Blood typing

Question 1

What are the 2 main blood typing systems?

Answer 1

ABO and Rhesus system

Question 2

ABO System

Answer 2

O- Neither A/B antigen on rbc, and both Anti- A and Anti- B ABs in plasma
A- A antigens, and Anti- B only
B- B antigens, and Anti- A only
AB- A and B antigens, neither antibody in plasma

E.G if Anti-A abs contact A antigens, they will bind

Question 3

Rhesus system

Answer 3

Rh+ has the D-antigen present on RBC surface, no D Ab in plasma

Rh- does not have the D-antigen, nor the D-antibody in the plasma
No one is born with Rh antibodies in plasma-
1. if Rh- individual transfused with positive blood
2. Rh- mother with Rh+ baby- some of babies blood may mix with babies’ blood- mother makes antibodies
problem if another Rh+ baby born
(Blue baby syndrome/ haemolytic disease of newborn)

Question 4

How many different blood types are there?

Answer 4

8- O+/-, A+/-, B+/- and AB+/-

Question 5

Why is it important to transfuse compatible blood?

Answer 5

When an antibody meets specific antigen, a cross reaction occurs- agglutination (clumping together of erythrocytes- can lead to blockages of vessels/ haemolysis can take place)
Haemoglobin released which is toxic to body tissue

Question 6

How to type blood?

Answer 6

Take a drop and mix with Anti- A/B and D serums. (Serum is plasma with no clotting factors)

Agglutination occurs in these serums e.g in A+,
it will occur in Anti- A and Anti- D

Question 7

What is cross matching?

Answer 7

A process which establishes the compatibility between donor and recipient, minimising risk of haemolytic reactions

Patient serum is mixed with Donor RBC, centrifuged and ABO compatibility determined

Question 8

What is haemostasis?

Answer 8

The series of reactions that occur to stop blood loss.

1. Vascular phase- Immediate response is vascular spasm (local vasoconstriction) to reduce the speed of blood flow through the injured vessel. Spasm triggered by injury itself + chemicals released by endothelial cells and platelets and by sensations of pain- e.g platelets release serotonin and thromboxane A2 (TXA2) (potent vasoconstrictors)
2. Platelet phase-
   Adherence: platelets rapidly begin to collect at site of injury and bind to exposed collagen in the vessel wall. Aided by von Willebrand factor (vWF), which attaches the platelets to the collagen.
   Activation: Platelets become activated when binded with collagen- swell to increase their SA, and become star-shaped and more sticky. Anionic phospholipids relocate from inner aspect of the membrane bilayer to outer aspect of the platelet membrane. Relocation provides the net negatively charged phospholipid surface required for key reactions of clotting cascade.
   Aggregation: Developing meshwork of platelets traps more platelets, which becomes activated and recruit more platelets. This positive feedback loop results in a platelet plug efffectively stopping bleeding from injured vessel.
3. Clotting phase- coagulation: Reinforces/ stabilizes platelet plug to produce a blood clot that effectively seals large vessel injuries. The blood clot is formed in a series of steps that involve clotting factors, or procoagulants knock on effect of activated factors, thrombin formed and important in fibrin clot formation. More fixed than platelet plug.