Blood Groups And Haemostasis (Physiology)

Question 1

Describe ABO and Rhesus blood grouping

Answer 1

ABO

• Formed by the blood types A, B, AB, and O.
• An ABO blood type is determined by the presence or absence of the A and B antigens on the red blood cells.
• Each blood group derives its name from the antigens present on the surface of the red blood cells.
• The plasma of each group contains antibodies against the antigens not present on the surface of the red blood cells.

Rhesus

• 3 main antigens involved - C, D (most common and most reactive), and E.
• Rhesus positive if the D antigen is present on red blood cells and rhesus negative if the D antigen is not present on red blood cells.
• Anti-D antibodies are not normally present in the blood but instead only form when an Rh- individual is exposed to Rh+ blood.

Question 2

Explain why its is important that blood is typed and cross matched

Answer 2

• If blood is not typed or cross matched, then the infusion of incompatible blood can cause an antigen-antibody cross-reaction.
• This can lead to the agglutination of red blood cells and haemolysis (destruction of red blood cells) which can be fatal.

Question 3

Explain the consequences of infusing incompatible blood

Answer 3

• If blood group A blood was given to a patient who is blood group B, then an antigen-antibody cross-reaction would occur.
• The anti-A antibodies in the patient’s blood would agglutinate the A antigens on the donor’s red blood cells.
• This can lead to haemolysis which can be fatal.

Question 4

Explain the meaning of the terms Universal Donor and Universal Recipient

Answer 4

Universal donor

• Refers to blood group O-.
• Blood group O- has no A, B or D antigens.
• This means that O- blood can be donated to all other blood groups because the donated blood has no antigens to cause an antigen-antibody cross-reaction and subsequently agglutination.
• Individuals with O- blood can therefore donate blood to individuals of any blood type.

Universal recipient

• Refers to blood group AB+.
• AB+ blood has all antigens (A,B, and D),
• Therefore AB+ blood has no antibodies and so could not cause agglutination of the antigens of any other blood type.
• Individuals with AB+ blood can therefore receive blood from individuals of any blood type.

Question 5

Describe the potential difficulty of a Rhesus positive mother bearing the child of a Rhesus negative father

Answer 5

• The Rh+ blood from the mother crosses the placenta.
• If the foetus is Rh-, then the immune system of the foetus will become sensitised to produce anti-D antibodies.
• The anti-D antibodies react with the D antigens in the mother’s blood and cause the mother’s blood to agglutinate.
• May cause haemolysis.

Question 6

What condition may result in the second child if a rhesus negative mother gives birth to two rhesus positive children

Answer 6

Haemolytic disease of the newborn (HDN)

Question 7

Define the term haemostasis and list its four stages

Answer 7

• Haemostasis is the prevention of blood loss.

Four stages

• Vascular spasms
• Platelet plug formation
• Coagulation
• Scar formation

Question 8

Define the terms vascular spasm, platelet plugging, blood clotting, and scar formation, and explain the underlying processes

Answer 8

Vascular spasm

• Prompt vasoconstriction of the damaged blood vessel.
• An injury stimulates pain receptors, some of which directly innervate nearby blood vessels causing them to contract.
• Injury to the smooth muscle of the blood vessel causes a longer-lasting vasoconstriction, and platelets release serotonin which is a chemical vasoconstrictor.

Platelet plugging

• Refers to when platelets stick to the endothelium.
• Platelets do not normally stick to the endothelium as it is normally very smooth and coated with a platelet repellant called prostacyclin.
• When a blood vessel is broken, collagen fibres of its walls are exposed. When platelets come into contact with collagen, they grow pseudopods that adhere to the vessel and to other platelets. The pseudopods then contract and draw the walls of the vessel together. The mass of platelets that forms is called a platelet plug.
• von Willebrand factor (vWF) is released by damaged endothelial cells which acts as a glue to stick platelets to the site of injury.
• Activated platelets release ADP, thromboxane A2, and serotonin. Thromboxane enhances ADP release from activated platelets which causes passing platelets to become sticky and adhere to the site of injury.

