Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 80 patients with Pneumocystis pneumonitis, the intial signs and symptoms of infection were usually fever and cough, followed by tachypnea and coryza. Flaring of the nasal alae and cyanosis occurred later. Blood gas composition was markedly altered in its acid-base profile in most patients at admission. There was moderate to severe respiratory alkalosis and hypoxia. Clinical manifestations were correlated with the extent of histopathologic changes in the lung. (Deprivation of protein in the diet of rats provoked P. carinii infection.) P. carinii infection was found in children with kwashiorkor; evidence of protein-calorie malnutrition is closely associated with P. carinii pneumonitis in children wiht cancer and other primary diseases. P. carinii pneumonitis proved unique in that the causative organisms remained limited to the lungs even in fatal cases. No toxins have been identified, and systemic effects of the infection were only those that could be related to hypoxia and fever.
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PMID:Signs, symptoms, and pathophysiology of Pneumocystis carinii pneumonitis. 1 4

In summary, HAPE is a potentially fatal form of noncardiogenic PE seen in a small number of individuals visiting above 9,000 ft in elevation. The pathophysiology is uncertain but is probably due, at least in part, to hydrostatic and capillary permeability abnormalities of the pulmonary vascular bed in response to hypobaric hypoxia. A subclinical form above 14,000 ft is common (15% to 23% incidence), but the incidence of HAPE itself is unclear. Possible risk factors include rapid ascent, strenuous activity on arrival, reascent to altitude by highlanders after a short stay lower, previous HAPE, cold, respiratory tract infections, sedation, youth, and the peripheral edema of AMS. Clinical presentation is similar to that of pneumonia: tachypnea, tachycardia, cyanosis, cough, fever, and chest discomfort. Symptoms often worsen with sleep. WBC count is usually elevated, and arterial blood gases reveal a respiratory alkalosis and an alarmingly low hemoglobin saturation. Chest radiographs reveal bilateral patchy infiltrates. Radiographic findings are dissimilar to those from cardiogenic PE. Differential diagnosis includes pneumonia, PE and HAB. Treatment modalities include early descent, bed rest, oxygen therapy, and EPAP. Mortalities range from 4% to 27% depending on the rapidity of descent and evacuation.
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PMID:High-altitude pulmonary edema: a collective review. 266 Aug 18

A 76-year-old on long-term Lasix and Pyrogastrone presented with stridor. This became worse with local irritation, e.g. on coughing or during indirect laryngoscopy. Indirect laryngoscopy showed a narrow glottis with an otherwise normal larynx. Blood investigation showed a low serum potassium with a raised bicarbonate level, and a serum calcium level just within the acceptable normal range. A diagnosis of laryngospasm secondary to drug-induced hypokalaemic alkalosis was made. This was treated with the withdrawal of the above drugs and supplementing potassium orally.
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PMID:Stridor due to drug-induced hypokalaemic alkalosis. 357 25

The published reports of patients with the acquired immunodeficiency syndrome (AIDS) with disseminated histoplasmosis come mostly from institutions located in endemic areas for histoplasmosis, where disease is thought to occur by either primary infection or reactivation. The characteristics of reactivation disease are not well delineated. We describe the clinical features of reactivation disseminated histoplasmosis in 46 residents of San Francisco, California, with AIDS who did not report recent travel to an area endemic for histoplasmosis. Patients presented with illness lasting days to months, manifested most frequently by fever, chills, sweats, cough or dyspnea, gastrointestinal complaints, malaise, and weight loss. Physical examination and imaging studies were notable for hepatosplenomegaly, lymphadenopathy, or abnormal pulmonary findings in more than half of patients. Laboratory studies revealed a high rate of cytopenia, elevated serum lactate dehydrogenase levels, abnormal liver function test values, respiratory alkalosis with hypoxemia, and a median CD4 lymphocyte count of 36 x 10(9) per liter. The clinical presentation of reactivation disseminated histoplasmosis in patients with AIDS living in San Francisco is similar to that of disseminated histoplasmosis reported in patients with AIDS living in endemic areas. Reactivation disseminated histoplasmosis should be considered in any AIDS patient with a low CD4 lymphocyte count, a febrile illness, and a history of travel or residence in an endemic area.
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PMID:AIDS-related disseminated histoplasmosis in San Francisco, California. 939 79

