WORLD JOURNAL OF ADVANCE
HEALTHCARE RESEARCH

Devanshi Khare*, Rifat Qureishi, Lokesh Tripathi, S. K. Sutrakar

ABSTRACT

Platelets are anucleate cytoplasmic fragments derived from bone-marrow megakaryocytes that form the first line of defence against microvascular and macrovascular bleeding by adhering to injured endothelium and aggregating into a haemostatic plug.[1] Thrombocytopenia, defined as a platelet count below 150x109/L, is one of the commonest haematological abnormalities encountered in clinical practice and predisposes patients to bleeding complications ranging from mild mucocutaneous haemorrhage to life-threatening internal bleeding.Mechanistically, thrombocytopenia can be grouped under three broad headings: Hypo proliferative thrombocytopenia, arising from impaired bone-marrow production, as in aplastic anaemia, megaloblastic anaemia, myelodysplastic syndrome, and post-chemotherapy marrow suppression; Hyperdestructive thrombocytopenia, resulting from accelerated peripheral destruction or consumption of platelets, as in immune thrombocytopenic purpura (ITP), dengue, malaria, and sepsis; and splenic sequestration, in which platelets are pooled within an enlarged spleen secondary to portal hypertension, myeloproliferative disease, or haemoglobinopathy.[2,3] Because management, monitoring, and prognosis differ substantially across these mechanistic categories, accurate subtype classification carries direct clinical relevance.

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