Foundations Year 2 Flashcards
(85 cards)
What is the primary source of bilirubin in the body?
from the breakdown of haem from aged red blood cells
What is the first step in bilirubin metabolism after haem is broken down?
Haem is converted to biliverdin, then to unconjugated bilirubin (indirect bilirubin)
How is unconjugated bilirubin transported to the liver?
Unconjugated bilirubin binds to albumin and is transported to the liver
How is conjugated bilirubin excreted from the body?
Conjugated bilirubin is secreted into the
1. bile
2. then enters the intestine
- where it is either converted to urobilinogen or excreted asstercobilinin faeces
What is the key difference between unconjugated and conjugated bilirubin?
Unconjugated bilirubin is lipid-soluble and bound to albumin, while conjugated bilirubinis water-soluble and can be excreted in bile/urine
What are the three main categories of causes of jaundice?
- Pre-hepatic
= haemolysis - Hepatic
= hepatitis, Crigler-Najjar - Post-hepatic
= biliary obstruction
What is the primary cause of hepatic jaundice?
Impaired liver function, such as in hepatitis, cirrhosis, or genetic conditions like Crigler-Najjar and Gilbert’s syndrome
What is the primary cause of pre-hepatic jaundice?
Haemolysis (destruction of RBCs) leading to increased unconjugated bilirubin
What causes post-hepatic jaundice?
- Biliary obstruction = such as from gallstones, pancreatic cancer
- biliary atresia = leading to increased conjugated bilirubin
At what age is neonatal jaundice considered pathological?
Neonatal jaundice is considered pathological if it appears before 24 hours of age
What is the most common cause of pathological neonatal jaundice?
Haemolytic disease of the newborn
= ABO incompatibility
= Rh incompatibility
How is neonatal jaundice investigated?
- serum bilirubin
- Coombs test
- blood group(mother and baby)
- FBC
- infection screen (blood cultures)
What is the first-line treatment for neonatal jaundice?
Phototherapy, which uses blue light to convert unconjugated bilirubin to a water-soluble form
When is exchange transfusion indicated for neonatal jaundice?
serum bilirubin levels are extremely high or phototherapyis ineffective
What is Dubin-Johnson syndrome?
A rare condition with impaired excretion of conjugated bilirubin, leading toconjugated hyperbilirubinaemia and a black liver on histology
It’s typically benign
What is Gilbert’s syndrome?
A benign condition with mild deficiency of UDP-glucuronyl transferase
= leading to intermittent unconjugated hyperbilirubinaemia, often triggered by stress, fasting, or illness
What is Rotor syndrome?
A condition similar to Dubin-Johnson, but without the pigmented liver
It also causes conjugated hyperbilirubinaemia but is typically benign
What is the difference betweenCrigler-Najjar syndrome Type I and Type II?
- Type I
= Complete absence of UDP-glucuronyl transferase →severe unconjugated hyperbilirubinaemia
= high risk of kernicterus - Type II
= Partial enzyme activity →milder hyperbilirubinaemia
What is the mechanism of Rhesus (Rh) incompatibility?
Rh-mothers can become sensitised during the first pregnancy with an Rh+ foetus, producing IgG antibodies.
In subsequent pregnancies, IgG crosses the placenta and causes haemolysis of the foetal RBCs
How do you prevent rhesus haemolytic disease?
Give Anti-D immunoglobulin to Rh-mothers after delivery or any sensitising event
= miscarriage, trauma etc
What does a Coombs test detect?
The direct Coombs test detects antibodies on neonatal RBCs, while the indirect Coombs test detects maternal anti-Rh antibodies
Rh- mother + Rh+ baby leads to what happening?
Immune sensitisation
- First pregnancy
= IgM (no placental crossing) - Subsequent pregnancies
- IgG crosses placenta → foetal haemolysis
What are the typical LFT findings in pre-hepatic jaundice?
(1) ↑ Unconjugated bilirubin
(2) Normal ALT, AST, ALP, and GGT
(3) Cause
= Excess haemolysis
(eg, haemolytic anaemia)
What are the typical LFT findings in hepatic jaundice?
(1) ↑ ALT and AST (often > ALP)
= hepatocellular pattern
(2) Mixed rise in conjugated and unconjugated bilirubin
(3) ALP and GGT may be mildly elevated or normal
(4) Cause: Hepatocellular damage
(eg, hepatitis, cirrhosis, Gilbert’s)
