Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiopulmonary dysfunction has been observed after the removal of benign hydatidiform mole. Of 60 cases reviewed with benign trophoblastic disease, five developed respiratory complications. Two patients developed pulmonary edema that progressed to adult respiratory distress syndrome. Autopsy of two patients showed no evidence of pulmonary trophoblastic emboli. Possible etiologies for the pulmonary findings, including trophoblastic emboli, hypervolemia, disseminated intravascular coagulation, and hyperthyroidism, are discussed.
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PMID:Benign molar pregnancies: pulmonary complications. 697 15

A previously healthy 37-year-old Latin American female presented at 17 6/7 weeks gestation with clinical manifestations of preeclampsia. Ultrasound revealed a growth-retarded fetus with hypoechoic bowel, a thickened cystic placenta, bilateral multicystic adnexal masses, and oligohydramnios. The patient had laboratory evidence of hyperthyroidism and the maternal serum alpha-fetoprotein was 12.3 multiples of the mean. Subclinical disseminated intravascular coagulation rapidly ensued and an induction of labor was performed. This was productive of a 110-g female fetus with a markedly distended abdomen and syndactyly. The placenta weighted 650 g with gross hydropic changes throughout. The clinical aspects of this case and review of the literature on partial molar pregnancies will be discussed.
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PMID:Partial hydatidiform molar pregnancy presenting with severe preeclampsia prior to twenty weeks gestation: a case report and review of the literature. 774 35

Molar pregnancy is a gestation in which the ovum is transformed into a fleshy tumor mass or mole. Of all gynecologic tumors, it is one of the most feared. It is characterized by first trimester bleeding, hyperemesis, and toxemia and can be diagnosed using pelvic ultrasound. Suction currettage is the treatment of choice for molar pregnancy when a patient desires to have more children; however, hysterectomy may be necessary. Abdominal hysterectomy reduces the risk of malignant sequelae. Complications associated with molar pregnancy usually are a result of suction curettage and include pulmonary insufficiency syndrome, choriocarcinoma, hyperthyroidism, theca lutein cysts, and disseminated intravascular coagulation. The perioperative nurse can be instrumental in assessing, planning, organizing, and directing intervention for potential complications associated with the management of a molar pregnancy crisis. The perioperative nurse is encouraged to review all aspects of molar pregnancy to understand the ramifications of the surgical procedures.
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PMID:Intraoperative molar pregnancy crisis. 794 18

After clinical assessment, pertinent history, and family history, the clinician often has a good idea concerning the cause of a patient's bleeding. The most appropriate laboratory tests can then be ordered. Routine screening tests include a complete blood cell count, platelet count, and evaluation of a peripheral blood sample, a prothrombin time, and an activated partial thromboplastin time. Thrombocytopenia may result from idiopathic thrombocytopenic purpura, disseminated intravascular coagulation, or, less commonly, acute leukemia, aplastic anemia, thrombotic thrombocytopenic purpura, or a particular drug that a patient is taking. Again, the patient's history, physical findings, and evaluation of a well-prepared peripheral blood smear will be helpful in determining the cause of the patient's thrombocytopenia. An isolated prolongation of the activated partial thromboplastin time may result from low levels of factors VIII, IX, or XI. A slightly prolonged activated partial thromboplastin time and a moderate decrease in factor VIII may reflect von Willebrand disease or the "carrier" state for hemophilia A. In women a greatly prolonged activated partial thromboplastin time and very low levels of factor VIII (< 3%) most often result from an acquired factor VIII inhibitor (autoantibody against factor VIII) or from severe (type III) von Willebrand disease. If von Willebrand disease is suspected (because of menorrhagia with or without other mucous membrane bleeding, a positive family history, and a prolonged activated partial thromboplastin time), more specific laboratory tests for this disease should be done. These include assays of factor VIII, von Willebrand factor antigen, von Willebrand factor activity (measured by the ristocetin cofactor assay), and template bleeding time. In von Willebrand disease the defect is in von Willebrand factor. The affected individual may have subnormal levels of structurally and functionally normal von Willebrand factor (this is called "classic" or type I von Willebrand disease) or may produce von Willebrand factor that is structurally and functionally abnormal (von Willebrand disease type 2). Individuals who inherit a gene for von Willebrand disease from both parents have severe (type 3) von Willebrand disease and will have extremely low levels (< 3%) of von Willebrand factor and factor VIII and will have a very prolonged bleeding time. In most populations type I disease is the most common form, whereas type 3 is the least commonly encountered form. It should be noted that levels of von Willebrand factor can be influenced by the patient's blood type (persons who have blood type AB have 60% to 70% higher levels than do persons who have blood type O) and can be elevated during pregnancy, stress, and hyperthyroidism. The two major functions of von Willebrand factor are to serve as a "bridge" between platelets and injury sites in blood vessel walls and to protect circulating factor VIII from rapid proteolytic degradation. Thus, if a patient has either too little or functionally abnormal von Willebrand factor, the bleeding time will be prolonged and factor VIII will be decreased (because it is not being protected by von Willebrand factor). It should be determined which type of von Willebrand disease a particular patient has because treatment depends on type. Multimeric analysis of von Willebrand factor can be done with use of sodium dodecyl sulfate gels, radiolabeled antibody to von Willebrand's factor, and autoradiography. This will allow visualization of the multimeric structure of von Willebrand factor. In type I disease all bands are present, whereas in the type 2 variants 2A and 2B no high-molecular-weight multimers are seen. Desmopressin acetate (which is available in parenteral form for intravenous use and in a highly concentrated intranasal spray formulation) is the treatment of choice for classic type I disease. The drug effects a rapid release of von Willebrand factor from endothelial cell stor
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PMID:Screening and diagnosis of coagulation disorders. 882 61

A 41-year-old man with a history of hyperthyroidism had been treated with methimazole and propranolol for the past 2 months. He developed multiorgan dysfunction with acute liver failure, severe lactic acidosis, disseminated intravascular coagulation, heart failure and acute pulmonary edema with rapid deterioration of renal function. The patient had no history of alcoholism, drug abuse, blood transfusion, or exposure to hepatitis A, B, or C. Extrahepatic obstruction was ruled out with an abdominal ultrasonogram. Serologic studies and immunologic tests were negative. This case illustrates the sudden and abrupt deterioration of multiorgan dysfunction due to antithyroid drug administration and thyroid storm. The thyroid storm score of Burch and Wartofsky was 90/140. The multiorgan dysfunction was reversed by discontinuation of the methimazole and treat with hemodialysis, steroids, cholestyramine, nonselective beta-blocker, fresh frozen plasma infusion and supportive management in the intensive care unit. The patient was discharged from the hospital with normal coagulation parameters, renal and liver function tests.
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PMID:Multiorgan dysfunction accompanied with metimazole and thyroid storm. 2228 65