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1. Dr. Ayaz Lone

2.  Decreased Production:
 Nutritional Deficiencies
 B12, Folate
 Bone marrow failure
 Aplastic anaemia
 Bone marrow infiltrations
 Leukaemia
 Metastasis
 Granulomatous disease

3.  Ineffective haematopoiesis
 Myelodysplastic syndromes
 Selective Impairment
 Drud induced (alcohol, Thiazides, cytotoxic)
 Infections ( Measles, HIV)
 Sequestration
 Hypersplenism

4.  Decreased Survival:
 Immunological destruction
 Primary autoimmune
 Acute ITP
 Chronic ITP
 Secondary Autoimmune
 SLE

5.  Alloimmune
 Post transfusion
 Neonatal
 Drug associated
 Quinidine, heparin, Sulfa compounds
 Infections
 HIV, Dengue fever, Infectious mononucleosis

6.  Nonimmunologic
 DIC
 TTP
 Giant haemangiomas
 Dilutional
 Massive transfussions

7.  Autoimmune disorder in which platelet
sensitization by autoantibodies takes
place, leading to destruction of opsonized
platelets primarily by the mononuclear
phagocytic system.

8.  Primary:
 Acute
 Chronic
 Secondary:
 Lymphoproliferative disorders
 SLE
 HIV
 Evan’s syndrome

9.  Thrombocytopenia in ITP is mediated by anti-
platelet antibodies directed against the
platelet specific glycoproteins (GP) IIb-
IIIa, Ib-IX or Ia-IIa.
 Antibodies against viral protein antigen that
are cross reactive against platelet antigens.

10.  Antibody coated platelets are susceptible to
phagocytosis by the cells of the mononuclear
phagocytic system.
 Spleen plays a crucial role for 2 reasons;
 Anti-platelet antibody production site
 Destruction of sensitized platelet
 IgG

11.  Petechiae
 Easy bruising
 Epistaxis
 Bleeding gums
 Melena
 Hematuria

12.  A diagnosis of ITP should be made only
after other causes of platelet deficiences
have been ruled out.
 CBC:
 Anaemia
 Thrombocytopenia
 BT
 Coagulation studies

13.  Bone marrow examination:
 Megakaryocytic hyperplasia with both mature
and maturing forms increased.