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Yr 3 - Skills & Extras > Interpreting LFTs > Flashcards

Interpreting LFTs Flashcards

1
Q

What are the two primary reasons for requesting LFTs?

A
  1. To confirm a clinical suspicion of potential liver injury or disease
  2. To distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic obstructive jaundice)
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2
Q

What is cholestasis?

A

The reduction or blockage of bile flow. Can be caused by disorders of the liver, bile duct or pancreas.

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3
Q

What are the 7 components of LFTs?

A
  1. Alanine transaminase (ALT)
  2. Aspartate aminotransferase (AST)
  3. Alkaline phosphatase (ALP)
  4. Gamma-glutamyl transferase (GGT)
  5. Bilirubin
  6. Albumin
  7. Prothrombin time (PT)
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4
Q

Which components of LFTs are used to assess the liver’s synthetic function?

A

Albumin, prothrombin time, bilirubin

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5
Q

Which components of LFTs are used to distinguish between hepatocellular damage and cholestasis?

A

AST, ALT, ALP and GGT

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6
Q

LFT reference ranges:

A
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7
Q

Where is ALT found in high concentrations?

A

Hepatocytes

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8
Q

When would ALT enter the blood (i.e. raised ALT)?

A

Following hepatocellular injury

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9
Q

Where is ALP concentrated?

A

Liver, bile duct and bone tissues

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10
Q

Is ALT or ALP more specific for liver disease?

A

ALT (as ALP also found in bile duct and bone tissues)

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11
Q

What is ALP often a useful marker of?

A

Cholestasis (due to increased synthesis)

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12
Q

What would a greater than 10-fold increase in ALT and a less than 3-fold increase in ALP be suggestive of?

A

Predominantly hepatocellular injury

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13
Q

What would a less than 10x increase in ALT and more than 3x increase in ALP indicate?

A

Cholestasis

Note; it is possible to have a mixed picture involving both hepatocellular injury and cholestasis

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14
Q

If there is a rise in ALP, which enzyme is it important to review?

A

GGT

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15
Q

Where is GGT predominantly found?

A

Liver and gallbladder

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16
Q

What are 4 causes of a raised GGT?

A
  1. Biliary epithelial damage
  2. Bile flow obstruction
  3. Response to alcohol
  4. Response to drugs e.g. phenytoin
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17
Q

What is a markedly raised ALP with a raised GGT highly suggestive of?

A

Cholestasis

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18
Q

What is a raised ALP in the absence of a raised GGT suggestive of?

A

Non-hepatobiliary pathology

ALP is also present in bone so anything that causes increased bone breakdown can elevate ALP

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19
Q

Give 2 bone causes of a high ALP?

A
  1. Bone mets
  2. Healing fracture
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20
Q

How would hyperthyroidism affect ALP levels? Why?

A

May increase ALP levels

Overt hyperthyroidism is associated with accelerated bone remodeling, reduced bone density, osteoporosis, and an increase in fracture rate

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21
Q

What are causes of an isolated rise in ALP?

A
  • Bone metastases
  • 1ary bone tumours (e.g. sarcoma)
  • Vitamin D deficiency
  • Recent bone fractures
  • Renal osteodystrophy
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22
Q

What is renal osteodystrophy?

A

A form of metabolic bone disease seen in patients with chronic renal insufficiency characterised by bone mineralisation deficiency due to electrolyte and endocrine abnormalities.

Patients present with osteomalacia, osteonecrosis and pathologic fractures.

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23
Q

Compare ALT to ALP levels in a primarily hepatocellular pattern of injury

A

ALT is raised markedly compared to ALP

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24
Q

Compare ALT to ALP levels in a primarily cholestatic pattern of injury

A

ALP is raised markedly compared to ALT

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25
Q

If the patient is jaundiced but ALP and ALT levels are normal, what is going to be risen?

A

Bilirubin

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26
Q

What is the most common cause of an isolated rise in bilirubin?

A

Gilbert’s syndrome

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27
Q

What is Gilbert’s syndrome?

A

An inherited condition where the liver’s ability to conjugate bilirubin is impaired. In times of fatigue/stress etc, that patient can become temporarily jaundiced. It is often not serious with no side effects.

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28
Q

What is another cause of an isolated rise in bilirubin?

A

Haemolysis e.g. haemolytic anaemia

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29
Q

What blood tests should be done in suspected cases of haemolysis?

A
  • Blood film
  • FBC
  • Reticulocyte count
  • Haptoglobin
  • LDH levels
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30
Q

What is the normal life span of a RBC?

