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clinical lab > evaluation of liver function > Flashcards

evaluation of liver function Flashcards

1
Q

unconjugated bilirubin is particularly high among who ?

A

neonates - whose glucorynyl transferase activity is low

Indirect / unconjugated bilirubinemia

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2
Q

other than haemolytic anaemia what are other causes for elevated uncongugated bilirubin ?

A

Gilbert syndrome - mild uncongugated hyperbilirubinemia
does not affect females
young - 20-30

CRIGLER- NAJJAR SYNDROME
high serum levels of indirect bilirubin
multiple mutations

causing jaundice

affected infants - severe indirect hyperbilirubinemia - develops into kernicterus , deposition of bilirubin in brain (particularly basal ganglia , lenticular nucleus - severe retardation and motor dysfunction)

less sever form type 2 - survival to adulthood possible

Fasting

hepatitis

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3
Q

causes of elevated DIRECT bilirubin ?

A

excretion deficicts - DUBIN JOHNSON SYNDROME

ABC (atp binding casette)organic iron transporter - MRP2

billary obstruction - cholelithaisis
females

septicemia

ascending cholangitis

Paraenteral nutrition

androgen drugs - increase of conjugated bilirubin

hepatitis - both increase in direct and indirect bilirubin

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4
Q

what are the clinical manifestation of DUBIN JOHSNON SYNDROME?

A

MILD JAUNDICE

dark pigmentation of liver due to lipofuscin

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5
Q

DUBIN JOHSNON SYDROME CAN BE CONFUSED WITH WHAT OTHER SYNDROME ?

A

rotor syndrome - viral origin
block in excretion of conjugated bilirubin but no liver pigmentation !

liver biopsy reveals cytosolic inclusion bodies of organic ion transporter can be detected

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6
Q

in billary obstruction what is there a rise of swell?

A

rise in alkaline phsophatase and GGT

normal :
AsAT
AlAT

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7
Q

ascending chlangitis gives also concomitant rise to what ?

A

alkaline phosphatase is high

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8
Q

what are urine and decal findings in jaundice ?

A

normal
urinary bilirubin is absent
urinary urobilinogen - is present
fecal color is dark

obstruction to bile flow
urnary bilirubin is increased
urinary urobilinogen if neoplasm low
is gallstones - variable
fecal colour - pale - with gall stones in bile duct
persistant wih eoplasm in duct or pancreas

hemolytic anemia
urinary bilirubin is absent
urinary urobilinogen is high
fecal colour - is dark

liver damage - hepatitis /cholestasis

urinary bilirubin is increased in early stage
urinary urobilinogen is decreased in early stage
and increased early stage

decal colour is pale early
and dark late in hepatitis
pale with cholestais

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9
Q

how is bilirubin measured ?

A

using diazotized sulfulanic acid
forms conjugates as compound with porphyrin rings of bilirubin

make products that absorb strongly ate 540 nm

uncongugated bilirubin reacts slowly - caffeine or methanol given to fasten the process
deletion of accelerants determines if bilirubin if direct or indirect

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10
Q

bilirubin typically reaches peak value when ?

A

14-18 years old
stable and falls at age 25
higher in makes

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11
Q

which ethnic group has bilirubin levels significantly lower ?

A

african americans

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12
Q

which are the proteins which are to synthesised in the liver ?

A

immunoglobulin and von willebrand factor

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13
Q

why does portal hypertension dcause diminished protein production

A

decrease delivery of amino acids to liver

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14
Q

what are the two vital measurements of liver function ?

A

total Proteins and albumin levels in serum

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15
Q

what are other causes other than liver for low serum protein ?

A

renal disease
alnutrition
protein loss enetropathy
chornic inflammtory diseases

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16
Q

which diagnostic method is used as a model for end stage liver disease (meld) score evaluating priority of liver transplantation ?

A

prothrombin time
also values of bilirubin , creatinine
INR

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17
Q

what are the MELD SCORE MORTALITY RATES

A

higher than 40 - 100 percent mortality

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18
Q

MELD score is used to predict what ?

A

predict accuratley 3 month mortality of cirrhotic patients awaiting liver transplant

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19
Q

what tests are placed for liver injury?

A

lactate dehydrogenase
aspartate aminotransferase
alanine aminotransefrase
mitochondrial isoenzymes of AST- mitochondrial damage - caused by ethanol

canicular enzymes:
- alklaine phosphatase
y- glutamyl transferase - GGT
increased by obstructive process - accumulation of bile salts release of membrane fragments that have these enzymes attached to them

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20
Q

increased GGT and to a lesser extent alkaline phosphates is increased due to ?

A

medication inducing microsomal enzyme synthesisi - ethanol , phenytoin , carbamazepine

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21
Q

what is the half life of AST ?

A

17 hours

mitochondrial ast - 87 hours

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22
Q

what is the half life of ALT ?

A

47 hours

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23
Q

where is AST LOCATED ?

A

intramitochondrial and extramitochndrial

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24
Q

where is ALT located ?

A

only extramitochondrial

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25
Q

other than the liver where is AST found ?

A

everywhere , heart , muscle

26
Q

other than the liver where is ALT found ?

A

only in the liver , and significant amount in kidney

27
Q

acute forms of hepatitis can be diagnosed how ?

