Exam 1 Flashcards
(112 cards)
AST/ALT
Hepatocellular pattern when these transaminases predominate
Alk phos
If GGT elevated also, then hepatic
Associated with obstruction, “cholestatic pattern”
Conjugation of bilirubin
Made to be more polar so that it can be absorbed better
Painless jaundice
Pancreatic/biliary cancer until proven otherwise
Jaundice levels
Total bili >2
Conjugated jaundice
Dark, tea colored urine (because direct bili can be excreted)
Light clay colored stools (no bili in the gut)
First imaging for the liver
Ultrasound
Reasons for nonpathologic increase in unconjugated bilirubin in a newborn
High HCT and short lifespan of fetal RBC
Low bilirubin clearance in first week
Increased enterohepatic circulation of bilirubin
Face vs feet jaundice in a newborn
Feet jaundice is a much higher level of bilirubin
Kernicterus
Bilirubin is neurotoxic to basal ganglia
Conjugated hyperbilirubinemia in a newborn
Abnormal and requires work up
Usually cholestasis
Kasai procedure
Remove damages bile duct to create roux en Y in neonatal jaundice from cholestasis
Gilbert syndrome general
Benign, asymptomatic jaundice
Autosomal dominant
UGT gene promoter defect
Criggler-Najjar syndrome general
Inherited unconjugated hyperbilirubinemia
Complete loss of UGT, autosomal recessive
Type 1 criggler-najjar
Persistent hyperbilirubinemia after birth, normal liver otherwise
Usually fatal from kernicterus
Type 2 crigler najjar
Later onset than type 1, milder elevations, traetment often not needed
Reye’s syndrome general
Usually pediatric and postinfections
Triad of encephalopathy, fatty liver/failure, transaminitis
Avoid ASA!!
Hemochromatosis general
Autosomal recessive HFE gene
Commonly white patients
Increased Fe uptakeas hemosiderin in liver, pancreas, heart, etc.
Hemochromatosis symptoms
Fatigue, impotence, arthralgia, hepatomegaly, hyperpigmentation(common), DM
Hemochromatosis genetics
Test all 1st degree relatives of the person diagnosed
Hemochromatosis treatment
Phlebotomy if symptomatic
Fast iron/decrease intake
Avoid vitamin C supplements
Wilson disease general
Autosomal recessive, less than 40 years old
Disrupted copper transport
Deposited copper in the liver and brain
Looks like parkinson’s in a young patient
Kayser fleischer ring
Pathognomonic for wilson disease, granular. Copper deposits around iris
Low ceruloplasmin
Alpha 1 antitrypsin deficiency general
Can lead to cholestasis
Otherwise acts mostly in the lung, manifests as early onset of emphysema