Fxnl Liver tests (5) Flashcards

1
Q

AST is a hepatocellular dmg marker, where else is it located?

A

Liver
heart
muscle
blood

(ALT is liver only)

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2
Q

Typical AST:ALT ratio is ____
___ is cirrhosis
___ is alcoholic liver disease

A

1

>2

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3
Q

Alkaline phosphatase

A

present in nearly all tissue

Elevated in:

  • Cholestatic or infiltrative dis of liver
  • obstruction of biliary system
  • bone disease
  • pregnancy
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4
Q

Prothrombin time

prolongation is significant for?

A

assess extrinsic clotting pathway

  • prolonged jaundice
  • malabsorption
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5
Q

what liver chemistry test elevation is seen with:
hepatocellular
cholestatic

A

hepatocellular: AST/ALT elevation
Cholestatic: alk phos elevation

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6
Q
Conjugated bilirubin (\_\_\_\_\_)
Unconjugated bilirubin (\_\_\_\_\_)
A
  • Conjugated bilirubin (indirect)

* Unconjugated bilirubin (direct)

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7
Q

Etiology of Mild (

A
  1. Acute viral hepatitis (A-E, herpes)
  2. Meds/toxins
  3. Ischemic hepatitis
  4. Autoimmune hepatitis
  5. Wilson’s disease
  6. Budd-chiari syndrome
  7. hepatic artery ligation or thrombosis
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8
Q

If pt has ↑ AST & ALT

A
  1. Hx and Physical →
  2. discontinue hepatotoxic meds→
  3. 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

  1. Lifestyle mod
  2. 3-6 mo repeat liver chem
  3. if abnl run step 4a
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9
Q

How can you tell if the problem is from the liver (hepatobiliary) or not from the liver (nonhepatobiliary)?

A

5’ nucleotidease
- elevated only in liver disease

GGT

  • not in bone
  • elevated after -oh consumption
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10
Q

Hemolytic jaundice

A

[overwhelmed conjugation]

Hemolytic anemia → 
lyse RBC →
lots of UNCONJUGATED bili →
liver tries to get rid of as much as poss →
lots of CONJUGATED bili
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11
Q

Gilbert’s disease

A

[decreased unconjugated bilirubin uptake]

Mut in gene encoding for UDP-GT → reduced activity → elevated total bilirubin that is mainly composed of unconjugated bilirubin

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12
Q

Crigler-Najjar syndrome

A

[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

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13
Q

HBcAb

A

marker of active or prior infection. If you have this you were previously infected

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14
Q

Goal of Treatment for Hep B

A

HBeAg seroconversion, Interferon,
*Nucleoside analog (Tenofovir) - majority

[loss of HBeAg and development of HBeAb associated with negative HBV DNA when treatment is stopped]

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15
Q

Chronic HBV infection: indications for treatment

A

(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!)

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16
Q

Hep C infxn

  • chronic HCV?
  • Goal of tx?
A

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

17
Q

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?

A

Anemic pts do not tolerate phlebotomy well.

Chelation therapy instead with desfuroxamide

18
Q

Tx for primary biliary cirrhosis

A

Ursodeoxycolic acid (UDCA)

  • improves bile acid transport
  • detoxifies bile and provides cytoprotection
  • reduce need for liver transplant
19
Q

AMA + (anti mitochondrial ab) is strongly indicative of?

A

primary biliary cirrhosis