Liver Function Tests Flashcards
ALT / AST
shows injury to hepatocyte
Alkaline Phosphatase
shows injury to cholangiocytes- meaning obstruction to bile flow
Injury to hepatocyte (Hepatocellular)
Viral hepatitis Drugs affecting hepatocytes Alcohol liver disease Non-alcohol liver disease Autoimmune hepatitis Hereditary diseases (hereditary hemochromatosis, Wilson disease)
Obstruction of bile flow
Gallstones in common bile duct
Pancreatic/ hepatic mass
Drugs affecting bile flow
ALT > AST
all hepatocellular conditions
AST > ALT
conditions caused by alcohol
AST > ALT (2:1) with AST in 100-200 u/L
- Alcoholic liver disease
- Review alcohol hx
ALT > AST, with ALT in 1000 u/l
- Acute viral hepatitis (A, B), acute drug induced injury, (acetaminophen >7.5 g/d)
- Hepatitis A, B panel, acetaminophen level
ALT > AST, with ALT in 100s u/l
- Chronic viral hepatitis (B, C), drug-related injury (TB medications, antiepileptic, methotrexate, statins, amiodarone, acetaminophen, amoxicillin-clavulanate), non-alcoholic fatty liver disease, congestive liver disease, autoimmune hepatitis
- Hepatitis B, C panel, autoantibodies (ANA), review medication history (obesity, T2DM, hyperlipidemia)
Alkaline phosphatase (<120 u/L)
Marker of cholestatic injury (intrahepatic and extrahepatic)
Maybe slightly elevated in hepatocellular injury
Requires evaluation of biliary tree ( US-initial test, MRCP is more accurate
Elevated Alkaline Phosphatase - Ductal dilation on imaging - extrahepatic cholestasis
- Choledocholithiasis: sharp pain
2. Pancreatic Cancer: painless/dull pain
Elevated Alkaline Phosphatase - No Ductal dilation on imaging - intrahepatic cholestasis
metastatic disease (colon, prostate)- hepatocellular carcinoma
PT/INR (11-15 sec/1.0)
Most sensitive marker of synthetic function of the liver
Most sensitive marker of acute liver injury
Marker of prognosis
Increase in PT/INR= decrease in the synthetic liver capacity
**ACUTE CHANGES
Albumin (3.5-5.3 g/dl)
**NOT FOR ACUTE CHANGES
Marker of synthetic function of the liver
Decrease in albumin = decrease in the synthetic liver capacity
Albumin is not specific for the liver( decrease in albumin in nephrotic syndrome or malnutrition)
Maybe normal in acute injury
Total bilirubin (0.5 -1.0 mg/dL)
Marker of synthetic function
Indicator of severity of disease
Bilirubin >2mg/dl
Jaundice
Hepatitis A
- Transmission: Fecal oral
- At risk: Traveling to endemic areas (fecal contamination of water, food)
- Only acute form; self-limiting. Fulminant hepatitis is rare
Hepatitis B
- Transmitted by Blood, Unprotected sex, Mother-baby
- At risk: Unprotected sex, IVD users
- Acute and chronic. Chronic in 90% of infected infants and only 5% of infected adults.
Cirrhosis (in 20% of chronically infected 20 years after exposure)
Hepatocellular carcinoma (HCC 2% risk per year)
Hepatitis C
- Transmitted: Blood, Unprotected sex (very rare)
- At risk: IVD users, Healthcare workers
- 85% of infected individuals will have chronic infection.
