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Biochemistry > Organ Function Tests - Liver > Flashcards

Organ Function Tests - Liver Flashcards

1
Q

What 2 things does the liver do in carbohydrate metabolism?

A

Synthesis and storage of glycogen. Glucose synthesis (glycogenolysis, gluconeogenesis).

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2
Q

What 3 things does the liver do in fat metabolism?

A

Synthesis of lipoproteins, phospholipids and cholesterol. Fatty acid metabolism = ketogenesis. Bile acid synthesis.

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3
Q

What does the liver do in protein/amino acid catabolism and metabolism (and state which ones)?

A

Catabolism of proteins/amino acid metabolism. Synthesis of proteins (but NOT immunoglobins) inc. albumin, prothrombin, clotting factors, other transport proteins, ‘acute phase’ proteins of immune response.

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4
Q

What are the roles of the liver?

A

Excrete, detoxify drugs and foreign compounds. Storage (iron, glycogen). ‘Conjugating’ bilirubin and bile acid secretion. Steroid hormone metabolism and excretion. Polypeptide hormone metabolism. Acid-base balance by removing lactate from blood and NH3 detoxification, urea synthesis.

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5
Q

What vitamins affect the liver when in decline?

A

A, D, E, K, B12

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6
Q

Liver disease can be acute or chronic. Name 5 diseases that affect the liver.

A

Hepatitis (viral or autoimmune), gallstones, tumours, toxic/drug induced damage. Other conditions such as haemolytic anaemia may cause disruption to liver-related test results.

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7
Q

What can be affected due to blockages?

A

Bile canaliculi and ducts.

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8
Q

What can liver function tests assess? And what 3 things can it help to differentiate between?

A

Hepatic cell damage and can help to differentiate between 1) obstruction of the biliary tract 2) acute hepatocellular damage 3) chronic liver disease

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9
Q

What are 3 liver function tests?

A

1) serum albumin and clotting time 2) serum bilirubin 3) serum enzyme activities

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10
Q

What 4 enzymes are observed during a serum enzyme liver function test?

A

ALP (alkaline phosphatase), GGT (gamma-glutamyltransferase), AST (aspartate aminotransferase), ALT (alanine aminotransferase).

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11
Q

What is the structure of the liver (cells and vasculature)?

A

Central vein, portal vein hepatic artery, sinusoids, bile duct. Hepatocytes, endothelial cells, kupffer cells, bile canaliculus.

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12
Q

Which 2 enzymes are largely associated with the membranes of the bile canaliculus and are released in very small amounts in hepatocellular damage?

A

ALP and GGT.

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13
Q

When are ALP and GGT released and synthesised in large amounts?

A

Cholestasis, when bile ducts are blocked.

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14
Q

What are the approx adult ref. ranges for ALP and GGT?

A

ALP: 40-125 U/L GGT: 10-55 U/L

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15
Q

How long of a lag period before AST and ALT are released into plasma after hepatocellular damage?

A

Around 24hrs after hepatocellular damage.

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16
Q

What are the approx adult. ref ranges for AST and ALT:

A

AST: 5-50 U/L ALT: 10-50U/L

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17
Q

What other 2 parts of the body produce ALP isoenzymes? And in what instances will they be elevated?

A

Bone and placenta. Bone-proliferation diseases, pregnancy, childhood.

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18
Q

What other conditions can raise AST levels?

A

AMI, plus other conditions.

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19
Q

What 2 drugs can induce GGT production?

A

Alcohol and anticonvulsants.

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20
Q

What is the approx reference range for albumin?

A

35-50g/L

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21
Q

What can impaired synthesis of albumin indicate?

A

Hepatocellular damage, progress of disease.

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22
Q

Why are levels of albumin not affected by acute conditions?

A

Due to half life (20 days).

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23
Q

Why can high levels of albumin not always indicate hepatocellular damage?

A

Maybe affected by other conditions.

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24
Q

What can cause reduced synthesis of clotting factors? What is its half-life? How is it assessed?

A

Hepatocellular damage. 6 hours (early indicator). By testing clotting time (prothrombin time or INR).

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25
Q

What is INR?

A

International normalised ratio. A ratio of prothrombin time to a control value.

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26
Q

How is bilirubin produced?

A

Produced as a breakdown product of haem.

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27
Q

Where is bilirubin excreted from and what into?

A

Liver, into bile.

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28
Q

How can jaundice result?

A

If there are problems with the liver - hepatocellular damage or a blockage to the biliary tract. Also by increased bilirubin production.

29
Q

Is unconjugated bilirubin soluble in water?

A

No, it is insoluble and transported in the blood bound to albumin to the liver.

30
Q

Where is bilirubin stored, carried by and used for?

A

Stored in bone marrow or liver, carried by transferrin, used for erythropoiesis in bone.

31
Q

What is added to bilirubin to make it water soluble and easily transported in the bile?

A

Glucuronic acid.

32
Q

What is unconjugated bilirubin?

A

Before the liver - bilirubin bound to albumin.

33
Q

What is conjugated bilirubin?

A

After the liver - bilirubin bound to glucuronic acid.

34
Q

What enzyme catalyses the transfer of glucuronic acid component of UDP-glucuronic acid?

A

UDP-glucuronyltransferase

35
Q

What is used to measure bilirubin?

