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Harvard MIT Division of Health Sciences and Technology HST 121 Gastroenterology Fall 2005 Instructors Dr Martin Carey Dr Raymond Chung Dr Daniel Chung and Dr Jonathan Glickman November 2005 HST 121 Gastrointestinal Pathophysiology Midterm Review Topics 5 0 Section 1 Overview of Embryology Glickman Important embryologic abnormalities Esophageal atresias Congenital pyloric stenosis non bilious projectile vomiting in month old infant Duodenal atresia affects premature Trisomy 21 infants more than normal Annular pancreas duodenal obstruction in infancy pancreatitis malignancy in adulthood Omphaloceles umbilical hernias gastroschisis MIDgut abn Ileal diverticulum Meckel s A portion of the bowel along the Ileum that may be left over from development More common in males the rule of 2 s 2 in length 2 from ileocecal valve 2 of population most Sx before 2 years old Volvulus Anorectal anomalies Hirschsprung s disease dilation of proximal colon due to narrowing increased luminal pressure in distal colon due to absence of autonomic ganglion cells in distal colon the most common cause of neonatal colonic obstruction Remember your pathology anatomy Layers of digestive tract wall epithelium lamina propria muscularis mucosae submucosa muscularis propria adventitia serosa Extrinsic nervous systems Parasympathetic usually EXCITATORY leads to smooth muscle contraction vasodilation secretion of enzymes pepsin etc SLUDGE salivation lacrimation urination defectaion GI upset and emesis symptoms if parasympathetic over stimulation Vagus nerve to upper large intestine pelvic nerve Sympathetic usually INHIBITARY Inhibits smooth muscle contraction and causes vasoconstriction Enteric Intrinsic nervous systems Auerbach s aka myenteric plexus between two layers of muscularis propria primarily controls motility of GI smooth muscle Meissner s in submucosa primarily controls secretion and blood flow Blood supply in via celiac to duodenum SMA from duodenum to proximal 1 3 of transverse colon IMA from there to the rectum out via portal vein to liver Section 2 Overview of Physiology Glickman How is the function of the GI tract reflected in its structure A simple understanding of the overall structure function specialization of the GI tract will help you reason through some of the pathophysiological derangements encountered later in the course Things to know and that underlie much of your understanding of the later material What are the four layers of the prototypical wall of the GI tract Do know the four major GI hormones Gastrin CCK Secretin think of it as the counter hormone of Gastrin and GIP Think about the functions of the GI tract and how they are necessary for organismal survival 2 Section 3 Gastroduodenal Pathophysiology Strate Acid Secretion The Parietal Cell Why do we need acid in our stomachs to convert pepsinogens to pepsins which digest 15 of dietary protein prepare iron for absorption prevent bacterial overgrowth activate gastric lipase What happens if there too much too little acid production How can the former be treated pharmacologically and what is its role in peptic and duodenal ulcer disease How does the parietal cell secrete acid Increased cAMP and Ca stimulate the parietal cell tubulovesicles fuse with secretory canaliculus and H K ATPase proton pump is activated to secrete H into lumen secreted in circadian pattern higher in evening basal level regulated by vagal tone and local histamine Parietal cell regulation from inside out and the pharmacologic targets in treating PUD 1 How to acid secretion a Histamine paracrine stimulation H2 receptor is linked to Gs which stimulates adenylate cyclase increasing cAMP Histamine release also stimulated by acetylcholine b Gastrin endocrine stimulation and acetylcholine receptor and acetylcholine receptor M3 are linked to Gp which stimulates phospholipase C PLC leading to increased Ca 2 How to acid secretion a Somatostatin and prostaglandins E are linked to Gi which inhibits adenylate cyclase decreasing cAMP b Secretin also decreases acid production through not entirely clear mechanism 3 Histamine is the dominant controller of acid secretion Contro l of Ac i d Secret i on Histamine Rs Gs AC ATP SS PGE Gastrin ACH Ri R Gi Gp GTP Pertuss is Tox in PIP 2 IP 3 Ca cAMP PLC Ca H Figure by MIT OCW Mucosal Integrity a balance between protective and damaging factors Protective factors Bicarbonate mucus secretion by surface foveolar cells stimulated by luminal acid cholinergic vagal 3 stimulation and prostaglandins Bicarbonate is decreased by histamine anoxia NSAIDs bile salts Mucus is decreased by aspirin NSAIDs ethanol bile salts Blood flow brings bicarbonate growth hormones like EGF FGF which help stimulate quick epithelial renewal Prostaglandins and nitric oxide stimulate mucus bicarbonate secretion increase blood flow and inhibit acid secretion Rapid epithelial cell renewal Injurious factors which damage the protective barrier Main physiological one is acid Pepsin Aspirin and other NSAIDs damage cell directly and indirectly by blocking the good prostaglandins as well as the bad ones responsible for inflammation Cox 1 PGHS 1 begins pathway leading from arachidonic acid to cytoprotective prostaglandins Cox 2 PGHS 2 leads from AA to inflammatory mediators Can lead to peptic ulcers treat by stopping NSAID or by giving misoprostol synthetic prostaglandin H2 blocker ranitidine proton pump inhibitor omeprazole Cigarette smoking Bile acids activated pancreatic enzymes Duodenal physiology brief discussion Main histologic features Tall columnar absorptive epithelium with microvili Crypts with stem cells for epithelium and Paneth cells immunological function at base Mucus secretion by goblet cells and Brunner s glands in submucosa I cells also in jejunum secrete CCK S cells secrete secretin Peptic Ulcer Disease can present in stomach or duodenum Risk factors include the injurious factors listed above plus chronic renal lung liver disease 10 lifetime risk in US population not all symptomatic H pylori is associated with 90 of peptic ulcers H pylori causes chronic superficial gastritis which may progress to chronic atrophic gastritis and gastric adenocarcinoma chronic infection also associated with MALT lymphoma 1 Drugs to treat H pylori use a combination of bismuth antibiotics proton pump inhibitor Trivia MALT lymphoma probably the only cancer curable with antibiotics most cases recede after the eradication of H pylori The rest treated with XRT 2 To reduce acid Antacids


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MIT HST 121 - Midterm Review Topics

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