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Anatomy and physiology of GIT. 5m. Foregut. Coeliac artery. Pharynx to duodenum. Superior mesenteric artery. Midgut. Duodenum to first 2/3 of transverse colon. Inferior mesenteric artery. Hindgut. Last 1/3 of transverse colon to upper half of anal canal. Accessory digestive organs.

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Coeliac artery

Pharynx to duodenum

Superior mesenteric artery


Duodenum to first 2/3 of transverse colon

Inferior mesenteric artery


Last 1/3 of transverse colon to upper half of anal canal

accessory digestive organs
Accessory digestive organs
  • Teeth
  • Tongue
  • Salivary glands
  • Liver
  • Gallbladder
  • Pancreas

Nerve: Ant + post gastric nerves (vagi) , sympathetic branches of thoracic trunk.

Internal circular and external longitudinal layers of muscle

1/3: voluntary

1/3: mix

1/3: smooth muscle



A: L gastric artery (from celiac trunk)

V: Portocavalanatomososes

stratified squamous non-keratinized epithelium

Lymph: Lt gastric nodes

Drain mainly to celiac lymph nodes


function oral cavity and esophagus
Function: Oral cavity and esophagus
  • Mechanical: Chew  swallow  peristalsis to stomach
  • Secretion: Saliva (lysozyme, defensins, andIgAab), amylase, lipase
  • Digestion: Carbohydrates and fat (minimal)
  • Absorption: None

Lt of midline, T11

Simple columnar

Covered by mucous layer

Cardiac orifice


Lesser curvature


Greater curvature


Rt of midline, L1 (Transpyloric plane)


Can hold up to 2-3L


Lymph: follows arteries  celiac nodes

Celiac trunk

Nerves: Celiac plexus – both sympathetic and parasympathetic

Portal vein

Pain – poorly localised

Referred – gastric ulcer – T7,T8 sensory ganglia

  • The stomach is divided into three histological regions based on the nature of the glands.
  • Cardiac region: near the opening of the oesophagus. Mucus-secreting cells. Protects the oesophagus against gastric reflux.
  • Fundic region: long glands, narrow neck and a short, wider base.
    • Cell types found
    • Mucous neck cells
    • Parietal (oxyntic) cells: HCL and intrinsic factor (B12).
    • Chief cells: pepsinogen and a weak lipase
    • Enteroendocrine cells: more prevalent near the base. Secrete products into lamina propria where it is taken up by blood vessels. Secretes gastrin – stimulates production of HCL.
  • Pyloric region: mucous
function stomach
Function: Stomach
  • Mechanical: mixing and propulsion
  • Secretion:
    • Parietal cells: HCl
    • Chief cells: Pepsinogen and lipase
    • Surface mucus cells: Mucus and HCO-3
    • G cells: Gastrin
    • ECL cells: Histamine
  • Digestion: Proteins and fats
  • Absorption: Lipid soluble (alcohol, aspirin etc)

Coeliac art

Sup mesenteric art

Lymph: Coeliac+ Sup mesenteric nodes

Through mesentry, forming arcades

Nerve: Coeliac + sup mesenteric plexus

small intestine epithelium
Small intestine epithelium
  • Villi covered by simple columnar epithelium
  • Intestinal glands
  • Enterocytes (absorptive cell)
  • Goblet cells: mucus secreting
  • Paneth cells: regulate intestinal flora
  • Enteroendocrine cells: CCK, secretin (bicarb), GIP (gastric inhibitory peptide- inhibits gastric acid)
function small intestine
Function: Small intestine
  • M: Mixing – enzymes from pancreas and liver; propulsion – segmentation.
  • S:
    • Goblet cells: Mucus
    • Hormones: CCK, Secretin, GIP
  • D: Carbohydrates, fats, protein and nucleic acids.
  • A: Peptides by active transport; amino acids, glucose and fructose by secondary active transport; fats by simple diffusion; water by osmosis; ions, minerals and vitamins by active transport

sup mesenteric nodes.

Sup mesenteric nerve plexus

infmesenteric nodes.

Inf mesenteric plexus:

Sympathetic (lumbar splanchnic nerves)

Parasympathetic S2-S4

function large intestine
Function: Large intestine
  • M: Segmental mixing; propulsion – mass movement.
  • S: mucus by goblet cells.
  • D: None.
  • A: Ions, water, minerals, vitamins produced by bacteria.
physiology of absorption carbohydrate
Physiology of absorption: Carbohydrate
  • Glucose rapidly absorbed before terminal part of ileum.
  • Transport affected by Na+ in intestinal lumen  sodium-dependent glucose cotransporter.
    • Secondary active transport
    • Congenital defective – glucose/galactosemalabsorption (severe diarrhoea)
  • Fructose different mech, independent of Na+.
  • Insulin little effect on sugar absorption in intestine  not depressed during DM.
physiology of absorption protein
Physiology of absorption: Protein
  • 7 diff syst for amino acids: 3  Na+ dependent, 2  Na+ & Cl-dependent.
  • Di/tripeptides H + dependent.
  • Hartnup disease: defect in AA absorption from intestine and tubules in the kidneys.
  • Cystinuria: inadequate reabsorption of cystine in PCT of kidneys.
  • Infants: undigested proteins absorbed  maternal IgA by transcytosis.
    • Adults: causes allergies.
  • Absorption of antigen by microfold (M) cells  transport to Peyer’s patches, lymphocytes activated.
physiology of absorption lipid
Physiology of absorption: Lipid
  • Passive diffusion  esterified.
  • Uptake of bile salts by jejunal mucosa low  form new micelles.
  • Process not fully matured in infants  fail to absorb 10-15% of ingested fat.
    • More susceptible to fat malabsorption diseases.
  • Cholesterol: needs bile, fatty acids and pancreatic juice.
    • Sterols of plant origin poorly absorbed  compete with cholesterol and reduce cholesterol absorption.
physiology of absorption water and electrolytes
Physiology of absorption: water and electrolytes.
  • 98% of fluid reabsorbed,~200mL excreted in stool.
    • Mainly in small and large intestine.
  • Na+ diffuses across small intestine through gradient; basolateral surface has Na+-K+ATPase actively absorbed.
  • Cl-  enterocytes via Na+-K+-2Cl-cotransporters  secreted via channels.
    • Cholera bacillus: increased Cl- secretion, reduced Na+ absorption.
  • Glucose / cereal containing carbs (tx of diarrhoea).
physiology of absorption water and electrolytes1
Physiology of absorption: water and electrolytes.
  • Jejunum – osmolality of content close to that of plasma  absorption of osmotically active particles.
  • Saline cathartics (Mg2+ sulfates)  poorly absorbed salts, increase intestinal volume  laxatives.
  • K+ secreted into intestinal lumen as mucus. H+-K+ATPase in distal colon reabsorbs.
    • Loss of ileal or colonic fluid (diarrhoea) can lead to severe hypokalaemia.