GI - Medicine & Surgery Flashcards
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
What is ischemic hepatic injury/shock liver?
Occurs in setting of hypotension or Budd Chiari syndrome (hepatic vein thrombosis) and manifests as acute, massive increases in transaminases (thousands, 25-250x normal, >10k) w/ milder increases in t bili and ALP
Presentation: diffuse liver injury, RUQ pain
Hallmark: rapid and significant increase in transaminases w/ modest accompanying elevations in total bili and ALP.
Liver enzymes return to normal in 1-2w
Liver enzymes in acute viral hep, alcoholic liver disease, autoimmune hep
Acute viral hep: large AST/ALT elevations (thousands) w/ significant hyperbilirubinemia
Alcoholic liver disease: AST/ALT ratio >2, AST rarely >300
Iron overload: low-grade increase in transaminases
Autoimmune hep: large increases in AST/ALT (thousands), dramatic increase in serum bili
Acetaminophen: thousands
What are colon cancer screening recommendation in pts at increased risk?
Fhx of adenomatous polyps or CRC - age 40 or 10y before age of dx in affected relative, repeat q5y
IBD: 8-10y postdx (12-15y if disease only in L colon and rectum), repeat q1-3y
FAP: age; 10-12, repeat annually
HNPCC (Lynch syndrome): age 20-25, repeat q1-2y
What is laxative abuse?
Presentation: water, frequent 10-20 episodes of diarrhea, nocturnal BMs and abdominal cramps
Labs: metabolic alkalosis, hypokalemia
Dx: positive stool screen for diphenolic (eg bisacodyl) or polyethylene containing laxatives; melanosis coli on colonoscopy, pigemented Macs of lamina propria on histology
What is acute liver failure?
Etiology: viral hep (eg HSV, CMV, hep ABDE), drug toxicity (acetaminophen overdose potentiated by chronic etoh use, idiosyncratic), ischemia (eg shock liver, budd-chiari), autoimmune hep, wilson’s, malignant infiltration
Presentation: fatigue, lethargy, anorexia, nausea, RUQ pain, pruritus and jaundice due to hyperbilirubinemia, renal insufficiency, thrombocytopenia, hypoglycemia in pt w/o cirrhosis or underlying liver disease
Dx: triad of severe acute liver injury - (ALT/AST >1000s), signs of hep enceph (eg confusion, asterixis), synthetic liver dysfunction (prolonged PT w/ INR >=1.5)
Complications: cerebral edema, most common cause of death; renal insufficiency
Tx: N acetylcysteine for acetaminophen overdose; liver transplant
What is angiodysplasia?
Dilated submucosal veins and arteriovenous malformation; assoc. w/ advanced renal disease, vWf disease, and Aortic Stenosis
Presentation: recurrent, painless GI bleeds, maroon-colored stools
Dx: colonoscopy, though frequently missed
Tx: not required if asx; anemia or bleeding can be treated with cautery
What is the relationship between NSAIDs and iron deficiency anemia?
NSAIDs are a common cause through chronic blood loss from the GI tract. Fe deficiency anemia should prompt thorough evaluation for the cause as early low-grade bleeding can herald later catastrophic hemorrhage. Elderly pts often have a low-grade chronic anemia at baseline and may not tolerate additional blood loss.
What is Dubin-Johnson syndrome?
Benign, hereditary condition; defect in hepatic excretion of conjugated bilirubin
Presentation: icterus and positive urine bilirubin assay; discovered in puberty or early adulthood
Histology: grossly black liver w/ dark, lysosomal pigment
Labs: elevated conjugated bilirubin; normal AST, ALT, ALP
What is acute erosive gastropathy?
The development of hemorrhagic lesions after ischemia or the exposure of gastric mucosa to injurious agents (alcohol, aspirin, cocaine).
Aspirin: decreases protective prostaglandin production; Cocaine: results in vasoconstriction, reducing blood flow;
aspirin + etoh cause direct mucosal injury
Presentation: hematemesis and abdominal pain
What is ulcerative colitis?
