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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
HCC screening and treatment
- cirrhotic patients: ultrasound q 6mos +/- serum alpha fetaprotein - treatment: liver transplant if limited tumor burden, local Rx, systemic Rx
26
Liver transplantation in HCC
- can be life saving - timing of transplant is KEY - MELD score used to predict 3 month mortality, thus priority for transplant
27
Model for end stage liver disease: MELD Score
- based on 3 lab scores: objective | - serum creatinine, serum bilirubin, INR
28
Liver function tests
- not tests of liver function - estimate metabolic function - indicate cholestasis - reflective of hepatocellular injury
29
Indices of metabolic function
- serum albumin, bilirubin, prothrombin time | - estimate severity of liver disease in pts WITH cirrhosis
30
Cholestasis lab values
- 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
Alkaline phosphatase
- 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
Causes of cholestasis
- extrahepatic biliary obstruction - drug induced - cholestatic liver diseases - infiltrative diseases - sepsis
33
Gilbert's syndrome
- genetic condition effecting 5% of population - causes isolated unconjugated hyperbilirubinemia - not a disease; needs no treatment
34
Indices of hepatocellular injury
- alanine aminotransferase - aspartate aminotransferase - highest levels of ALT in liver so specific - AST found in other places
35
Elevated aminotransferases
- correlation b/w height of elevation and degree of necrosis is poor - normal values don't preclude significant liver injury
36
AST:ALT ratio
- AST:ALT usually 2 suggestive of alcoholic liver disease
37
Differential diagnosis of AST/ALT > 1000
- acute viral hepatitis - toxin (mushroom poisoning) - drug (acetaminophen) - ischemia ("shock liver")
38
Major complications of cirrhosis
- ascites - variceal bleeding - hepatic encephalopathy - hepatocellular carcinoma
39
Morphology of alcohol related liver disease
- fatty change: steatosis - steatohepatitis - cirrhosis
40
Alcoholic steatohepatitis vs. NAFLD/NASH: clinical
- alcohol: EtOH, AST>>ALT, GGT high, elevated MCV | - NAFLD/NASH: metabolic syndrome, obesity, or diabetes, ALT>AST, low titre positive ANA
41
Alcoholic steatohepatitis vs. NAFLD/NASH: histology
- alcohol: more ballooned hepatocytes, more mallory hyaline, more neutrophilic inflammation - NAFLD/NASH: more fat, numerous glycogenated nuclei, less active
42
Autoimmune hepatitis
- 4:1 female predominance - can be associated with other autoimmune conditions - treatment: immunosuppression-prednisone
43
Autoimmune hepatitis: aspects in favor
- female - high protein (globulin) - HLA DR3 or DR4 - other autoimmune disease
44
Drug induced liver injury: types
- 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
Clinical features and diagnosis of DILI
- 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
Treatment of DILI
- stop the drug - only specific antidote is N-acetyl-cysteine (acetaminophen) - liver transplant for fulminant hepatic failure
47
DILI histology
- mimics of all patterns of liver disease | - recognition based on temporal relationship: when was drug started, when was jaundice or abnormal test noted
48
Antidote to acetaminophen
N-acetyl-cysteine | - most effective within 8 hours of ingestion
49
Herbal liver injury
- just because its natural doesn't mean it won't cause damage
50
Hemochromatosis
- autosomal recessive disorder - leads to iron overload - multiple organs effected: bronze diabetes
51
Hemochromatosis mutations
- 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
Hemochromatosis: diagnosis, caveat, biopsy, treatment
- 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
Primary biliary cirrhosis (PBC)
- damage to small bile ducts - most pts not cirrhotic at presentation: "primary biliary cholangitis" - autoimmune etiology
54
PBC presentation, serology, consequences, treatment
- 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
Primary sclerosing cholangitis (PSC)
- 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
PSC: presentation, risks, treatment
- 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
Diseases affecting intrahepatic biliary tree
- PBC: intrahepatic only | - PSC: intra/extrahepatic
58
Features common to PBC and PSC
- elevated alkaline phosphatase and GGT - patchy involvement of triads - destruction of interlobular bile ducts
59
Features differentiating PBC and PSC
- 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
Autoimmune liver disease
- autoimmune hepatitis + PBC (more likely) or PSC

MODHIII - Unit 3 (20 decks)

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