4. Fxnl Liver Tests and tx of Chronic Hepatitis Flashcards
LO1: AST abnl
1) signals hepatocellular damage
LO1: ALT abnl
1) Hepatocellular damage
231480
LO1: Alk phos abnl
1) Cholestasis
2) Infiltrative dz
3) biliary obstruction
LO1: Bili Abnl
1) Cholestasis
2) Impaired conjugation
3) biliary obstruction
LO2: Hepatocellular pattern of labs
1) Predominantly Elevated ALT and AST
LO2: Cholestatic pattern of labs
Predominantly Alk phos elevation
LO3: Bilirubin metabolism
NL heme degradation product
1) unconjugated bili (unBR) exits sinusoid into hepatocyte
2) unBR + UDP glucuronyl transferase (UDP GT) = Conjugated bili (cBR)
3) cBR pumpred into bile canaliculus via ATP
LO3: Jaundice: Conjugated bili
1) hemolytic jaundice - overwhelmed conjugation
2) biliary obstruction -intra or extrahepatic
3) Dubin-Johnson Defective secretion of conjugated bili -rare, MRP-2 mutation, benign
LO3: Jaundice: Unconjugated bili
1) Gilbert’s Dz -decreased bili uptake
- mutation in gen for UDP GT
2) Crigler-Najjar Syndrome -impaired bili conjugation
- -rare
3) Increased RBC destruction in cirrhosis
LO4: abnl Liver algorithm: AST and ALT < 5x NL
1) Hx and PE
2) D/c hepatotoxic meds
3) alk phos, bili, INR, albumin, viral hepatitis serologies, iron studies
4a) neg serologies, symptomatic
- US, ANA, Anti-SM Ab, ceruloplasmin, Alpha-1-antitrypsin
5a) Liver biopsy
4b) neg serologies, asymptomatic
- lifestyle modification
5b) Repeat liver chemistry in 3-6 months, if abnl -> 4a
LO6: Hep B Tx
1) Interferon
- 1 yr
2) Nucleoside/tide analoges-tenofovir
- fewer SE
LO6: Hep C Tx
Ledipasvir/sofosbuvir +/- Ribavirin
LO6: Hereditary hemochromatosis: Tx, indications for tx and cause
1) Therapeutic phlebotomy, endpt= ferritin of 50 ng/mL or chelation tx
2) HFE gene- homozygote C282Y
3) Inherited disroder -> increased inestinal Fe absorption
LO6: Autoimmune Hepatitis: Tx, indications for tx and cause
1) Corticosteroids, azathioprine. Relapse common
2) ANA +, symptomatic
3) Chronic hepatitis -immunologic and autoimmune
LO6: Primary Biliary Cirrhosis: Tx, indications for tx and cause
1) Ursodeoxycolic acid (UDCA)-improves bile acid transport, detoxify bile, and cytoprotective
- -improve liver chem
- -improve survival
- -reduce liver transplant
2) cholestatic w/o increased bili. AMA +
3) Immune mediated -damage to small intrahepatic bile ducts
LO6: Primary Sclerosing cholangitis: Tx, indications for tx and cause
1) No effective med tx. Manage obstruction - stenting strictures, antibx for cholangitis
2) Strictures and obstruction of bile duct can lead to cirrhosis
2a) increased risk of cholangiocarcinoma
3) Inflamm of intr and extrahepatic large bile ducts
4) CT dilated bile ducts
LO6: Wilson Dz: Tx, indications for tx and cause
1) copper chelation
-D-penicillamine
-Trientine
Maintenance tx - zinc
2) Low ceruloplasmin
Kayser-Fleisher rings -eyes
3) AR. Decreased hepatocellular Cu excretion - > hepatic Cu accumulation and injury
LO6: non-alcoholic steatohepatitis: Tx, indications for tx and cause
1) Modify risk factors
-Obesity
-DM2
Dyslipidemia
? DM meds, Vit E
2)
3) NASH- hepatic steatosis and inflamm w/ hepatocyte injury (ballooning)
Albumin and PT abnl
1) Signals synthetic dysfxn
PT time deficiency vs dysfxn
1) Administer SQ Vit K
- -no correction -liver dysfxn
- -normalzie -Vit K deficient
4 patterns of dz that LFT can indicate
1) Hepatocellular injury or necrosis
2) cholestasis
3) synthetic dysfxn -mixed
4) Infiltrative -predominant alk phos elevated
AST vs. ALT: Location in hepatocyte
AST- cytosol and mitochondria
ALT - Cytosol
AST vs. ALT: Organ expression
AST - Liver, heart, muscle, blood
ALT -liver only
AST: ALT patterns
> 1 =cirrhosis
2 = ETOH
-lower ALT from B6 deficiency, which is cofactor for ALT
-preferential injry to mitochondria w/ AST
Alk phos
1) cleaves phosphates
2) Present in nearly all tissues
3) Elevation causes
- cholestatic or infiltrative
- biliary obstruction
- bone dz
- Pregnancy
Alk phos: hepatobiliary vs. nohepatobiliary
1) 5-nucleotidease -only up in liver dz, highest in cholestatic dz
2) GGT
- not in bone
- up in ETOH and all types of liver dz
Infiltrating dz leading to alk phos up
1) sarcoidosis
2) Tuberculosis
3) fungal infxn
4) Amyloidosis
5) Lymphoma
6) mets
7) HCC
Elevated Alk phos algorithm
1) Hx and PE
2) Liver chemistries
3a) NL AST and ALT
4a) GGT or 5’-nucleotidease-> 4b if elevated
5a) Nl -not hepatobiliary
3b) abnl liver chem
4b) RUQ US for biliary dilation
5bi) biliary dilated - ERCP or MRCP
5bii) not dilated - AMA
6bii) Positive =PBC
6bii1) Negative - test for elevated ALT, liver biopsy, and/or ERCP or MRCP
HBsAg
1) active infection
2) > 6 mo = chronic hepatitis B
HBsAb
Immunity to Hep B
HBcAb
Marker of active or prior infxn
HBeAg
surrogate of high viral load
HBeAb
associated w/ lower viral load
HBV DNA
Active viral replication
Goal of HBV Tx
1) Loss of HBeAg, develop HBeAb, neg HBV DNA
2) Prevent decompensated cirrhosis
Goal of HCV Tx
1) Chronic HCV = HCV RNA in blood > 6 mo after infxn
2) HCV RNA neg 12 weeks after d/c tx
3) Sustained SVR = cure