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56 Cards in this Set
- Front
- Back
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most potent stimulus for meal-stimulated HCl acid secretion
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gastrin
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what receptor does gastrin bind and at what two locations
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CCK-B receptor on:
ECL cells - increase histamine synthesis and secretion Parietal cells - stimulate acid secretion |
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what produces histamine
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enterochromaffin-like (ECL) cells
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most important regulator of HCl acid secretion
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vagus nerve
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how does gastrin releasing peptide (GRP) directly and indirectly stimulate parietal cells
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directly - binds to GRP receptor on parietal cells to stimulate HCl secretion
indirectly - binds GRP receptor on G cell to increase gastrin secretion which binds CCK-B receptor on parietal cell |
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which phase does a vagotomy completely abolish
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cephalic phase - acid secretion initiated by sight, smell, taste, and thought of food
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3 Actions of somatostatin
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1. directly inhibits gastrin release by G cells
2. indirectly inhibits histamine by decreasing gastrin secretion 3. directly inhibits acid secretion by decreasing intracellular cAMP in parietal cells |
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what produces somatostatin
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antral/body D cells
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how can somatostatin act as an endocrine and paracrine hormone
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endocrine - when Free ions directly stimulate secretion by antral D cells
paracrine - when corpus (body) D cells are stimulated by neurohumoral stimuli |
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Actions of secretin
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inhibits HCl secretion by decreasing G cell gastrin release
increases somatostatin release |
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what produces secretin
what activates secretin production |
release from duodenal S cell in response to decreased intestinal pH
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where is gastric HCl and HCO3 derived from
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CO2, combines with H20 and forms H and HCO3 via carbonic anhydrase.
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what happens to the blood pH following a meal
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alkalizes due to HCO3 getting returned to the blood for every H secreted in the parietal cell
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4 receptors and second messanger system for gastric acid secretion by parietal cell
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1. CCK-B receptor binds gastrin and increases IP3 and DAG leading to increased intracellular Ca
2. H2 receptor binds histamine which increases adenyl cyclase and cAMP 3. M3 muscarinic receptor binds ACh which increases IP3 and DAG 4. GRP receptor binds GRP causing increased IP3 and DAG |
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pre-epithelial protective mechanism
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mucus layer that allows little diffusion and contains HCO3 to counteract the pepsin
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epithelial protective mechanism
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tight junctions and cellular restitution to replace damaged cells
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sub-epithelial protective mechanism
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regulated by PGE2 and NO:
increased blood flow, increased mucus secretion, stimulates HCO3 secretion, inhibits HCl secretion by parietal cells (PGE2) |
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how does CagA+ H. pylori disrupt the gastric mucosal protective mechanism
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protease - alters the viscosity and permeability of the mucus barrier
cytotoxin - disrupts the tight junctions between adjacent epithelial cells and allow back diffusion of H ion |
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how does chronic NSAID therapy disrupt gastric mucosal protective mechanism
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decreases COX activity to decrease PGE2 synthesis. Leads to thinning of mucus layer, decreased HCO3 secretion, and decreased blood flow
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3 phenotypes of H. pylori infection and types of disease produced
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1. mild pangastritis - usually asymptomatic with no disruption of acid secretion
2. antral-predominant - increased gastrin and acid secretory predisposing them to ulcers 3. corpus-predominant - gastric atrophy with decreased gastric acid production, predisposes them to gastric ulcers and adenocarcinoma |
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patient presents with dyspepsia, awakens at night, and pain is relieved within minutes of food ingestion
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peptic duodenal ulcer
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patient presents with dyspepsia that worsens upon eating, they have nausea, vomiting, and weight loss
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peptic gastric ulcer
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how does antral infection with H. pylori lead to peptic duodenal ulcer
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H. pylori destroys somatostatin producing D cells, increases gastrin production by G cells, and increases histamine production by ECL cells. Hypergastrinemia increases number of parietal cells leading to gastric metaplasia of duodenum where H. pylori can thrive
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How doe H. pylori activate inflammation
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tirggers epithelial cells to secrete IL-8 which recruits and activates neutrophils
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how does corpus infection with H. pylori lead to peptic gastric ulcer
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organism penetrates the mucus layer and alters the mucus secretion and epithelial layer leading to self-digestion of epithelial cells. hypersecretion of acid is not necessary for this process to occur
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which H. pylori associated ulcer is hypersecretion of acid necessary
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antral-predominant - hypersecretion of acid causes gastric metaplasia of duodenum
corpus-predominant - causes ulcer via normal acid secretion in an area with compromised mucus layer |
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what are the virulence factors of H. pylori
