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Vascular-occlusive disease

Alpha-receptor-blocking drugs do not seem to be effective in the treatment of peripheral vascular occlusive disease characterized by morphologic changes that limit flow in the vessels. Occasionally, individuals with Raynaud s phenomenon and other conditions involving excessive reversible vasospasm in the peripheral circulation do benefit from prazosin or phenoxybenzamine, although calcium channel blockers may be preferable for most patients. [Pg.204]

Several extended-release devices able to deliver a consistent level of corticosteroid to the retina have been devised. Two will be presented in this chapter, although other devices are under evaluation or in the development pipeline at the time of writing. The primary indications for these devices are persistent macular edema associated with several conditions, including diabetic retinopathy, retinal vascular occlusive disease, cataract surgery, and posterior uveitis. [Pg.309]

Five of 160 children with nephrotic syndrome developed distinctive vascular purpura (45). They had taken levamisole for a mean of 24 months when they developed purpuric erythematous macules, which evolved to ecchy-motic and necrotic purpura. The lesions were mostly on the external ear. Biopsies obtained from the ear lesions in four patients showed vasculopathic reaction patterns, ranging from leukocytoclastic and thrombotic vasculitis to vascular occlusive disease without true vasculitis. There were anticardiolipin, antinuclear, and/or antineutrophil cytoplasmic antibodies in four patients. The lesions resolved within 2-3 weeks after levamisole withdrawal, whereas anticardiolipin and antineutrophil cytoplasmic antibodies disappeared after 2-14 months only. A direct effect of levamisole on the endothehal cells or levamisole-induced or unmasked latent immunological abnormalities was suspected. [Pg.2032]

Gardner AW, Skinner JS, Smith LK. Effects of handrail support on claudication and hemodynamic responses to a single-stage and progressive treadmill protocols in peripheral vascular occlusive disease. Am J Cardiol 1991 68 99-105. [Pg.255]

In most animal models, the course of experimentally induced vascular occlusive disease is independent of risk factors such as smoking, diabetes, or hypertension this is not the case in humans. Animal mperiments are only rough indications of human conditions, and the postulated protective mechanisms of ct>-3 polyunsaturated fatty acids may differ substantially from those in humans. Therefore, results of animal studies are obviously not directly applicable to pathophysiologic or therapeutic concepts in human disease. [Pg.17]

Thrombolytic Enzymes. Although atherosclerosis and the accompanying vascular wall defects are ultimately responsible for such diseases as acute pulmonary embolism, arterial occlusion, and myocardial infarction, the lack of blood flow caused by a fibrin clot directly results in tissue injury and in the clinical symptoms of these devastating diseases (54). Thrombolytic enzyme therapy removes the fibrin clot by dissolution, and has shown promise in the treatment of a number of thrombo-occlusive diseases (60). [Pg.309]

Platelets play an important role in hemostasis and are involved in the pathogenesis of many diseases, such as artherosclerosis and asthma. Moreover, an inadequately controlled aggregation may lead to vascular occlusion. [Pg.335]

T. Tamura, S. M. Bergman, and S. L. Morgan, Hyperhomocysteinemia as a cause of vascular occlusion in end-stage-renal disease, Int. J. Artificial Organs. 21, 72-74 (1998). [Pg.324]

Retinal vascular diseases, such as vascular occlusions, hemorrhage, retinal venous thrombosis Retinal hemorrhage... [Pg.725]

Previous ocular disease such as cataracts, uveids, dia-bedc rednopathy or vascular occlusions... [Pg.422]

Ischemic strokes account for around 80-85% of all strokes and are caused by arterial vascular occlusions rarely occlusion in the cerebral venous system may result in ischemic and/or hemorrhagic stroke. Arterial occlusions resulting from cerebral embolism are the most common causes of ischemic strokes, and by about one week after stroke as many as 70-90% of occlusions will have spontaneously recanalized. Emboli typically originate from atherosclerotic stenoses in the internal carotid artery or from sources in the heart such as clots in the left atrium or the left ventricle. Hypertension-induced vascular disease of the small perforating intracerebral arteries is a common cause of lacunar strokes. A classification of the major stroke subtypes is shown in Table 31.1. [Pg.431]

The APT 1994 overview showed that any excess risk of intracranial bleeding with antiplatelet therapy was small, at most one or two per 1000 patients per year in trials of long-term (more t one month) treatment (8). Among patients at high ri of arterial occlusive disease, therefore, the large absolute reductions in serious vascular events produced by antiplatelet therapy (Figure 24.2) fer outweigh any absolute hazards. [Pg.543]

The study of cerebrovascular disease has advanced markedly in recent years with advances in non-invasive imaging methods such as MR angiography and CT angiography as well as an improved understanding of the immune system in the pathogenesis of atherosclerosis. Atherosclerotic cerebrovascular disease is a common cause of strokes and shows a predilection for sites such as the bifurcation of the common carotid artery into the internal and external carotid arteries and the aortic arch and the major intracranial arteries such as the basilar artery and the middle cerebral arteries. Occlusive atherosclerotic vascular disease of these large extracranial arteries is responsible for as many as 20-30% of ischemic strokes and intracranial steno-occlusive disease causes around 5-10% of ischemic strokes. [Pg.437]


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See also in sourсe #XX -- [ Pg.230 ]




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