A

120 days

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31
Q

What may a FBC show in haemolysis?

A

Reduced haemoglobin indicates anaemia (normocytic or macrocytic)

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32
Q

What may a blood film show in haemolysis?

A

Abnormal RBCs e.g. spherocytes, schistocytes etc

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33
Q

What may a reticulocyte count show in haemolysis?

A

Elevated reticulocytes

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34
Q

What is haptoglobin?

A

Haptoglobin is the protein produced by the liver that in humans is encoded by the HP gene. In blood plasma, haptoglobin binds to free haemoglobin.

35
Q

What may haptoglobin levels show in hameolysis?

A

Reduced haptoglobin

36
Q

What may LDH levels show in haemolysis?

A

LDH levels elevated as LDH is intracellular so released when RBCs rupture

37
Q

Is the bilirubin conjugated or unconjugated in haemolytic anaemia?

A

Unconjugated (no effect on urine/stools)

38
Q

What are the 4 main synthetic functions of the liver?

A
  1. Conjugation and elimination of bilirubin
  2. Albumin
  3. Clotting factors
  4. Gluconeogenesis
39
Q

What 4 investigations can be done to assess synthetic liver function?

A
  1. Serum bilirubin
  2. Serum albumin
  3. Prothrombin time (PT)
  4. Serum blood glucose
40
Q

What is bilirubin?

A

Breakdown product of haem

41
Q

Describe the conjugation process of bilirubin

A
  1. RBC breakdown in spleen gives unconjugated bilirubin
  2. Unconjugated bilirubin is conjugated in the liver to give conjugated bilirubin
  3. Conjugated bilirubin then is excreted in bile into the 2nd part of duodenum (ampulla of vater)
  4. In the colon, bacteria convert conjugated bilirubin into urobilinogen
  5. Most urobilinogen is converted into sterocobilin and excreted via faeces
  6. Some urobilinogen is reabsorbed to be recycled or sent to kidneys where it is converted to urobilin and excreted via urine
42
Q

Which form of bilirubin gives faeces its brown colour?

A

Stercobilin

43
Q

Which form of bilirubin gives urine its yellow colour?

44
Q

What is the cause of dark urine in post-hepatic jaundice?

A

Urobilinogen

45
Q

What type of jaundice does malaria cause?

A

Pre-hepatic (haemolytic anaemia)

46
Q

In pre-hepatic jaundice:

a) what type of bilirubin is raised?
b) colour of skin?
c) colour of urine?
d) colour of stool?

Why?

A

a) unconjugated bilirubin
b) yellow
c) normal
d) normal

As unconjugated bilirubin is insoluble

47
Q

In post-hepatic jaundice:

a) what type of bilirubin is raised?
b) colour of skin?
c) colour of urine?
d) colour of stool?

Why?

A

a) conjugated
b) yellow
c) dark
d) pale

As conjugated bilirubin is soluble so can pass into urine as urobilinogen (causes dark urine)

48
Q

In obstructive post-hepatic pathology, how many stools appear? Why?

A

Stools appear pale, bulky and difficult to flush

As bile and pancreatic lipases are unable to reach the bowel because of the blockage so fat cannot be absorbed

49
Q

What type of jaundice is indicated by;

a) normal urine + normal stools
b) dark urine + normal stools
c) dark urine + pale stools

A

a) pre-hepatic
b) intra-hepatic
c) post-hepatic

50
Q

What are 3 mechanisms behind unconjugated hyperbilirubinaemia?

A
  1. Haemolysis → haemolytic anaemia
  2. Impaired conjugation → Gilbert’s syndrome
  3. Impaired hepatic uptake → drugs, congestive cardiac failure
51
Q

What are 2 major causes of conjugated hyperbilirubinaemia?

A
  1. Hepatocellular injury
  2. Cholestasis
52
Q

What is albumin? Function?

A

Albumin is synthesised in the liver and helps to bind water, cations, fatty acids, and bilirubin. It also plays a key role in maintaining the oncotic pressure of blood.

53
Q

What are 3 mechanisms causing hypoalbuminaemima?

A
  1. Excessive losses → loss of protein due to protein losing enteropathies or nephrotic syndrome
  2. Decreased production → liver disease e.g. cirrhosis
  3. Inflammation
54
Q

What is a protein losing enteropathy?

A

A pathological condition in which there is an increased loss of proteins through the gastrointestinal tract, which leads to low serum proteins.

E.g. severe burns

55
Q

Why can inflammation lead to hypoalbuminaemia? Is this permanent?

