{"id":7230,"date":"2013-07-23T18:58:15","date_gmt":"2013-07-23T23:58:15","guid":{"rendered":"http:\/\/medicinainterna.com.mx\/?p=7230"},"modified":"2013-07-23T18:58:15","modified_gmt":"2013-07-23T23:58:15","slug":"clasificacion-de-las-alteraciones-hemostaticas-y-las-causas-de-sangrado-patologico","status":"publish","type":"post","link":"https:\/\/medicinainterna.com.mx\/?p=7230","title":{"rendered":"Clasificaci\u00f3n de las alteraciones hemost\u00e1ticas y las causas de sangrado patol\u00f3gico."},"content":{"rendered":"<p align=\"center\">\n<table width=\"95%\" border=\"1\" cellspacing=\"0\" cellpadding=\"0\">\n<tbody>\n<tr>\n<td valign=\"top\" width=\"100%\">1. Alteraci\u00f3n de las plaquetas:<br \/>\n1.1. Alteraciones cuantitativas (trombocitopenia):<br \/>\n1.1.1. Trombopoyesis insuficiente o anormal:<br \/>\n1.1.1.1. Anemia apl\u00e1sica.<br \/>\n1.1.1.2. D\u00e9ficit de B12 o de folato.<br \/>\n1.1.2. Destrucci\u00f3n acelerada, p\u00e9rdida o distribuci\u00f3n anormal:<br \/>\n1.1.2.1. Inmunol\u00f3gico: p\u00farpura trombocitop\u00e9nica idiop\u00e1tica, drogas.*<br \/>\n1.1.2.2. No inmunol\u00f3gica: p\u00farpura tromb\u00f3tica trombocitop\u00e9nica,* coagulaci\u00f3n intravascular diseminada.*<br \/>\n1.2. Alteraciones cualitativas:<br \/>\n1.2.1. Cong\u00e9nitas:<br \/>\n1.2.1.1. Defectos de adhesi\u00f3n: enfermedad de von Willebrand.<br \/>\n1.2.1.2. Defectos de secreci\u00f3n: enfermedad de almacenamiento de las plaquetas.<br \/>\n1.2.1.3. Defecto de agregaci\u00f3n: tromboastenia.<br \/>\n1.2.2. Adquiridas:<br \/>\n1.2.2.1. Defectos de adhesi\u00f3n: uremia,* drogas.*<br \/>\n1.2.2.2. Defectos de secreci\u00f3n: enfermedad mieloproliferativa, drogas.*<br \/>\n1.2.2.3. Defecto de agregaci\u00f3n: paraproteinemia, drogas,* productos de degeneraci\u00f3n de fibrina\/fibrin\u00f3geno.*<br \/>\n2. Alteraciones de la coagulaci\u00f3n:<br \/>\n2.1. Deficiencia de factores:<br \/>\n2.1.1. Defectos de producci\u00f3n:<br \/>\n2.1.1.1. Cong\u00e9nito: hemofilia.<br \/>\n2.1.1.2. Adquirido: d\u00e9ficit de vitamina K,* enfermedades hep\u00e1ticas,* drogas\u00a0 (cumar\u00ednicos).*<br \/>\n2.1.2. Destrucci\u00f3n acelerada:<br \/>\n2.1.2.1. Consumo: fibrinolisis, coagulaci\u00f3n intravascular diseminada.*<br \/>\n2.1.2.2. P\u00e9rdida: s\u00edndrome nefr\u00f3tico.<br \/>\n2.1.2.3. Multifactorial: postoperatorio de cirug\u00eda card\u00edaca.<br \/>\n2.1.3. Dilucional: reposici\u00f3n masiva de sangre.*<br \/>\n2.2. Inhibidores (anticoagulantes):<br \/>\n2.2.1. Anticuerpos contra factores de coagulaci\u00f3n: inhibidor factor VIII.<br \/>\n2.2.2. Anticuerpos anti fosfol\u00edpidos: inhibidor &#8220;lupuslike&#8221;.<br \/>\n2.2.3. Disproteinemia.<br \/>\n2.2.4. Productos de degeneraci\u00f3n de fibrina\/fibrin\u00f3geno.*<br \/>\n2.2.5. Heparina*.<\/td>\n<\/tr>\n<tr>\n<td valign=\"top\" width=\"100%\">(*) alteraciones comunes en UCI.<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n<p>Fuente: Ansell JE. Acquired bleeding disorders. En: Rippe JM, Irwin RS, Fink MP, Cerra FB (eds.): Intensive Care Medicine (3rd ed). Little, Brown. 1996: 1357-1368<\/p>\n","protected":false},"excerpt":{"rendered":"<p>1. Alteraci\u00f3n de las plaquetas: 1.1. Alteraciones cuantitativas (trombocitopenia): 1.1.1. Trombopoyesis insuficiente o anormal: 1.1.1.1. Anemia apl\u00e1sica. 1.1.1.2. D\u00e9ficit de B12 o de folato. 1.1.2. Destrucci\u00f3n acelerada, p\u00e9rdida o distribuci\u00f3n anormal: 1.1.2.1. Inmunol\u00f3gico: p\u00farpura trombocitop\u00e9nica idiop\u00e1tica, drogas.* 1.1.2.2. No inmunol\u00f3gica: p\u00farpura tromb\u00f3tica trombocitop\u00e9nica,* coagulaci\u00f3n intravascular diseminada.* 1.2. Alteraciones cualitativas: 1.2.1. Cong\u00e9nitas: 1.2.1.1. 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