GI - Medicine & Surgery Flashcards
(155 cards)
What is hepatic hydrothorax?
Complication of cirrhosis. A transudative pleural effusion not due to underlying cardiac or pulmonary abnormalities. Occurs due to small defects in the DIAPHRAGM, more common on the R side due to less muscular hemidiaphragm.
Dx: documentation of effusion
Tx: salt restriction and diuretic administration
What is hepatopulmonary syndrome?
It results from intrapulmonary vascular dilation in setting of chronic liver disease. Pt frequently has evidence of platypnea (increased dyspnea while upright) or orthodeoxia (O2 desaturation while upright).
What is Primary Biliary Cholangitis?
Pathogenesis: autoimmune destruction of intrahepatic bile ducts leading to intrahepatic cholestasis
Clinical features: affects middle aged women, insidious onset of fatigue and pruritis, progressive jaundice, hepatomegaly, cirrhosis, cutaneous xanthomas and xanthelasmas
Labs: increased ALP, a little AST, ALT; AMA, severe hypercholesterolemia
Dx: anti-mitochondrial antibody (AMA) titers
Tx: ursodeoxycholic acid (delays progression and may improve sxs and possible survival), liver transplantation for advanced disease
Assoc. w/ ulcerative colitis
Complications: malabsorption, fat soluble vitamin deficiencies, metabolic bone disease (osteoporosis, osteomalacia), hepatocellular carcinoma
Assoc. w/ autoimmune thyroid disease
What is spontaneous bacterial peritonitis?
Suspected in any patient with cirrhosis and ascites who presents with: temp >= 100F, abdominal pain/tenderness, altered mental status (abnormal connect the numbers test), hypotension, hypothermia, paralytic ileus with severe infection
Diagnosis from ascitic fluid: paracentesis; PMNs >= 250, positive culture, often gram-negative organisms (E. coli, Klebsiella), protein <1, SAAG >= 1.1
Tx: empiric antibiotics - 3rd gen cephalosporins (cefotaxime),
Fluroquinolones for SBP prophylaxis
What is dyspepsia?
Intermittent epigastric pain and postprandial discomfort.
Caused by NSAIDs, gastric or esophageal cancer, functional dyspepsia, GERD, PUD w/ H. pylori
Dx: endoscopy
What is chronic pancreatitis?
Etiology: etoh use, cystic fibrosis (common in children), ductal obstruction (e.g., malignancy, stones), autoimmune
Presentation: chronic epigastric pain radiating to the back w/ intermittent pain-free intervals, relieved by leaning forward, malabsorption-steatorrhea, weight loss, DM
Labs/imaging: amylase/lipase can be normal and non-diagnostic, plain film, CT scan or MRCP can show calcifications, dilated ducts, and enlarged pancreas
Low fecal elastase is diagnostic
Tx: pain mgmt, etoh and smoking cessation, frequent/small meals, pancreatic enzyme supplements
What is metastatic liver disease?
The most common site of colon cancer metastasis is to the liver.
Presentation: RUQ pain, mildly elevated liver enzymes, firm hepatomegaly
Dx: CT of abdomen
What is alcoholic cirrhosis?
Liver is often shrunken and edge is not palpable.
AST:ALT >2:1, <500
What is autoimmune hepatitis?
Presentation: young to middle aged women, acute or chronic hepatitis, significant hepatocellular injury
Labs: transaminases often >1000 U/L;
ANA, Anti-smooth antibodies
Tx: oral glucocorticoids
What is acute pancreatitis?
Etiology: chronic alcohol use, gallstones, hypertriglyceridemia, drugs (azathriprine, valproic acid, thiazides), infections (CMV, legionella, aspergillus), iatrogenic (post-ERCP, ischemic/atheroembolic), cholesterol emboli
Presentation: acute epigastric pain radiating to back, eruptive xanthomas (yellow-red papules due to subq fat deposition), livedo reticularis; severe disease - fever, tachypnea, hypoxemia, hypotension
Labs: fasting lipid profile, ALT >150 = biliary pancreatitis
Imaging: abdominal U/S (most sensitive and specific), then ERCP if that is nondiagnostic
Imaging: CT findings may remain normal for up to 48h
Dx: 2 of the following - acute epigastric pain radiating to back, increased amylase or lipase >3x normal limit (rise w/in several hours), abnormalities on imaging consistent with pancreatitis
Tx: IV fluids and supportive care
What is cirrhosis?
