Thrombocytopenia pathophysiology
|
Thrombocytopenia Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Thrombocytopenia pathophysiology On the Web |
|
American Roentgen Ray Society Images of Thrombocytopenia pathophysiology |
|
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, M.D.
Overview
Basically, thrombocytopenia is the result of one of these mechanisms or a combination of some of them:
- Reduced production of platelets due to bone marrow dysfunction
- Increased destruction of platelets in the body
- iatrogenic
- entrapment of platelets in spleen
Several conditions, some of which mentioned below, can activate the mechanisms that ultimately lead to thrombocytopenia.
Pathophysiology
Physiology
Platelets are produced in hematopoiesis by budding off from megakaryocytes, which are produced by pluripotent hematopoietic stem 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 four main 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.
Some conditions cause thrombocytopenia through a combination of these mechanisms. For instance, primary ITP is associated with antibody-mediated platelet destruction, but it can also cause suppression of megakaryocytes, which is considered a bone marrow dysfunction.
| main cause | mechanism and further explanations | examples |
|---|---|---|
| Bone marrow dysfunction | Bone marrow abnormalities that cause decreased platelet production commonly reduce the production of RBCs and WBCs as well, resulting in pancytopenia. Common presentations include symptoms of thrombocytopenia (eg, bleeding, petechiae) or symptoms associated with anemia and/or leukopenia (eg, shortness of breath, fatigue and recurrent infections). | |
| Platelet destruction/consumption | Several mechanisms can accelerate the normal platelet degradation process in the body:
Anti-platelet antibodies seen in both primary ITP and its secondary form (associated with systemic autoimmune disorders such as SLE) play a main role. Antibody-mediated reactions can also cause a reduction in other blood cell lines, resulting in combined cytopenias. Some medications and ingested substances can also cause thrombocytopenia through this mechanism. |
|
| Dilution | Dilutional thrombocytopenia is an iatrogenic form of thrombocytopenia caused by massive fluid resuscitation or massive blood transfusion. There is a correlation between the decrease in platelet count and the number of RBC units transfused during the course of a day.[2][3] |
|
| Redistribution/splenomegaly | In individuals with normal splenic function, approximately one-third of the platelet mass is found in the spleen, in equilibrium with the circulating platelet pool. Any condition resulting in splenomegaly and/or splenic congestion due to portal hypertension may lead to a reduced platelet count, while the total platelet mass in the body is intact.[4] Severe thrombocytopenia or bleeding accompanied by splenomegaly is an indication for further diagnostic investigations. |
|
References
- ↑ 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.
- ↑ Counts RB, Haisch C, Simon TL, Maxwell NG, Heimbach DM, Carrico CJ (1979). "Hemostasis in massively transfused trauma patients". Ann Surg. 190 (1): 91–9. PMC 1344465. PMID 464685.
- ↑ Leslie SD, Toy PT (1991). "Laboratory hemostatic abnormalities in massively transfused patients given red blood cells and crystalloid". Am J Clin Pathol. 96 (6): 770–3. PMID 1746495.
- ↑ Aster RH (1966). "Pooling of platelets in the spleen: role in the pathogenesis of "hypersplenic" thrombocytopenia". J Clin Invest. 45 (5): 645–57. doi:10.1172/JCI105380. PMC 292742. PMID 5327481.