We describe the case of a 61-year-old male patient, in which the search for the cause of chronic respiratory failure, severe pulmonary hypertension and secondary erythrocytosis resulted in a diagnosis of combined pulmonary fibrosis and emphysema (CPFE). This is a unique, recently characterised syndrome with upper-lobe emphysema and pulmonary fibrosis of the lower lungs. The cause is unknown, but one of the main risk factor remains smoking. The patient was a heavy smoker (over 40 pack-years). He complained of dyspnoea on exertion and cough. Physical examination revealed basal crackles and cyanosis. The patient had severe reduction in diffusing capacity, out of proportion to his lung volumes (DLCO 27% of predicted value, FEV1 2.95 l (100%), FVC 4.41 l (118%), FEV1/FVC (66%). The blood gas showed hypoxemia (pO2 37 mm Hg), hypocapnia and respiratory alkalosis. Diagnosis was based on chest computer tomography, which revealed upper lobe emphysema and lower lobe ground glass changes and honeycombing. Severe pulmonary hypertension (SPAP 80 mm Hg) was confirmed by echocardiography and right cardiac catherisation. The patient received long-term oxygen therapy, inhaled corticosteroid and Ca-blocker.
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PMID:[Combined pulmonary fibrosis and emphysema - case report and literature review]. 1946 58

Jenny, a nonsmoker, 54 years of age, presents with 3 years of dry cough, progressive breathlessness and reducing exercise tolerance. Two years ago she was diagnosed with asthma and treated with inhaled bronchodilators (which have been marginally effective). Jenny has worked in a tile factory for 22 years; 15 years in the grinding department, transferring to the chipping department 7 years ago. On examination she is tachypnoeic with a prolonged expiratory phase. There are bilateral rhonchi and a few fine crepitations at the left infrascapular region. Jenny's full blood count and electrocardiogram are normal. Arterial blood gas show mild hypoxia with respiratory alkalosis. Spirometry demonstrates mixed moderate obstructive and restrictive impairment. The diffusion capacity for carbon monoxide is reduced. Mantoux is negative and erythrocyte sedimentation rate is 10 mm/hour. A chest X-ray is taken.
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PMID:A tile factory worker presenting with breathlessness and dry cough. 1989 21

Biotinidase deficiency (BTD) is a rare yet treatable metabolic autosomal recessive (AR) disorder in which the body is unable to recycle the vitamin biotin. Early diagnosis and treatment can be life-saving, but some symptoms of the disease are irreversible, and the condition can even prove to be fatal if not correctly diagnosed and managed. Here we present a case of a six-month-old child who presented with cough, fever, and difficulty in breathing. Respiratory examination revealed deep subcostal and intercostal recessions, bilateral crepitations, and wheezes. On central nervous system (CNS) examination, the baby had a low Glasgow Coma Scale (GCS) score of 10 while the tone was decreased, and bulk was increased in all four limbs. Chest X-ray revealed haziness at the right middle and lower lobes. Antibiotics were started keeping pneumonia, bronchiolitis, and sepsis in mind along with an initial diagnosis of inborn error of metabolism (IEM). As the patient's condition deteriorated, nasal bubble continuous positive airway pressure (CPAP) and nebulization were provided and later put on a ventilator. Arterial blood gases (ABGs) showed severe metabolic acidosis and compensatory respiratory alkalosis with an anion gap of 15. Urine profile for organic acid was performed, and the diagnosis of sepsis with BTD was made. Unfortunately, our patient expired on the fourth day of admission before a biotin injection could be searched and administered. Moreover, our patient was also suspected of a possible Sotos syndrome, which is a rare genetic disorder characterized by excessive growth in the initial years of life. The case highlights the significance of the diagnosis of such metabolic disorders in the natal period of life and their immediate management.
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PMID:Biotinidase Deficiency With Suspected Sotos Syndrome: A Rare Entity. 3252 54