Presents between 15-40 and 50-80, bimodal
Abdominal pain, bloody diarrhea, tenesmus, and fecal incontinence
Endoscopy: erythema, friable mucosa, pseudopolyps, involvement of rectosigmoid (always), continuous colonic involvement (no skip lesions)
Biopsy: mucosal and submucosal inflammation, crypt abscesses, NO granulomas
Labs: leukocytosis, Fe deficiency anemia, reactive thrombocytosis, increased ESR
Complications: toxic megacolon, primary sclerosing cholangitis, colorectal cancer, erythema nodosum, pyoderma gangrenosum, spondyloarthritis, uveitis
Tx: 5ASAs (mesalamine, sulfasalazine, balsalazide) mesalamine enema/suppository (preferred) for mild UC, oral for more extensive disease
NSAIDs relieve arthritis but worsen underlying bowel disease
What is oropharyngeal dysphagia?
Difficultly initiating swallowing due to inability to transfer food from mouth to pharynx.
Etiologies: stroke, advanced dementia, oropharyngeal malignancy, neuromuscular disorders (myasthenia gravis) Presentation: coughing, choking, nasal regurgitation on swallowing
Complications: aspiration pneumonia + weight loss
Dx: videofluororscopic modified barium swallow study to evaluate swallowing mechanics, degree of dysfunction, + severity of aspiration
What is esophageal dysphagia?
Sensation of food getting stuck in esophagus (not throat) a few seconds after a swallow.
Does not cause difficulty initiating swallowing.
What is carcinoid syndrome?
Presentation: skin - flushing, telangiectasias, cyanosis; GI - diarrhea, cramping; cardiac - valvular lesions (R>L; murmur of tricuspid regurg; episodic pounding sensation due to flushing and assoc. rise in pulse rate); pulm - bronchospasm; miscellaneous: Niacin deficiency (dermatitis, diarrhea, dementia)
Dx: elevated 24h urinary excretion of 5HIAA, CT/MRI of abdomen + pelvis to localize tumor, octreoScan to detect metastases, echocardiogram (if sxs of carcinoid heart disease are present)
Tx: octreotide for symptomatic pts; prior to surgery/anesthesia; surgery for liver metastases
What is infective endocarditis?
R sided infective endocarditis is assoc. w. IV drug use.
Presentation: fever, malaise, arthralgias, vascular or immunologic phenomena, and new valvular regurgitant murmur
No flushing or diarrhea present.
What is celiac disease?
Suspect if there is malabsorption and diarrhea.
Features of malabsorption:
general - bulky, foul-smelling, floating stools; fat and protein - loss of muscle mass, loss of sub-q fat, fatigue; Fe - pallor (anemia), fatigue; Ca and Vit. D - bone pain (osteomalacia), fracture (osteoporosis); Vit. K - easy bruising, Vit. A - hyperkeratosis
Confirmatory tests - antibodies and duodenal biospy
Biospy: villous atrophy
Labs: IgA anti-tissue transglutaminase, IgA anti-endomysial antibodies
Selective IgA deficiency is common, so measure total IgA or IgG
What is collagenous colitis?
Chronic watery diarrhea.
Colon is frequently involved, but colonoscopy shows normal mucosa.
Biopsy: subepithelial collagen depositon
What is an endoscopic retrograde cholangiopancreatogram (ERCP)?
Primarily used for suspected choledocholithiasis
Usually performed in pts when initial U/S or CT scan suggests presence of obstruction due to cholelithiasis or malignancy; used to visualize and intervene upon biliary and pancreatic ducts; widely used for stone removal, tissue sampling, stent placement, and sphincterotomy
ERCP in these settings can be both diagnostic and therapeutic by relieving obstruction and facilitating biliary drainage.
Indicated for gallstone in common biliary duct causing CBD dilation; acute cholangitis.
Most common complication is post-ERCP pancreatitis
What is alcoholic hepatitis?
