Download Anat n phys of GIT

Anatomy and physiology of GIT
5m
Foregut
Coeliac artery
Pharynx to duodenum
Midgut
Superior
mesenteric artery
Duodenum to first 2/3 of transverse colon
Hindgut
Inferior
mesenteric artery
Last 1/3 of transverse colon to upper half of anal canal
Accessory digestive organs
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Teeth
Tongue
Salivary glands
Liver
Gallbladder
Pancreas
Nerve: Ant + post
gastric nerves
(vagi) ,
sympathetic
branches of
thoracic trunk.
Esophagus
Pharynx
25cm
A: L gastric artery (from celiac
trunk)
V: Portocaval anatomososes
Lymph: Lt gastric
nodes
Drain mainly to celiac
lymph nodes
Internal circular and
external longitudinal layers
of muscle
1/3: voluntary
1/3: mix
1/3: smooth muscle
stratified squamous
non-keratinized
epithelium
Stomach
Function: Oral cavity and esophagus
• Mechanical: Chew  swallow  peristalsis to
stomach
• Secretion: Saliva (lysozyme, defensins, and
IgA ab), amylase, lipase
• Digestion: Carbohydrates and fat (minimal)
• Absorption: None
Lt of midline, T11
Cardiac
orifice
Lesser
curvature
Fundus
Body
Simple columnar
Covered by mucous layer
Greater
curvature
Pylorus
Rt of midline, L1
(Transpyloric plane)
Antrum
Can hold up to
2-3L
Celiac trunk
Lymph: follows
arteries 
celiac nodes
Nerves: Celiac
plexus – both
sympathetic and
parasympathetic
Portal vein
Pain – poorly localised
Referred – gastric ulcer –
T7,T8 sensory ganglia
Glands
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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
• 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
Nerve: Coeliac +
sup mesenteric
plexus
Through
mesentry,
forming arcades
Small intestine epithelium
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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
• 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
nerve plexus
sup mesenteric
nodes.
inf mesenteric
nodes.
Inf mesenteric
plexus:
Sympathetic
(lumbar splanchnic
nerves)
Parasympathetic
S2-S4
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
• 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/galactose
malabsorption (severe diarrhoea)
• Fructose different mech, independent of Na+.
• Insulin little effect on sugar absorption in
intestine  not depressed during DM.
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
• 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.
• 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
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.