A

Spectrophotometric methods are used, which create a colour-change.

36
Q

Is jaundice a symptom or an illness and describe its characteristics.

A

Symptom. Yellow discolouration of the eyes/skin caused by an increase in plasma bilirubin concentration.

37
Q

What concentration does bilirubin have to be for jaundice to be detectable? And what is the reference range?

A

> 50umol/L. Reference range < 22umol/L.

38
Q

What are the 3 main reasons bilirubin levels rise?

A

Haemolysis, hepatocellular damage, cholestasis.

39
Q

How is jaundice caused by haemolysis?

A

Increased haemoglobin breakdown which produced more bilirubin and overloads the mechanism of conjugation in the liver = high levels of unconjugated bilirubin as liver’s capacity is exceeded.

40
Q

How is jaundice caused by hepatocellular damage?

A

Failure of the conjugating mechanism in the liver = mainly high levels of unconjugated bilirubin.

41
Q

How is jaundice caused by cholestasis?

A

Obstruction of the biliary system = high levels of conjugated bilirubin.

42
Q

What causes haemolysis (pre-hepatic jaundice)?

A

Haemolytic anaemia and haemolytic disease of the newborn.

43
Q

What causes neonatal jaundice?

A

Normal haemolysis with immature liver function.

44
Q

What can high levels of unconjugated bilirubin cause in babies (although research suggests genetic factors may be involved)? What might be needed?

A

Kernicterus (brain damage). Phototherapy (biliblankets) or exchange transfusion might be needed.

45
Q

What can delay a diagnosis of kernicterus in babies?

A

Individuals with more melanin as jaundice is less noticeable.

46
Q

What are the most common causes of acute jaundice in adults? What 4 things will be raised?

A

Viral hepatitis and paracetamol poisoning. Total bilirubin, unconjugated bilirubin, AST and ALT levels.

47
Q

What 2 things will rise if damage to hepatocytes begins to cause intrahepatic biliary obstruction?

A

ALP and GGT.

48
Q

What will raised AST and ALT mean?

A

Acute hepatocellular jaundice.

49
Q

What will raised GGT mean?

A

Possible slight intrahepatic biliary obstruction.

50
Q

What will raised total bilirubin show?

A

Jaundice.

51
Q

What are serologic tests?

A

Blood tests that look for antibodies in your blood to diagnose various disease conditions. Serologic tests all focus on proteins made by your immune system.

52
Q

What can happen to the bile duct in cholestasis jaundice?

A

The bile duct can be completely or partially blocked by gallstones.

53
Q

What 4 things will be raised in cholestasis?

A

Total bilirubin, conjugated bilirubin, ALP and GGT. In partial blockage bilirubin levels may be normal or slightly raised.

54
Q

How will stools appear and what is there little off in the urine, when diagnosed with cholestasis?

A

Pale. Little urobilinogen in the urine. These symptoms disappear if the blockage is removed.

55
Q

What are the most well-documented poisons that lead to liver disease and where are they found?

A

Paracetamol and carbon tetrachloride (tetrachloromethane - used in fridges, fire extinguishers and dry cleaning).

56
Q

Why are small quantities of paracetamol and tetrachloride ok but higher concentrations toxic?

A

Small = can be metabolised by the liver. High concentrations produce toxic metabolites causing hepatocyte destruction. This cell damage causes considerable release of enzymes.

57
Q

Why is it not recommended to draw a paracetamol serum level before 4 hours of OD’ing?

A

A paracetamol level drawn in the first four hours after ingestion may underestimate the amount in the system because paracetamol may still be in the process of being absorbed from the gastrointestinal tract.

58
Q

What is the normal plasma half-life when taking paracetamol? And when is it extended as long as in OD’s?

A

Around 2 hours. Extended to as long as 12 hours in OD.

59
Q

What can hepatic necrosis lead to after 2-3 days?

A

Delayed acute hepatic failure and death.

60
Q

What 2 things peak at 72-96 hours post paracetamol OD and what increases?

A

ALT and AST. INR increases.

61
Q

Who is at a higher risk after OD’ing on paracetamol?

A

Individuals with pre-existing liver disease or after enzyme-inducing drugs.

62
Q

What is the treatment for paracetamol OD?

A

N-acetylcysteine if indicated.

63
Q

What are the 6 symptoms for acute hepatic failure?

A

Inadequate clotting factors, electrolyte imbalance, decrease in Na and Ca levels, acid/base problems, hypoglycaemia and raised ammonia levels (lack of urea cycle) = all leading to a severe emergency.

64
Q

What causes oedema and/or abdominal fluid build up in acute hepatic failure?

A

Decreased albumin levels. Prognosis is poor without a transplant.

65
Q

Why are ammonia levels difficult to measure accurately in acute hepatic failure?

A

Not usually used as a routine test as very labile (liable to change).

66
Q

What are the causes of chronic liver disease?

A

Hepatitis B, autoimmune conditions, infiltration of liver by tumour, alchoholic fatty liver disease.

67
Q

What can chronic liver disease lead too?

A

Cirrhosis (scar tissue in liver) and terminal liver failure.

68
Q

What 2 methods can help to diagnose CLD?

A

Biochemical markers, imaging techniques.

69
Q

What are liver function tests used to assess and NOT used for?

A

Hepatocellular damage, not biochemical function.

Biochemistry (7 decks)

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