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Yr 3 - January lectures 19 > Interpreting liver function tests > Flashcards

Interpreting liver function tests Flashcards

1
Q

What are the main roles of the liver?

A

detoxification - metabolism and excretion of drugs
process and storage of - amino acids, proteins (most produced by the liver, except immunoglobulins), carbohydrate, cholesterol and vitamins
synthesis of bile acids -cholesterol catabolism
catabolic site for many of the hormones - insulin, glucagon, oestrogens, glucocorticoids, GH, PTH, conversion of VITd to 25-OHD
contribution to the immune response

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2
Q

What routine biochemical tests are there to assess liver function?

A 
bilirubin 
hepatocellular enzymes - ALT (AST - less specific)
hepatobiliary enzymes - ALP, gamma-GT
albumin 
total protein
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3
Q

What clinical questions need to be asked when assessing the liver?

A

is the liver disease present?
what is the aetiology?
what is the severity?
can the disease be monitored?

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4
Q

What are the possible symptoms in which liver disease may present?

A

jaundice
abdo distension
ankle swelling - odema due to altered albumin
haemetemesis
pruritis
pale stools and dark urine - due to obstruction

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5
Q

What important factors should you ask about in the history if you suspect liver disease?

A 
recent travel 
duration of illness
drug use
alcohol consumption 
family history 
weight loss 
BMI - fatty liver
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6
Q

What are the normal ranges for:

  • total bilirubin
  • ALP
  • ALT
  • AST
  • Albumin
  • gamma-GT (M and F)
A
  • total bilirubin = <21 micromol/L
  • ALP = 30-130 U/L = also found in bone and intestine, varying levels in adolescents
  • ALT = 5-40 U/L
  • AST = 5-43 U/L
  • Albumin = 35-50g/L
  • gamma-GT (M and F) = 9-50u/l and 9-40u/l
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7
Q

What is bilirubin a product of?

A 
haem catabolism - 85%
red cell precursors
myoglobin 
cytochromes
peroxidase 
daily production = 170-300 micromol/day
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8
Q

What are the different types of hyperbilirubinaemia?

A

pre-hepatic = haemolytic conditions cause raised bilirubin (unconjugated) but with no bilirubinaemia

hepatic = bilirubin (unconjugated and conjugated) is elevated at some stage of most hepatobiliary disease (with biliruburia)

post-hepatic = raised bilirubin (conjugated) due to bile outflow obstruction - bilirubinaemia

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9
Q

When is jaundice noticeable?

A

about 50 micromol/L

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10
Q

What are the main causes of pre-hepatic unconjugated hyperbilirubinaemia?

A

Production from haem
- haemolysis - hereditary, acquired or rapid turnover in neonates

Reduced delivery of unconjugated bilirubin in plasma
- R sided CCF, portocaval shunt

Reduced uptake of unconjugated bilirubin across liver membrane

  • competitive inhibition e.g. drugs
  • Gilbert’s (UGT1A1*28)
  • Sepsis, fasting
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11
Q

What are the main causes of post-hepatic conjugated hyperbilirubinaemia?

A

Reduced secretion of conjugated bilirubin into the canaliculi

  • hepatocellular disease - hepatitis, intrahepatic cholestasis
  • drugs

Reduced drainage
- extrahepatic obstruction - stones, carcinoma, stricture, atresia

Sclerosing cholangitis intrahepatic obstruction

  • drugs
  • granuloma
  • PBC
  • tumour
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12
Q

What are the different types of jaundice?

A

haemolytic
cholestatic
hepatocellular

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13
Q

What criteria suggest haemolytic jaundice?

A 
bilirubin usually <75 micromo/L 
no bilirubin in urine 
Reticulocytosis 
Reduced Hb 
Reduced haptoglobin 
LDH may increase
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14
Q

What criteria suggest cholestatic jaundice?

A

Bilirubin may be really increased
Bilirubin in urine
ALP > x3 ULN
AST, LDH and ALT moderately increased

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15
Q

What criteria suggest hepatocellular jaundice?

A

AST + ALT significantly increased
Bilirubin increased later
Bilirubin in urine
ALP raised later

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16
Q

What are the differences between AST/ALT and ALP/gamma-GT?

A

AST and ALT = cytosolic enzyme (50% AST is mitochondrial)
- increased with hepatic damage

ALP / gamma-GT = membrane bound glycoprotein enzyme
- increased with cholestatic damage

17
Q

What happens to the enzymes in liver cell damage ?

A

AST released more quickly in liver disease
ALT more chronic release and may reflect length of disease
- fatty liver causes rises in ALT more often than AST

18
Q

What happens to the enzymes in cholestasis ?

A

ALP increased
gamma-GT increased - can be induced by lots of alcohol
Alcohol and Gamma-GT
- increases are noted BUT increased gamma-GT is often found in pts with increased triglyceride and fatty liver, diabetes

19
Q

Where is AST found?

