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- Gastric Tumors
H. pyloricolonizes duodenum in areas of gastric metaplasia / can synergize with NSAID to create DUC / can cause iron-deficiency anemia from (erosions with blood loss and malabsorption from atrophic gastritis) Diagnosis: serology (85-95% sensitive) / positive result usually indicates active infection (if symptomatic and not already treated; serology remains positive for years after treatment) C13 urease breath test (95% sensitivity, 95% specificity) ($200) / 30% false negative if on PPI (must hold PPI 2 wks before testing, hold any antibiotics 4 wks before testing) direct urease detection from EGD biopsy specimen 90% s/s ($15) stool cultures, tissue biopsy, dental plaque? 90% s/s ($15) Differential diagnosis: non-related lymphoma, Crohn’s, GERD, bile reflux gastritis Treatment: use of NSAIDS should not alter treatment / document eradication (also reduces risk of future bleeding) / Note: H. pylori found incidentally – many would treat just to remove any future cancer risk (H. pylori is carcinogengastric lymphoma) Treatment (various preparations) (initial efficacy 90%) metronidazole + PPI + other clarithromycin + PPI + other Note: resistance to clarithromycin and metronidazole is prevalent after previously given to patient although clarithromycin resistance is more frequently implicated in subsequent treatment failure Note: elevated pH has theoretical risk of affecting IgG and MIC for certain antibiotics Recurrence: 75% untreated, 25% treated, 5% with eradication (antibody titre falls 50% by 6 months) NSAID induced ulcers very common cause of recurrent GI ulcers / may affect any portion of GI tract / dyspepsia 15% / gastric erosions / reactive gastropathy – can be differentiated from other chronic types / develop in 5% - even after just 1 week of NSAID use Risk Factors: pre-existing ulcer, higher age, females, cardiovascular disease, high dose/potency NSAID, duration of treatment, smoking, alcohol, steroids / advanced age associated with less pain (no warning symptoms), more rebleeding Prevention: use lowest possible dose, enteric coating, prophylactic adjuvant treatment / buffering appears ineffective Treatment: stop or minimize NSAID use, eradicate H. pylori if present proton pump inhibitor (work faster, NNT 6 / may be better for maintenance), prostaglandin, H2 antagonists Duodenal ulcer 90% due to H. pylori / relieved by food / triple therapy for H. pylori / double (omeprazole, clarithromycin) / NO risk of malignancy (unlike gastric H. pylori) Other Acid hypersecretory states (hypertrophic gastropathy) Mechanism: gastrin stimulates gastric acid secretion / trophic effects regulating GI mucosal-cell proliferation / G17 more potent, shorter half-life / G34 less potent, predominates Zollinger-Ellison Syndrome (ZES) gastric gland hyperplasia (gastrinoma) / hypertrophic-hypersecretory gastropathy (parietal and chief cells) / gastrinoma triangle Presentation: epigastric pain, weight loss, vomiting, severe diarrhea/malabsorption / extra pancreatic tumors Clinical: gastrinoma, pancreatic tumor, PUD with diarrhea, recurrent following surgery, FH, multifocal PUD, distal duodenal or jejunal ulcer (may occur anywhere though), rugal hypertrophy, hypercalcemia or multiple endocrine abnormalities (MEA) (¼ of cases) Diagnosis: serum gastrin level / secretin challenge causes paradoxical increase in gastrin (> 200 pg/mL; often > 1000 pg/mL) (must have 2 negatives to r/o ZES) [$200 test] / find tumor with MRI, U/S, CT, venous sampling Treatment: H2, PPI, octreotide / confined to lymph nodes resect nodes (good prognosis) Prognosis: very good if resected early / debulking also prolongs survival Gastric Carcinoma (see below) 5th most common worldwide, 10% greater than 80 yrs / may present as GI ulcer confirm findings histologically (biopsy edge)
