✓GIT is the most common site of cancer development
✓10% For indigestion and 1 in 14 come for GP consultation in UK
✓Functional bowel disease affects 10-15% and IBD 1in 250 population
✓Oesophagus 25 cm from cricoid cartilage to cariac orifice of stomach having ,2 construction upper and lower has perstaltinc activity which passages food to stomach.
✓Stomach act as hopper retains and grins food then propel to small intestine
✓From G cell of stomach secreted gastrin stimulate acid sevretion,somatostatin from D cell inhibit it's actionand Ghrelin from oxyntic cell increase appetite,gastric emtying and also acid secretion.
✓Protective factor from from ulcerative property of acid and pepsin are prostaglandins,mucin and trefoil factor family peptides
✓Small bowel starts from ligament if treitz to ileocal valve which has peristaltic activity in empty stomach every 1-2 hours during fasting which increase after eating.
✓Function of small bowel include digestion of food,absorption of mineral,electrolytes,water,protection from toxins and immune regulation
✓Fat digestion include several phases that include
1.Luminal phages: where secretion of CCK from dudenum acting on GB causing contraction and relaxing Sphincter of Oddi ultimately secretion of bile.CCK also causes secretion of enzymes like amylase,protease,collipase from pancreas
2.Fat solubilization: Mixed micelle formation combining dietery fat containing cholesterol,phospholipids,fat suble vitamins and bike acid and salts.
3.Digestion: By pancreatic lipase and cofactor collipase triglycerides to monoglyceride and fatty acid
4. Absorption: When micerle comes to the brush border of enterocyte fat soluble vitamins, cholesterol,phospholipids,short chain fatty acids absorbed directly where as long chain fatty acid binds with protein and absorbed.Bile salts remain in the lumen and enter into enterohepatic circulation
5.Re estirification and chylomicrons formation:In the enterocyte fatty acid resterified to form triglycerides.Triglycerides,other fats,appoproteins together form chylomicrons.
6.Transport:By exocytosis chylomicrons leaves the enterocytes,enters into the mesenteric lymphatics,then to thoracic duct and ultimately to systemic circulation
✓Carbohyrate starch by pancreatic to and salivary hydrolyzed forming alfadextrin,maltose,maltotriose.Disaccharides by microvillus membrane enzyme converted to form monosaccharides,galactose,fructose and glucose.Fructose enters the cell by simple diffusion but glucose and galactose enter by engery requiring processs.
✓Protein digestion starts by gastric pepsin though minor contribution but it stimulate CCK secretion which stimulate pancreases to sevrtete protease enzyme such as trypsinogen, chymotrypsinogen, pro-elastases and procarboxypeptidases.Trypsinogen in the small intestine by enterokinase converted to Trypsin which further activate other enzymes.Action these enzymes form peptides,amino acid Peptde in the cell by peptidase enzyme converted to amino acid and amino acid finally actively transported to portal circulation through basal border of enterocytes.
✓Control of acid secretion: Gastrin released from antral G cells in response to food (protein) binds to cholecystokinin receptors (CCK-2R) on the surface of enterochromaffin-like (ECL) cells, which in turn release histamine. The histamine binds to H2 receptors on parietal cells and this leads to secretion of hydrogen ions in exchange for potassium ions at the apical membrane. Parietal cells also express CCK-2R and it is thought that activation of these receptors by gastrin is involved in regulatory proliferation of parietal cells. Cholinergic (vagal) activity and gastric distension also stimulate acid secretion; somatostatin, vasoactive intestinal polypeptide (VIP) and gastric inhibitory polypeptide (GIP) may inhibi it.
Reference:
El-Oar E, McLeam MH..Gastroenterology.In.Ralston SH,Penman ID,Strachen MW, Hobson RP.Davidson's principles & practice of medicine.23rd edition.Elsevier.Elssevier Ltd.2018.p.764-769
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