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37 Cards in this Set
- Front
- Back
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Gastrin |
1- G cells (antrum of stomach, duodenum) 2- Action 1- Increase gastric H secretion 2- Increase growth of gastric mucosa 3- Increase gastric motility 3- Regulation 1- Stomach distention/alkalization, amino acid, peptides, vagal stimulation via Gastrin releasing peptide (GRP) 2- decrease pH <1.5 4- Nots 1- Increase in chronic PPI use, chronic strophic gastritis (H. Pylori) and Zollinger Ellison syndrome |
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Somatostatin |
1- D cells (pancreas and GI mucosa) 2- Action 1- Decrease acid and Pepsinogen secretion 2- Decrease pancreatic and small intestine fluid secretion 3- Decrease gallbladder contraction 4- Decrease insulin and glucagon release 3- Regulation 1- Increase by acid 2- Decrease by vagal stimulation 4- Notes 1- Inhibits secretion of various hormones 2- Octreotide is an analog used to treat acromegaly, carcinoid syndrome and varicella bleeding |
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Cholecystokinin |
1- I cells (duodenum, jejunum) 2- Action 1- Increase pancreatic secretion 2- Gallbladder contraction 3- Decrease gastric emptying 4- Increase sphincter of oddi relaxation 3- Regulation 1- increase by fatty acids, amino acids 4- Acts on neural Muscarinic pathways to cause pancreatic secretion |
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Secretin |
1- S cells (duodenum) 2- Action 1- Increase pancreatic HCO secretion 2- Decrease gastric acid secretion 3- Increase bile secretion 3- Regulation 1- Increase by acid, fatty acid on lumen of duodenum 4- Increase HCO neutralizes gastric acid in duodenum, allowing pancreatic enzymes to function |
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Glucose dependent insulinotropic peptide |
1- K cells (duodenum, jejunum) 2- Action 1- Exocrine - decrease gastric H secretion 2- Endocrine - increase insulin release 3- Regulation 1- Increase by fatty acids, amino acids oral glucose 4- Also called gastric inhibitory peptide (GIP) 2- Oral glucose load increase insulin compared to IV equivalent due to GIP secretion |
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Motility |
1- Small intestine 2- Action- Produced migrating motor complexes 3- Regulation 1- Increase in fasting state 4- Motilin receptors against (eg erythromycin) are used to stimulate intestinal peristalsis |
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Vasoactive intestinal polypeptide |
1- Parasympathetic ganglia in sphincters, gallbladder, small intestine 2- Action 1- Increase intestinal water and electrolyte secretion 2- Increase relaxation of intestinal smooth muscle and sphincter 3- Regulation 1- Increase by distention and vagal stimulation 2- Decrease by adrenergic input 3- VIPoma- non alpha, non beta islet call pancreatic tumor that secrets VIP, associated with watery diarrheal, Hypokalemia, Achlorhydria |
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Nitric oxide |
1- Action 1- Increase smooth muscle relaxation, including lower esophageal sphincter 2- loss of NO secretion is implicated in increase LES time of Ach Alaska |
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Ghrelin |
1- Stomach 2- Action 1- Increase appetite 3- Regulation 1- Increase in fasting state 2- Decrease by food 3- Increase in Prader-Willi syndrome Decrease after gastric bypass surgery |
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Intrinsic factor |
1- Parietal cells 2- Action 1- Vitamin B12 binding protein (required intrinsic factor for B12 absorption in terminal ilium) 3- Autoimmune destruction of parietal cells - chronic gastritis and pernicious anemia |
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Gastric acid |
1- Parietal cells (stomach) 2- Action - Decrease stomach pH 3- Increase by 1- Histamine 2- Vagal stimulation (Ach) 3- Gastrin Decreased by 1- GIP 2- Secretin 3- Somatostatin 4- Prostaglandin
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Pepsin |
1- Chief cells (stomach) 2- Action 1- Protein digestion 3- Regulation 1- Vagal stimulation (Ach) 2- Local acid 4- Pepsinogen (inactive) conceded to pepsin in the presence of H |
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Bicarbonate |
1- Mucosa (saliva, stomach, duodenum, pancreas) Bruner gland (duodenum) 2- Action - Neutralizes acid 3- Regulation 1- Pancreatic and gallbladder secretion with secretin 4- Trapped in mucus that covers the gastric epithelium |
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On which cells does Gastrin act |
Enterochromaffin like cells and parietal cells |
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Where are parietal cells located |
Body of the stomach |
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Where are Chris cells located |
Body of the stomach |
