Idiopathic thrombocytopenic purpura pathophysiology

Idiopathic thrombocytopenic purpura Microchapters
Home
Patient Information
Overview
Historical Perspective
Classification
Pathophysiology
Causes
Differentiating Idiopathic thrombocytopenic purpura from other Diseases
Epidemiology and Demographics
Risk Factors
Screening
Natural History, Complications and Prognosis
Diagnosis
Diagnostic Study of Choice
History and Symptoms
Physical Examination
Laboratory Findings
Electrocardiogram
X Ray
CT
MRI
Ultrasound
Other Imaging Findings
Other Diagnostic Studies
Treatment
Medical Therapy
Radiation
Surgery
Primary Prevention
Secondary Prevention
Cost-Effectiveness of Therapy
Future or Investigational Therapies
Case Studies
Case #1
Idiopathic thrombocytopenic purpura pathophysiology On the Web
Most recent articles
Most cited articles
Review articles
CME Programs
Powerpoint slides
Images
American Roentgen Ray Society Images of Idiopathic thrombocytopenic purpura pathophysiology All Images X-rays Echo & Ultrasound CT Images MRI
Ongoing Trials at Clinical Trials.gov
US National Guidelines Clearinghouse
NICE Guidance
FDA on Idiopathic thrombocytopenic purpura pathophysiology
CDC on Idiopathic thrombocytopenic purpura pathophysiology
Idiopathic thrombocytopenic purpura pathophysiology in the news
Blogs on Idiopathic thrombocytopenic purpura pathophysiology
Directions to Hospitals Treating Idiopathic thrombocytopenic purpura
Risk calculators and risk factors for Idiopathic thrombocytopenic purpura pathophysiology

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

Pathophysiology

Physiology

AAA

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 atopic dermatitis:
• Chronic atopic dermatitis:

Microscopic Pathology

On microscopic histopathological analysis, characteristic findings of itp include:

• Acute vesicular lesions:
• Chronic lichenified plaque: