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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is often a misguide of chronic bronchitis and passive pulmonary hypertension. In 42 patients with chronic bronchitis a revision of the results was made and it was found that in 28 (67%) patients the former diagnosis of chronic bronchitis was confirmed, while in 8 (19%) patients a new diagnosis was established--a passive pulmonary hypertension and in 6 (14%) patients a combination of chronic bronchitis and passive pulmonary hypertension was found. It is considered that the symptoms like cough, sputum and dyspnea as well as the similar physical finding may lead the clinician to change the diagnoses.
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PMID:[Pathogenic and clinical differences between stasis and chronic bronchitis]. 279 64

Chronic obstructive pulmonary disease (COPD) is equated with chronic bronchitis and emphysema as one disease entity. In COPD airflow limitation is relatively persistent--unlike asthma. Tests for "small-airways disease" form no part of routine practice, for their accuracy in detecting pathological change is debatable. The proteolytic theory of the pathogenesis of emphysema highlights the role of neutrophil elastase, antielastases, oxidants, antioxidants, and thus of potential new treatments. Clinical features of COPD include breathlessness, cough, and sputum, with airflow obstruction and lung hyperinflation. The differential diagnosis includes bronchiectasis, cystic fibrosis, and pulmonary hypertension, but pulmonary fibrosis, etc., is distinguished by radiological infiltrates. Plain chest radiography cannot reliably diagnose emphysema in life, but a new method measuring lung density from the computed tomographic (CT) scan allows location, quantitation, and diagnosis of emphysema (defined by enlargement of distal air spaces) in humans in life. "Pink puffers" with breathlessness, hyperinflation, mild hypoxemia, and a low PCO2 are contrasted with "blue bloaters" with hypoxemia, secondary polycythemia, CO2 retention, and pulmonary hypertension and cor pulmonale. Antismoking measures are a major aim in management. A bronchodilator regimen combining a slow-release oral theophylline with an inhaled beta 2-agonist, ipratropium, and high-dose inhaled steroids is proposed because even modest improvement in obstruction can help these patients. In acute exacerbations with purulent sputum, antimicrobials against Streptococcus pneumoniae and Hemophilus influenzae are used with controlled oxygen therapy aiming to keep the arterial PO2 over 50 mm Hg without the pH falling below 7.25. Influenza prophylaxis is recommended, but pneumococcal vaccination remains debatable. Chronic under-nutrition in "emphysema" implies controlled trials of feeding regimens--but these remain to be assessed. Long-term oxygen therapy is the only treatment known to prolong life in blue bloaters, and oxygen concentrators and transtracheal oxygen delivery are discussed. Pulmonary vasodilators (e.g., beta 2-agonists, hydralazine, nifedipine, angiotensin-converting enzyme [ACE] inhibitors, etc.) have not yet been proved to provide long-term reduction in pulmonary arterial pressure. Blue bloaters have severe nocturnal hypoxemia in rapid eye movement (REM) sleep that is corrected by oxygen or the investigational drug almitrine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Chronic obstructive pulmonary disease. 304 40

The choice of a contrast agent for pulmonary angiography has important implications for patient comfort, image quality, and perhaps the safety of the procedure, particularly for "high-risk" patients. In a prospective study the nonionic, low-osmolality agent iopamidol eliminated the problem of image degradation due to coughing, and patients showed excellent tolerance for it. However, pressure measurements obtained within 3-5 minutes of injection of iopamidol and diatrizoate sodium meglumine 76% showed no significant difference in the hemodynamic effects of the two contrast agents, either for normotensive or for pulmonary hypertensive patients. Contrary to a common presumption, pulmonary hypertension by itself did not appear to increase the risk of pulmonary angiography. The theoretic presumption of greater hemodynamic stability with low-osmolality contrast agents was not clinically evident in this trial with iopamidol. At present, enhanced patient comfort and improved image quality remain the only confirmed bases for choosing this contrast agent for pulmonary angiography.
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PMID:Pulmonary angiography with iopamidol: patient comfort, image quality, and hemodynamics. 365 54

The clinical signs associated with heartworm disease are the result of changes in the pulmonary arterial system. These clinical signs are the result of either pulmonary hypertension or lung parenchymal disease associated with vascular changes. An increase in pulmonary arterial pressure produces an increase in right ventricular afterload, which may lead to exercise intolerance, syncope, and right-sided congestive heart failure. Coughing, dyspnea, and hemoptysis are the results of pulmonary parenchymal disease.
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PMID:Pulmonary manifestations of heartworm disease. 390 12

A case of congenital aneurysm of the left pulmonary artery in a 52-year-old Nigerian woman is presented. She presented with a transient history of cough and epigastric pains. A chest radiograph revealed a rounded left hilar mass just superior to the left main bronchus, and pulmonary angiography confirmed the presence of fusiform aneurysm of the left pulmonary artery. At cardiac catheterization, there was pulmonary hypertension (80 mmHg). There was no associated congenital cardiac malformation. The electrocardiograph showed right ventricular hypertrophy. The patient remains asymptomatic to date. This is the fourth known report of pulmonary aneurysm in an African. The rarity of pulmonary artery aneurysms is stressed.
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PMID:Congenital aneurysm of the pulmonary artery: a case report. 628 84

