, vitamin B12.
Villi and microvilli increase surface area.

Large Intestine (Colon)

Absorbs water, electrolytes, and vitamins (especially from gut flora).
Forms and stores feces.

Question 2

Describe the physiology of underlying oesophageal motility and discuss the pathophysiology of GORD

Answer 2

Normal Oesophageal Motility

1. Coordinated peristaltic waves move bolus to stomach.
2. Lower oesophageal sphincter (LES) relaxes during swallowing and contracts afterward to prevent reflux.

Gastro-Oesophageal Reflux Disease (GORD)

Pathophysiology:

Incompetent LES → gastric contents reflux into oesophagus.

Causes:
LES hypotonia
Hiatus hernia
Increased intra-abdominal pressure (obesity, pregnancy)
Leads to mucosal damage and inflammation.

Symptoms:
Heartburn, regurgitation, dysphagia.

NICE Guidelines:

First-line: lifestyle advice (weight loss, avoid triggers).
PPIs (e.g. omeprazole): reduce acid.
Refer for endoscopy if:
Age >55 with new symptoms.
Alarming features (weight loss, dysphagia, anaemia).

Question 3

Describe the production of gastric acid & mucus secretion and the pathophysiology of gastric ulcers

Answer 3

Gastric Acid Production

Parietal cells: H⁺/K⁺-ATPase pumps secrete H⁺ into the stomach.

Stimulated by:
1. Gastrin (from G cells)
2. Histamine (from enterochromaffin-like cells)
3. Vagal stimulation (ACh)

Mucus Secretion:

Mucous neck cells produce mucus and bicarbonate → protect epithelium from acid.

Gastric Ulcers (Peptic Ulcer Disease)

Causes:

1. H. pylori infection (disrupts mucus barrier).
2. NSAIDs (reduce prostaglandin synthesis).
3. Stress, smoking, alcohol.

NICE:

1. Test and treat for H. pylori (urea breath test or stool antigen).
2. Use PPIs for acid suppression.
3. Eradicate H. pylori with triple therapy (PPI + 2 antibiotics).

Question 4

Describe the production and regulation of bile in digestion and absorption

Answer 4

Bile:

Produced by hepatocytes, stored in the gallbladder, released into duodenum.

Components:

1. Bile salts (from cholesterol): emulsify fats.
2. Bilirubin: waste from haemoglobin breakdown.
3. Water, cholesterol, phospholipids.

Regulation:

1. CCK stimulates gallbladder contraction and bile release.
2. Secretin promotes bile production.

Role:

1. Bile salts form micelles to aid fat absorption in the small intestine.
2. Reabsorbed in ileum (enterohepatic circulation).

Question 5

Outline the function of microbial flora in the alimentary tract and how pathogens can cause diarrhoea.

Answer 5

Gut Microbiota Functions:

1. Ferment undigested carbohydrates → produce SCFAs.
2. Synthesize vitamins (e.g. vitamin K, biotin).
3. Prevent colonization by pathogens (colonization resistance).
4. Modulate immune responses.

Pathogens Causing Diarrhoea:
Disrupt absorption and/or increase secretion.

Mechanisms:
1. Toxin production (e.g., cholera, E. coli): ↑ Cl⁻ secretion → osmotic water loss.
2. Invasion/inflammation (e.g., Shigella, Salmonella): mucosal damage → blood/mucus in stool.
3. Malabsorption: rotavirus → enterocyte destruction.

Question 6

Describe the mechanism behind nausea and vomiting

Answer 6

Vomiting Centre (in medulla):

1. Coordinates muscle contractions and autonomic responses.
2. Input from:
   - Chemoreceptor Trigger Zone (CTZ) in area postrema: detects toxins in blood/CSF.
   - Vestibular system (motion sickness): via histamine, ACh.
   - GI tract: vagal afferents (e.g. distension, irritation).
   - Higher centers: emotions, sights, smells.

Neurotransmitters Involved:

Dopamine (D2)
Serotonin (5-HT3)
Histamine (H1)
Acetylcholine (muscarinic)
Substance P (NK1)

Clinical Management (NICE CKS):

Antiemetics chosen based on cause:
1. Ondansetron (5-HT3 antagonist) – chemotherapy-induced.
2. Cyclizine – motion sickness.
3. Metoclopramide, domperidone – gastroparesis.