A

Inflammation triggers an acute phase response which temporarily decreases the liver’s production of albumin

56
Q

What is prothrombin time? Which pathway is it measuring?

A

A measure of the blood’s coagulation tendency (i.e. clotting time).

Directly assesses the extrinsic pathway.

57
Q

What are two 2ary causes of an increased PT?

A
  1. Anticoagulant drug use
  2. Vitamin K deficiency
58
Q

Why can a vitamin K deficiency lead to an increased PT time?

A

Some clotting factors are vitamin K dependent

59
Q

How can hepatic pathology affect PT? Why?

A

Increase - liver synthesises clotting factors

60
Q

What is gluconeogenesis?

A

A metabolic pathway that results in the generation of glucose from certain non-carbohydrate substrates

61
Q

Why can assessment of serum blood glucose provide an indirect assessment of the liver’s synthesis function?

A

The liver plays a significant role in gluconeogenesis

62
Q

Is gluconeogenesis affected early or late in liver failure?

A

Late - one of the last functions to be impaired

63
Q

Common patterns of LFT derangement

64
Q

In acute hepatocellular damage, describe;

a) ALT levels
b) ALP levels
c) GGT levels
d) bilirubin

A

a) markedly raised
b) normal or slightly raised
c) normal or slightly raised
d) slightly or markedly raised

65
Q

In chronic hepatocellular damage, describe;

a) ALT levels
b) ALP levels
c) GGT levels
d) bilirubin

A

a) normal or slightly raised
b) normal or slightly raised
c) normal or slightly raised
d) normal or slightly raised

66
Q

In cholestasis, describe;

a) ALT levels
b) ALP levels
c) GGT levels
d) bilirubin

A

a) normal or slightly raised
b) markedly raised

c) markedly raised

d) markedly raised

67
Q

What are 3 common causes of acute hepatocellular injury?

A

a) Poisoning (paracetamol overdose)
b) Infection (hep A & B)
c) Liver ischaemia

68
Q

What types of hepatitis can progress to chronic?

A

Hep B and C

69
Q

What are 4 common causes of chronic hepatocellular injury?

A
  1. Chronic infection (Hep B or C)
  2. Alcoholic fatty liver disease
  3. Non-alcoholic fatty liver disease
  4. Primary biliary cirrhosis
70
Q

What are 3 less common causes of chronic hepatocellular injury?

A
  1. Wilson’s disease → copper build up damages liver)
  2. Haemochromatosis → excess iron stored in liver damages it
  3. Alpha-1 antitrypsin deficiency → 15% develop cirrhosis
71
Q

What is a liver screen?

A

A batch of investigations focused on ruling underlying causes of liver disease out or in.

72
Q

What does a typical liver screen include?

A
  • LFTs
  • Coagulation screen
  • Hepatitis serology (A/B/C)
  • Epstein-Barr virus (EBV)
  • Cytomegalovirus (CMV)
  • 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
73
Q

What is the purpose of serum copper levels in a liver screen?

A

To rule of Wilson’s disease

74
Q

What is ceruloplasmin?

A

Ceruloplasmin is a protein that is made in the liver.

Ceruloplasmin is the major copper-carrying protein in the blood, and in addition plays a role in iron metabolism.

75
Q

What is ceruloplasmin?

A

Ceruloplasmin is a protein that is made in the liver.

Ceruloplasmin is the major copper-carrying protein in the blood, and in addition plays a role in iron metabolism.

76
Q

What disease can be included/excluded by assessing ceruloplasmin in liver disease?

A

To rule out Wilson’s disease

77
Q

How is ceruloplasmin affected in Wilson’s? Why?

A

Reduced levels

In Wilson disease, copper is not put in ceruloplasmin (carrying protein).

78
Q

What disease can be included/excluded by assessing ferritin in liver disease?

A

Haemochromatosis

79
Q

What disease can be included/excluded by assessing alpha-1 antitrypsin in liver disease?

A

alpha-1 antitrypsin deficiency

80
Q

Anti-mitochondrial antibodies (AMA) are highly specific of which pathology?

A

Anti-mitochondrial antibody are highly sensitive and specific marker of Primary Biliary Cirrhosis

81
Q

What do high levels of anti-smooth muscle antibodies (ASMA) likely indicate?

A

Autoimmune hepatitis

82
Q

What disease can a positive ANA test indicate?

A

Autoimmune; e.g. SLE

83
Q

What can a positive p-ANCA test indicate?

A

Autoimmune vasculitis e.g. Granulomatosis with polyangitis (formerly known as Wegners Granulomatosis)

Yr 3 - Skills & Extras (7 decks)

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