ESOPHAGEAL OBSTRUCTION - rEMERGs

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GASTRITIS ACUTE ‣ Alcohol ‣ NSAIDs ‣ Bacteria ‣ Food poisoning ‣ Stress CHRONIC ‣ Autoimmune - congenital pernicious anemia ‣ Bacteria - HP ‣ Chemical - bile relux (following Sx,EtOH) ‣ Drugs - NSAIDs ‣ Eosinophillic - eosinophillic gastroenterities ‣ Follicular - HP ‣ Granulomatous - TB, Chron’s ‣ Hypertrophic - menetrier’s dz *Chronic gastritis 10Xs more likely to get gastric Ca* MANAGEMENT ‣ Endoscopic diagnosis ‣ Management depending on condition present SUPERIOR MESENTERIC ARTERY SYNDROME ‣ ‣ SMA crosses the duodenal segment of small intestine and leads to obstruction Pain precipitated by eating HELICOBACTER PYLORI (HP) MICROBIOLOGY ‣ Gram -ve rod, spiral, flagellated, giesma +ve, urease producing ‣ Source unknown but person-person spread most likely ‣ most acquired in childhood ‣ family spread ‣ fecal-oral spread most likely ‣ Risk factors for infection are mainly low SES and age ‣ Prevalence increase w/ age (1% per year of life when >30yo); plateaus at approximately 40 -50% at > 50yo ‣ Multiple genotypes w/ virulent strains causing ulcer disease. This explains why not all individuals w/ the HP infection get ulcer disease ‣ Only 15% of infected b/c symptomatic (all have gastritis, 15% develop PUD) ‣ Lives in mucus layer ‣ a few adhere to mucosa but DO NOT penetrate mucosa
‣ urease splits urea and produces ammonia which neutralizes the acid H.PYLORIA AND HUMAN DISEASE ‣ Definite Associations ...... ‣ Gastritis: all HP infected patients have gastritis which resolves w/ HP eradication ‣ Gastric Ulcers: 90% of nonmalignant, nonNSAID ulcers are associated w/ HP; eradication prevents recurrence; nearly 100% recurrence w/o eradication ‣ Duodenal Ulcers: 95% of nonNSAID ulcers are associated w/ HP, eradication reduces recurrence to zero; failure of eradication leasds to 100% recurrence ‣ Possible Associations ...... ‣ Nonulcer dyspepsia ‣ NSAID induced gastropathy ‣ MALT (Mucosal Associated Lymphoid Tissue) lymphoma ‣ Gastric Adenocarcinoma: increase risk 9Xs ‣ Nonassociated Conditions ‣ GERD ‣ Irritable bowel syndrome ‣ Cholecystitis DIAGNOSIS ‣ Biopsy histology: gold standard ‣ Biopsy urease gel: rapid, less expensive ‣ Urea breath test: inexpensive, doesn’t detect ulcer, should not be used for initial dx, reserved for confirmation of eradication ‣ Serology: inexpensive, test of choice when endoscopy not needed, remains +ve awhile :. cannot be used to confirm eradication, false -ves: Abx, bismuth compounds, PPIs w/i last month WHO SHOULD BE TESTED? ‣ Radiologically/Endosopically confirmed gastric or duodenal ulcer —> NO testing necessary b/c it is assumed that HP is present and eradication is indicated w/o testing ‣ Confirmation of eradication is generally not necessary ‣ Confirm eradication w/ urea breath test @ 4 - 8 wks following eradication therapy if high risk (ex: previous ulcer complications or multiple medical problems) ERADICATION WITH TRIPLE THERAPY ‣ Amoxicillin (1gm bid) X 7d ‣ Clarithromycin (500mg bid) X7d **3 drugs, 2 times a day, for 1 week** ‣ Omeprazole (30mg bid) X 7d ‣ Who should be treated? (1) Recommended ..... ‣ nonmalignant, nonNSAID gastric/duodenal ulcer confirmed by radiology or endoscopy (2) Recommended by some ..... ‣ nonulcer dyspepsia (ulcer - like subgroup) ‣ strong fhx of gastric cancer
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 and 16: ‣ ‣ May present w/ Complication
Page 17 and 18: NSAID INDUCED ULCERS EPIDEMIOLOGY
Page 19: MEDICATION OPTIONS ‣ Gastric Acid

ESOPHAGEAL OBSTRUCTION - rEMERGs

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