Thrombocytopenia pathophysiology

Revision as of 14:16, 25 June 2018 by Farbod Zahedi (talk | contribs)
Jump to navigation Jump to search

Thrombocytopenia Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Thrombocytopenia from other Diseases

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Diagnostic Study of Choice

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

X-ray

Echocardiography and Ultrasound

CT

MRI

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Thrombocytopenia pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Thrombocytopenia pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Thrombocytopenia pathophysiology

CDC on Thrombocytopenia pathophysiology

Thrombocytopenia pathophysiology in the news

Blogs on Thrombocytopenia pathophysiology

Directions to Hospitals Treating Thrombocytopenia

Risk calculators and risk factors for Thrombocytopenia pathophysiology

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

Overview

Pathophysiology

Physiology

Platelets are produced in hematopoiesis by budding off from megakaryocytes, which are derived from multipotent hematopoietic progenitor cells.[1] Each megakaryocyte produces 1000 to 5000 platelets. Platelets circulate for approximately one week, and are then destroyed by the spleen and by Kuppfer cells in the liver.

Pathogenesis

It is thought that thrombocytopenia is the result of either of these mechanisms:

  • decreased production of platelets in the bone marrow,
  • destruction of platelets outside of bone marrow,
  • blood dilution from fluid resuscitation or massive transfusion,
  • sequestration of platelets in the spleen due to portal hypertension and/or splenomegaly.

References

  1. Klein LS, Shih HT, Hackett FK, Zipes DP, Miles WM (1992). "Radiofrequency catheter ablation of ventricular tachycardia in patients without structural heart disease". Circulation. 85 (5): 1666–74. PMID 1572025.

Template:WS Template:WH