profound hyperplasia of rugal folds (epithelial cells/glands) / middle aged men / malignant transformation / protein-losing may cause edema / linked with type A blood (less secretion/protection) Gastric Varices (see GI bleed) associated w/ esophageal varices / portal hypertension / deep location, resemble enlarged rugae Treatment: endoscopic ligation (most effective treatment), B-blockers and nitrates are less effective (but still useful as single therapy and even more so when combined with ligation) Portal Gastropathy (see GI bleed) Kassabach-Merrit Diabetic gastroparesis [NEJM] Presentation: fullness, bloating, nausea, vomiting, delayed or accelerated gastric emptying / may occur in absence of other overt diabetic complications (although usu. part of broad spectrum of autonomic dysfunction) Exacerbated by: may be worsened by acute hyperglycemia, medications (pramlintide, exenatide), calcium channel blockers, clonidine, anticholinergics (e.g. antidepressants) Diagnosis: delayed gastric emptying suggested by splashing sound on abdominal succession one hour after meal / EGD / barium swallow / scintiscanning (modified protocol with hourly scans often done; retention over 10% at 4 hours is abnormal; sensitivity 93%, specificity 62%) / CO2 breath test (sensitivity 86%, specificity 80%) Course: symptoms generally stabilize indefinitely; no increase in mortality Treatment: try dietary modifications / erythromycin or metoclopramide or domperidone (not FDA approved), cisapride (requires special authorization) / may need pain relief (antidepressants, Neurontin) / severe cases may require nutritional support including G or J-tubes (2% serious complication rate of J-tubes: bowel perforations, jejunal volvulus, major bleeding, aspiration) / gastric electrical stimulation (being developed; showing some promise 1/07) / tegaserod (5HT4 receptor antagonist) being studied Gastric TumorsGastric polyps 90% non-neoplastic / 10% gastric adenomas / sessile or pedunculated / may become carcinoma Gastric carcinomas (very bad prognosis) 1 in 40,000 / onset in 50’s / diet (early exposure most important) / geographic setting Presentation: many are asymptomatic or fullness/anorexia (1st) or steady RUQ pain +/- anorexia, nausea, weight loss, iron deficiency anemia, B12 deficiency? / N/V pylorus, dysphagia cardiac / upper GI bleeding (hematemesis or melena) Risk factors: pernicious anemia, chronic atrophic gastritis Associations: migratory thrombophlebitis, microangiopathic hemolytic anemia, acanthosis nigricans Pathology: lesser curvature, antropyloric / exophytic, flat, excavated / invasion most important factor linitis plastica (diffuse, leather bottle appearance) Location: 30% distal / 20% mid / 40% proximal / 10% total / ovary mets (a.k.a. Krukenberg tumors) Method of Spread: direct, lymphatic (supraclavicular, L>R, Virchow’s node), hematologic Prognosis: very bad unless tumor is limited to submucosa/submucosa 80% survival (so get biopsy on all ulcers) intestinal diminishing in frequency in U.S. (may change with use of H2-blockers) / chronic gastritis / gastric adenoma / antrum, lesser curvature / expanding growth pattern / fungated, ulcerated diffuse prevalence unchanging in U.S. / younger onset / infiltrative growth pattern worse prognosis / signet-ring appearance, linitis plastica / mucin lakes reactive fibrosis Treatment: resection radiation only palliative taxol + radiation under investigation for advanced gastroesophageal CA post-op radiation + chemo under investigation as is pre-op (to increase respectability)
average – 10% 5 yr survival Gastric lymphomas (good prognosis) MALT/B-cell or high grade/large cell / hard to distinguish clinically from gastric carcinoma / associated with H. pylori Diagnosis: gastric biopsy to look for H. pylori and tissue histology (make sure gastric biopsy is deep enough!) Treatment: 2 wks antibiotics for H. pylori, recheck breath test; if (-) observe for improvement (usu. by 2-18 months, 75% regress by 6 months, longest 2 yrs) and follow-up any gastric lesions with EGD or U/S; if no improvement, rebiopsy; if more aggressive histology seen, consider combination chemotherapy (50% cure rate) Other gastric tumors gastric sarcoma neuroendocrine cell (carcinoid) tumors mesenchymal (stromal, lipomas, neurofibromas) breast and lung mets may cause linitis plastica Trends: gastric bypass surgery more effective than nonsurgical treatments for morbid obesity (BMI > 40 kg/m2) Small and Large Intestine Causes of intestinal hyperpermeability: celiac sprue, IBD (CD>UC), Trauma/Burns/Sepsis, other (chemotherapy, diabetes, schizophrenia, sarcoidosis, cystic fibrosis, major surgical operations) Labs: increased lactulose/mannitol ratio (small molecules absorbed less, larger molecules absorbed more) Vascular GI Disorders Gastroesophageal Varices [NEJM] 40-60% of patients with cirrhosis / 33% will bleed Ddx: gastric varices may occur from splenic venous thrombosis (consider in non-cirrhotics)
