Platelets are derived from megakaryocytes of bone marrow. These are oval and thin, non-nucleated discs 2 to 3 microns in diameter. Normal count – 250,000 – 500,000 per c.mm. of blood. Agglutination of platelets is favoured by substances exuded by injured tissue, and inhibited in vitro, by anticoagulants like citrate or oxalate, or in vivo, by heparin and dicoumarol. Their number is increased by the acute blood loss, trauma, partial asphyxia and splenectomy. The platelets play important part in the arrest of haemorrhage from minute vessel, promoting the coagulation of blood, securing firm adhesion and retraction of clot. The normal chemical function of the platelets is to initiate the coagulation process by their disintegration, when they liberate several factors, all concerned with the chemistry of blood coagulation. Thus , (1) platelet AcG equivalent to serum Ac-globulin in activity (2) a factor accelerating the action of thrombin on fibrinogen (3) an antifibrinolysin (4) a factor which neutralizes heparin activity (5) a powerful vasoconstrictor (6) a factor which acts in conjunction with PTC (7) a factor ( thromboplastinogenase) that acts with the antihaemophilic globulin (or thromboplastinogen) to form active thromboplastin. The normal physical function of platelet, in the healthy man, is to seal off minute lesions in the blood vessel that are continually occurring as the result of daily wear and tear of life due to mechanical or metabolic stresses. When, therefore, platelets become sufficiently reduced in number, they can no longer seal off the minute leaks in the wall of the vessel, with the result that purpuric spots begin to appear spontaneously. Tourniquet test is positive in such cases of thrombocytopenia, because the platelets are insufficient in number to plug the minute gaps in the capillaries produced by the increased intravascular pressure. In thrombocytopenic purpura, the bleeding time is increased to several minutes or even hours because the platelets are not only insufficient in number but also fail to agglutinate due to loss lf their property of adhesiveness, and thus are unable to occlude the gap in the vessel wall produced by needle puncture. The coagulation time and prothrombin time are normal in such cases. Clot retraction, which is effected by an excess of platelets, because of their formation of complex knots at the points of intersection of the interlacing strands of fibrin, is diminished or absent when the platelet count falls to 70,000 per c.mm. or less.
The thrombocytopenic purpura may be primary, known as essential or idiopathic, or it may be secondary to some known causes of platelet reduction, such as are found in the initial stage of an acute infection, on the first or second day of menstruation, and in allergy to food or drugs. Thus, organic arsenicals, sulphonamides and especially sedormid, have been proved beyond doubt to produce sensitivity in certain person, who, after a few minutes of readministration of small doses of these drugs, show a pronounced fall in the count of blood platelets and subsequent development of extensive purpura. Thrombocytopenia may frequently be secondary to any cause directly affecting the bone marrow. Bone marrow inhibitors like benzol, arsphenamine, stilbestrol, gold compound, radium or x-ray produce reduction in platelet count. Similar result is seen in invasion of bone marrow by foreign cells, which cause pressure atrophy of the megakaryocytes, and consequent thrombocytopenia, in peripheral blood, eg. , metastatic cells of cancer, immature white cells of leukaemia, the lipoid containing cells of Gaucher’s or Niemann-Pick disease, the fibrous tissue of nonleukaemic myelosis or osteosclerotic anaemia and the megaloblastic proliferation in pernicious anaemia. Bleeding may occur when the platelet count is 100,000 per c.mm. and is profuse when the count is less than 50,000 per c.mm.
In idiopathic thrombocytopenic purpura(Werlhof’s disease), the aetiological factor though not definitely established is thought by most observes to lie in the spleen. Some workers believe that increased destruction of platelets by the spleen is cause of thrombocytopenia. An alternative hypothesis is that the spleen exerts an inhibitory effect on bone marrow on its platelet-formation function. Splenectomy, therefore, in thrombocytopenic purpura, should, by raising the number of platelets, cause two effects, viz., (1) quick reduction in bleeding time and (2) increase in capillary resistance as found by the tourniquet test. A positive tourniquet test signifies , either or both of two things : (1) weakness of the capillary wall to withstand increased hydrostatic pressure and (2) deficiency in platelets either in number or their adhesiveness, or in both, to plug the lesion in the capillary walls produced by increased intravascular pressure.
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