LFTs and Hepatitis Flashcards
Liver inflammation/hepatocellular damage
Elevated ALT (more specific), AST, &GGT (worry if associated with other elevations or if elevated 3-5fold)
Most common in primary care
Any vitamins (esp. ephedra, kava, vit A) can cause elevations, many prescription meds too
Hepatitis, alcoholic liver disease, fatty liver/NASH, meds, hemochromatosis
Elevations in cholestasis
bilirubin, bilirubin direct (conjugated), alkaline phosphatase, GGT, LOW urobilinogen (white poop)
common cause-choledocholithiasis
Gamma-Glutamyl Transpeptidase (GGT)
used to determine source of ALP (alkaline phosphate) elevation (bone or liver), if GGT also elevated its likely liver
alcohol consumption makes it unclear
Reduced Liver function
Low albumin, low total protein, high/prolonged PT (more important than ALT/AST levels)
Common cause-cirrhosis or severe acute injury
Choledocholithiasis
gallstones in common bile duct from gall bladder
present with pain, jaundice, clay-colored stool, cola urine
Painless jaundice
pancreatic cancer/tumor until proven otherwise
Hepatic Obstruction
Elevated ALT/bilirubin, high/normal ALP, normal urobilinogen with bilirubin
Post-hepatic obstruction
normal/high ALT, high ALP/bilirubin, no urobilinogen, bilirubin in urine
Gilbert Syndrome
elevated Indirect (unconjugated) bilirubin Benign, defect of gene usually only in homozygotes jaundice episodes in times of stress, diagnosis made by ruling out other causes of ^indirect bilirubin
Alkaline phosphatase elevation
if GGT elevated-source is liver
if GGT not elevated-source is bone
Cirrhosis
Scarred liver (can’t be repaired)
Fatigue, portal hypertension, ascites, jaundice, easy bruising/bleeding
Definitive diagnosis/staging requires liver biopsy
High AST, normal ALT
ETOH liver disease, esp if GGT >2x normal
High ALT, normal AST
Acute/chronic viral hepatitis (normal GGT)
NASH
High Alk Phos with High ALT/AST
Cholestatic disease (choledocolithiasis)
Fatty Liver (NAFLD/NASH)
fatty infiltration with inflammation-NASH
Can lead to cirrhosis/liver failure
75% of liver disease
Most asymptomatic/fatigue
Hepatomegaly
Low albumin, high PT/ALT/AST, may have high Alkphos; can have normal labs
Ultrasound first test, definitive diagnosis needs hepatic steatosis by image/biopsy, exclusion of alcohol/other causes
Hereditary Hemochromatosis
Hereditary disorder of iron metabolism, autosomal recessive, HFE gene
Increased iron absorption in gut>accumulation of iron in liver, kidney, pancreas, heart, adrenals, testes, pituitary
Mostly caucasians (0.5%homozygotes, 10%hetero)
Symptoms in 50’s, earlier in men (periods dump iron)
Classic triad-cirrhosis, DM, bronze skin
High ALT/AST, poss alkphos, symptoms, 1st degree relative; TS >45 check for HFE
Managed with phlebotomy, avoid iron/alcohol
Major cause of death cirrhosis, HCC, D, cardiomyopathy
Autoimmune Hapatitis
Rare, more common in females
Low albumin, high PT/ALT/AST/IgG, antibodies
Diagnose with blood and liver biopsy to confirm
Manage with corticosteroids (pred)
Wilson Disease
Hereditary, autosomal recessive
impaired biliary copper excretion>accumulation of copper in organs
1/30,000
Children present with liver disease/hepatitis
Adults present with dysarthria, gait, dystonia, tremor, Parkinson’s, drooling
Kayser-fleischer rings in 1/2 pst
High ALT/AST/PT, low albumin/platelets/ceruloplasmin
Refer to specialist for diagnosis
Approach to asymptomatic with high ALT/AST
Risk factors, labs (TS/Iron>specialist)
Consider other causes (celiac, hypothyroid, adrenal insufficiency)
Screen for rare liver conditions (autoimmune/wilson)
Refer to specialist
Hepatitis A
Causes infectious/endemic fecal-oral 10-15 day incubation Excreted in feces 2 weeks before clinical illnessdaycares/sex/high risk areas >90% childhood infections asymptomatic, 25-50% adults asymptomatic 99% recover Treat symptoms Prevent with hygiene/vaccinations High ALT/AST/bilirubin, antibodies
Hepatitis B
Transmitted through blood/sex/injection
Leading cause of cirrhosis/hepatocellular carcinoma
Acute-fever, jaundice, rarely fatal; high ALT/AST/bilirubin
Chronic-asymptomatic until late, 90% infected as babies
Premature death due to cirrhosis or HCC, treat with antivirals; High ALT/AST, no other abnormals until late
Hep B surface antigen
present if currently infected
Hey B Surface antibody
appears during recovery; if present pt immune due to vaccine or infection (if core is present)
Total Hep B Core antibody
appears at onset of symptoms and stays forever-current or previous infection