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urease - buffers HCl
catalase - neutralizes H2O2 |
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3 complications associated with peptic ulcer disease and location of each
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bleeding - posterior duodenum
perforation - anterior duodenum ulcer penetration - posterior duodenum |
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rate of acid secretion seen in:
duodenal peptic ulcer gastric peptic ulcer gastric carcinoma |
duodenal ulcer - high acid secretion due to hypergastrinemia
gastric ulcer - low acid secretion due to gastric atrophy gastric carcinoma - associated with achlorhydria (very low acid secretion) |
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3 conditions associated with elevated gastrin levels
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gastrinoma
peptic ulcers gastric carcinoma |
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signs that point to gastrinoma present
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plasma gastrin concentration > 200 pg/mL
basal acid secretory rate > 15 mmol/hr ulcers with diarrhea multiple ulcers develop simultaneously |
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what electrolyte abnormalities develop from nasogastric suctioning or persistent vomiting
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leads to loss of HCl and K causing hypokalemic metabolic alkalosis. the intravascular depletion further worsen this by activating RAAS
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what two things are responsible for preventing reflux of gastric contents into the lower esophagus
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LES
diaphragmatic crux |
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what pathophysiologic mechanisms lead to mild and severe forms of GE reflux disease
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transient lower esophageal ralaxation, decreased LES pressure leads to mild form
anatomic disruption of GE jxn such as hiatal hernia leads to severe form |
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patient presents with chest pain, nocturnal coughing, wheezing, laryngitis
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GERD
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how you differentiate chest pain from GERD vs. angina
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acid suppression therapy with proton pump inhibitor resolves the symptoms of GERD
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three major causes for peptic ulcers
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H. pylori
chronic NSAID use gastrinoma |
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what is predominantly responsible for the cephalic phase of acid secretion
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vagal activity
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what are the three phases of acid secretion
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cephalic - initiated by sight, smell, taste, and thought of food. Mediated by ACh and GRP from vagal activity (30%)
gastric - chemical products of digestion stimulate gastrin release (60% of acid secretory response to feeding) intestinal - amino acids and peptides stimulate gastrin release from G cells in the duodenum (10%) |
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what converts pepsinogen into pepsin
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acid catalyzes this conversion
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what secretes pepsinogen
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chief cells
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what can disrupt the epithelial tight junctions and cause back leak of H ions into gastric epithelial lining
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bile agents
alcohol aspirin CagA+ H. pylori |
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mal effects of NSAIDs on the mucosal layer of the stomach
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decrease mucosal blood supply
damaged the tight junctions augments histamine-stimulated acid secretion in parietal cells increase production of oxygen-derived free radicals |
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risk factors for developing peptic duodenal ulcers
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genetic - increased number of parietal cells or concentration of pepsinogen
smoking - nicotine inhibits pancreatic bicarbonate secretion emotional stress |
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urease breath test
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ingestion of radiolabeled urea which H. pylori hydrolyzes it into NH3 and radiolabled HCO3. The radiolabeled HCO3 is absorbed into the blood and excreted as radiolabeled CO2 into the breath
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where do gastric ulcers tend to be malignant
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body/fundus
benign in the antrum |
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what contributes to mucosal tissue damage in corpus-predominant gastritis
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mucosal antibody response caused by H. pylori
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what is seen in corpus-predominant gastritis
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decreased number of parietal cells
autoimmune antibody tissue damage increased gastrin secretion reflux of duodenal contents (bile, lysolecithin, pancreatic enzymes) |
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differentiate how COX-1 and COX-2 inhibitors lead to increased prevalance of gastric peptic ulcers
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COX-1 inhibitor - decreased mucus secretion, bicarbonate secretion, and blood flow
COX - 2 inhibitor - blocks the normal inhibition of leukocyte adherence and the normal epithelial proliferation when damage occurs |
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what correlates more with ulcerogenic potention, COX-1 or COX-2
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COX-1
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associated with MEN type I
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gastrinoma (zollinger-ellison syndrome)
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what normally increases LES tone
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ACh and gastrin
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what normally decreases LES tone
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VIP
NO PGE2 |
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what aberrantly decreases LES tone
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caffeine
nicotine alcohol fatty meal |
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most common cause of severe GERD and erosive esophagitis
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combination of hypotensive LES plus and abnormal diaphragmatic sphincter
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what can trigger reactive airway disease and pulmonary fibrosis in a patient with GERD
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aspiration of refluxed material into the tracheobronchial tree
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