ESOPHAGEAL OBSTRUCTION - rEMERGs

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GASTRIC ULCERS EPIDEMIOLOGY ‣ Incidence peaks in 50s (10yrs later than DU) ‣ Incidence NOT decreasing ‣ 3 males: 2 females ‣ Less common clinically than DU ‣ Increase risk of Ca (1/200): Must R/O Ca ETIOLOGY ‣ 80% associated w/ HP ‣ 15% associated w/ NSAIDs ‣ 5% other: stress, ischemia, infections, ZES PATHOLOGY ‣ Imbalance b/w protective and damaging factors ‣ Interplay b/w HP, drugs, smoking, alcohol, caffeine, stress, ‣ Pathophysiological Characteristics ‣ Normal or reduced acid secretion rates ‣ NOT associated w/ hypergastrinemia or hyperchloremia ‣ Decreased parietal cell mass ‣ Decreased pyloric sphincter pressure (in response to acid , secretin, fat, and CCK in duo) leading to increased duogastric reflux thus increased bile acids and pancreatic enzymes in stomach (bile + Hcl very damaging) ‣ Location ‣ Majority found at fundic-antral junction on lesser curvature ‣ Ulcers on greater curvature and cardia are more likely to be Ca CLINICAL FEATURES ‣ Pain ‣ Epigastric pain is MC symptom but the pattern is less characteristic ‣ Less consistent relief w/ food or antacids ‣ N+V may occur in absence of gastric outlet obstruction ‣ May present with complications ‣ Hemorrhage ‣ Gastric outlet obstruction DIAGNOSIS ‣ UGI series: note that NSAID induced ulcers are often too superficial to be seen and cannot dx benign vs malignant ‣ Endoscopy: must be done to R/O Ca, important to determine in HP is present TREATMENT ‣ Lifestyle ‣ Eradication triple therapy + Maintenance therapy ‣ D/C NSAIDs
NSAID INDUCED ULCERS EPIDEMIOLOGY ‣ Cause 15% of gastric ulcers ‣ Cause 7% of duodenal ulcers ‣ Cause gastric mucosal petechieae in virtually all, erosions in most, and ulcers in some (2% with symptomatic ulcers/complications) PATHOGENESIS ‣ Local effect: non-ionized drug (HA) in stomach acid can enter gastric epithelial cell ‣ Systemic effect: absorption into blood, distribution to stomach epithelial cells (note some systemic effects required for ulcer formation; reason why enteric coated can still cause ulcers) ‣ Common pathway: inhibition of cyclo-oxygenase and inhibition of PG synthesis which results in decreased mucus production, decreases mucosal blood flow, decreased HCO3 production, and decreased cell healing ‣ Selective COX-2 inhibitors selectively block COX-2 (joints) > COX -1 (stomach) ‣ Predisposing factors ‣ Age ‣ Previous PUD ‣ High dose NSAID ‣ Corticosteroid use ‣ Severe medical conditions MANAGEMENT ‣ D/C NSAIDs ‣ Misoprostol ‣ Evaluate for H. pylori ‣ Acid reduction: H2 antagonist or PPI Stress Ulcerations ‣ Mostly ICU patients ‣ Stomach (fundus) most common ‣ Usually only recognized by UGI bleeding ‣ Pathogenesis?: ishcemia, hypersecretion of acid especially in CNS diseaase (“Cushing’s ulcers”) ‣ Prophylaxis decreases ulcers but increases pneumonia: ‣ Treatment same as for bleeding peptic ulcers Risk Factors: Mechanical ventilation, multiorgan failure, septic, severe surgery/trauma, CNS insult, burns > 35% BSA.
Page 1 and 2: ESOPHAGEAL OBSTRUCTION ANATOMY ‣
Page 3 and 4: ESOPHAGEAL PERFORATION INTRODUCTION
Page 5 and 6: DYSPHAGIA DEFINITIONS ‣ Dysphagia
Page 7 and 8: INVESTIGATIONS ‣ Neck Xrays: look
Page 9 and 10: ‣ Resp Complications: recurrent c
Page 11 and 12: GASTROESOPHAGEAL REFLUX DISEASE Int
Page 13 and 14: ABDO PAIN: GASTRIC OR DUODENAL ORIG
Page 15: ‣ ‣ May present w/ Complication
Page 19 and 20: MEDICATION OPTIONS ‣ Gastric Acid
Page 21 and 22: ‣ urease splits urea and produces

ESOPHAGEAL OBSTRUCTION - rEMERGs

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