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Name 3 secretory cells located in the antrum of the stomach |
G cells (Gastrin) D cells (Somatostatin) Mucous cells |
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Pancreatic secretion |
Isotonic fluid Low flow- high CL High flow- high HCO |
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Alph amylase |
1- Starch digestion 2- Secreted in its active form |
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Lipase |
Fat digestion |
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Protease |
1- Protein digestion 2- Include trypsin, chymotrypsin, elastase, carboxypeptidases 3- Secreted as a proenzymes also called zymogens |
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Trypsinogen |
1- Converted to its active form trypsin - Activation of other pro enzymes and cleavage of additional trypsinogen molecules to active trypsin (Positive feedback loop) 2- Converted to trypsin by enterokinase/enteropeptidase a brush border enzymes in duodenum and jejunal mucosa |
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Carbohydrate absorption |
1- Only monosaccharides (glucose, galactose, fructose) are absorbed by enterocytes 2- Glucose and galactose are taken up by SGT1 (Na dependent) 3- Fructose take up via facilitated diffusion by GLUT5 4- All are transported to the blood by GLUT2 |
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D-xylose absorption test |
1- Simple sugars require an intact mucosa for absorption but does not require digestive enzymes 2- Helps to distinguish GI mucosal damage from other causes of malabsorption |
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Where are GLUT located |
Apical - GLUT5 and SGLT1 Basolateral- GLUT2 |
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Vitamin and mineral absorption |
1- Iron 1- Absorbed as Fe2+ 2- Absorbed in duodenum 2- Folate - Absorbed in jejunum 3- Vitamin B12- Absorbed in terminal ileum as well as bile require intrinsic factor |
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How is iron stored in the liver |
Ferritin |
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What molecule binds iron and allows it to travel through blood |
Transferrin |
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What molecule provides negative feedback on ferroportin-1, thereby preventing release of iron into the bloodstream |
Hepcidin |
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Peyer patches |
1- Unencapsulated lymphoid tissues in the lamina propria and submucosa of the ilium 2- Contain specialized M cells that sample and present antigen to the immune system 3- B cells stimulated in the germinal center of the Peyer patches differentiate into IgA secreting plasma cells with inch resides in lamina propria 4- IgA receive proctective secretory component that move across epithelium into the gut to deal with intraluminal antigens |
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Bile |
1- Composed of 1- Bile salt ( conjugated to glycine or tourine making them water soluble) 2- Phospholipid 3- Cholesterol 4- Bilirubin 5- Iron 6- Water 2- Cholesterol 7alpha hydroxylase catalyzed the rate limiting steps for bile acid synthesis 3- Decrease normal absorption of bile in terminal ileum prevents normal fat absorption- steatorrhea 4- Calcium which normally binds to oxelate now binds to fat and free oxalate is absorbed by the gut - increase frequency of calcium oculars kidney stones |
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Function of bile |
1- Antimicrobial activities (via membrane disruption) 2- Cholesterol excretion (body’s 1’ source of eliminating cholesterol) 3- Digestion and absorption of lipid and fat soul ale vitamin |
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Bilirubin |
1- Unconjugated bilirubin is removed from the blood by the liver 2- Conjugated with gluconate and excreted in bile 3- Direct bilirubin - Conjucayed with glucuronic acid, water soluble 4- Indirect bilirubin- unconjugated , water insoluble 5- Heme (Heme oxidase)— biliverdin (biliverdin reductase)— unconjugated bilirubin (glucuronate)— conjugated bilirubin |
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What enzyme catalyzes bilirubin conjugation |
UDP- glucuronosyltransferase |
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Of the 20% urobilinogen that goes to the kidney how much enters the enterohepatic circulation Nx how much is excreted renally |
90% enters enterohepatic circulation 10% excreted as urobilin in urine (produce yellow color) via kidney |
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How much of urobilinogen is excreted as steric oil in in Feces |
80% as stercobilin, giving stool it’s brown color |
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What are the 3 fates of urobilinogen |
1- Excreted in Feces 2- Excreted in urine via kidney 3- Recycles via enterohepatic circulation |