A

AST higher than ALT

ongoing damage 24-48 hours ALT becomes higher than AST

28
Q

what is the diagnosis for alcohol induced hepatitis ?

A

gives mitochondrial damage
release of mitochondrial AST

de ritis ratio
AST/ALT
3-4:1

29
Q

inc hronic hepatitis injury such as cirrhosis what is the diagnostic values ?

A

chronic injury - alt more than ast

as fibrosis progresses ALT declines and AST gradually increases

cirrhsis present - AST higher that ALT

end stage cirrhosis - AST and ALT low

30
Q

AST is used for monitoring therapy with

A

hepatotoxic drugs

more than three times the upper border of normal should signal stopping of therapy

31
Q

chronic elevate of AST and ALT other than alcohol is due ?

A

chronic alcohol use
medication
chronic viral heptatis
non alcoholic fatty liver disease

32
Q

how many isoenzymes of LD exists ?

A 
5 
tetrameters of two form H and M 
H having high affinity for lactate 
M having high affinity for pyruvate 
progressing from HHHH-->MMMM
33
Q

which LD are predominate in cardiac muscle , KINDEY AND ERYTHROCYTES ?

A

Ld 1 - HHHH

ld2- HHHM

34
Q

which ld are the major isoenzymes in lover and skeletal muscle

A

Ld4 - HMMM

Ld 5 - MMMM

35
Q

when does serum LD become elevated ?

A

in hepatitis - transient and return to normal at clinical presentation

selective increases - metastatic carcinoma , primary hepatcellular carcinoma
rarely benign lesion such as hemagioma adenoma

36
Q

alkaline phosphatse is present in what tissue besides the liver ?

A

bone - heat liable , kidney , small intestines , placenta

each containing distinct isoenzymes

37
Q

ALP in liver has what half life ?

A

about 3 days

38
Q

bulk of ALP n serum of normal patient is made up of what ?

A

liver and bone ALP

39
Q

what causes increase in ALP?

A

billary tract obstruction - by stones
ascending cholangitis
lesions

also eleavted in jaundice

cholestatsis reveield ALP falls more slowly than bilirubin

40
Q

what is the function of y glutamyl transferase ?

A

regulate the transport of amino acids across cell membranes

41
Q

if ALP is elevated and GGT is also elevated what does that tell you

A

the source of elevated ALP is due to billiard tract

42
Q

high values of GGT are due to ?

A

chronic cholestasis - primary billary cirrhosis

sclerosing cholangitis

43
Q

GGT is elevated due to ?

A

chronic abuse of alcohol
drugs - acetaminophen phenytoin

all of these without nay apparent liver injury

44
Q

what is the half live of GGT?

A

10 days
recovery from alcohol - 28 days
higher in obstructive disorders

45
Q

serum levels of GGT differ from ALP during cholestasis in who ?

A

during pregnancy

GGT remains normal even during cholestaisis

46
Q

what is AFP

A

alpha fetportein - synthesised by embyoic hapetocytes

and fetal yolk sac cells

47
Q

when does AFP peak normally in individuals ?

A

second trimester in pregnancy

48
Q

AFP peak elevated to abnormal levels in pregnancy due to ?

A

fetal neural tube defect

49
Q

AFP increases after what type of injury ?

A

acute injury in liver from regenerating liver cells

hepatocellular carcinoma - 90 percent of the time it is this

50
Q

in hepatocellular tumor other than AFP WHAT ELSE IS INCREASED

A

HCC

51
Q

AFP is also a marker for what type of tumor other than the live ?

A

rare germ cell tumor - yolk sac - endodermal in infants

or sertoli leydig cells

52
Q

what is the most common autoimmune liver disease ?

A

primary billary cirrhosis - often accompanied by other autoimmune disease such as sjorgren syndrome

antibodies are directed against mitochondrial antigens from M2 inner mitochondrial membrane- 100 percent specific for primary billiard cirrhosis

53
Q

how is primary billiard cirrhosis diagnosed ?

A

through immunofluroence /elsa

serum autoantibodies

54
Q

antimitochrondiral antigen are found in M1 in what ?

A

syphilus

55
Q

what is marker for primary sclerosing cholangitis ?

A

perinuclear -ANCA - antineutrophil cytoplasmic antbodies
ANA - antinuclear antibodies
ASMA - anti smooth muscle antibodies

56
Q

what is the pathology of primary sclerosing cholangitis ?

A

autoimmune destruction of extra hepatic and and intrahepatic bile ducts

often associated with chronic inflammatory bowel disease - ulcerative colitis

57
Q

what is the diagnostic marker for type 1 autoimmune hepatitis ?

A

usa - ANA
ASMA - to actin

titres of ANA or ASMA greater than 1:80 support diagnosis

58
Q

type 2 autoimmune hepatitis usually affects whom?

A

children and europeans

59
Q

what is the diagnostic criteria for type 2 autoimmune hepatitis ?

A

ANA AND ASMA often negative

antibodies to lover and kidney microsomal antigens are positive

60
Q

m=both types of autoimmune hepatitis usually affects who ?

A

women

61
Q

wieght reduction lowers what?

A

ALT

clinical lab (9 decks)

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