Liver disease Flashcards
Increased alk phos and bilirubin signify what kind of injury?
Cholestasis
Increased AST and ALT signify what kind of injury?
Hepatocellular injury
Progression of alcoholic liver disease
Fatty liver -> hepatitis -> cirrhosis
Fatty liver is asymptomatic
Hepatitis has an increased AST/ALT/alk phos/GGT/bilirubin
Cirrhosis has all the signs of ESLD
Workup of isolated hyperbilirubinemia
Direct (conjugated) hyperbilirubinemia: Dubin-Johnson and Rotor
Unconjugated hyperbilirubinemia: hemolytic anemia, Criggler-Najjar, and Gilberts
Gilberts disease
Unconjugated hyperbilirubinemia
Asymptomatic most of the time
May present with mild jaundice when stressed, sick, etc.
2/2 decreased activity of glucuronyl transferase
Crigler-Najjar
The only form of hyperbilirubinemia which can be dangerous
Unconjugated hyperbilirubinemia
Type I: severe, often p/w permanent neuro damage
Type II: less severe
Tx: phototherapy or plasmapharesis
Phototherapy helps which kind of bilirubinemia?
Unconjugated
Dubin-Johnson disease
Conjugated hyperbilirubinemia
Asymptomatic, can p/w icterus. Triggered by URI, OCPs, pregnancy
Black liver pigmentation on biopsy
Labs: normal urine coproporphyrin level but the breakdown is very altered (normally, 80% is coproporphyin III, in this dz 80% is coproporphyin I)
Rotor syndrome
Asymptomatic conjugated hyperbilirubinemia
Defect of hepatic storage leads to leakage into plasma
Elevated direct and indirect bili w/ nl LFTs
No pigmented granules
Ddx of increased alk phos and bilirubin
Cholestasis:
- Ductal dilation present: biliary obstruction (stone, stricture, cancer)
- No ductal dilation: intrahepatic cholestasis (postop, sepsis, medications)
Metabolic syndromes that can cause chronic hepatitis
Hemochromatosis
Wilson’s dz
Alpha 1 antitrypsin deficiency
Clinical presentation of acute hepatitis
Viral prodrome (fever, nausea, vomiting, malaise) followed by jaundice and RUQ tenderness
Lab differences between acute and chronic hepatitis
Acute: markedly elevated AST, ALT and elevated bili/alk phos
Chronic: persistently elevated ALT and AST for 3-6 months
Timeline of HBV serologies
Acute infection: HBsAg +
As infection progresses: HBeAg starts to appear
Then a large titer of Anti-HBc (anti-core antigen) presents (2 months)
HBsAg and HBeAg start to decrease and disappear at 5 months
Anti-HBe starts to present around this time also
Window period: between disappearance of HBsAg and appearance of Anti-HBs
You are not immune unless you have Anti-HBs
Viral serology for HAV infection
Look for IgM antibody to HAV
Autoimmune hepatitis serologies
Anti-smooth muscle antibodies
Labs for hemochromatosis
High ferritin, high transferrin saturation (>50%)
Labs for Wilson’s disease
Low ceruloplasmin, high urine copper
Treatment of chronic HBV infection
Interferon and lamivudine (3TC) or adefovir
Treatment of chronic HCV infection
Interferon and ribavirin
Definition of cirrhosis
Fibrosis and nodular regeneration 2/2 chronic hepatic injury
Budd-Chiari syndrome
Hepatic vein thrombosis 2/2 hypercoaguable state
Non-hepatitis causes of cirrhosis
Right sided heart failure, biliary disease (primary sclerosing cholangitis or primary biliary cirrhosis), Budd-Chiari syndrome, constrictive pericarditis
Effects of portal HTN
Varices (esophageal, hemorrhoids) Melena (2/2 variceal bleeding) Splenomegaly Caput medusae (blood vessels near the umbilicus) Ascites
Effects of liver cell failure
Neuro: AMS and asterixis
Synthetic: gynecomastia, loss of sexual hair, and testicular atrophy, hypercoagulation, anemia, edema
Others: spider nevi, scleral icterus, jaundice
Serum-ascites-albumin-gradient
Serum albumin - ascites albumin
If > 1.1: 2/2 portal HTN
If < 1.1: 2/2 nephrotic syndrome, Tb, malignancy with peritoneal carcinomatosis
Causes of portal HTN
Pre-sinusoidal: splenic or portal vein thrombosis, schistosomiasis
Sinusoidal: cirrhosis
Post-sinusoidal: RHF, Budd-Chiari, constrictive pericarditis
MOA of lactulose
Lactulose is digested by gut bacteria
This acidifies the gut and converts NH3 -> NH4+, which is not absorbed
MOA and use for neomycin
Antibiotic that destroys ammonia producing gut bacteria
Short term use for hepatic encephalopathy and liver failure
SE: ototoxicity and nephrotoxicity
Complications of cirrhosis
Variceal bleeding Coagulopathy Hepatic encephalopathy Hepatorenal syndrome Spontaneous bacterial peritonitis Ascites
Diagnosis of SBP
PMNs > 250/mL and a + Gram stain
Tx of SBP
IV antibiotics ie 3rd generation cephalosporin
IV albumin
PPx w/ fluoroquinolone to prevent future infections
How to treat coagulopathy in liver disease
FFP. Vitamin K will not help
Primary biliary cirrhosis: what is it
An autoimmune disorder characterized by destruction of intrahepatic bile ducts
Presentation of primary biliary cirrhosis
Jaundice, pruritis, and fat-soluble vitamin deficiency (A, D, E, K)
Lab findings of primary biliary cirrhosis
Increased alk phos, increase bilirubin
+ antimitochondrial antibody
Increased cholesterol
Treatment of primary biliary cirrhosis
Ursodeoxycholic acid slows progression
Liver transplant
Biopsy findings of primary biliary cirrhosis
Ductopenia which can be caused by failing liver transplant, Hodhkins, CMV, sarcoid, HIV
Lab values in hepatocellular carcinoma
Abnormal LFTs
Significantly elevated AFP levels
Presentation of hemochromatosis
Diabetes, abdominal pain, hypogonadism, arthropathy of the MCP joints, heart failure, restrictive cardiomyopathy, cirrhosis
Bronze skin pigmentation, hepatomegaly, and testicular atrophy
Labs in hemochromatosis
Elevated serum iron, elevated ferritin, decreased transferrin Transferrin saturation (serum Fe/TIBC) > 45% is highly indicative
Tx of hemochromatosis
Weekly phlebotomy until iron levels normalize, phlebotomy every 2-4 months
Deferoxamine (iron chelator) can be used as maint therapy
Presentation of Wilson’s disease
Hepatitis/cirrhosis
Neurologic dysfunction: ataxia and tremor
Psychiatric abnormalities: psychosis, anxiety, mania, depression
PE: Kayser-Fleischer rings, jaundice, hsm, asterixis, rigidity
Wilson’s disease labs
Decreased serum ceruloplasmin, increased urinary Cu excretion
How to treat Wilson’s disease?
Penicillamine: copper chelator that increases urinary excretion
Zinc: increases fecal excretion
