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MODHIII - Unit 3 > Liver & Biliary Disorders > Flashcards

Liver & Biliary Disorders Flashcards

1
Q

Ascites

A
  • most common complication of cirrhosis
  • 50% of cirrhotics will die within 2 yrs of onset of ascites
  • physical exam worthless, ultrasound is the way to go
  • paracentesis part of physical exam
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2
Q

Indications for paracentesis

A
  • new onset ascites
  • signs of infection
  • any evidence of clinical deterioration
  • relief of symptoms due to tense ascites
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3
Q

Lab tests on ascitic fluid

A
  • cirrhotic: serum ascites-albumin gradient, cell count w/ differential, ascitic fluid cultures in addition to the above
  • absence of liver disease: cytology, AFB culture, triglycerides, amylase
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4
Q

Serum-ascites albumin gradient (SAAG)

A
  • SAAG > 1.1 = portal hypertension

- SAAG

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5
Q

SAAG levels

A
  • SAAG > 1.1: high portal pressure; portal HTN or CHF

- SAAG

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6
Q

Spontaneous Bacterial Peritonitis (SBP)

A
  • result of bacterial translocation from gut due to impaired barrier
  • 2/3 of pts present with abdominal pain, fever, diarrhea NOT peritonitis
  • 1/3 asymptomatic
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7
Q

Diagnosis of SBP

A
  • > 250 PMNs/mm3 in ascitic fluid
  • cultures negative 50% of the time
  • monomicrobial: E coli, klebsiella
  • polymicrobial: anaerobic or fungal (secondary peritonitis i.e. perforated viscus)
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8
Q

Treatment of SBP

A
  • antibiotic: Cefotaxime
  • IV albumin infusion: 1.5g/kg bw on day 1, 1g/kg bw on day 3
  • aminoglycosides should NOT be used
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9
Q

Candidates for prophylaxis of SBP

A
  • hospitalized cirrhotics w/ GI bleeding
  • non bleeding cirrhotics w/ ascites and: protein 2.5, SBP
  • various antibiotic regimen are effective
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10
Q

Management of Ascites

A
  • sodium restricted diet (2g/d)
  • diuretics: spironolactone (K+ sparing) with furosemid (K+ wasting)
  • NO IV diuretics: too rapid volume loss = renal hypoperfusion
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11
Q

Causes of poor response to treatment of ascites

A
  • inadequate sodium restriction

- inadequate diuretic dosage

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12
Q

Endpoints of ascites treatment

A
  • weight loss of .5-1 kg/day
  • urinary Na:K ratio > 1 indicates good response
  • fluid restriction not necessary except for significant hyponatremia (Na 120, creatinine >2, or encephalopathy
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13
Q

Large volume paracentesis

A
  • rapid relief of symptoms but does not treat underlying cause
  • if used w/ out sodium restriction ascites reaccumulates
  • not first line therapy
  • albumin infusions used to blunt changes in volume (8g/L removed)
  • smaller volume taps
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14
Q

Variceal bleeding

A
  • 1/3 who have varices will bleed from them
  • bleeding associated w/ 30% risk of mortality
  • accounts for 80% of GI bleeding in cirrhotics
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15
Q

Management of suspected variceal hemorrhage

A
  • life threatening event: admit to ICU
  • hemodynamic resuscitation: large bore IVs, blood products
  • consider intubation, call GI
  • begin somatostatin or octreotide (decreases portal pressure)
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16
Q

Treatment of variceal bleeding

A
  • endoscopic therapy: ligation
  • TIPS when can’t be stopped endoscopically
  • antibiotic prophylaxis (quinolone)
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17
Q

Transjugular intrahepatic portosystemic shunt (TIPS)

A
  • shunt to bypass the liver vasculature: portal vein to IVC
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18
Q

Primary prophylaxis of variceal hemorrhage

A
  • screen cirrhotics for varices
  • nonselective B-blockers: propranol or nadolol
  • Goal: reduction in hepatic venous pressure gradient by 25%/below 12
  • Alternate: 25% decrease in HR or HR of 50-60bpm
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19
Q

Hepatic encephalopathy (HE)

A
  • due to impaired hepatic clearance of neurotoxic molecules (ammonia)
  • most cases precipitating cause can be identified, treatment of cause usually results in complete resolution
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20
Q

