Fxnl Liver tests (5) Flashcards
AST is a hepatocellular dmg marker, where else is it located?
Liver
heart
muscle
blood
(ALT is liver only)
Typical AST:ALT ratio is ____
___ is cirrhosis
___ is alcoholic liver disease
1
>2
Alkaline phosphatase
present in nearly all tissue
Elevated in:
- Cholestatic or infiltrative dis of liver
- obstruction of biliary system
- bone disease
- pregnancy
Prothrombin time
prolongation is significant for?
assess extrinsic clotting pathway
- prolonged jaundice
- malabsorption
what liver chemistry test elevation is seen with:
hepatocellular
cholestatic
hepatocellular: AST/ALT elevation
Cholestatic: alk phos elevation
Conjugated bilirubin (\_\_\_\_\_) Unconjugated bilirubin (\_\_\_\_\_)
- Conjugated bilirubin (indirect)
* Unconjugated bilirubin (direct)
Etiology of Mild (
- Acute viral hepatitis (A-E, herpes)
- Meds/toxins
- Ischemic hepatitis
- Autoimmune hepatitis
- Wilson’s disease
- Budd-chiari syndrome
- hepatic artery ligation or thrombosis
If pt has ↑ AST & ALT
- Hx and Physical →
- discontinue hepatotoxic meds→
- alk phos, albumin, bili, INR, viral hep serologies, iron →
NEGATIVE SERO + SYMPTOMATIC
4a. US, ANA, ASMA, ceruloplasmin, a1-antitrypsin
5a. Liver biopsy
NEG SERO + ASYMPTOMATIC
- Lifestyle mod
- 3-6 mo repeat liver chem
- if abnl run step 4a
How can you tell if the problem is from the liver (hepatobiliary) or not from the liver (nonhepatobiliary)?
5’ nucleotidease
- elevated only in liver disease
GGT
- not in bone
- elevated after -oh consumption
Hemolytic jaundice
[overwhelmed conjugation]
Hemolytic anemia → lyse RBC → lots of UNCONJUGATED bili → liver tries to get rid of as much as poss → lots of CONJUGATED bili
Gilbert’s disease
[decreased unconjugated bilirubin uptake]
Mut in gene encoding for UDP-GT → reduced activity → elevated total bilirubin that is mainly composed of unconjugated bilirubin
Crigler-Najjar syndrome
[Impaired bilirubin conjugation]
rare - AR
UDP-GT deficiency/low levels (cant conj bili)
Type I: severe jaundice, neuro impairment
Type II: lower serum bili, no neurologic impairment
HBcAb
marker of active or prior infection. If you have this you were previously infected
Goal of Treatment for Hep B
HBeAg seroconversion, Interferon,
*Nucleoside analog (Tenofovir) - majority
[loss of HBeAg and development of HBeAb associated with negative HBV DNA when treatment is stopped]
Chronic HBV infection: indications for treatment
(1) HBsAg (+) [surface antigen] in blood for >6 months
(2) serum HBV DNA > 105 copies/mL
(3) persistent or intermittent elevation in ALT and AST levels [likelihood of HBeAg seroconversion with normal ALT is very low]
- if elevated serum ALT is high, they respond better to tx
IF PT HAS CIRRHOSIS WITH LIVER BIOPSY TX WITH NUCLEOSIDE/TIDE ANALOG (TENOFOVIR!)
Hep C infxn
- chronic HCV?
- Goal of tx?
Chronic HCV is presence of HCV RNA in blood >6 mo after infxn
Goal: clear HCV RNA so that remain HCV RNA negative 12 weeks after stopping therapy
- sustained virological response (SVR) = cure
TX: 1 pill
If pt has hereditary hemochromatosis and they have increased intestinal iron absorption. You would normally suggest therapeutic phlebotomy (to keep ferritin 50-100ng/mL). But you find out the pt is anemic, what do you do?
Anemic pts do not tolerate phlebotomy well.
Chelation therapy instead with desfuroxamide
Tx for primary biliary cirrhosis
Ursodeoxycolic acid (UDCA)
- improves bile acid transport
- detoxifies bile and provides cytoprotection
- reduce need for liver transplant
AMA + (anti mitochondrial ab) is strongly indicative of?
primary biliary cirrhosis
