| Term 
 
        | What is the purpose of the mesenteric membranes? |  | Definition 
 
        | Keep the stomach in place -- lesser and greater omentums |  | 
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        | Term 
 
        | What is the anatomy of the stomach? |  | Definition 
 
        | - Cardial stomach - portion right after the stomach. Produces ONLY mucus - Fundus - raises up. Mucus, gastric acid, enzymes, and intrinsic factor
 - Body/corpus - main part - MOST amount of gastric acid, mucus, and intrinsic factor.
 - Antrum - just before pyloric. Mucus, enzymes, and the HORMONE gastrin
 - Pyloric canal- empties into duodenum, ending at the pyloric sphincter. ONLY mucus.
 ** folds called rugae, allow for expansion
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        | Term 
 
        | What parts of the stomach secrete intrinsic factor? What is it? |  | Definition 
 
        | The fundus and the body/corpus. Required for absorption of b12 |  | 
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        | Term 
 
        | What is the anatomy of gastric glands? |  | Definition 
 
        | - Chief cells - produce enzymes - Parietal cells - produce acid and intrinsic factor
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        | Term 
 
        | How large can the stomach expand to? |  | Definition 
 
        | Up to 4 L, expanded by chyme and gastric juice |  | 
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        | Term 
 
        | What provides blood flow to the stomach? |  | Definition 
 
        | Right and left gastric arteries Right and left gastropiploid arteries
 Not much nutrient absorption, what is absorbed goes to the hepatic portal vein.
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        | Term 
 
        | What are the major functions of the stomach? |  | Definition 
 
        | - Temporary storage of food - receptive relaxation through VIP, NO, CCK. MAIN FUNCTION - Mechanical breakdown of PROTEINs by HCl and pepsin
 - Mixing - formation of chyme
 - Propulsion towards intestines
 - Production of intrinsic factor
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        | Term 
 
        | How is gastric emptying controlled? |  | Definition 
 
        | - By BOTH stomach distention and duodenum - Vagal PSNS stimulation increases motility
 - Gastrin - slows emptying, signalled by proteins
 - Enterogastrones are inhibitory - CCK, Secretin, GIP
 - Duodenum has reflexes to the presence of acid, irritation, foods, and distention --> inhibition
 ** goal is to slow emptying, allow stomach to work longer.
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        | Term 
 
        | Where is acid secreted in the stomach? |  | Definition 
 
        | In the gastric lumen. Beneath that is (should be) a mucous/bicarbonate layer to protect the COLUMNAR/goblet cells of the stomach. Goblet cells produce mucus, columnar cells produce bicarb.
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        | Term 
 
        | How are parietal cells activated? |  | Definition 
 
        | Activated during meals - TV turn into microvilli and intracellular canaliculus is developed. Hydrogen/potassium ATPase pump is active. **An active parietal cell secretes acid and intrinsic factor!
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        | Term 
 
        | What secretagogues are responsible for acid release? |  | Definition 
 
        | - Ach -- on M3 receptors - act directly and indirectly by releasing histamine - GASTRIN - from G cells in antrum - directly and indirectly by histamine release
 - Histamine - from EC-like cells
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        | Term 
 
        | What are mechanisms for direct acid release from parietal cells? |  | Definition 
 
        | - Ach acts on M3 --> IP3/Calcium --> ATPase pump - Histamine acts on H2 --> cAMP/PKA --> ATPase pump
 - Gastrin acts on CCKb --> IP3/calcium --> ATPase pump
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        | Term 
 
        | What are mechanisms for indirect release of acid from parietal cells? |  | Definition 
 
        | - Ach or gastrin stimulate EC-like cells to release histamine --> histamine acts of H2 receptor of parietal cell --> cAMP/PKA and activation of ATPase pump |  | 
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        | Term 
 
        | What are the steps to the parietal cell forming HCl? |  | Definition 
 
        | - Gastrin, histamine, or Ach directly or indirectly stimulate the cell, activating the ATPase pump - carbonic acid breaks down bicarb into hydrogen ions.
 - ATPase exchanges H/K, while and exchanger brings Cl inside the cell in exchange for HCO3-
 - Chlorine and K channels exist, allowing the Cl- and K+ to leave. H+ + Cl- = ACID!
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        | Term 
 
        | What are functions of high acidity in the stomach? |  | Definition 
 
        | - KILL microorganisms present in food - Denature proteins
 - Break down plant cell walls
 - Activation of pepsinogen released from chief cells.
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        | Term 
 
