Gastroenterology
Showing 32 of 32 topics
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Acute cholangitis is bacterial infection of an obstructed biliary system. The combination of infection and impaired bile drainage can progress rapidly to sepsis, shock, acute kidney injury, coagulopathy, and altered mental status. Management therefore has two equally important components: early antimicrobial and physiologic support, and timely biliary decompression when obstruction persists or disease is moderate to severe.
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Charcot triad (fever, jaundice, RUQ pain) ± hypotension/AMS suggests cholangitis. Use Tokyo Guidelines for severity grading. Start broad IV antibiotics and arrange urgent biliary drainage—ERCP preferred; percutaneous transhepatic biliary drainage if ERCP not feasible.
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Systemic inflammation + cholestasis + imaging define diagnosis. Start early broad‑spectrum antibiotics and fluids; perform ERCP drainage urgently for Grade II–III disease and after stabilization for Grade I; tailor timing to sepsis severity and comorbidity.
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Acute pancreatitis is diagnosed when at least two of three features are present: characteristic abdominal pain, serum lipase or amylase at least three times the upper limit of normal, or characteristic imaging. Early care emphasizes risk assessment, lactated Ringer's solution when fluids are needed, early oral feeding as tolerated, analgesia, and treatment of the cause rather than routine antibiotics or routine early CT.
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Acute pancreatitis is diagnosed when at least two of three features are present: characteristic abdominal pain, lipase or amylase at least three times the upper limit of normal, or characteristic imaging. Early management emphasizes cause identification, moderately aggressive lactated Ringer's resuscitation with frequent reassessment, analgesia, early oral feeding as tolerated, and selective imaging or ERCP rather than routine invasive testing.
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Epigastric pain radiating to the back with elevated lipase/amylase (>3× ULN) and imaging findings. Provide early goal-directed fluids (prefer lactated Ringer’s), adequate analgesia, and early enteral nutrition; avoid prophylactic antibiotics. Identify gallstone etiology and perform cholecystectomy before discharge for mild cases.
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Diagnose pancreatitis with 2 of 3: characteristic pain, lipase >3× ULN, or imaging. Give early goal-directed lactated Ringer’s, adequate analgesia, and start early enteral nutrition; treat causes (gallstones, alcohol, hypertriglyceridemia). Avoid routine antibiotics unless infected necrosis is suspected.
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Early care centers on LR fluids, analgesia, and early enteral nutrition; ERCP reserved for cholangitis or persistent biliary obstruction.
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Hospitalize for intensive monitoring, start IV corticosteroids, perform early flexible sigmoidoscopy, and escalate to infliximab or cyclosporine if steroid-refractory; coordinate with colorectal surgery for timely colectomy when failure criteria are met.
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Outpatient management focuses on fiber, topical therapies, and office procedures; escalate to surgery for refractory cases or complications.
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Accidental or intentional ingestion of acids/alkalis causes esophageal/gastric injury. Keep NPO, avoid neutralizing/emesis/NG placement blindly, and perform early endoscopy (within 12–24 h) to grade injury; manage severe injuries in ICU with perforation surveillance and staged nutrition.
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Test with tTG‑IgA and total IgA; confirm with duodenal biopsy (unless pediatric no‑biopsy criteria met). Lifelong gluten‑free diet; monitor serology, micronutrients, and bone health.
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Differentiate slow‑transit constipation from pelvic floor dyssynergia; pursue anorectal testing and targeted therapy (biofeedback) before empiric laxatives alone.
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Acute diverticulitis ranges from localized uncomplicated colonic inflammation to abscess, perforation, obstruction, fistula, or diffuse peritonitis. CT is the preferred diagnostic study when the diagnosis or severity is uncertain. Stable immunocompetent patients with mild uncomplicated disease may not require antibiotics, whereas complicated disease, systemic illness, immunocompromise, or high-risk features require antimicrobial therapy and often admission or procedural management.
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Confirm delayed gastric emptying (4‑hour scintigraphy). Manage with dietary measures, glycemic control, and prokinetics; consider pyloric therapies for refractory disease.
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Use an 8‑week PPI trial for typical GERD without alarms; then step‑down to lowest effective dose or on‑demand. Deprescribe PPIs when no ongoing indication; reinforce lifestyle measures.
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Severe abdominal pain with TG >1000 mg/dL—hypertriglyceridemia‑induced acute pancreatitis (HTG‑AP).