A

in the liver - predominantly mitochondrial
in the muscle - predominantly cytoplasmic
in red blood cells - gross haemolysis

20
Q

Where is ALT found?

A

cytoplasmic enxyme

21
Q

Where is ALP found in ?

A

bone
placenta
growth phases in childhood and adolescence
when bone is remodelled (after fracture)

22
Q

What are plasma proteins usually included in?

A

LFTs

  • NOT specific
  • albumin - hypoalbuminaemia very common in hospitalised patients
  • immunoglobulinaemia can reflect liver disease- also a general indicator of chronic infection
23
Q

What are some other examples of plasma proteins?

A

caeruloplasmin = reduced in wilson’s disease (problem with copper metabolism)
alpha-1 antitrypsin - protease inhibitor, deficiency states lead to liver/lung disease

coagulation proteins - short half life, use INR

24
Q

What liver function test is used for liver tumours?

A

AFP (alpha-fetoprotein) 75% cases

25
Q

What liver function tests are used for metabolic liver disease?

A

alpha-1 antitrypsin deficiency
haemochromatosis
iron, total iron binding capacity (transferrin) ferritin
Wilson’s disease - serum copper, caeruloplasmin

26
Q

What is the AST:ALT ratio?

A

normal ration of AST to ALT = ABOUT 0.8

>1 = EVIDENCE OF CIRRHOSIS

27
Q

What would you want to check if you suspected hepatocellular disease?

A

check transaminase > about 5xULN

ALP normal or slightly increased

28
Q

What would you want to check if you suspected cholestatic disease?

A

ALP >200U/L

Transaminase normal or slightly raised <200U/L

29
Q

If there was mixed liver disease what would you expect to see?

A

significant increases in ALP and transaminase

both greater than 200U/L

30
Q 
Case 1:
- 24 F, no meds
- mild jaundice, pallor, malaise, 6/12 hx heavy irregular menstrual periods 
- no spleno or hepatomegalu 
investigations:
- TProt: 77g/l
- Alb : 35g/L
- ALP: 110U/L 
- ALT: 42 U/L
- Bili: 48 umol/L

What are the differential diagnosis?

A

haemolytic disease
iron deficiency anaemia
gilbert’s syndroe
hepatobiliary disease

on futher testing:

  • Tbil: 48
  • Cbil: 11
  • LDH: 149U/L (increased)
  • Iron: 5 (decreased)

iron deficiency anaemia

31
Q

What is gilbert’s syndrome?

A 
autosomal dominant (7%)
intermittant mild jaundice with unconjugated bilirubin 
periods of fasting and illness
32
Q 
Case 2: 
- 14 M treated for broken arm 
- mildly jaundiced 
- splenomegaly 
Investigations:
- Tprot: 75
- Alb: 40
- ALP: 98
- ALT: 14
- Bili: 68 
- Hb:10.3 
- Cbil:  <5 
- LDH: 560U/L (increased) 
- haptoglobin: 0.1 (reduced)

What are the differential diagnoses?

A

unconjugated hyperbilirubinaemia, LDH and haptoglobin=> haemolytic process

hereditary spherocytosis

33
Q 
Case 3:
- 35 F 
- 4/52 hx malaise, anorexia, upper abdo pain 
- dark urine 
- overt jaundice for 3/7 
Investigations:
- Tprot - 71 g/dl
- Alb- 42
- ALP - 180
- GGT - 331
- ALT 2090
- AST 1788
- bilirubin - 126 
What is the potential diagnosis?
A

Serology:

  • hep A and C negative
  • hep b positive
34
Q 
Case 4:
- 65 M 
- AAA repair 
- after OP developed severe chest pain and shock 
- BP unrecordable 
- Acute MI 
INVESTIGATIONS:
- T prot: 69 to 63
- ALP: 125 to 13
- GGT: 50 to 169
- ALT: 43 to 955
- AST: 30 to 812 
- Bili: 14 to 17 
Rapid development of hepatocellular damaage, no jaundice and hypoxic damage to liver
What are the main causes of acute hepatocellular damage?
A

hypoxia
chemicals
drugs
acute hepatitis

35
Q 
Case 5:
- 49 F 
- pneumonia and septicaemia 
- started on erythromycin and 5 days later become jaundiced and complained of pruritis 
- no pain 
investigations:
- TProt: 72 to 69
-ALP: 120 to 328 
- GGT: 43 to 402
- ALT: 24 to 67
- AST: 30 TO 89 
- Bili:13 to 156

What is the diagnosis?

A

Erythromycin associated cholestasis
re-challenge the patient when LFTs have normalised
stopped it and when back to normal

36
Q

What is the classical picture of obstructive jaundice?

A

significantly elevated ALP with mild elevations of transaminase
stone in common bile duct

Yr 3 - January lectures 19 (30 decks)

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