Health Information

Red blood cells normally live for 120 days.
Some diseases cause premature breakdown of red blood cells.
At the end, cell is too fragile.
Cell membrane rupture.
Destroyed by macrophages in the spleen and bone marrow – Reticuloendothelial system.

What is haemolysis?
Haemoglobin splits and globin and heme release.
Heme consists of four pyrrole rings.
Heme ring open and release pyrrole rings.
Pyrrole will under go several reaction and bilirubin form.
Conjugated bilirubin turn to urobilinogen by bacteria in the intestine.
Excrete via stool.
Urobilinogen can be reabsorbed to blood.
5% excrete via urine.

Urobilinogen turn to urobilin by oxidization when expose to air.
Stercobilinogen turn to stercobilin by oxidization when expose to air.
Jaundice
Excess bilirubin in the extracellular fluid.
Detectable when the serum bilirubin >30-60 µmol/letter.

Haemolysis
increase unconjugated bilirubin in plasma.
Urobilinogen increase

Intrahepatic cholestasis
acute and chronic liver diseases including cirrhosis, hepatitis, drugs,
increase in both type bilirubins

Congenital hyperbilirubinaemias
Glibert’s syndrome
common type
2-5% of population with mild increase unconjugated bilirubin.
Asymptomatic
Crigler-Najjar syndrome
rare
Problem of conjugation
Increase unconjugated bilirubin.
Dubin-johnson syndrome
Defect in bilirubin handling.
Increase conjugated bilirubin.

Haemolysis
Red blood cells normally live for 120 days.
Some diseases cause premature breakdown of red blood cells.
At the end, cell is too fragile.
Cell membrane rupture.
Destroyed by macrophages in the spleen and bone marrow – Reticuloendothelial system.
Haemoglobin splits and globin and heme release.
Heme consists of four pyrrole rings.
Heme ring open and release pyrrole rings.
Pyrrole will under go several reaction and bilirubin form.
Unconjugated bilirubin enter to hepatic cells.
Conjugate
80% - bilirubin glucuronide.
10% - bilirubin sulfate.
10% - other substances.

Form biliverdin.
Further reduced to bilirubin.
First form is unconjugated/free bilirubin.
Release from macrophage to plasma.
Not soluble and bind to protein.

Rh Factor
Detected only on the red cell surface.
Sub groups - C, c, D, E, e
D is more antigenic.
If D antigen is present Rh +, if absent Rh –
Antibodies (agglutinins) to Rh factor is not developed spontaneously in Rh – individuals without having exposure to Rh antigen.
Sensitisation to Rh Factor
May occur
Following transfusion of Rh + blood to Rh – individuals
In events related to pregnancy (abortion, anti-partum haemorrhage, delivery) having Rh + fetus in Rh - mother
Haemolytic Disease of the Newborn
Rh incompatibility is less commoner – severe.
Other causes for haemolytic disease of newborn.
ABO blood group incompatibility.
“minor” blood group incompatibilities.

Rh Incompatibility
Occurs in Rh+ babies born to Rh- mothers.
No Rh agglutinins in non sensitised Rh negative individuals.
Antibodies developed following exposure to the Rh antigen.
Rh antibodies are Ig-G type, it crosses the placenta
If Rh antibody crosses the placenta of Rh+, haemolysis occurs in fetal blood.

Consequences of Rh Incompatibility
Haemolytic disease of the newborn
(Erythroblastosis fetalis)
Death inutero
Hydrops fatalis
Kernicterus
Usually 1st child is normal
≈17% children in 2nd pregnancy of Rh – mothers are affected

Prevention
Prevention of sensitisation in Rh – mothers to Rh factor
Avoiding transfusion of Rh+ blood to Rh – women
Treating with Rh antibodies to mothers who have exposed to Rh antigen within 48 hours of exposure (following miscarriage, still birth or delivery).
Rh immune globulin (RhIG) or Rhogam.
Passively acquired antibodies destroy any fetal cells in her circulation before they can elicit an active immune response.
Treatment for Rh Incompatibility
Mild disease - no treatment.
if jaundice is significant - need to treat.
Why
Kernicterus (Bilirubin can cross the blood brain barrier and causes damage to basal ganglia
It may leads to deafness
Treatment for Rh Incompatibility
Phototherapy
Convert bilirubin into water soluble isomers
Exchange transfusion

Incompatibility make clumps/agglutinates.
Cells (antigen) from donor will react with recipient antibody.
One antibody can bind several antigen.
Can plug in small blood vesicles and Cell will be destroyed by macrophage or physical distortion.

Transfusion reaction
Antibody from donors not make problem due to dilution.
Can be immediate hemolysis.
Delayed hemolysis – need high titer of antibody for lysis to occur.
Can results jaundice.
Can be minor reaction to death.

AB type – ‘universal recipients’
O type – ‘universal donors’
But always need cross match.

Blood types
Karl Landsteiner discovered blood groups, 1901.
Membrane of red blood cell contain blood group antigens - agglutinogens
Several types of antigens.
Most important – ABO system and Rh.
Less important - MNSs, Lutheran, Kell, Kidd

ABO system
4 major blood groups.
A – antigen A
B – antigen B
AB – antigen A & B
O – no antigen
Found in other tissue – Kidney, liver, lungs.
All type contain H antigen on cell surface.
A type – acetylgalactosamin
B type – galactose
AB – Both
O – only H antigen

Antibody against RBC antigen – agglutinins.
Antibody develop after birth due GIT bacteria/food
No antibody development against antigen present in own cells.

Inheritance of ABO system
Inherited as mendelian allelomorphs.
Phenotype B – Genotype BB (homozygous) or BO (heterozygous).
When blood type of parents know possible genotypes can be predicted.
If mother’s and child’s blood type know, it can be prove that a man can’t be father.

Rh blood group
Rh factor named for rhesus monkey.
Only found in RBC.
C,D,E (and more) antigen – Most important is D.
Rh positive mean antigen D present.
85% Caucasians, 99% Asians are Rh positive.
Rh blood group
Rh negative person can produce anti-D antibody when expose to antigen D.
Anti-D antibody will not develop without expose antigen D.
To develop anti-D need transfusion
from other person
from fetal blood to mother.

Collection of Lymphoma-Leukemia slides.

Here provide good collection of slides of all types of anemias and lukemias.