Disease States Involving Disturbances of Haemostasis. (Nursing Project)

Disease States Involving Disturbances of Haemostasis.

Normal Human Haemostatic Mechanisms

Haemostasis is the control of linage loss from the circulation, involving a fall of sepa set events including coagulation.

The process is as follows:

1. Vasoconstriction (Vasospasm).

When the initial injury occurs to a blood vessel, it constricts with enough intensity to close the vessel. It occurs as the essence of 2 separate mechanisms:

a) local reflexes of the nervous system.

b) biochemical- serotonin and epinephrine are released by aggregated thrombocytes causing vasoconstriction.

Histamine is released subsequent to meander damage by mast cells in the inflammation process and has a vasodilator effect.

TXA2 also produces vasoconstriction as mentioned later.

2. Sticking of the Endothelial Surfaces.

When vasoconstriction occurs, the clear endothelial surfaces of the blood vessels adhere keeping the blood vessel closed. Adhesiveness of the damaged membranes is facilitated by the altered surface properties of the injure blood vessel.

3. Formation of a Platelet Plug.

Platelets are cytoplasmic fragments which are released into the circulation by megakaryocytes formed in the bone marrow. (The ordinary survival time of platelets is 10 days.) Platelets stick to exposed subendothelial surfaces of blood vessel walls.

The platelet receptor binds to the von Willebrand Factor (a blood plasma protein) which bridges the platelet to the injury site. They then degranulate ie.



release the contents of their granules. Their are 2 types of granules in their cytoplasm: alpha granules containing coagulation factors and a growth factor, and dense granules containing ADP, ATP, Ca2+, and serotonin.

Erythrocyte involvement - erythrocytes increase the rate of platelet adherence by facilitating migration of platelets toward vascular surfaces and by evacuant ADP (adenodiphosphate- a by-product of the Krebs Cycle) which enables platelets to adhere to exposed collagen - platelet aggregation. This process would non stop if the effects of ADP were not counteracted.

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