Jaundice DSA - McGowan Flashcards Preview

2.2Elizi ex 2 GI 2 Exam 2 COPY > Jaundice DSA - McGowan > Flashcards

Flashcards in Jaundice DSA - McGowan Deck (113)
Loading flashcards...
1

transfusion reactions, sickle cell anemia, thalassemia (inadequate Hg), autoimmune disease

prehaptic

2

hepatitis, cancer, cirrhosis, congenital disorders, drugs

intrahepatic

3

gallstones, inflammation, scar tissue or tumors that block the flow of bile into the intestines

posthepatic

4

primary injury is to the hepatocytes
- **primarily AST/ALT elevation**
- ALT more specific for liver injury than AST

hepatocellular injury

5

primary injury is to the bile ducts
- **primarily Alk Phos and bilirubin elevated**
- failure of bile to reach duodenum
- jaundice and pruritis
- pure cholestasis (no signs of hepatocellular necrosis)

cholestatic injury

6

what are the TRUE liver function tests that McGowan wants us to know?

NOTE: AST/ALT, Alk Phos and bilirubin (LDH, GGT) can come from other sources and are not accurate to determine liver's function

- PT/INR
- albumin
- cholesterol
- ammonia

7

what are the 4 main DDx for unconjugated (indirect) jaundice?

1. hemolytic syndrome (anemia/reaction)
2. Gilbert syndrome
3. Criggler-Najjar syndrome
4. viral hepatitis

8

what are the 5 main DDx for conjucated (direct) jaundice?

1. hepatitis (acute/chronic, infectious/non-infectious)
2. cirrhosis
3. obstruction
4. Dubin-Johnson syndrome
5. Rotor syndrome

9

what are the first steps in evaluating pt with jaundice?

1. determine conjugated vs unconjugated
2. other biochemical liver tests are normal

10

how to diagnose jaundice

- order CBC to look for anemia and thrombocytopenia
- order chemistry labs: AST/ALT, total bilirubin, Alk phos (will need to request fractionated bilirubin to tell you indirect vs. direct)

11

when ALP is elevated, what is your next step?

fractionate by ordering gamma glutamyl transferase (GGT)

12

what if ALP and GGT are elevated?

most commonly coming from liver source

13

what if ALP elevated, but GGT is normal?

consider bone or other source (placenta) for elevated ALP

14

what would you order to look for anemia and thrombocytopenia?

CBC
- can check for hemolysis: haptoglobin (low), reticulocyte count (elevated) and LDH (elevated)

15

reduced activity of uridine diphosphate glucuronyl transferase
- unconjugated (indirect) bilirubin
- benign, asymptomatic hereditary jaundice, hyperbilirubinemia increased by 24-36 hour fast

Gilbert syndrome
- no tx required
- assoc with reduced mortality from cardiovascular disease

16

AR, absent UGT1A1 activity
- no liver pathology
- fatal in neonatal period

Crigler-Najjar Type 1

17

AD with variable penetrance, decreased UGT1A1 activity
- no liver pathology
- generally mild, occasional kernicterus

Crigler-Najjar Type 2

18

AR, decreased UGT1A1 activity
- no liver pathology
- innocuous (not harmful) clinical course

Crigler-Najjar Type 3

19

AR, impaired biliary excretion of bilirubin glucuronides due to mutation in canalicular multidrug resistance protein (MRP2)
- pigmented cytoplasmic globules
- innocent clinical course

Gilbert Syndrome

20

what is the main serum antibody present in acute viral hepatitis?

IgM

21

what is the main serum antibody present in chronic?

IgG

22

viral, drugs, ischemia, Budd-Chiari
- pt has aversion to smoking
- stools my be acholic (no bile = pale yellow)
- dx: CVC, CMP, PT/INR, acetaminophen level (use rumack-matthew nomogram)

acute hepatitis

23

- ssRNA virus
- aversion to smoking
- 2-3 week incubation
- enlarged tender liver, jaundice, acholic stools
- fecal-oral transmission
- **elevated bilirubin and alk phos = cholestasis**
- both IgM and IgG are detectable in serum soon after onset

Hep A
- vaccine!

NOTE: detection of IgN anti-HAV is excellent test for dx acute Hep A

24

- partially dsDNA
- acute illnes usually subsides over 2-3 weeks, 5-10% chronic
- low-grade fever, enlarged and tender liver, jaundice
- **assoc with polyarteritis nodosa**
- parenteral, sexual, perinatal transmission
- endemic in sub-saharan Africa and SE Asia
- **HBsAg-positive mothers may transmit HBV at delivery, risk of chronic infection in infant is 90%**
- elevated aminotransferases early in course (higher than HAV infection)
- substantial risk for cirrhosis -> HCC

Hep B
- vaccine!

25

what is the window period of HBV infection?

between HBsAg disappearing and HBaAb appearing, which may take several weeks
- pt is still considered to have acute HBV
- infection is only detectable with **HBcAb IgM**

NOTE: VERY important when screening blood donations

26

persistence of HBsAg more than 6 months after acute illness signifies what?

chronic Hep B

27

what appears in most individuals after clearance of HBsAg and after successful vaccination against Hep B?

anti-HBsAb

28

what does IgM anti-HBc indicate?

acute Hep B
- may also reappear during flares of previously inactive chronic Hep B

29

what appears during acute Hep B but persists indefinitely?

IgG anti-HBc

30

what is HBeAg?

Hep B envelope Ag = secretory form of HBcAg
- in serum shortly after detection of HBsAg
- indicated viral replication and infectivity
- persistence of HBeAg beyond 3 months = increased likelihood of chronic Hep B