Cirrhosis (in 20% of patients 20 years after exposure). Hepatocellular carcinoma (HCC 2% risk per year)
Hepatitis D
- Co-exist with B
- Same as B
Hepatitis E
Transmission: Fecal-oral
- Same as A
Clinical manifestation of Acute Hepatitis
- Maybe completely asymptomatic
- in severe cases:
Fatigue
Anorexia
Weight loss
Nausea, +/- vomiting
Abdominal discomfort
Low-grade fever
(+/-) arthralgia
Signs: Jaundice, scleral icterus, dark urine, pale stool, liver tenderness, hepatomegaly
Clinical manifestations of chronic hepatitis
Asymptomatic (discovered by abnormal liver enzymes/ abnormal US imaging)
Or
Mild symptoms (fatigue, abdominal discomfort “ fullness”, anorexia)
Or
Symptoms of decompensated cirrhosis (ascites…)
Signs and symptoms of decompensated liver cirrhosis: Hepatic Insufficiency
coma jaundice spider nevi pectoral alopecia gynecomastia liver damage palmar erythema altered hair distribution testicular atrophy hemorrhagic tendency ankle edema
Signs and symptoms of decompensated liver cirrhosis: portal hypertension
esophageal varices splenomegaly distension of abdominal veins ascites bone marrow changes extremity muscle wasting hemorrhoids
Ascites: physical examination
bulging flanks, fluid wave, shifting dullness
Workup for suspected hepatitis
Consider travel history, risk factors, alcohol consumption, medications review, history of diabetes, obesity, hyperlipidemia
LFTs and bilirubin (increased direct bilirubin, increased ALT more than AST, minor elevation of Alk phosphatase)
Viral hepatitis serology (A,B,C)
Consider CMV serology (CMV IgM), EB (EB IgM)
(+) IgM means
active disease
Hepatitis A serology
Patient 1: (+) anti-HAV IgM, (+) anti-HAV IgG = active
Patient 2: (+) anti-HAV IgM, (-) anti-HAV IgG = early active
Patient 3: (-) anti-HAV IgM, (+) anti-HAV IgG = immune due to vaccine or hep A resolved
Hep B antigens and antibodies
- HBs Ag: indicates ACTIVE INFECTION
- Anti HBs: resolution of active infection and immunity & successful vaccination
- HBc Ag: NOT detected in blood
- IgM Anti HBc: ACUTE INFECTION
- IgG Anti HBc: RESOLUTION OF INFECTION
- HBe Ag: high level of infectivity
- Anti HBe: low level of infectivity
Acute Hep B
HBs Ag, IgM anti HBc
Resolution of Acute Hep B
anti HBs, IgG anti HBc
Chronic Hep B
HBs Ag, IgG anti HBC
Hep C Serology
Patient 1: (-) anti-HCV = no disease
Patient 2: (+) anti-HCV , followed by (+) HCV RNA = active disease
Patient 3: (+) anti-HCV , followed by (-) HCV RNA = resolved/ treated
Treatment of acute viral hepatitis (A and B)
- Supportive (anti-emetics, adequate hydration, adequate nutrition)
- AVOID alcohol
- Steroids, high-carbohydrate and low-protein diets ARE NOT recommended
Treatment of chronic hepatitis B
Oral direct antiviral therapy monotherapy, 20-25% achieve suppression of viral load
Only patients with significant viral activity (HBeAg and high viral load should be treated
Goal is suppression Hep B replication (low viral load -HBV DNA) and HBeAg seroconversion
Long-term therapy is necessary (4-5 years and more)
Treatment of chronic hepatitis C
Oral direct antiviral therapy (one pill once a day), >90% patients achieve cure
Goal is to achieve undetectable HCV RNA for at least 6 months after cessation of therapy (= cure)
The treatment and the duration is based on Hepatitis C genotype (genotype 1 accounts for 70%), usually 12-24 weeks
All patients with active HCV infection would benefit, with the exception of those with life expectancy less than 12 months
Treatment of compensated cirrhosis
Surveillance of HCC every 6-12 months (ultrasound)
Screening for esophageal varices (endoscopy)
Avoidance alcohol (no safe level !)
HAV, HBV, pneumococcal pneumonia, and influenza immunizations
Statins can be safely used
Acetaminophen may be used in persons with cirrhosis in doses of up to 2 g daily
Aspirin and other NSAIDs should be avoided
High-caloric small meals
Treatment of decompensated cirrhosis
Esophageal varices – non-selective beta-blockers ( decrease portal flow)
Ascites – diuretics (Spironolactone) and sodium restriction diet
Hepatic encephalopathy- lactulose (decrease absorption of ammonia)
Screening for Hep C
- born 1945-1965 regardless of risk
- IV drug users
- HD pt
- HIV pt
- MSM
- Abnormal liver enzymes
Screening Hep B
- all pregnant women
- IV drug users
- HIV
- MSM
- abnormal liver enzymes
Hep A Vaccine (2 doses)
- travelers to endemic areas
- MSM
- drug users (poor housing conditions, high hep c prevalence)
- pt with chronic liver disease
Hep B vaccine (3 doses)
- IVD users
- multiple sex partner
- MSM
- Healthcare/ public safety workers
- Patients with chronic liver conditions
- Patients on HD
- Patients with DM 19-59 y. (sharing needles, finger stick devices, syringes , needles)
Post-exposure Hep A
- for close household and sexual contact during outbreak
For healthy adults <40y/o»_space; Hepatitis A vaccine (x 2 doses)
For > 40y/o»_space; HAIG followed by vaccination
Post-exposure Hep B
- percutaneous exposure, sexual contact
HBIG and Hepatitis B vaccine (x 3 doses)
