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Query: UMLS:C0019079 (hemoptysis)
 6,129 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevation of pulmonary arterial pressure may be secondary to many diseases of the lungs, chest wall, and heart. From a pathophysiologic viewpoint, pulmonary hypertension is secondary to vascular obstruction, vasoactivity, increased circulation, and passive forces. Clinically, the entities that result in secondary pulmonary hypertension present with a picture that identifies the primary disease. Patients with primary pulmonary hypertension may be difficult to identify. Pulmonary hypertension may present early with dyspnea and fatigue, while syncope and hemoptysis are late symptoms. In many instances, pulmonary hypertension can be diagnosed utilizing physical examination and noninvasive tests. Eventually, right heart catheterization is necessary to confirm the diagnosis and to monitor trials of therapy with vasodilators. Treatment may be specific (closure of a septal defect, thromboendarterectomy) or generic (vasodilators). These have been used recently for both secondary and primary pulmonary hypertension in an effort to reduce pulmonary vascular resistance, thereby decreasing right ventricular afterload and improving cardiac output and oxygen delivery. The success of these treatments has not been demonstrated.
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PMID:Pulmonary hypertension: etiology and clinical evaluation. 333 61

Pulmonary embolism is nearly always a complication of deep venous thrombosis. The evaluation of risk factors for venous thromboembolism not only aids diagnosis but also guides decisions about the intensity of prophylactic measures. As both the extent and chronicity of pulmonary vascular obstruction vary widely, pulmonary embolism can produce widely differing clinical pictures. From the clinical, pathophysiological and therapeutical point of view, it is convenient to classify pulmonary embolism into four types: acute minor embolism (dyspnoea with or without pleuritic pain or haemoptysis), acute massive embolism (hemodynamic instability), subacute massive embolism (mimicking heart failure or indolent pneumonia), and chronic thromboembolic pulmonary hypertension (slowly progressing dyspnoea). This classification is of importance not only for the rational diagnosis and differential diagnosis, but also for the institution of adequate therapy. Because the disease has many nonspecific manifestations but no pathognomonic symptoms or signs, it is impossible to prove the diagnosis of pulmonary embolism alone on the basis of clinical presentation.
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PMID:[Clinical characteristics of pulmonary embolism]. 1121 69

A 34-year-old woman with bilateral pulmonary infiltrates was diagnosed with sarcoidosis. She refused corticosteroid treatment despite a worsening of the pulmonary infiltrate, and thereafter developed dyspnea following hemoptysis 6 years later. The upper lobe branches of the pulmonary artery were obstructed and the left main pulmonary artery was narrowed by mediastinal soft tissue, thus complications of granulomatous mediastinitis and fibrosing mediastinitis were suspected. The mediastinal soft tissue regressed, following the administration of corticosteroids, whereas the vascular obstruction and narrowing remained unchanged. Although the obstruction or stenosis of major pulmonary vessels is rare in sarcoidosis, such potential developments should be considered when mediastinal soft tissue appears in follow-up examinations.
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PMID:Sarcoidosis complicated with major pulmonary artery obstruction and stenosis. 2303 73