 |
|
Management of Thrombocytopenic States
MARIO STEFANINI, M.D.
AMA Arch Intern Med. 1955;95(4):543-556.
|
|
| Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings. |
|
|
|
Either defect of production of platelets from the bone marrow megakaryocytes or excess of their destruction or utilization in the peripheral circulation may result in thrombocytopenia. These two basic pathogenetic mechanisms are reflected into two main types of this syndrome, amegakaryocytic and megakaryocytic (Table 1). Whatever the pathogenetic mechanism of thrombocytopenia in the individual patient may be, platelet deficiency results in serious breakdown of the hemostatic process, involving all of its phases and mechanisms 1: A. The "resistance" of the vascular wall appears decreased. The tourniquet test becomes positive. B. The ability of the vessel to contract effectively after injury is also impaired, owing to lack of serotonin, an agent liberated by platelet disintegration. Perhaps for this reason, the bleeding time is prolonged. C. The fibrin clot retracts poorly. D. The coagulation of blood becomes abnormal, since platelet deficiency causes impaired formation of thromboplastin, and this, in turn, results in
. . . [Full Text PDF of this Article]
Author Affiliations
Boston
From Saint Elizabeth Hospital, the New England Center Hospital, and the Department of Medicine, Tufts College Medical School; Established Investigator, American Heart Association.
Footnotes
Presented, in part, at the "Symposium on Hemorrhagic Diseases," Marquette University School of Medicine, Milwaukee, Wis., May 21 and 22, 1954, in honor of Dr. Armand J. Quick.
The original work presented in this article was completed with assistance by grants-in-aid from the Atomic Energy Commission, the United States Public Health Service, National Institutes of Health, and the American Heart Association.
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati
What's this?
|
