LFTs Flashcards

1
Q

Why do you order LFTs?

What can it help distinguish?

A

To confirm clinical suspicion of potential liver injury/disease

To distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic or obstructive jaundice).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

There are 7 component of the LFTs.

Which tests are used to distinguish between hepat-cellular damage and cholestasis? - 4

A

ALT - alanine transaminase
AST - aspirate aminotransferase
ALP - alkaline phosphate
GGT - gamma-glutamyltransferase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ALT and ALP levels:

Which one is raised in hepato-cellular inflammation or damage and which one is cholestatic?

What 3 places is ALP found in high concentrations?

A

ALT - Liver
ALP - cholestatic

ALP - PIPES SO BILIARY
ALT - TISSUE SO LIVER

Liver
Bile ducts
Bone tissues**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ALT and ALP levels:

Why is ALT a good marker of hepat-cellular injury?

Why is ALP raised in cholestasis?

What 3 pathologies will cause an ALT that is very raised (>1000 IU/L)?

It is also possible to have a mixed picture!!!

AST/ALT ratio:

What does an AST/ALT ratio>2 suggest the cause is?

What does an AST/ALT ratio<1 suggest the cause is?

A

It is at high concentrations within hepatocytes so enters the blood in hepatocellular injury (AST is found in other places around the body)

Liver pathology causes increased ALP synthesis in response to cholestasis

Ischaemia - AF can cause this!!
Drugs (Most commonly Paracetamol)
Viruses (Hepatitis A, B, C and E)

Alcoholic liver disease

Non-alcoholic liver disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ALT and ALP levels:

What if the patient is jaundiced but ALT and ALP levels are normal?

What can be used to measure severity of jaundice?

A

Pre-hepatic cause of jaundice

BR - bilirubin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

ALP:

An isolated raise in ALP (without GGT) suggests non-hepatobiliary pathology.

What is the main cause an isolated rise in ALP?

Other causes:

  • A deficiency
  • Something that could have happened recently
  • Renal
  • ALP is also found in the placenta. What is it also therefore raised in?
A

Bone metastases/primary bone tumours (sarcoma)

Vit D deficiency - unable to oppose PTH, increased resorption, raised ALP

Recent bone fractures

Renal osteodystrophy - an alteration of bone morphology in patients with chronic kidney disease (CKD).

Pregnancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GGT:

What pathology does GGT primarily suggest? - 2

Therefore, what is GGT used for?

What else can raise GGT?

A

Biliary epithelial damage
Bile flow obstruction

If there is a rise in ALP, if GGT is also high, then it is very likely to be a cholestatic pathology.

Alcohol and drugs (e.g. phenytoin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Useful tip:

When Transferases (ALT/AST)&raquo_space; ALP and GGT, what pathology does it suggest?

Where ALP and GGT&raquo_space; Transferases (ALT/AST)

A

Hepatic cause

Obstructive/biliary

COMMON SENSE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Patterns of chronic LFT changes:

What pathology would cause all enzymes to be raised”?

What enzyme is very raised in both Alcoholic LD and MI? What other enzyme is slightly raised that is liver-specific?

What enzyme is very raised in NAFLD?

2 enzymes that are very raised in drug, viral or autoimmune hepatitis?

A

Cirrhosis

↑ ↑ AST - found in the heart and the liver so released when the cells are damaged - A(S)T = sauce - starts with s

↑ ↑ALT (Lipid)

↑ ↑ ALT
↑ ↑ AST

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

A liver screen can be done to rule out underlying causes one you have identified liver pathology.

List a few of the components of this - 8

A

LFTs

Coagulation screen

Viral screen:

  • Hepatitis serology (A/B/C)
  • Epstein-Barr Virus (EBV)
  • Cytomegalovirus (CMV)
Autoantibodies:
- Anti-mitochondrial antibody (AMA)
- Anti-smooth muscle antibody (ASMA)
- Anti-liver/kidney microsomal antibodies (Anti-LKM)
- Anti-nuclear antibody (ANA)
p-ANCA

Immunoglobulins – IgM/IgG

Alpha-1 Antitrypsin

Serum Copper
Ceruloplasmin

Ferritin – Haemochromatosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hyperacute - Encephalopathy occurs within 7 days of onset of jaundice

Acute liver failure – 8 to 28 days from jaundice to encephalopathy

Sub acute failure - Hepatic encephalopathy occurs within 5-12 weeks of onset of jaundice.

Severe Acute liver injury –
Elevated transferases, prolonged PT and jaundice. But NO hepatic encephalopathy

A

Basically:

Hyperacute = <7

Acute = 1 wk - 4 wks

Subacute = 5-12 wks

Chronic = >12 wks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly