Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0751295 (memory loss)
 3,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Our understanding of the pathophysiology of ITP owes to pioneering work of W J Harrington in 1951, delineating the immunologic nature of platelet destruction. In ITP, antibody-coated platelets are destroyed by macrophages of RES. However, other mechanisms are also implicated: C-mediated platelet lysis and newly described C-independent peroxide injury. Both induce platelet fragmentation and lysis, generating procoagulant platelet microparticles (PMP). A third mechanism of platelet consumption in the microvasculature is proposed, based on overlapping syndromes of ITP and TTP in some patients. In assessing hemostasis in ITP, platelet counts alone is not sufficient. Evaluation of platelet clumping, giant platelets, and platelet activation, marked by increased PMP is useful. Patients with platelet activation or giant platelets bleed less and detection of clumping prevents unwarranted therapy. Thrombotic complications may develop in ITP. A syndrome, characterized by recurrent TIA-like symptoms, progressive memory loss due to ischemic small vessel disease is described. The management of ITP should include the search for and elimination of underlying causes and careful evaluation of hemostasis. Therapy is divided into definitive vs symptomatic measures. The former including splenectomy, danazol, chemotherapy offers lasting remission after therapy was stopped, while the later including glucocorticoids, gammaglobuin, antiD antibodies and others increases platelet counts but seldom sustains remission upon withdrawal. Danazol therapy is up-dated since it is an effective and safe definite measure in ITP.
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PMID:Idiopathic thrombocytopenic purpura: pathophysiology and management. 1243 Sep 12

Adverse neurologic outcomes after cardiac surgery can have devastating consequences, among them increased mortality risk and, among survivors, loss of independence and a diminished quality of life. They also represent a burden on the health-care system, requiring prolonged hospitalizations and additional aftercare and, therefore, greater costs. Adverse outcomes are classified by their severity. Frank stroke is the most serious. This complication is associated with patient age; however, the presence of significant ascending aortic disease represents the greatest hazard. Multivariable analysis also indicates that prior neurologic events, diabetes, chronic obstructive pulmonary disease, preoperative status, and diffuse vascular disease are predictive. The second type of adverse cerebral outcome includes neurocognitive abnormalities such as memory loss and diminished emotional health. The strongest predictors of these abnormalities are hypertension and a history of alcohol use, as well as age. These predictive factors have been incorporated into the Multicenter Study of Perioperative Ischemia stroke-risk index, which clinicians can use to better assess the risk of adverse neurologic events. Clinical research examining the relationship between the predictive variables for neurologic adverse events and cerebral blood flow has suggested some surgical strategies for minimizing risk, such as limiting manipulation of the ascending aorta. The benefits of strategies such as using low or high mean arterial pressures and manipulating pump flow remain unclear. Off-pump coronary bypass surgery has been proposed as a means of reducing neurologic risk, but its effectiveness is unproved in this area. One pharmacologic strategy, the administration of aprotinin, has been shown to reduce the incidence of stroke in high-risk patients.
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PMID:Predicting and preventing adverse neurologic outcomes with cardiac surgery. 1649 92