Anatomy and physiology of GIT

1. Anatomy and physiology of GIT

2. 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

4. Accessory digestive organs • Teeth • Tongue • Salivary glands • Liver • Gallbladder • Pancreas

5. Esophagus 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 Pharynx 25cm A: L gastric artery (from celiac trunk) V: Portocavalanatomososes stratified squamous non-keratinized epithelium Lymph: Lt gastric nodes Drain mainly to celiac lymph nodes Stomach

6. 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

7. Lt of midline, T11 Simple columnar Covered by mucous layer Cardiac orifice Fundus Lesser curvature Body Greater curvature Pylorus Rt of midline, L1 (Transpyloric plane) Antrum Can hold up to 2-3L

8. 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

9. Glands • 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

10. 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)

11. Coeliac art Sup mesenteric art Lymph: Coeliac+ Sup mesenteric nodes Through mesentry, forming arcades Nerve: Coeliac + sup mesenteric plexus

12. 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)

13. 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

14. sup mesenteric nodes. Sup mesenteric nerve plexus infmesenteric nodes. Inf mesenteric plexus: Sympathetic (lumbar splanchnic nerves) Parasympathetic S2-S4

15. Function: Large intestine • M: Segmental mixing; propulsion – mass movement. • S: mucus by goblet cells. • D: None. • A: Ions, water, minerals, vitamins produced by bacteria.

16. 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.

17. 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.

18. 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.

19. 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).

20. 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.