Liver Disease

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Clinical Chemistry
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1

necrosis

results from injurious environment; cellular swelling and loss of membrane integrity, toxic injury from aspirin or acetominophen, and further inflammatory response and cell injury

2

apoptosis

programmed cell death-hepatitis

3

aminotransferases and ALP

distinguish pattern of injury

4

serum albumin

tests chronicity

5

PT or factor V

detects severity

6

biopsy

detects fibrosis of the liver

7

hepatocellular

functional liver disease

8

obstructive

mechanical liver disease

9

ALT, AST, ALP, GGT, LD

five useful liver lab tests

10

aspartate aminotransferase (AST)

converts aspartate to oxaloacetate

11

alanine aminotransferase (ALT)

converts alanine to pyruvate

12

ALT

more liver specific enzyme since it is found primarily in the liver

13

ALT and AST

aminotransferases

14

2-6 weeks

how long aminotransferases remain elevated

15

acute conditions (viral hepatitis, drug and toxin-induced liver necrosis, hepatic ischemia)

raise aminotransferases to the highest levels

16

ALT>AST

ALT/AST relationship in acute conditions

17

obstructive liver disease

raise aminotransferases moderately or not at all

18

alkaline phosphatase, y-glutamyltransferase, 5'nucleotidase, and lactate dehydrogenase

four serum phosphatases

19

alkaline phosphatase

zinc metalloenzymes that differentiate hepatobiliary disease from bone disease; significantly increased in extrahepatobiliary obstruction and intrahepatic cholestasis; slight to moderate increase in hepatocellular disorders-hepatitis and cirrhosis, bone disorders, and pregnancy

20

y-glutamyltransferase

helps to differentiate ALP elevated levels; higher levels in biliary obstrcution, alcohol and drug ingestion

21

5'nucleotidase

hydrolysis; increased in hepatobiliary disease, metastatic liver disease; no bone source

22

lactate dehydrogenase

not very helpful; moderately raised in acute viral hepatitis and cirrhosis, metastatic carcinoma of liver; slightly raised in biliary tract disease

23

ALP, GGT

higher levels in obstructive disease than hepatocellular disease

24

AST, ALT

higher in acute hepatocellular disease rather than obstructive disease

25

LDH

elevated only slightly in either condition

26

hepatitis

injury to liver characterized by inflammation in liver tissue; caused by virus, bacteria, parasite infections, radiation, drugs, chemicals, autoimmune disease, and toxins; jaundice, dark urine, fatigue, nausea, vomiting, abdominal pain

27

hepatitis A

most common form of viral hepatitis worldwide; caused by infection with HAV via contaminated or improperly handled food; fecal-oral

28

hepatitis B

can cause both acute and chronic hepatitis; caused by infection with HBV via parenteral, perinatal, and sexual transmission; serologic markers core, surface, and envelope

29

hepatitis C

caused by infection with HCV via parenteral transmission (blood transfusions)

30

hepatitis D

unique subvirus of HBV; requires HbsAg for replication

31

hepatitis E

caused by infection with HEV; nonenveloped RNA virus; very small; fecal-oral; water borne epidemics in developing countries

32

HBV

only DNA hepatitis virus

33

HbsAg

early acute infection marker

34

HbsAg, anti-HBc, anti-HBc IgG

acute infection

35

HbsAg and anti-HBc

chronic infection

36

anti-HBc

recovery from past infection