Understanding LFTs Flashcards

1
Q

Function of LFTs

A

To distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic or obstructive jaundice)

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2
Q

Tests used in LFTs

A
Alanine transaminase (ALT)
Aspartate aminotransferase (AST)
Alkaline phosphatase (ALP)
Gamma-glutamyltransferase  (GGT)
Bilirubin
Albumin
Prothrombin time (PT)
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3
Q

Distinguishing between Hepatocellular Damage and Cholestasis

A

ALT
AST
ALP
GGT

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4
Q

Assessing Liver’s Synthetic Function

A

Bilirubin
Albumin
PT

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5
Q

ALT

A

Marker of hepatocellular injury

Concentrated in hepatocytes
Enters blood after hepatocellular injury

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6
Q

ALP

A

Marker of cholestasis

Concentrated in liver/bil duct/bone tissues
Raised in live pathology due to incr synthesis in response to cholestasis

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7
Q

ALT and ALP in Predominantly Hepatocellular Injury

A

Greater than 10-fold increase in ALT and a less than 3-fold increase in ALP

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8
Q

ALT and ALP in Cholestasis

A

Less than 10-fold increase in ALT and a more than 3-fold increase in ALP

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9
Q

GGT

A

Suggests biliary epithelial damage and bile flow obstruction

Raised in resp to alcohol and drugs e.g. phenytoin

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10
Q

Highly raised ALP plus raised GGT?

A

Cholestasis

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11
Q

Causes of Isolated Rise of ALP

A
(Anything involving bone breakdown)
Bony metastases or primary bone tumours (e.g. sarcoma)
Vitamin D deficiency
Recent bone fractures
Renal osteodystrophy
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12
Q

Causes of Isolated Rise in Bilirubin

A

Gilbert’s syndrome: the most common cause.

Haemolysis: check a blood film, full blood count, reticulocyte count, haptoglobin and LDH levels to confirm.

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13
Q

Investigation of Liver’s Main Synthetic Functions

A

Conjugation and elimination of bilirubin (serum bilirubin)
Synthesis of albumin (serum albumin)
Synthesis of clotting factors (PT)
Gluconeogenesis (serum blood glucose)

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14
Q

Cause of Jaundice from Urine/Stool Colour

A

Normal urine + normal stools = pre-hepatic cause
Dark urine + normal stools = hepatic cause
Dark urine + pale stools = post-hepatic cause (obstructive)

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15
Q

Causes of Unconjugated Hyperbilirubinaemia

A

Haemolysis (e.g. haemolytic anaemia)
Impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
Impaired conjugation (e.g. Gilbert’s syndrome)

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16
Q

Causes of Conjugated Hyperbilirubinaemia

A

Hepatocellular injury

Cholestasis

17
Q

Function of Albumin

A

Helps bind water/cation/FAs/bilirubin

Maintains oncotic pressure of blood

18
Q

Causes of Decreased Albumin

A

Liver disease resulting in a decreased production of albumin (e.g. cirrhosis).
Inflammation triggering an acute phase response which temporarily decreases the liver’s production of albumin.
Excessive loss of albumin due to protein-losing enteropathies or nephrotic syndrome

19
Q

Prothrombin Time (PT)

A

Measure of the blood’s coagulation tendency, specifically assessing the extrinsic pathway

20
Q

Causes of Increased PT

A

(In absence of anticoags and vit K defic)
Liver disease and dysfunction
Failure to produce clotting factors

21
Q

AST/ALT Ratio

A

ALT > AST is associated with chronic liver disease

AST > ALT is associated with cirrhosis and acute alcoholic hepatitis

22
Q

Serum Glucose

A

Measures liver’s generaton of glucose from non-carb substrates (gluconeogenesis)
One of the last to be impaired in liver failure

23
Q

Common Causes of Acute Hepatocellular Injury

A

Poisoning (paracetamol overdose)
Infection (Hepatitis A and B)
Liver ischaemia

24
Q

Common Causes of Chronic Hepatocellular Injury

A

Alcoholic fatty liver disease
Non-alcoholic fatty liver disease
Chronic infection (Hepatitis B or C)
Primary biliary cirrhosis

25
Q

Less Common Causes of Chronic Hepatocellular Injury

A

Alpha-1 antitrypsin deficiency
Wilson’s disease
Haemochromatosis