Session 6: Jaundice and LFTs Flashcards

1
Q

Define jaundice

A

Clinical manifestation of raised bilirubin presenting as yellowish sclera and skin.

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2
Q

What is bilirubin?

A

Breakdown product of haem.

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3
Q

What are the two forms of bilirubins found in the body?

A

Unconjugated and conjugated bilirubin.

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4
Q

What is unconjugated bilirubin?

A

Not water soluble and bound to albumin.

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5
Q

What is conjugated bilirubin?

A

Conjugation of bilirubin in the liver making it water soluble.

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6
Q

What are the options of bilirubin to go in the body?

A

Kidneys as urobilinogen and get excreted. Urobilinogen excreted in faeces. (What makes faeces brown) Enter the enterohepatic circulation with bile and then excreted.

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7
Q

Causes of jaundice (very broad).

A

Pre-hepatic Hepatic Post-hepatic

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8
Q

Pathogenesis of pre-hepatic jaundice.

A

Due to too much haem. This is because increased degradation of haemoglobin. The liver conjugating is still fine and the excretion pathway also. However there is too much demand on the liver and this leads to an increased level of bilirubin that is unconjugated.

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9
Q

Common causes of pre-hepatic jaundice.

A

Haemoglobinopathies like sickle cell, thalassaemia and spherocytosis. Damage to red blood cells like haemolysis like MAHA

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10
Q

What is hepatic jaundice due to?

A

Reduced hepatocyte function.

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11
Q

Explain hepatic jaundice.

A

Caused by reduced conjugating ability of the liver. This is due to damage of the hepatocytes where the amount of bilirubin is fine and the excretion pathway is fine. This leads to a mix of conjugated and unconjugated bilirubin.

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12
Q

Common causes of hepatic jaundice.

A

Cirrhosis like alcoholic fatty liver disease, NAFLD, drugs, autoimmune, depositions, hepatitis, infections, hereditary haemochromatosis, Wilson’s disease etc… Can also be caused by acute liver damage like paracetamol toxicity, viral hepatitis etc…

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13
Q

Explain post-hepatic jaundice.

A

Caused by obstruction to the excretion pathway. Amount of bilirubin is fine and the conjugating ability is usually fine as well. This means that there will be an increase in conjugated bilirubin.

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14
Q

How can you distinguish between raised levels of unconjugated bilirubin and conjugated?

A

Unconjugated will still eventually make it into the normal pathway in normal doses to become conjugated. It just takes more time. Unconjugated will not be excreted in urine because it is not water soluble. Raised conjugated levels will lead to increased bilirubin excreted in kidney and therefore darker urine and pale stools.

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15
Q

Common causes of post-hepatic jaundice.

A

Gallstones Biliary stricture Pathology of the head of the pancreas. Intrahepatic pathology can also lead to compression of the intrahepatic bile ducts. Like in the case of oedema, malignant growth or scarring.

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16
Q

LFTs

A

Bilirubin - conjugated vs unconjugated Albumin ALT AST ALP

17
Q

Will albumin levels rise or decrease in reduced liver function?

A

Less albumin

18
Q

What does low albumin cause?

A

A reduction in oncotic pressure leading to oedema and ascites.

19
Q

What other body system might lead to low albumin levels?

A

Kidney injury

20
Q

What is ALT and AST?

A

Alanine transaminase Aspartate transaminase Hepatic enzymes that increase in conc. when the hepatocytes are damaged.

21
Q

What is more specific to the liver; ALT or AST? Why?

A

ALT is more specific AST can also be found in cardiac/skeletal muscle as well as in red blood cells.

22
Q

What rises more in acute liver damage? ALT or AST?

A

ALT > AST

23
Q

What rises more in cirrhosis and alcoholic hepatitis? ALT or AST?

A

AST > ALT

24
Q

Where can ALP be found?

A

Found in the cells lining the bile ducts.

25
Q

When do the levels of ALP rise?

A

In cholestasis i.e. bile duct obstruction.

26
Q

ALP is not specific to bile duct obstruction. When else can it be found?

A

It is also used to assess bone turnover.

27
Q

What can be used to specify the source of increased ALP?

A

Gamma-Glutamyl Transferase (Gamma GT) to specify the source as liver.

28
Q

LFTs of pre-hepatic jaundice.

A

Usually no abnormalities of LFTs other than raised levels of unconjugated bilirubin and associated anaemia.

29
Q

LFTs of hepatic jaundice.

A

Mixed bilirubin. High lvls of ALT and AST Usually normal ALP

30
Q

LFTs of post-hepatic jaundice.

A

Raised levels of conjugated bilirubin. Raised ALP Usually normal ALT/AST

31
Q

17 yr old admitted having ingested two packets of paracetamol.

They are drowsy, have some abdo pain and feel nauseous. They appeard jaundiced.

A

Hepatic jaundice

Shows hepatocellular damage

Acute liver damage as ALT is raised considerably.

32
Q

42 y old admitted with epigastric pain radiating to her back.

Odd niggly with stomach pain every now and then but not as bad at this. Feels nauseous and has vomited this morning.

A

Raised ALP indicating obstructive pattern. No signs of jaundice.

Test Cullen’s sign, Grey Turner’s sign, Gamma GT as well as amylase and lipase to confirm acute pancreatitis.

33
Q
A

C

34
Q
A

E