Seen in pts w/ hx of chronic heavy alcohol use
Presentation: jaundice, anorexia, fever, RUQ or epigastric pain, abdominal distension due to ascites, proximal muscle weakness from muscle wasting (if malnourished), possible hepatic encephalopathy
Labs/imaging: Elevated AST/ALT, 300-500, AST:ALT >=2, elevated gamma-glutamyltransferase, ferritin (acute phase reactant), bilirubin, MCV, and/or INR, leukocytosis, predominantly neutrophils, decreased albumin if malnourished, abdominal imaging may show fatty liver
What can exacerbate hepatic encephalopathy?
Hypokalemia: resultant intracellular acidosis (excreted intracellular K replaced by H ions to maintain electroneutrality) causes increased NH3 production (glutamine conversion) in renal tubular cells Metabolic alkalosis (elevated bicarb): promotes conversion of NH4+ (ammonium), which cannot enter CNS, to NH3 which can enter CNS NH3 made to offset decrease in H
What is primary sclerosing cholangitis?
Presentation: fatigue and pruritis; majority of pts are asx at time of dx; about 90% have underlying IBD, mainly UC
Labs/imaging: cholestatic liver function pattern, elevated ALP (serum aminotransferases typically <300), multifocal stricturing/dilation of intrahepatic and/or extrahepatic bile ducts on MRCP
Elevated ESR, IgM; positive perineutrophil cytoplasmic antibody (ANCA)
Liver biopsy: fibrous obliteration of bile ducts w/ concentric replacement by connective tissue in an “onion-skin” pattern
Complications: intrahepatic and/or extrahepatic biliary stricture, cholangitis and cholelithiasis (cholesterol and/or pigment stones), cholangiocarcinoma (10-15% lifetime risk), cholestasis (e.g., decrease in fat-soluble vitamins, osteoporosis), colon cancer
What is medication-induced/pill esophagitis?
Etiology: tetracyclines - acid effect; aspirin and NSAIDs - disruption of gastroesophageal protection; alendronate, risedronate; KCl, Fe - osmotic tissue injury
Presentation: sudden onset of retrosternal pain and severe odynophagia
Pts may be unable to swallow saliva due to PAIN
Most common in mid-esophagus due to compression by aortic arch or an enlarged L atrium
Dx: endoscopy which shows discrete ulcers w/ relatively normal-appearing surrounding mucosa
Tx: stopping offending medication
What is pancreatic adenocarcinoma?
Assoc. b/n psychiatric manifestation (something bad is going to happen; feeling low for no reason) and pancreatic cancer is well documented
New onset DM, thin, older pts = pancreatic cancer
Risk factors: smoking (most significant; reversible), hereditary pancreatitis 1st degree relative with pancreatic cancer, germline mutations (BRCA1,2, peutz-jeghers syndrome), environmental (nonhereditary chronic pancreatitis, obesity and lack of physical activity)
Presentation: most common (epigastric gpain that is progressive and constant often radiating to the flanks or the back); systemic sxs (e.g. wt loss, anorexia), epigastric abdominal pain radiating to the back (worse at night, w/ eating, or when lying supine), jaundice, recent onset atypical DM in thin/older pt, unexplained migratory superficial thrombophlebitis/Trousseau’s, hepatomegaly and ascites w/ metastasis; distended gb/painless jaundice (head), ab pain/no jaundice (body/tail)
Labs: cholestasis (increased ALP and direct bilirubin, intra and extrahepatic dilation), increased cancer assoc. antigen 19-9 (not as a screening test), abdominal U/S if jaundiced (= cancer in head of pancreas), CT scan w/ contrast (if no jaundice = cancer in body and tail of pancreas)
Dx workup: CT scan of the abdomen
What is Zollinger-Ellison Syndrome?
