interpretation of LFTs

Question 1

LFTs include

Answer 1

Alanine transaminase (ALT)
Aspartate aminotransferase (AST)
Alkaline phosphatase (ALP)
Gamma-glutamyltransferase (GGT)
Bilirubin
Albumin

Question 2

ALT reference range

Answer 2

3-40 iu/L

Question 3

AST reference range

Answer 3

3-30 iu/L

Question 4

ALP reference range

Answer 4

30-100 umol/L

Question 5

GGT reference range

Answer 5

8-60 u/L

Question 6

Bilirubin reference range

Answer 6

3-17 umol/L

Question 7

Albumin

Answer 7

35-50 g/L

Question 8

ALT is

Answer 8

alanine aminotransferase

Question 9

AST is

Answer 9

aspartate aminotransferase

Question 10

raised AST and ALT means

Answer 10

occur in pathologies that cause liver cell (hepatocyte) inflammation or damage
marker of hepatocellular injury

Question 11

common causes of hepatocellular injury

Answer 11

hepatitis (viral, alcoholic, ischaemic)
liver cirrhosis
drug/toxin-induced liver injury (e.g. paracetamol overdose)
malignancy (hepatocellular carcinoma)

Question 12

AST:ALT ratio

Answer 12

if it is >2:1 this is classical of alcoholic liver disease

Question 13

ALP is

Answer 13

alkaline phosphatase

Question 14

GGT is

Answer 14

Gamma-glutamyltransferase

Question 15

ALP is derived from

Answer 15

biliary epithelial cells (cells lining the biliary tract) and bones

Question 16

raised ALP levels may be caused by

Answer 16

cholestasis or bone disease

Question 17

what is cholestasis

Answer 17

Cholestasis describes an interruption in the bile flow from hepatocytes to the small intestine.
Common causes include gallstone disease, external compression of the biliary tract (e.g. pancreatic malignancy) or medication side effects. Bilirubin may or may not be raised depending on the severity of cholestasis.

Question 18

GGT is found in

Answer 18

hepatocytes and also biliary epithelial cells

Question 19

GGT is a marker of

Answer 19

non-specific but highly sensitive marker of liver damage and cholestasis

Question 20

ALP rise with normal GGT

Answer 20

suggests bone disease eg. paget’s disease, vit D deficiency, bony metastasis

Question 21

ALP rise with associated GGT rise is more suggestive of

Answer 21

cholestasis

Question 22

isolated GGT rise is associated with

Answer 22

alcohol excess

Question 23

where does bilirubin come from

Answer 23

a waste product of haemoglobin breakdown

Question 24

what do hepatocytes do to bilirubin

Answer 24

Hepatocytes take up unconjugated bilirubin and metabolise it to form conjugated (soluble) bilirubin

Question 25

where does conjugated bilirubin go

Answer 25

Hepatocytes excrete conjugated bilirubin into the biliary tract, where it flows into the bowel lumen as bile

Question 26

what happens to conjugated bilirubin in the gut

Answer 26

Gut bacteria further metabolise bilirubin in bile to form urobilinogen, which is eventually excreted in the stools as stercobilinogen
A small amount of urobilinogen is reabsorbed from the intestine into the portal venous system, and as urobilinogen is water-soluble, the kidney is able to excrete some of this into the urine.

Question 27

stercobilinogen

Answer 27

Stercobilinogen gives stools their dark colour

Question 28

urobilinogen

Answer 28

Urobilinogen is colourless in the urine. However, if the urine is left exposed to the air, oxidation will occur, creating a dark colour. Under normal physiological conditions, urobilinogen will be present in the urine, however conjugated bilirubin will not be present.

Question 29

what type of bilirubin should be present in the urine

Answer 29

Under normal physiological conditions, urobilinogen will be present in the urine, however conjugated bilirubin will not be present.

Question 30

raised levels of bilirubin in the blood can be caused by

Answer 30

Excess bilirubin production (pre-hepatic jaundice)
A breakdown in bilirubin metabolism (hepatocellular jaundice)
A blockage in the bile excretion pathway (cholestatic jaundice)

Question 31

pre-hepatic jaundice occurs when

Answer 31

Pre-hepatic jaundice occurs when increased red blood cell breakdown produces excess bilirubin. This can overwhelm metabolism/excretion pathways, leading to jaundice.

Question 32

most common cause of increased red blood cell breakdown

Answer 32

haemolysis

Question 33

what does LFTs for haemolysis look like

Answer 33

Bilirubin is unconjugated in the blood, as the hepatocytes have not yet metabolised it. The remainder of LFTs are generally normal, as the liver is otherwise working well.

Question 34

what is Gilbert’s syndrome

Answer 34

Gilbert’s syndrome is a congenital disorder present in up to 5% of the population. It results from a deficiency of glucosyltransferase, the enzyme responsible for the conjugation of bilirubin within hepatocytes.

Question 35

how does Gilberts syndrome present

Answer 35

Gilbert’s syndrome classically presents following viral infection with raised bilirubin but normal LFTs/ full blood count. The disease is benign and requires no specific management.

Question 36

Hepatocellular jaundice occurs when

Answer 36

when hepatocytes are damaged and dysfunctional, leading to an inability to metabolise unconjugated bilirubin from the bloodstream. This leads to high levels of unconjugated bilirubin in the blood.

Question 37

LFT appearance of hepatocellular jaundice

Answer 37

very high ALT / AST levels, marking hepatocyte damage.

Question 38

common causes of hepatocellular injury

Answer 38

hepatitis, cirrhosis, malignancy, drug or toxin insult
When liver injury is severe, there are not enough functioning hepatocytes to metabolise bilirubin, and jaundice will develop.

Question 39

what is cholestasis

Answer 39

an interruption in bile flow from hepatocytes to the gut. When this interruption is severe, bilirubin levels will build up in the blood. The bilirubin has been metabolised in the liver, and thus the bilirubin in the blood is predominantly conjugated bilirubin.

Question 40

what type of bilirubin will build up in the blood in cholestasis

Answer 40

conjugated

Question 41

what type of bilirubin will build up in the blood in hepatocellular jaundice

Answer 41

unconjugated

Question 42

what kind of bilirubin will be in the blood in pre-hepatic jaundice

Answer 42

unconjugated

Question 43

LFTs appearance of cholestatic (obstructive) jaundice

Answer 43

There will generally also be high ALP levels with associated high GGT, marking dysfunction of the biliary system.

Question 44

clinical symptoms of cholestatic (obstructive) jaundice

Answer 44

Obstructive jaundice will classically lead to dark urine and pale stools.

Question 45

why does cholestatic jaundice lead to dark urine and pale stools

Answer 45

Bilirubin cannot enter the gastrointestinal tract due to cholestasis, leading to low stercobilinogen excretion in stools.
The bilirubin in the blood is conjugated and can be filtered by the kidneys. The presence of conjugated bilirubin gives the urine a very dark colour.