Platelets and blood coagulation

Question 1

Name blood clotting factors, from factor I to factor XIII.

Answer 1

Factor I - fibrinogen
Factor Ia - fibrin
Factor II - prothrombin
Factor IIa - thrombin
Factor III - tissue factor (found in subendothelial outer plasma membranes)
Factor IV (Ca2+)
Factors V, VII, VIII, IX, X, XI, XII AND XIII - ACTIVE FORMS ADD AN 'a'. eg factor Va 
(there is no factor VI)

Question 2

What three reactions does thrombin catalyse?

Answer 2

1. The conversion of fibrinogen(factor I) to fibrin(factorII)
2. The activation of factor XIII (factor XIII to factor XIIIa) XIIIa then catalyses loose fibrin to stabilized fibrin
3. +ve feedback - activates proteins and platelets of cascade - leading to more thrombin formation

Question 3

Name two ways that factor IX can be converted to factor IXa (intrinsic and extrinsic)

Answer 3

1. Intrinsic pathway
   - exposed collagen activates factor XII to XIIa
   -XIIa catalyses conversion of XI to XIa.
   (-XIa catalyses conversion of X to Xa. Xa catalyses prothrombin to thrombin)
2. Extrinsic pathway
   - Tissue factor is exposed to blood due to damaged endothelium activating factor VII to VIIa.
   - the tissue factor=VIIa complex catalyses:
   a) factor X activation to Xa (Xa catalyses prothrombin to thrombin)
   b) factor IX to IXa (this activates more factor X)

The extrinsic is the usual way of initiating clotting, this generates thrombin which triggers +ve feedback on the intrinsic pathway. This eliminates need for factor XII.

Question 4

What is hemostasis?

Answer 4

Hemostasis is the process of clot fomation

Question 5

What action can help slow rate of venous bleed?

Answer 5

-Raising bleed above the heart

decrease in hydrostatic pressure may stop hemorrhage

Question 6

What is a hematoma?

Answer 6

A hematoma is when blood accumulates internally due to an internal bleed - this may eliminate the pressure gradient so that the bleed stops)

Question 7

Why does a blood vessel constrict when it is injured?

Answer 7

Blood flow to the area slows down so that less blood is lost, the constriction also presses the opposed endothelial surfaces together inducing a ‘stickiness’

1) formation of platelet plus
2) blood coagulation

(constriction is likely to be due to changes in local vasodilator and vasoconstrictor substances released by endothelial cells and blood cells)

Question 8

How is the platelet plug formed?

Answer 8

Platelet plug.
1) damage to endothelium exposes collagen
2)vWF binds to collagen and changes its conformational shape so that it can bind to platelets (von Willebrand factor, a plasma protein secreted by endothelial cells and platelets)
3) vWF forms a bridge between the damaged vessel wall and platelets
4) The platelet binding triggers the platelets to release the contents of their secretory vesicles
5) These contain
a) Adenosine diphosphate (ADP)
b) serotonin
both of which act locally to change platelets, activating them causing platelet aggregation
6) This creates a platelet plug
7) Platelet aggregation induces them to synthesize thromboxane A2 (thromboxane A2 is from eicosoncid family, it is made from arachidonic acid in the platelet plasma membrane)
8) thromboxane A2 is released into the ECF where it stimulates platelet aggregation and secretory vesicle release
9) Platelet activation also exposes fibrinogen-receptors, so that fibrinogen forms bridges between aggregating platelets
10) Platelets contain large amounts of actin and myosin - these are stimulated to interact causing compression and strengthening
11) While the plug is being formed the smooth muscle in the damaged vessel is stimultaneously being stimulated to contract (This is descreases blood flow and pressure) This action is mediated by thromboxane A2 and other chimcals in platelet vesicles.

Question 9

How do adjacent endothelial cells prevent platelet aggregation along undamaged endothelium?

Answer 9

1) Adjacent endothelial cells synthesize and release PROSTACYCLIN (an eicosoncid also known as prostagladin I2). This inhibits platelet aggregation along undamaged endothelium.
2) They also release NITRIC OXIDE - this is a vasodilator and inhibitor of platelet adhesion and activation.

Question 10

What is the importance of the liver in blood clotting?

Answer 10

Liver produces

1) Plasma clotting factors
2) Bile salts (important for vit K absorption, vit K is needed to produce prothrombin and other clotting factors)

Question 11

What is disseminated intravascular coagulation?

Answer 11

Disseminated intravascular coagulation is when there is widespread activation of the clotting cascade..
This means that blood clots form in the small blood vessels =decreased blood flow and organ failure
-Also disrupts normal clotting so can lead to serveve bleeding
1. Sepsis (sereve infection) 2. Obstetrics, eg eclampsia 3. Malignacy

Question 12

What could cause a problem with a person’s blood clotting/cause a blood disease?

Answer 12

• Liver disease as it is the site of fibrinogen and coagulation factor synthesis
• VitK deficiency as it is needed to synthesize clotting factors in liver
• Drugs eg asprin, heparin, warfarin, steroids