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chem path > Liver function tests > Flashcards

Liver function tests Flashcards

1
Q

how are LFTs separated

A

1) markers of liver cell damage
2) markers of synthetic function

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2
Q

what are the markers of liver cell damage

A

ALT, AST, ALP, GGT, bilirubin

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3
Q

what are the markers of synthetic function

A

clotting (INR) = specifically prothrombin time
albumin
glucose

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4
Q

what 2 ways can you measure synthetic function

A

T1/2 of INR = short (acute phase - hours)
T1/2 of albumin - long term function (days)

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5
Q

what causes transaminitis in the 1000s

A

1) acute viral hepatitis
2) toxins/drug (eg. paracetamol)
3) ischaemic hepatitis (rare due to good blood supply)

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6
Q

what is the best marker of liver function in acute liver injury

A

prothrombin time

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7
Q

what does raised AST > ALT indicate

A

alcoholic liver disease (usually >= 2:1)

AST = STELLA (beer)

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8
Q

what does raised ALT > AST indicate

A

chronic liver disease (NASH), chronic Hep C, hepatic obstruction, advanced fibrosis/cirrhosis

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9
Q

what does equally raised ALT = AST indicate

A

viral hepatitis

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10
Q

what does raised GGT and ALP indicate

A

cholestatic/obstructive picture

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11
Q

when is GGT raised

A

chronic alcohol use, bile duct disease and mets (used to determine hepatic cause of raised ALP)

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12
Q

what causes isolated raised ALP

A

1) physiological: pregnancy, childhood (growth spurt)
2) pathological: if >5xULN = bone (pagets, osteomalacia), liver (cholestasis, cirrhosis)
if <5xULN = bone cancers, hepatitis renal osteodystrophy

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13
Q

where is GGT found

A

hepatocytes, biliary cells, kidney, pancreas

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14
Q

where is ALP found

A

liver, bone (osteoblastic), intestine, placenta

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15
Q

why is ALP normal in myeloma

A

plasma cells suppress osteoblasts

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16
Q

what does low albumin indicate

A

chornic liver disease, malnutrition, protein losing enteropathy, nephrotic syndrome, sepsis (3rd spacing)
(inflammation - negative acute phase protein - low in inflammation)

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17
Q

what does low urea indicate

A

severe liver disease (synthesized in liver), malnutrition, pregnancy

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18
Q

what does raised urea indicate (>10x ULN)

A

1) upper GI bleed (or large protein meal)
2) dehydration/AKI (urea excreted really)

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19
Q

why is ALT more specific to liver than AST

A

AST also found in cardiac tissue + muscle

20
Q

what are some drugs that cause an increase in GGT

A

alochol, phenyotin, carbamazepine, phenobarbital

21
Q

main cause of drug induced cholestasis

A

co-amoxiclav

22
Q

why is low albumin not a good marker of synthetic dysnfuntion>?

A

1/2 life = 20 days
low albumin common in critically ill patients due to inflammation & malnutrition

23
Q

which clotting factors are made in the liver

A

all except 3 & 8
(this includes fibrinogen & prothrombin)

24
Q

what is INR

A

Prothrombin time standardised for age and population expressed as a ratio of normal

25
Q

what is the life path of bilirubin

A

-produced as breakdown product of heme (haemoglobin)
-conjugated in hepatocytes
-secreted into bile ducts & GI tract
-metabolised further in GI tract
-urobilinogen partially reabsorbed and exreted in kidneys as urobilin
-rest of urobilinogen converted to stercobilin (brown pigment in faeces)

26
Q

how are causes of jaundice broken down

A

-pre-hepatic (raised bili production)
-hepatic (decreased ability to conjugate bili)
-post-hepatic (decreased ability to excrete conjugated bili)

27
Q

what are causes of pre-hepatic jaundice?

A

-haemolytic anaemia
-ineffective erythropoesis (eg. thalassaemia)
-congestive heart failure

28
Q

what is present/absent in pre-hepatic jaundice?

A

-absent conjugated bilirubin (cos too much unconjugated for liver to handle)
-increased unconjugated bilirubin
-urobilinogen increases (more reaching gut)
-absent urine bilirubin & conjugated urine BR
-normal urine, stool colour
-splenomegaly

29
Q

what are the causes of hepatic jaundice?

A

1) hepatocellular dysfunction (viral/alc hep)
2)impaired conjugation / BR excretion (gilberts, crigler najjar syndrome)

30
Q

what is gilberts syndrome

A

autosomal dominant - UDP glucuronyl transferase deficiency
-causes raised unconjugated bilirubn & all normal LFTs

31
Q

how is gilberts confirmed

A

by fasting bilirubin (jaundice triggered by infection, stress)

32
Q

what is crigler najjar syndrome

A

dysfunctional UDP glucuroyl transferase (type 1 is non-functional) type 1 is milder)
-much worse phenotype than gilberts

33
Q

what is the first investigation if suspecting pre-hepatic jaundice

A

blood film + FBC

34
Q

what is present/absent in hepatic jaundice?

A

-increased conjugated & unconjugated bilirubin (cant conjugate as much + cholestasis)
-increased urobilinogen
-dark urine (conjugated BR & urobilingone)
-normal/pale stools (reduced conversion to stercobilin in gut)
-spenomegaly

35
Q

why is splenomegaly present in pre and hepatic jaundice but absent in post-hepatic

A

due to increased haemolysis (in pre-heapatic) or portal hypertension/liver congestion (in hepatic). main issue in post-hepatic is bile obstruction

36
Q

causes of post-hepatic jaundice?

A

obstruction of biliary tree
1)intraluminal (stones, strictures)
2) luminal (mass, neoplasm, inflammation eg. PBC, PSC)
3)dextra-luminal (pancreas/cholangiocarcinoma)

37
Q

what is present/absent in post-hepatic jaundice

A

-increased conjugated bilirubin
-normal unconjugated bilirubin
-decreased/absent urobilinogen
-dark urine (conjugated BR leaking through)
-pale stools (no stercobilinogen)
-increased ALP
-no splenomegaly

38
Q

what do you expect in increased haemolysis?

A

raised LDH
reduced haptoglobin

39
Q

causes of hepatomegaly with smooth margin?

A

viral hep, biliary tree obstruction, hepatic congestion (heart failure, budd chiari)

40
Q

causes of hepatomegaly with craggy border?

A

hepatic metastasis, polycystic disease, cirrhosis (will shrink)

41
Q

which cause of jaundice would lead to itching and why?

A

only post-hepatic
-from bile salts (stercobilinogen & urobilinogen)

42
Q

difference in signs between compensated & decompensated cirrhosis?

A

-Compensated cirrhosis is when the liver is still functioning adequately despite damage, with signs like spider naevi and gynaecomastia.

Decompensated cirrhosis occurs when the liver fails to cope with its damage, leading to more severe symptoms like jaundice, ascites, encephalopathy, peripheral edema, and bleeding from varices.

43
Q

how do you determine proportion of conjugated vs unconjugated BR

A

van der bergh test
-direct rxn measured conjugated
-indirect rxn measured unconjucated
-it specifically measures conjugated BR levels by adding a reagent to plasma which reacts with conjugated BR to form colour (intensity of colour depends on conc of BR)

44
Q

formula linking total, conj & unconj BR?

A

unconjugated BR = total - conjugated

45
Q
A

chem path (20 decks)

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