        | What can inhibit secretion of acid endogenously? |  | Definition 
 
        | - Prostaglandins - from stomach. reduce cAMP - Stomatostatin - from D cells
 - Enterogastrones: Secretin (S cells), CCK (I cells), GIP (K cells), VIP (enteric nerves)
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        | Term 
 
        | How do infant chief cells differ from adult physiology? |  | Definition 
 
        | Pepsinogen is not produced - rennin is produced that breaks down only milk. |  | 
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        | Term 
 
        | What is the only function of the stomach necessary for life? |  | Definition 
 
        | Manufacture of intrinsic factor |  | 
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        | Term 
 
        | How is cobalmin handled by the stomach/small intestine? |  | Definition 
 
        | - Bound to proteins in food, released in the stomach by acid. - Parietal cells secrete intrinsic factor
 - Haptocorrin binds to B12 in the stomach, prevents degradation. Removed in the small intestine
 - In the small intestine, IF-B12 complex forms. B12 can now be absorbed.
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        | Term 
 
        | What are the 4 phases of digestion? |  | Definition 
 
        | - Cephalic phase - prepares the stomach for the arrival of food. 20% of acid secreted. Under Vagal control - Gastric phase - 60-70% of acid. Stimulation of receptors by food. PEPSIN breaks down protein. ENS and vagovagal reflexes inhibit D cell release of somatostatin
 - Intestinal phase - control rate of gastric emptying, last phase of acid release
 - Interdigestive phase
 **Acid is it's own negative feedback
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        | Term 
 
        | What are the function of Ach in the stomach? |  | Definition 
 
        | - Direct binding to parietal cell --> acid release - Binds to M3 on chief cells - pepsinogen release
 - M3 on EC-like cells - histamine release --> parietal cells
 - Bind to G cells to release gastrin --> parietal cells
 ** Ach moderates acid cleavage of pepsinogen to pepsin!
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        | Term 
 
        | What happens if acid or fat gets into the small intestine? |  | Definition 
 
        | Neural response - increase in SNS, constriction of pyloric sphincter. Decrease in PNS Release of CCK, Secretin, and GIP to slow gastric emptying.
 Enhanced digestion in the STOMACH.
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        | Term 
 
        | What do enterogastrones stimulate? |  | Definition 
 
        | - CCK (I cells) - stimulates pancreas acinar cells and gallbladder - Secretin (S cells) - stimulates pancreas duct and liver - bicarbonate and bile
 - All 3 - Inhibits stomach release of gastrin, acid, and pepsinogen.
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        | Term 
 
        | How are ghrelin levels effected by consumption of meals? |  | Definition 
 
        | - Low during consumption of meals - High during fasting
 ** stimulates GH secretion
 ** stimulates appetite
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        | Term 
 
        | How does leptin control body weight? |  | Definition 
 
        | Leptin is released from adipose, turns off appetite. **More adipose, less of an appetite.
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        | Term 
 | Definition 
 
        | Inflammation of the rugae, can be caused by H. pylori |  | 
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        | Term 
 
        | What is peptic ulcer disease? |  | Definition 
 
        | An ulcer in the GI tract that is usually acidic. - Gastric ulcer - in the stomach. Usually decreased protection in MUCOSA rather than oversecretion of acid
 - Duodenal ulcer - in duodenum. Increased parietal cells = increased acid/pepsin, increased SENSITIVITY to gastrin
 - Esophageal ulcer - in esophagus, usually caused by GERD
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        | Term 
 
        | What are the major causes of PUD? |  | Definition 
 
        | - H.Pylori - more duodenal ulcers. MOST COMMON CAUSE - Impaired mucosa - NSAIDS!, steroids, stress
 - Hypersecretion - Zollinger-ellison --> elevated gastrin release
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        | Term 
 | Definition 
 
        | A lifelong infection of a bacteria that burrows into the stomach and intestinal lining. Burrows into the antrum or duodenum to protect itself from acid. ** Production of ammonia to neutralize acid
 ** Initiation of inflammatory response --> injection of CagA --> NFkB --> release of IL-8 attracts PMNs and release of TNF and IL-1.
 ** Humoral and Cellular immune rxn leads to chronic inflammation
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        | Term 
 | Definition 
 
        | - Loss of epithelial cell fxn - mitochondria uncoupling - Inhibition of prostaglandin synthesis through COX inhibition --> decreased mucus, bicarb, and increased acid
 - increased free radicals
 - direct toxicity
 **Attraction of NEUTROPHILS promotes inflammation
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        | Term 
 
        | What is zollinger-ellison syndrome? |  | Definition 
 
        | The least common source of PUD, tumors produce excessive gastrin --> increased acid release. NO negative feedback! |  | 
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