Lecture 21 Flashcards
What are platelets?
platelets or thrombocytesare one of the three cell types (with WBC and RBC), they are extremely small (2-4 micrometers) with irregular spindles/oval disc shapes which assume various shapes on contact.
What are the stages of haemostasis?
Haemostasis has three stages:
1. constriction of blood vessels, stopping blood flow to the area, followed by formation of a platelet plug. if this isn’t enough it moves on to stage two and three, the formation of a blood clot.
What are the steps in haemostasis stage 1?
vessel damage leads to an altered endothelial surface (exposed collagenn), this causes platelets to activate and aggregate as well as release mediators like ADP and thromboxane A2, contraction then occurs to the vessel
This all occurs on the surface of the platelet and is known as the clotting cascade.
What are the steps in stage 2 and 3 of haemostasis
in stage 2 prothombin is in our blood and is activated by prothrombin activator which is released by the platelets and calcium to produce thrombin which breaks fibrinogen into fibrin which can then cross link to form the blood clot in stage 3.
What are intrinsic pathways and extrinsic pathways?
for intrinsic pathways everything necessary for the pathway is in the blood, for extrinsic a cellular element outside the blood is needed (like tissue factor from the damaged tissue), both provide the catalyst for activation of prothrombin activator. Each step in either pathway requires the previous step to produce the catalyst for the next.
Both pathways join at the activated factor X. Which leads to stage 2.
How are platelets formed?
The formation of platelets is known as thrombopoieis and is generated from myeloid cells due to stimulation by thrombopoietin, they bud off from huge cells. They are used for haemostasis and blood coagulation to stop blood loss, they work with the blood vessels and blood coagulation factors.
How is haemophilia caused and what is a common deficiency which leads to impaired bleeding?
Haemophilia is a bleeding disorder which results in an inability to form blood clots, any missing factor will lead to this but it is typically absence of factor 8. Calcium deficiency also leads to bleeding disorders.
What are common opposing clot formation factors and why?
Opposing clot formation is important because we don’t want a clot to form where we don’t need it, many factors do this: e.g limiting platelet response, typically via endothelial surface being very smooth, prostacylin inhibits aggregation, nitric oxide vasodilates and inhibits aggregation. Tissue factor pathway inhibitor inhibits extrinsic pathway, thrombin is inhibited via antithrombins, warfarin impairs the livers use of vitamin K to retard clotting and aspiring inhibits platelet aggregation.
What is fibrinolysis?
Fibrinolysis is the mechanism that dissolves clots, they are released at the same time as the clot forms but occurs very slowly in comparison. This means the tissue has enough time to repair itself. It occurs via plasminogen and t-PA (tissue plasminogen activator) converting into plasmin.
How do blood systems and transfusions work?
REd blood cells have antigens on their membrane, they are genetically determined and inherited (this is the ABO and Rhesus blood group systems), our plasma contains natural antibodies which exist prior to exposure with antigens. Typer A has antigen A, B has B, AB has A and B and O has neither.
Type A plasma will have antibody B, B has A, AB has neither and O has both. This means O can recieve only type O blood (but can give to all), AB can only give to other AB people (but can recieve all) etc.
If we mix different types of blood (eg small amount of donor blood A with large amount of recipient B) The donor blood will stick together (agglutinate) and rupture, the B cells will not due to the much lower exposure to anti B antibodies.
There are however many other possible incompatibilities
What is the Rhesus system and how does this relate to pregnancy? Why is the ABO system not affected the same way?
The rhesus system is + or negative, it involves the D antigen, those with it are Rhesus positive (85% are positive). There are no preformed antigens but will slowly develop. This can be a problem for a pregnant - mother with a + fetus. The positive blood can go to the mother and develop anti rhesus antibodies which could come back to the fetus if there is enough time. This isn’t typically a problem for the first pregnancy but for a second + fetus the fetus will be in danger (leading to anaemia and haemolytic disease of the newborn). To deal with this anti-D antibody will be administered.
The ABO system is not as musch of a problem because the A and B antigens are not expressed as strongly in the fetus and won’t cross the placenta.
