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Digestive MBChB 2 > Lecture 18: Test of Liver Function > Flashcards

Lecture 18: Test of Liver Function Flashcards

1
Q

What are the four key enzymes of the liver?

A

AST and ALT = Intracellular enzymes, active only in hepatocytes but leak into plasma so are measurable

GGT and ALP = Enzymes in liver metabolism, found in bile ducts.

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2
Q

What are some biomarkers of liver function?

A

Albumin
Prothrombin ratio
Glucose
Ammonia (urea)

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3
Q

What are the two patters of liver damage/ enzyme patterns?

A

Hepatocellular (thus ALT, AST)

or

Biliary / Cholestatic (ALP, GGT and Bilirubin-sometimes)

Often a mixture of the two in presentation

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4
Q

What are some examples of hepatocellular damage? and how do we know its hepatocellular?

A

Viral hepatitis
Liver toxins/drugs

Damage leads to inflammation, enzymes (ALT, AST) released into plasma = hepatocellular process

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5
Q

Whats some examples of Biliary/cholestatic process?

A

Gallstones

Some drugs

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6
Q

Describe bilirubin metabolism;

A

RBC breakdown forming haem

  • Haem breaksdown into bilirubin and is complexed to albumin (Unconjugated, ~85%) (In blood)
  • Bilirubin is taken up by the liver as it is not water soluble when unconjugated.

Bilirubin is conjugated with glucuronide (~15%)

  • A small amount of this conjugate is enters the blood and then is excreted in the urine.
  • The remaining can enter the biliary system and be released into the gut. It then forms urobilinogen (via gut flora) in the feaces (hence colour). A lot of this urobilinogen is re-absorbed and secreted in the urine.
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7
Q

What happens to bilirubin metabolism in states of haemolysis?

A

Overdrive production of conjugated bilirubin in the liver because increased haeme in blood.

This increases the amount of conjugated-bilirubin entering the gut. Thus increased urobilinogen in the feaces and re-absorption/ secretion or urobilnogen in urine.

Generally no increase in bilirubin conjugate if liver is still healthy. (no detectable rise in blood or urine of bilirubin-glucuronide)

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8
Q

What happens to bilirubin metabolism when theres hepatitis or cancer?

A

Increased bilirubin-glucuronide in the blood and urine and less urobilinogen in the feaces.

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9
Q

Whats the problem with inflammation of the liver?

A

It is in a firbous capsule therefore cannot expand and inflammation can lead to loss of function / occlusion of the networks.

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10
Q

What is jaundice?

A

When the skin, eyes, mucous membranes turn yellow because the billiary system is compromised

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11
Q

What are some examples of unconjugated (indirect) jaundice?

A

Haemolysis

Gilberts syndrome

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12
Q

What are some examples of conjugated (direct) jaundice?

A

Inside liver;

  • Choleostasis (Drugs, pregnancy, thyroid disease)
  • Obstruction inside liver (Hepatitis, cirrhosis, biliary cirrhosis, liver masses)

Outside liver
- Obstruction outside liver (Gallstones, biliary/pancreatic cancer, Pancreatitis (because these inflame and obstruct)

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13
Q

What is ALP?

A

Alkaline phosphatase

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14
Q

What does ALP do?

A
  • Transfers/hydrolyses phosphate groups
  • Age variation
  • Mainly in liver and bone
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15
Q

Whats GGT?

A

Gamma-Glutamyl Transferase

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16
Q

What causes GGT to elevate?

A
  • Inflammation/obstruction of biliary system

- Induced by alcohol, drugs such as phenytoin, rifampicin

17
Q

Describe the relationship of CGT and alcohol;

A

GGT has huge variations and doesnt always reflect increased alcohol intake

Plasma GGT doesnt correlate with liver biopsy

Takes heavy drinkers /weekend bingers 6 weeks of abstinence for GGT to drop to normal

18
Q

What does ALT stand for?

A

Alanine aminotransfersase

19
Q

What does ALT do?

A

Involved in Gluconeogenesis

Ala + Alpha-ketogluterate Glutamate and pyruvate

Mainly in liver hepatocytes (in cytosol during infection i.e hepatitis)

20
Q

What is AST?

A

Aspartate Transaminase

21
Q

What does AST do?

A
  • Involved in gluconeogenesis
  • Found in liver
  • Less liver specific than ALT

(8hr halflife vs 48hr for ALT)

22
Q

Whats normal concentrations of albumin?

A

35-47g/L

Liver only source in adults

23
Q

When does albumin fall?

A
  • Decreased synthesis (Cirrhosis)
  • Increased loss (i.e kidney)
  • Illness (non-specific)
  • Redistribution
  • Negative acute phase reaction i.e inflam turns this process off.
24
Q

What do globulins show?

A

IgA etc

  • Reflect inflammation, subacute or chronic
  • Very high levels with chronic hepatitis or cirrhosis
25
Q

What does the prothrombin ratio (PR/INR) reflect?

A
  • Reflects clotting factor synthesis (2,7,9,10)

- Rise indicates vit K def. or liver failure (indirect test)

26
Q

What does blood glucose reflect?

A
  • Liver maintains fasting blood glucose

- Inability to maintain glucose is ominous

27
Q

What are general signs of liver scarring and declining function?

A
  • Persistant GGT, ALP elevation
  • Increased; AST/ALT ratio (>1), Globulins, bilirubin, prothrombin ratio (low vit K, cant produce), Ammonia
  • Decreased; Albumin, glucose
28
Q

What is important to remember about albumin?

A

Its a negative acute phase reaction protein

29
Q

What is a CEA on a blood test?

A

Carcinoembyronic antigen

Indicates cancer for; Colon, breast, lung, pancreas, thyroid
Indicates benign for; Hepatitis, cirrhosis, ulcerative collitis, renal failure, smoking

== Doesnt have adequate sensitivity for early disease and therefore limited as early screening tool

30
Q

What is gilberts syndrome?

A
  • Variant in bilirubin conjugation
  • Other liver tests normal
  • (mild bilirubin rise, mild jaundice)

Illness fasting can worsen

31
Q

What must you exclude to diagnose gilberts syndrome;

A
  • Haemolysis
  • thyroid disorders
  • Iron overload
  • Recent hepatitis
  • Drugs i.e steroids

Done by 48hr fasting and seeing bilirubin rise

32
Q

What are common causes of viral hepatitis?

A
  • Infectious mono (50%)
  • Hep A, B, C
  • Cytomegalovirus
33
Q

Go over the examples used to determine causes

A

In the guidebook

Digestive MBChB 2 (31 decks)

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