Etiology: sporadic or MEN1 gene mutation;
Recurrent peptic ulcer disease with multiple ulcers and jejunal ulceration + assoc. chronic diarrhea; excess gastric acid in small intestine causes diarrhea and steatorrhea due to inactivation of pancreatic enzymes and injury to mucosal brush border
Presentation: dyspepsia, reflux sxs, abdominal pain, wt loss, diarrhea, frank GI bleeds
Endoscopy: thickened gastric folds, multiple peptic ulcers, refractory ulcers despite PPI use, ulcers distal to duodenum in jej (suggesting excess gastric acid that can’t be fully neutralized in duo)
Labs: fasting serum gastrin >1000 in the presence of normal gastric acid (pH <4)
Work-up: endoscopy, CT/MRI and somatostatin receptor scintigraphy for tumor localization
What is a jejunal ulcer?
Usually due to gastric acid hypersecretion rather than local tumor invasion.
What is a duodenal ulcer?
Etiology: H. pylori or NSAIDs; a result of acid secretion in absence of food buffer
Presentation: epigastric pain occurs in absence of food buffer (e.g., 2-5h after meals, on an empty stomach, or at night), GI bleed, and anemia
Pain improves after eating.
Dx: endoscopic biopsy or urea breath test
Tx: PPI and antibiotic eradication therapy
What is a false-positive D-xylose test?
Low urinary D-xylose level despite normal mucosal absorption.
Seen in delayed gastric emptying, impaired glomerular filtration, small intestinal bacterial overgrowth (SIBO)
What is small intestinal bacterial overgrowth (SIBO)?
Occurs when bacteria from colon are inappropriately present in small intestine.
Alteration in small intestinal flora (due to abnormal intestinal anatomy or motility), leading to bacterial fermentation of the d-xylose before it can be absorbed.
Assoc. w/ underlying motility disorders (e.g., DM) or anatomical abnormalities (e.g., jejunocolic fistula)
Presentation: abdominal pain, bloating, flatulence, watery diarrhea, diarrhea is frequently greasy.
Dx: jejunal aspiration demonstrating high bacterial concentration, however test is invasive and not easily performed; more commonly diagnosed by positive carbohydrate breath test using either glucose or lactulose (pts w/ SIBO have an earlier peak in breath hydrogen/methane due to carb metabolism in SI, compared to those w/o SIBO where carb metabolism normally occurs in the colon)
Tx: rifaximin, neomycin to reduce bacterial load
What s esophageal (peptic) stricture?
Etiology: GERD, radiation, systemic sclerosis, caustic ingestions
Presentation: symmetric and circumferential narrowing of esophagus on barium swallow w/ dysphagia for solids but typically no wt loss
As it progresses, it can block reflux leading to improvement of heart burn symptoms
Dx: endoscopy (can be therapeutic)
What is barium swallow?
Useful for evaluating esophageal abnormalities (e.g., dysphagia, odynophagia) or documenting aspiration.
How do you manage gallstones?
Gallstones w/o sxs: no treatment necessary in most patients
Gallstones w/ typical biliary colic symptoms: elective laparascopic cholecystectomy, possible ursodeoxycholic acid in poor surgical candidates
Complicated gallstone disease (acute cholecystitis, choledocholithiasis, gallstone pancreatitis): cholecystectomy w/in 72h
What is a hiatal hernia?
Common disorder that occurs when contents of abdominal cavity herniate through diaphragm into thoracic cavity at esophageal hiatus.
Etiology: laxity of phrenoesophageal membrane due to age-related degeneration or repetitive stress (e.g., vomiting, coughing)
Asx pts require no further evaluation beyond obs.
Pts w/ reflux sxs should be medically managed (eg PPI), those with refractory GERD sxs can be considered for antireflux surgery (e.g. Nissen fundoplication)
CXR: retrocardiac opacity, often w/ air fluid level w/in thoracic cavity
Barium swallow is most sensitive test for dx if there are sxs.
What is emphysematous cholecystitis?
Life-threatening form of acute cholecystitis more common in IC.
