140 - Practical Use of Liver Enzymes in Diagnosing Liver Disease Flashcards

1
Q

Examples of liver-secreted blood proteins

A

Clotting factors

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2
Q

Breakdown of what marks cell death?

A

Cytoskeleton

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3
Q

Mild appearance of damaged cells

A

Cytoskeleton is damaged.

Blebs form from surface of cell, released into the blood

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4
Q
Features of apoptosis
1
2
3
4
A
  • Nuclear degeneration
  • Cytoskeletal degeneration
  • Membrane Blebbing
  • Shrinking
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5
Q

Things to consider with enzymes detected in the blood
1
2
3

A

1) Which cell did they escape from?
2) How did they get into the blood?
3) How will they be removed from the blood?

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6
Q

Cytoplasmic liver enzymes

A

ALT, AST, LD

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7
Q

Membrane liver enzymes

A

ALP, GGT

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8
Q

Organelle liver enzymes

A

Mitochondrial AST, lysosomal Superoxide dismutase

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9
Q

Things released from necrotic liver cells

A

ASL, AST, LD

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10
Q

Things released in biliary disease

A

AST, GGT

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11
Q

Things released with inducing drugs

A

GGT, ALP

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12
Q

ALT

A

Converts pyruvate to lactate (Cori cycle, anaerobic use of glucose)

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13
Q

Cori cycle

A

Occurs mainly in liver and muscle.

Anaerobic use of glucose

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14
Q

AST

A

Converts oxo-glutarate and aspartate to oxaloacetic acid and glutamate in the malate shuffle.

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15
Q

Where is ALT found?

A

Mostly in liver.
Slightly less in muscle and kidney.

More specific to liver than AST is.

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16
Q

Where is AST found?

A

In cytosol and in mitochondria.
Liver, muscle, blood cells.
Less specific to the liver than ALT is.

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17
Q

ALT half life

A

36 hours

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18
Q

AST half life

A

18 hours

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19
Q

GGT half life

A

5-7 days

20
Q

AST>ALT

A

Acute, affecting mitochondria.

EG: an acute virus, ethanol damage.

21
Q

ALT>AST

A

Chronic/resolving disease (because AST has a shorter half life than ALT).
EG: In hep B, C. With drugs, chronic viruses, metabolic problems.

22
Q

Examples of viral diseases that can damage liver cells

A

Hep A, B, C, D, E.

EBV, CMV, Q fever, rubells

23
Q

Normal ALT concentration in the blood

A

7 - 56 units/L

24
Q

ALT level at which a patient will start feeling sick

A

1000 units/L

25
Q

Maximum ALT possible in the blood

A

10, 000 units/L.

If patient has this, is in acute liver failure.

26
Q

Severe hep A ALT level

A

5000 units/L.

Significant, as indicates that about half the liver has been lost.

27
Q

Relationship between ALT levels and hep B core IgM and surface IgG levels

A

High ALT coincide with high core IgM, low surface IgG

28
Q

ALT levels of chronic hep B, C

A

Fairly low ALT (~100 units/L)

29
Q

Examples of hepatotoxic drugs

A
ANTIBIOTICS
– Flucloxacillin, amoxil
• STATINS
– Atorvastatin, Simvistatin,
Pravastatin, Fluvastatin
• ETHANOL
• PARACETAMOL
• OTHERS
– HERBAL TEA (Kombucha)
30
Q

Rough amount of paracetamol required for liver failure

A

~15g (about one packet of paracetamol - 30 tablets)

31
Q

What does significantly elevated ALT and AST indicate?

A

Liver cell death

32
Q

Weakness with Simvastatin, only AST is elevated.

A

Simvastatin isn’t damaging liver, as other transaminases are normal.
AST is in other tissues. Probably a muscular problem.

33
Q

What might it indicate if ALT is elevated, AST is normal?

A

Very chronic liver disease. ALT has a longer half life than AST.

34
Q

Liver function tests on end-stage cirrhosis

A

ALT, AST look normal. Everything else looks close to normal.
This is because so much of the liver has been destroyed that transaminases aren’t being released much anymore.

35
Q

Gamma GT role

A

Adds glutamyl groups to amino acids in the biliary membrane.

This forms glutamate, which goes on to form glutathione.

36
Q

Why is GGT induced by drugs and alcohol?

A

Liver tries to combat toxic effect by generating more glutathione through GGT pathway

37
Q

ALP role

A

Attaches a phosphate group to something on the biliary membrane.
Makes substrate more hydrophilic.

38
Q
Jaundice causes
1
2
3
4
5
6
A
• INCREASED PRODUCTION
– Haemolysis
• DECREASED EXCRETION
– Gilberts, Dubin Johnson
– Hepatitis
• OBSTRUCTION
– EXTRAHEPATIC CHOLESTASIS
• Elevated Conjugated Bilirubin
– INTRAHEPATIC CHOLESTASIS
• No Jaundice
• No increase in Bilirubin
39
Q

Intrahepatic biliary obstruction vs extrahepatic biliary obstruction GGT and ALP

A

GGT and ALP much higher with extrahepatic than intrahepatic

40
Q

How does GGT, ALP get into the blood from bile?

A

Through lymphatics in biliary tree

41
Q

Effect of alcohol metabolism on liver [NAD+]

A

Drops a lot.

Liver is using NAD+ to help mop up H+ from alcohol->acetaldehyde->acetic acid (forming NADH)

42
Q

What does the liver do when NAD+ is depleted?

A

Glutathione is mobilised more

43
Q

Significance of an extremely high GGT, and only slightly elevated AST and ALT

A

Mildly high AST and ALT not indicative of liver cell death.

Liver stress, but not widespread cell death

44
Q

Mixed pattern of hepatitis (hepatocellular and biliary)
1 a, b, c
2 a, b, c

A
• HEPATOCELLULAR DEATH
– Death of liver cells
– Inflammation & swelling
– Biliary Obstruction
• BILIARY OBSTRUCTION
– Inability to excrete toxins
– Accumulation of toxins in
hepatocyte
– Hepatocellular death
45
Q

Effect of weight on liver function tests

A

ALT, AST, GGT elevated

46
Q

Effect of liver metabolising glucose and fructose

A

Fructose can be converted to glucose, but in the presence of glucose, the liver won’t convert fructose.
The fructose is stored in the liver as fat.