Etiology: viral hepatitis B +C, chronic etoh abuse, NAFLD, hemochromatosis
Presentation: ascites, spider angiomata, gynecomastia, splenomegaly
Dx: Patients w/ cirrhosis should undergo screening endoscopy to exclude varices, indicate the risk of variceal hemorrhage, and determine strategies for primary prevention of variceal hemorrhage.
What are esophageal varices?
Tx: PPx - non-selective beta blocker (propranolol, nadolol) to decrease progression to large varices and the risk of variceal hemorrhage.
Octreotide is used to treat active variceal bleeding, no role in primary ppx. MOA - inhibits release of vasodilator hormones leading to indirect splanchnic vasoconstriction and decreased portal flow
Endoscopic variceal ligation can be used as alternative primary preventive therapy in pts with contraindication to beta blocker therapy
Goal Hgb is above 9.
What is Familial adenomatous polyposis?
Etiology: alteration in adenomatous polyposis coli (APC) gene
Presentation: development of >1000 polyps, universal development of CRC if left untreated
Screening sigmoidoscopies for children start at age 10-12, followed by annual colonoscopies once colorectal adenomas are detected or if pt is age >=50
Pts w/ attenuated version of FAP can have a delayed start of screening (age 25) and longer screening intervals (1-2 years)
Tx: increased screening and elective proctocolectomy
What is lactose intolerance?
Lactose is processed into glucose and galactose by lactase on brush border. Inability to absorb lactose found in milk and dairy products. Most common in Asian Americans, and pts of African, Latin American, or Native American descent.
Presentation: osmotic diarrhea, abdominal cramps, bloating, and flatulence after ingestion of dairy products; no steatorrhea
Labs: high osmotic gap due to unmetabolized lactose and organic acids; acidic stool pH due to fermentation products
Dx: lactose hydrogen breath test - positive test characterized by rise in measured breath hydrogen level after ingestion of lactose indicating bacterial carbohydrate metabolism; positive stool test for reducing substances
High osmotic gap due to unmetabolized lactose and organic acids
What is C. diff colitis?
Diarrhea and/or abdominal pain in pt who has been on antibiotics
Tx: Initial episode: vanc PO or fidaxomicin PO
Recurrence: 1st - vanc PO (taper) or fidaxomicin if vanc was used in initial episode;
multiple recurrences - van PO followed by rifaxmin, fecal microbiota transplant
Fulminant (e.g., hypotension/shock, ileus, megacolon): metro IV PLUS high dose vanc PO (or per rectum, if ileus is present), surgical evaluation
Dx: stool pcr for c. diff toxin
What is the management of cirrhosis?
Compensated: U/S surveillance for hepatocellular carcinoma +/- alpha fetoprotein q6mo, EGD varices surveillance
Decompensated - liver can’t keep up with needs of body: variceal hemorrhage - nonselective bblockers, repeat EGD annually; ascites - dietary Na restriction, diurectics, paracentesis, abstinence from etoh; hepatic encephalopathy - identify underlying cause (e.g., infection, GI bleeding), lactulose therapy
What is diffuse esophageal spasm?
Uncoordinated, simultaneous contractions of esophageal body
Presentation: intermittent chest pain, dysphagia for solids and liquids, regurgitation precipitated by emotional stress
Dx: manometry: intermittent peristalsis, multiple simultaneous contractions;
esophagram: “corkscrew” pattern
Tx: calcium channel blockers, alternatives: nitrates or TCAs
What is Nonalcoholic fatty liver disease?
Most common in pts with obesity and diabetes.
Hepatic steatosis on imaging or biopsy, exclusion of significant alcohol use, exclusion of other causes of fatty liver; related to peripheral insulin resistance leading to increased peripheral lipolysis, triglyceride synthesis; hepatic uptake of fatty acids, which increases oxidative stress and production of proinflammatory cytokines
Presentation: mostly asx, metabolic syndrome, +/- steatohepatitis (AST/ALT ratio <1), hyperechoic texture on U/S
Dx: biopsy for confirmation
Tx: diet and exercise, consider bariatric surgery if BMI >= 35; safe to continue statins
What is pellagra?
Due to niacin deficiency, prolonged isoniazid therapy
Niacin synthesized endogenously from tryptophan
Presentation: dermatitis, diarrhea, dementia; can be seen with carcinoid syndrome (depletion of trytophan) or HartNup disease (congenital disorder of tryptophan absorption)
What is severe acute pancreatitis?
Pancreatitis with failure of at least 1 organ
Presentation: fever, tachycardia, hypotension, dyspnea, tachypnea and/or basilar crackles, abdominal tenderness and/or distension, Cullen sign (periumbilical bluish coloration indication hemoperitoneum), Grey-Turner sign (Reddish-brown coloration around flanks indicating retroperitoneal bleed); pancreatic enzymes enter vascular sys –>increase vascular permeability–>hypotension
Assoc. w/ increased risk: age >75, obesity, alcoholism, CRP >150 48h after presentation, rising BUN and Cr in first 48h, CXR w/ pulmonary infiltrates or pleural effusion, CT scan/MRCP w/ pancreatic necrosis and extrapancreatic inflammation
Complications: pseudocyst, peripancreatic fluid collection, necrotizing pancreatitis, ARDS, acute renal failure, GI bleeding
Tx: several liters of IV fluid
What is a pseudocyst?
Complication of acute pancreatitis: A fluid collection containing pancreatic enzymes, blood, fluid, and tissue debris surrounded by a necrotic or fibrous capsule.
Typically takes 3-4w to develop after acute pancreatitis.
Can leak amylase-rich fluid into circulation and increase serum amylase
No sxs + no complications - expectant management
Sx - endoscopic drainage
What is fecal impaction?
Common in older pts w/ impaired mobility, chronic constipation, or decreased sensation of stool in rectal vault
Presentation: obstruction of fecal flow in rectum can cause backup of stool; passage of stool around impaction leads to incontinence
Tx: manual disimpaction + enemas to clear rectal vault
What is Crohn Disease?
Inflammatory Bowel Disease, mouth to anus (rectum is spared)
Risk factor: smoking
GI: abdominal pain, chronic nonbloody diarrhea (bloody if colitis), oral ulcers, malabsorption, weight loss, transmural inflammation, strictures, fistula/abscess formation, peri-anal skin tags, anal fissures, non-caseating granulomas, creeping fat
Extraintestinal: MSK (arthritis), eye (e.g., uveitis, scleritis, episcleritis), skin (e.g., erythema nodosum, pyoderma gangrenosum), lung disease, kidney stones
Dx: increased WBC, Fe deficiency anemia, increased inflammatory markers; endoscopy - focal linear ulcerations adjacent to normal mucosa (cobblestoning), skip lesions; radiography - strictures, bowel wall thickening
Tx: 5ASA drugs (w/o systemic sxs), corticosteroids, azathioprine, anti-TNF (severe disease), antibiotics
NSAIDs can relieve arthritis sxs but worsen underlying bowel disease
[5ASA drugs are ineffective and not recommended]
What is the serology for hep b?
First marker to appear - HBsAg (4-8w after infection)
IgM anti-HBc appears around time of clinical sxs (ALT/AST >25x normal limit)
Window period = time between disappearance of HBsAg and appearance of anti-HBs, only IgM anti-HBc detectable
HbsAg and anti-HBc: most approp. dx test for acute hepatitis B infection as both are elevated during initial infection and IgM anti-HBc will remain elevated during window period.
Resolved infection: positive for anti-Hbs and IgG anti-Hbc
Recovery phase: anti-Hbs, IgG anti-Hbc, anti-Hbe