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Positive diagnosis using Rome IV; screen for celiac disease in IBS‑D/M; limited testing otherwise. Management combines diet (low‑FODMAP), gut‑directed pharmacotherapy, and psychological therapies.
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Resuscitate, risk stratify, and obtain CTA for brisk bleeding when endoscopy is not immediately available; manage anticoagulants and coordinate GI and interventional radiology.
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Acute lower gastrointestinal bleeding most often presents with hematochezia and ranges from self-limited diverticular bleeding to life-threatening hemorrhage. Initial management is based on hemodynamic status rather than presumed anatomic source. Brisk upper GI bleeding can present as hematochezia and should be considered in unstable patients. CT angiography is the preferred localization test for ongoing hemodynamically significant bleeding in many contemporary pathways, while colonoscopy remains important
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Acute lower gastrointestinal bleeding most often presents as hematochezia from diverticular bleeding, angioectasia, hemorrhoids, ischemic or inflammatory colitis, neoplasia, or post-procedural sources. Initial management is based on hemodynamic severity rather than stool appearance alone. Stabilize significant hemorrhage, exclude a brisk upper-GI source when appropriate, and use CT angiography for ongoing hemodynamically significant bleeding. Colonoscopy remains important for diagnosis and therapy but does
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Chronic watery, non‑bloody diarrhea with normal colonoscopy; diagnosis requires random biopsies. Budesonide is first‑line; review medications and bile acid malabsorption.
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Severe pancreatitis complicated by necrosis requires early enteral nutrition, goal‑directed resuscitation, and organ support. Reserve antibiotics for proven infection. Delay intervention until walled‑off necrosis (~4 weeks) when feasible; employ a step‑up approach starting with percutaneous or endoscopic drainage and escalating to minimally invasive necrosectomy if needed.
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Hematemesis or melena with hemodynamic changes suggests upper GI bleeding. Resuscitate with balanced transfusion strategy, start high-dose IV PPI, risk-stratify (GBS/Rockall), and arrange early endoscopy with endoscopic hemostasis for high-risk stigmata; resume antithrombotics per risk.
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Resuscitate and risk‑stratify (Glasgow‑Blatchford). Administer high‑dose PPI and give pre‑endoscopy erythromycin when appropriate; perform early endoscopy with hemostasis. Transfuse at Hgb <7 g/dL unless exceptions; resume antiplatelets per risk/benefit.
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Acute nonvariceal upper gastrointestinal bleeding most commonly arises from peptic ulcer disease and presents with hematemesis, coffee-ground emesis, melena, or occasionally brisk hematochezia with shock. Stabilize circulation, use a restrictive red-cell transfusion strategy for most patients, stratify risk, give IV proton-pump inhibitor therapy when appropriate, and perform upper endoscopy within 24 hours after adequate resuscitation. Endoscopic hemostasis is required for high-risk ulcer stigmata, with tra
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Diagnose SIBO with breath testing (glucose/lactulose) or jejunal aspirate; treat with antibiotics and correct underlying motility/anatomic disorders.
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Superior mesenteric artery syndrome is compression of the third portion of the duodenum between the SMA and aorta after loss of the intervening mesenteric fat pad. It presents with postprandial pain, early satiety, nausea, vomiting, and further weight loss; CT demonstrates a narrowed aortomesenteric angle and distance, while initial treatment emphasizes decompression and nutritional rehabilitation.
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Nonvariceal upper gastrointestinal bleeding most often results from peptic ulcer disease, erosive disease, malignancy, or vascular lesions. Management prioritizes hemodynamic stabilization, restrictive transfusion in most patients, risk stratification, proton pump inhibitor therapy, and endoscopy within 24 hours after adequate resuscitation, with endoscopic hemostasis for high-risk lesions.
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Nonvariceal UGIB: resuscitate, risk‑stratify (GBS/Rockall), PPI therapy, and endoscopic hemostasis within 24 h; treat H. pylori; manage antithrombotics with clear restart strategy.
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Manage UGIB with ABCs, balanced transfusion targets (Hb ~7–8 g/dL), and early endoscopy (within 24 h; sooner if unstable). Use Glasgow‑Blatchford/Rockall for triage. High‑dose IV PPI for suspected non‑variceal bleeding; in suspected variceal bleeding, add octreotide and prophylactic antibiotics.
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Resuscitate with balanced strategy, start vasoactive therapy and antibiotics, and arrange urgent endoscopy; use balloon tamponade or self expanding stent as bridge when needed.
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