73) .FAILURE OF NORMAL CLOT RETRACTION MAY BE DUE

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a) abnormal platelet function
b) abnormal plasma calcium
c) hypoparathyroidism
d) low thrombin concentration
e) factor 7 deficiency

[Editor]

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There are 5 stages in haemostasis: 1) vessel spasm 2) platelet plug formation 3) blood coagulation (extrinsic pathway, intrinsic pathway, final common pathway resulting in fibrin formation) 4) clot retraction 5) clot dissolution. After platelets aggregate to form a clot, contractile proteins in the platelets contract to pull the edges of the wound together. This is a thrombin-dependent, platelet mediated process.
Platelets are responsible for forming the primary haemostatic plug. They adhere to sites of injury, change shape and release their granules (containing coagulation factors, adhesive proteins and growth factors). They then aggregate together forming the platelet plug.
Ca2+ is a key second messenger in platelet activation. Other Ca2+ dependent activities are platelet aggregation, clot retraction and secretion of the contents of the storage granules.
Parathyroid hormone, secreted by the parathyroid glands, elevates plasma calcium levels by:
-stimulating release of calcium from bone
-stimulating calcium reabsorption from the renal tubules
-increased urinary phosphate excretion
-accelerates rate at which vitamin D is converted to its active form
Thrombin cleaves fibrinogen to form fibrin monomers that then spontaneously aggregate to form fibrin strands that are cross-linked by factor XIIa to form a stable clot.
Factor VII is involved in the extrinsic pathway. Tissue factor, which is normally present outside the vascular system, acts as a co-factor in the extrinsic pathway increasing the activity of factors VII and VIIa in the cleavage of factors X-Xa. It initiates coagulation events in vivo.