somatostatin or octreotide are effective in 80% of cases, mechanism unclear, reduces GI blood flow, side effects include hyperglycemia, abdominal cramping / vasopressin as continuous IV infusion, may require use of nitroglycerine for systemic BP increase / terlipressin (not in U.S.) has longer half-life, can be given as bolus Endoscopy for ligation or sclerotherapy (ligation preferred due to fewer complications) Antibiotics (ceftriaxone) in acute cases due to risk of co-existent infection Balloon tamponade: Minnesota tube (only if you know what you’re doing) Ischemic Bowel Disease (mesenteric ischemia, ischemic colitis) Causes: atheromatous disease > cardiac disease > colonic surgery, DM, arrhythmias embolic arterial occlusion - usually more SMA nonocclusive ischemia - SMA-IMA (splenic flexure) and IMA-hypogastric watershed areas Presentation: acute mesenteric thrombosis acute bloody diarrhea chronic mesenteric ischemia bloody or watery diarrhea Diagnosis: often delayed due to more common appendicitis, peptic ulcer, cholecystitis Pathology: transmural infarction - often splenic flexure / hemorrhagic / gangrene and perforation at 1-4 days mural and mucosal infarction - hemorrhage and exudate absent from serosa / secondary acute and chronic inflammation / bacterial superinfection (pseudomembranous inflammation) / presents with intermittent bloody diarrhea chronic ischemia - submucosal chronic inflammation may cause stricture / segmental and patchy Note: colonoscopy appearance may resemble IBD [pic] Course: most often resolve without intervention Angiodysplasia (intestinal AVMs) tortuous dilatations / cecum, right colon / 20% of lower intestine bleeds / 50s Hemorrhoids varices of anal, perianal venous plexi / 40s / 5% of population / may reflect portal hypertension Enterocolitis (Infectious Diarrhea) Differential Diagnosis: malabsorption, antibiotic use, cystic fibrosis, inflammatory bowel disease, thyrotoxicosis Labs: electrolytes and renal function, abdominal radiographs usually non-specific, blood, mucus, fecal leukocytes indicate bacterial causes Rapid antigen for rotavirus Treatment: quinolones are good (except campylobacter macrolide) Viral Gastroenterocolitis Rotavirus Norwalk Adenovirus - 1 wk incubation / 7-10 day duration Astrovirus and Calicivirus - mostly children / systemic symptoms as well Bacterial, Enterocolitis [pic] Preformed toxins S. aureus, Vibrio sp., C. perfringens Toxigenic organisms C. difficile (invasion, hemorrhage) cause of antibiotic-associated colitis (pseudomembranous colitis; fibrinopurulent necrotic debris forms the pseudomembrane) ETEC (LT/ST) Vibrio (cholera toxin) (no invasion) EHEC (shiga-like, hemorrhage, but no invasion) Shigella (shiga toxin, hemorrhage, invasion) C. botulinum (neurotoxin) C. perfringens (no invasion) some strains produce severe necrosis or “pigbel” Salmonella (invasion) ileum, colon / bacteremia 5 - 10% / S. typhi causes chronic typhoid fever Campylobacter jejuni small intestine, colon, appendix, villous blunting, superficial ulcers, purulent exudate Yersinia enterocolitica pseudotuberculosis / hemorrhage and ulceration / necrotizing granulomas systemic spread with peritonitis, pharyngitis, pericarditis
Isospora belli – like cryptosporidium / bactrim Entamoeba histalyticum – bloody / metronidazole or
perforation, sepsis, shock) / fluid, electrolyte replacement or massive surgical resection Other inflammatory HIV enteropathy - opportunistic vs. direct (unproven) bone marrow transplantation - blunting, degeneration due to pre-transplant radiation or chemo. Graft versus host disease of GI tract (see GVHD) severe, acute secretory diarrhea / crypt cell necrosis / may progress to fluid, electrolyte derangement, sepsis, hemorrhage / chronic course may include dysphagia or malabsorption Malabsorption Syndromes Manifestations Download 3.95 Mb. Share with your friends:
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