Idiopathic thrombocytopenic purpura pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Pathophysiology

Physiology

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AAA:

• AAAA:
• AAA:

Pathogenesis

Increased platelet destruction:

• Autoantibody‐induced platelet destruction:
  • Abnormal IgG auto-antibody recognizes glycoprotein IIb/IIIa, glycoprotein Ib/IX complex, etc
  • IgG auto-antibody binds to the circulating platelet membranes through glycoproteins
  • Autoantibody-coated platelets induce Fcg receptors and bind to antigen-presenting cells (Splenic macrophages or dendritic cells) where the platelets undergoes phagocytosis.
  • Antigen-presenting cells degrade glycoproteins and and not only degrade glycoprotein IIb/IIIa (light blue oval), thereby amplifying the initial immune response, but also may generate cryptic epitopes from other platelet glycoproteins
  • Activated antigen-presenting cells
  • express these novel peptides on the cell surface along with costimulatory help (represented in part by the interaction between CD154 and CD40) and the relevant cytokines that facilitate the proliferation of the initiating CD4-positive T-cell clones (T-cell clone 1) and those with additional specificities (T-cell clone 2)
  • B-cell immunoglobulin receptors that recognize additional platelet antigens (B-cell clone 2) are thereby also induced to proliferate and synthesize anti–glycoprotein Ib/IX antibodies (green) in addition to amplifying the production of anti–glycoprotein IIb/IIIa antibodies (orange) by B-cell clone 1
• Autoreactive T lymphocyte‐mediated platelet lysis

Decreased platelet production:

• abnormal thrombopoiesis
• degenerative changes in both nuclei and cytoplasm

Associated Conditions

Conditions associated with

Gross Pathology

On gross pathology, characteristic findings of itp include:

• Acute
• Chronic

Microscopic Pathology

On microscopic histopathological analysis, characteristic findings of itp include:

• Acute
• Chronic