Evolution of hepatic encephalopathy

A
  • first sign: sleep disturbance
  • asterixis: flapping hand tremor
  • altered reflexes
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21
Q

Diagnosis of HE

A
  • CLINICAL diagnosis: based on signs of liver disease, asterixis, hyperreflexia
  • elevated blood ammonia levels NOT required to make diagnosis
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22
Q

Precipitants of hepatic encephalopathy

A
  • GI bleed, infection, constipation, hypoxia, electrolyte imbalance, use of sedatives, or tranquilizers
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23
Q

Treatments of HE

A
  • lactulose: osmotic laxative
  • neomycin or rifaximin: if no response to lactulose
  • sodium benzoate rarely used
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24
Q

Hepatocellular carcinoma (HCC)

A
  • primary liver cancer: 80% occur in setting of cirrhosis
  • incidence in cirrhotics is 3-5%/year
  • risk is even higher with cirrhosis due to chronic viral hepatitis
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25
Q

HCC screening and treatment

A
  • cirrhotic patients: ultrasound q 6mos +/- serum alpha fetaprotein
  • treatment: liver transplant if limited tumor burden, local Rx, systemic Rx
26
Q

Liver transplantation in HCC

A
  • can be life saving
  • timing of transplant is KEY
  • MELD score used to predict 3 month mortality, thus priority for transplant
27
Q

Model for end stage liver disease: MELD Score

A
  • based on 3 lab scores: objective

- serum creatinine, serum bilirubin, INR

28
Q

Liver function tests

A
  • not tests of liver function
  • estimate metabolic function
  • indicate cholestasis
  • reflective of hepatocellular injury
29
Q

Indices of metabolic function

A
  • serum albumin, bilirubin, prothrombin time

- estimate severity of liver disease in pts WITH cirrhosis

30
Q

Cholestasis lab values

A
  • hallmark is elevation of alkaline phosphatase: bone and placenta can be other sources as well
  • bilirubin need not be elevated for pattern to be cholestatic
31
Q

Alkaline phosphatase

A
  • heat fractionation: antiquated approach to identifying source of elevated alk phos that can yield equivocal results
  • isolated alkaline phosphatase: order GGT or 5’ nucleotidase, canalicular enzymes, so if elevated alk phos is coming from live
32
Q

Causes of cholestasis

A
  • extrahepatic biliary obstruction
  • drug induced
  • cholestatic liver diseases
  • infiltrative diseases
  • sepsis
33
Q

Gilbert’s syndrome

A
  • genetic condition effecting 5% of population
  • causes isolated unconjugated hyperbilirubinemia
  • not a disease; needs no treatment
34
Q

Indices of hepatocellular injury

A
  • alanine aminotransferase
  • aspartate aminotransferase
  • highest levels of ALT in liver so specific
  • AST found in other places
35
Q

Elevated aminotransferases

A
  • correlation b/w height of elevation and degree of necrosis is poor
  • normal values don’t preclude significant liver injury
36
Q

AST:ALT ratio

A
  • AST:ALT usually 2 suggestive of alcoholic liver disease
37
Q

Differential diagnosis of AST/ALT > 1000

A
  • acute viral hepatitis
  • toxin (mushroom poisoning)
  • drug (acetaminophen)
  • ischemia (“shock liver”)
38
Q

Major complications of cirrhosis

A
  • ascites
  • variceal bleeding
  • hepatic encephalopathy
  • hepatocellular carcinoma
39
Q

Morphology of alcohol related liver disease

A
  • fatty change: steatosis
  • steatohepatitis
  • cirrhosis
40
Q

Alcoholic steatohepatitis vs. NAFLD/NASH: clinical

A
  • alcohol: EtOH, AST»ALT, GGT high, elevated MCV

- NAFLD/NASH: metabolic syndrome, obesity, or diabetes, ALT>AST, low titre positive ANA

41
Q

Alcoholic steatohepatitis vs. NAFLD/NASH: histology

A
  • alcohol: more ballooned hepatocytes, more mallory hyaline, more neutrophilic inflammation
  • NAFLD/NASH: more fat, numerous glycogenated nuclei, less active
42
Q