Risk factors: DM, vascular compromise (obstruction/stenosis of cystic artery), immunosuppression, gallstones
Presentation: fever, RUQ pain, n/v, crepitus in abdominal wall adjacent to gallbladder
Complications: gangrene and perforation
Dx: air-fluid levels in gb, gas in gb wall, pneumobilia (air w/in heaptobiliary sys), cultures w/ gas-forming clostridium, e. coli, UCB (from clostridium induced hemolysis), mildly elevated aminotransferases
Tx: emergeny cholecystectomy, broad-spectrum antibiotics w/ clostridium coverage (e.g, amp-sulbactam)
What is a mallory weiss tear?
Often seen in assoc. w/ alcohol abuse and hiatal hernia
Etiology: upper GI mucosal tear, caused by forceful retching (increased pressure), submucosal arterial or venule plexus bleeding
Presentation: vomiting, retching, hematemesis, epigastric pain
Labs/imaging: EGD confirms dx
Tx: most tears heal spontaneously, endoscopic tx for continual bleed with electrocoagulation or local injection of epinephrine
What is boerhaave syndrome/spontaneous esophageal rupture?
Etiology: Esophageal transmural tear, caused by forceful retching (increased pressure), esophageal air/fluid leakage into nearby areas (e.g., pleura)
Presentation: vomiting, retching, chest + upper abdominal pain, odynophagia, fever, dyspnea + septic shock can ensue, subcutaneous emphysema may be seen
Labs/imaging: CT or contrast esophagography w/ gastrofin confirms diagnosis;
CXR: pneumomediastinum and L unilateral pleural effusions; pleural fluid analysis: exudative, low pH, very high amylase (>2500; due to saliva in the esophageal contents)
Tx: surgery - for thoracic perforations, conservative measures (eg, antibiotics) - for cervical perforations
What is perforated viscus?
GI perforation
Etiology: hx of NSAID and alcohol use, peptic ulcer disease
Presentation: severe abdominal pain, fever, tachycardia, signs of peritonitis (rigidity, reduced bowel sounds, rebound tenderness, guarding), positive stool guiac test
Dx: upright xray of chest and abdomen showing free intraperitoneal air under the diaphragm
Tx: urgent exploratory laparatomy
What is a psoas absecess?
Etiology: hematologic seeding from a distant infection or from direct extension of an intraabdominal infection (eg diverticulitis, vertebral osteomyelitis)
Risk factors: HIV, IV drug use, DM, Crohn disease
Presentation: subacute fever, abdominal/flank pain radiating to groin, anorexia, wt loss, abdominal pain w/ hip extension (psoas sign)
Dx: CT scan of the abdomen and pelvis, leukocytosis, elevated inflammatory markers, blood and abscess cultures
Tx: drainage, broad-spectrum antibiotics
What is cholangiocarcinoma?
Highly lethal malignancy of bile duct epithelium
Risk greatest in those w/ fibropolycystic liver disease or primary sclerosing cholangitis due to underlying UC
Presentation: UC, subacute RUQ pain, wt loss, biliary obstruction (eg jaundice, dark urine, pruritus, elevated ALP, dilated intrahepatic/common bile ducts), hepatomegaly/palpable RUQ mass
Labs: elevated carcinoembryonic antigen (CEA) and CA19-9, normal AFP
Dx: Endoscopic US or ERCP for tissue dx
What is esophageal rupture?
Etiology: spontaneous rupture (boerhaave syndrome), instrumentation (endoscopy; most common cause), esophagitis (infectious/caustic), esophageal ulcer
Presentation: chest/back and abdominal pain, sys findings (fever), subcutaneous emphysema in the neck, hamman sign (crunching sounds on chest auscultation); pleural effusion w/ atypical (eg green fluid)
Dx: CXR or ct scan - wide mediastinum, pneumomediastinum, pneumothorax, air around paraspinal muscles, L-sided pleural effusion (late)
CT scan - esophageal wall thickening, mediastinal air fluid level; water-soluble contrast esophagogram (gold standard) - leak at perforation site
Mgmt: NPO, IV antibiotics, PPIs, and supportive care for all pts, surgical repair for significant leakage with sys inflammatory response