A 23-year-old man was admitted because of an attack of chest pain and dry cough. Chest roentogenogram showed a solitary pulmonary nodule in the left upper lobe. Chest CT showed a nodule and a small pleural effusion on the same side. Pulmonary thrombosis was diagnosed by pulmonary Ventilation/perfusion scintigraphy and pulmonary arteriography. Deep vein thrombosis was not detected except in a distal pulmonary artery. The solitary nodule disappeared spontaneously without thrombolytic therapy. An anticardiolipin antibody (IgG) test was positive. Primary antiphospholipid syndrome was diagnosed, because of the absence of physical findings suggesting other collagen vascular diseases. Patients with antiphospholipid syndrome have a high frequency of pulmonary complications that include pulmonary hypertension and pulmonary embolism. Most of the patients with pulmonary embolism have deep vein thrombosis, and pulmonary vessel thrombosis as seen in the present case is a rare complication.
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PMID:[A case of pulmonary thrombosis associated with primary antiphospholipid syndrome]. 773 Nov 19

A 50-year-old woman was admitted to our hospital on April 4, 1992, because of progressive worsening of dry cough and exertional dyspnea. Moderate hypoxemia and obstructive ventilatory impairment were present. Her chest roentgenogram and CT films showed thickened bronchovascular bundles in the absence of significant parenchymal fibrosis. Transbronchial lung biopsy revealed the formation of noncaseous epithelioid cell granulomas. Pulmonary perfusion scintigraphy showed multiple perfusion defects predominantly in the upper lung fields. Pulmonary ventilation scintigraphy showed a normal pattern. After administration of prednisolone for 3 months, her chest roentgenogram and CT films demonstrated marked decrease of infiltrates, but there was no improvement of hypoxemia and perfusion defects on pulmonary perfusion scintigraphy. Pulmonary angiography revealed multiple stenoses and occlusions of segmental and subsegmental branches of pulmonary arteries. Long-term steroid treatment will be necessary for this rare form of pulmonary sarcoidosis to prevent the development of pulmonary hypertension.
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PMID:[A case of pulmonary sarcoidosis with circulatory insufficiency of segmental and subsegmental branches of pulmonary arteries]. 804 Oct 41

Pulmonary hypertension occurs frequently in patients with chronic obstructive lung diseases and contributes to a poor prognosis. Most common symptoms in addition to dyspnea, cough and expectoration are fatigue, syncopes, chest pain and peripheral oedema. No single non-invasive method such as lung function testing, blood gas analysis, ECG, chest x-ray, myocardial scintigraphy and isotopic radionuclide ventriculography is sufficiently reliable for predicting pulmonary hypertension. Only the combination leads to the diagnosis of pulmonary hypertension and cor pulmonale within acceptable limits. Echocardiography was found to be a reliable method of assessing right ventricular function. Doppler echocardiography is most useful with a specificity and sensitivity of about 80%. As "golden standard" cardiac catheterisation is still required for the measurement of pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR), cardiac output (CO) and pulmonary capillary wedge pressure (PCWP) at rest and exercise.
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PMID:[Current aspects in diagnosis of chronic cor pulmonale]. 829 Dec 70

A Haitian woman with the human immunodeficiency virus (HIV) presented with dyspnea, cough, fatigue and lower abdominal pain of recent onset. Clinical, radiologic and hemodynamic investigations demonstrated pulmonary hypertension. The patient died a few days later. The pathological findings were compatible with primary pulmonary hypertension. This case is similar to others that have been reported and indicates a possible link between HIV infection and rapidly progressive primary pulmonary hypertension.
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PMID:Primary pulmonary hypertension associated with HIV infection. 842 54

We report the clinical features, electrocardiographic and chest X-ray findings, and Doppler-measured pulmonary artery pressures in 22 children admitted to Goroka Base Hospital with primary pulmonary hypertension and compare them with findings in 10 controls. Symptoms frequently reported by patients were recurrent cough (95%) and shortness of breath (77%). 82% of the patients had increased intensity of the pulmonary component of the second heart sound. 45% of the patients had clinical evidence of right heart failure. Chest X-rays were readable in 14 patients: the mean cardio-thoracic ratio was 65% and in the controls 58%; the mean diameter of the descending branch of the right pulmonary artery was 9 mm and in the controls 6.4 mm. 13 patients and 8 controls had electrocardiograms: 11 patients had right axis deviation, 2 a normal axis, and all showed evidence of right ventricular hypertrophy; 7 controls had a normal axis, 1 had right axis deviation, and 3 controls had right ventricular hypertrophy. Pulmonary artery pressures in the patients ranged from 41 to 137 mmHg with a mean of 79 mmHg. The control group had a mean pulmonary artery pressure of 28 mmHg, but 5 of the 10 controls had pulmonary artery pressures greater than the accepted norm (peak systolic pressure less than 30 mmHg). Altitude and chest infection may be playing a role in the pathogenesis of pulmonary hypertension in patients in the highlands but further studies need to be done to define the causes and the pathological changes in the pulmonary vasculature, as well as to determine local norms and the natural history of pulmonary hypertension in highland children.
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PMID:Unexplained pulmonary hypertension in children in the highlands of Papua New Guinea. 857 77


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