Autoimmune hepatitis

A
  • 4:1 female predominance
  • can be associated with other autoimmune conditions
  • treatment: immunosuppression-prednisone
43
Q

Autoimmune hepatitis: aspects in favor

A
  • female
  • high protein (globulin)
  • HLA DR3 or DR4
  • other autoimmune disease
44
Q

Drug induced liver injury: types

A
  • type A: predictable, dose dependent toxicity, characteristic histology-EX: acetaminophen
  • type B: unpredictable, occur at therapeutic doses, may be accompanied by systemic features (fever, rash, eosinophilia, autoantibodies)-EX: nitrofurantoin
45
Q

Clinical features and diagnosis of DILI

A
  • hepatitis or cholestasis
  • diagnosis: exclusion of other causes, known effect of drug, chronology (onset within 90 days of beginning drug, may become evident after stopping drug)
46
Q

Treatment of DILI

A
  • stop the drug
  • only specific antidote is N-acetyl-cysteine (acetaminophen)
  • liver transplant for fulminant hepatic failure
47
Q

DILI histology

A
  • mimics of all patterns of liver disease

- recognition based on temporal relationship: when was drug started, when was jaundice or abnormal test noted

48
Q

Antidote to acetaminophen

A

N-acetyl-cysteine

- most effective within 8 hours of ingestion

49
Q

Herbal liver injury

A
  • just because its natural doesn’t mean it won’t cause damage
50
Q

Hemochromatosis

A
  • autosomal recessive disorder
  • leads to iron overload
  • multiple organs effected: bronze diabetes
51
Q

Hemochromatosis mutations

A
  • mutations affect transmembrane protein HFE (C282Y, H63D)
  • HFE mutations appear to disrupt sensing of iron status in hepatocytes
  • pts homozygous for C282Y defect or compound heterozygous C282Y/H63D
52
Q

Hemochromatosis: diagnosis, caveat, biopsy, treatment

A
  • diagnosis: transferrin saturation > 45% prompts HFE genotyping
  • caveat: iron studies frequently abnormal in patients liver disease
  • biopsy: pts with HFE mutations, or abnormal transferrin saturation
  • treatment: phlebotomy to mobilize iron stores
53
Q

Primary biliary cirrhosis (PBC)

A
  • damage to small bile ducts
  • most pts not cirrhotic at presentation: “primary biliary cholangitis”
  • autoimmune etiology
54
Q

PBC presentation, serology, consequences, treatment

A
  • presentation: WOMEN, most asymptomatic at dx
  • serology: anti mitochondrial Ab 90%
  • consequences: pruritis, hyperlipidemia, bone density, cirrhosis
  • treatment: ursodiol may slow progression of liver disease
55
Q

Primary sclerosing cholangitis (PSC)

A
  • chronic disease characterized by inflammation and fibrosis of intra AND extra hepatic bile ducts leading to STRICTURES
  • diagnosis: cholestatic chemistries plus multiple bile duct strictures and segmental dialtions (RADIOLOGIC diagnosis)
  • autoantibodies present (ANCA, ANA) but no required for diagnosis
56
Q

PSC: presentation, risks, treatment

A
  • up to 80% of cases occur in setting of IBD
  • symptoms: RUQ discomfort, fatigue, pruritis; look for stricture
  • risk: colon cancer, cholangio cancer
  • treatment: no medical treatment, transplant/surgical resection of obstruction
57
Q

Diseases affecting intrahepatic biliary tree

A
  • PBC: intrahepatic only

- PSC: intra/extrahepatic

58
Q

Features common to PBC and PSC

A
  • elevated alkaline phosphatase and GGT
  • patchy involvement of triads
  • destruction of interlobular bile ducts
59
Q

Features differentiating PBC and PSC

A
  • PBC: antibody-antimitochondrial, IBD-uncommon, cholangiogram-pruned biliary tree, extrahepatic ducts-not involved, distinctive lesion-florid duct, cholangiocarcinoma-no
  • PSC: antibody-UC ANCA, IBD-common, cholangiogram-beaded bile ducts, extrahepatic ducts-involved, distinctive lesion-fibro obliterative
60
Q

Autoimmune liver disease

A
  • autoimmune hepatitis + PBC (more likely) or PSC

MODHIII - Unit 3 (20 decks)

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