Blood clotting

• Also known as the coagulation cascade.
• Follows intrinsic and extrinsic pathways as well as a common pathway. (Intrinsic pathway uses clotting factors within the bloodstream whereas extrinsic pathway uses clotting factors outside of the bloodstream.)
• The objective is to convert the plasma protein fibrinogen into fibrin, a sticky protein that adheres to the walls of a vessel.
• As blood cells and platelets arrive, they stick to the fibrin. The resulting mass of fibrin, blood cells, and platelets seals the break in the blood vessel.

Scar formation

• The replacement of normal skin with fibrous tissue after an injury.
• After a clot has formed, pseudopods of the platelets adhere to strands of fibrin and contract, pulling on the fibrin threads and drawing the edges of the broken vessel together.
• This process of clot retraction allows the clot to become more compact within 30 minutes.
• Platelets and endothelial cells secrete a mitotic stimulant called platelet-derived growth factor (PDGF) which stimulates fibroblasts and smooth muscle cells to multiply and repair the damaged vessel.
• Fibroblasts also invade the clot and produce fibrous connective tissue which helps to strengthen and seal the vessel while it repairs.

Question 9

Distinguish between bleeding and clotting time

Answer 9

Bleeding time

• The duration of bleeding after controlled, standardised puncture of the earlobe or forearm.
• It measures capillary and platelet function.
• Normal bleeding time is between 1-3 minutes.

Clotting time (coagulation time)

• The time required for blood to clot in a glass tube.
• Mainly reflects the tine required for generation of thrombin.
• Prolonged if plasma concentration of prothrombin or other clotting factors is low.
• Normal clotting time is between 4-10 minutes.

Question 10

Explain the significance of thromboplastin, factor VII, thrombokinase, prothrombin, thrombin, fibrinogen, and fibrin in blood clotting

Answer 10

• The damaged blood vessel releases a lipoprotein mixture called thromboplastin (factor III).
• Thromboplastin combines with factor VII to form a complex that, in the presence of calcium, activates factor X.
• When platelets degranulate they release factor XII. Through a cascade of reactions, this leads to activated factors XI, IX, and VIII, in that order - each serving as an enzyme that catalyses the next step - and finally to factor X. This pathway requires calcium and platelet factor 3.
• Activated factor X combines with factors III and V in the presence of calcium and platelet factor 3 to produce prothrombin activator which converts prothrombin (factor II) to the enzyme thrombin.
• Thrombin converts fibrinogen into fibrin monomers which covalently bond with each other to form fibrin polymers.
• Factor XIII cross-links the fibrin polymers to create a dense aggregation that forms the structural framework of the blood clot.
• Once a clot begins to form, thrombin works with factor V in a positive feedback process to accelerate the production of prothrombin activator, which in turn produces more thrombin.

Question 11

Outline the process of fibrinolysis (clot removal)

Answer 11

• Factor XII catalyses the formation of a plasma enzyme called kallikrein.
• Kallikrein converts the inactive protein plasminogen into plasmin, an enzyme that breaks up the clot.
• Thrombin also activates plasmin, and plasmin indirectly promotes the formation of more kallikrein, thus completing a positive feedback loop.

Question 12

What are the causes of hyper- and hypocoagulation

Answer 12

Hypercoagulation

• Endothelial damage due to atherosclerosis, infection, or trauma.
• Slowly flowing or static blood due to leg immobilisation or atrial fibrillation.
• May result in myocardial infarction, deep vein thrombosis, and pulmonary embolism.

Hypocoagulation

• Deficiency of platelets (thrombocytopenia purpura).
• Deficiency of coagulation factors: haemophilia A (lack of factor VIII) and haemophilia B (lack of factor IX).
• Deficiency of vitamin K.