Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most common causes of hypoxic cor pulmonale are chronic bronchitis and emphysema. Although the clinical situation in some patients is characterized early by hypoxemia, oedema is rare in patients with an arterial pO2 above 60 mm Hg. The presence of oedema can be regarded as an unfavorable prognostic indicator. For many years, peripheral oedema had been considered an expression of congestive cardiac failure; it may be assumed, however, that neither right nor left ventricular failure is prerequisite to the development of oedema. Oedema formation can be attributed to excessive retention of salt and water or a redistribution of body water into the extracellular compartment. Hypercapnia and acidosis affect direct stimulation of renal hydrogen ion secretion. The resulting electrochemical imbalance is compensated by reabsorption of sodium. Hypercapnia and, in acute phases possibly, hypoxia lead to a fall in renal blood flow mediated by alpha-adrenergic stimulation through activation of the renin-angiotensin-aldosterone system. An increase in plasma ADH may also contribute to development of oedema. The development of cor pulmonale or respiratory insufficiency can be enhanced by nocturnal hypoventilation and hypoxia during sleep as well as by sleep apnoea. Nocturnal hypoxia, smoking and reduced oxygen tension in the relevant kidney cells responsible for erythropoietin release promote the occurrence of secondary polycythaemia. For treatment of acute exacerbations in cor pulmonale associated with infections bronchitis antibiotics such as amoxycillin and cotrimoxacol are drugs of first choice. While the use of digoxin is of doubtful value, the cautious administration of diuretics may bring symptomatic relief. In addition to physiotherapy, beta-2-selective bronchodilators and nebulized bronchodilator therapy can be useful; theophyllines dilate airways and increase cardiac output but they can cause arrhythmias and a deterioration of arterial blood gases in hypoxic patients. If the patient has been treated chronically with corticosteroids, the dosage will have to be incremented; if asthma is suspected, corticosteroid treatment is essential. Controlled oxygen therapy is the most important single therapy aimed at relief of severe arterial hypoxaemia. Oxygen should be titrated initially (for the first one or two days) to achieve an arterial tension of at least 48 mm Hg. Thereafter, the oxygen flow should be increased to yield an arterial tension in excess of 60 mm Hg during continued treatment for two to three weeks.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Hypoxic cor pulmonale: a review. 294 54

A 67-year-old man with SIADH complicated by slowly progressing autonomic failure was described. The patient noticed constipation at the age of 57. In the following years, he suffered from urinary incontinence, depletion of sweating, impotence, sleeplessness with snore, and dizziness while walking. Physical examination revealed a masked oily face with slight cerebellar disturbance. Abnormality of autonomic function tests was recognized and he was diagnosed as Shy-Drager syndrome with gradually progressing, diffuse autonomic failure accompanied by slight cerebellar ataxia and Parkinsonism. Both serum sodium level and plasma osmotic pressure were reduced, whereas daily sodium excretion was more than 100mEq and urinary osmolality was about 500mOsm/kgH2O. His renal function was intact, and the adrenocortical and thyroid hormone levels were normal, then criteria of SIADH was fulfilled. SIADH was thought to have occurred on the basis of Shy-Drager syndrome. Water load test showed failure of adequate water diuresis, but intravenous phenytoin administration following the water load test ameliorated the diuresis to normal. The relationship between plasma osmolality and the ADH response indicates that ADH was adequately secreted in response to the increase in plasma osmolality but not suppressed in response to the decrease in plasma osmolality below 280mOsm/kgH2O. These results suggest that ADH synthesis in the hypothalamus and its secretion from the pituitary gland were both intact. The response of ADH secretion to the orthostatic hypotension induced by head-up tilt was quite blunted, being compatible with Shy-Drager Syndrome. Sleep disturbance was studied by polysomnography and laryngoscopy, and was revealed to be based upon severe sleep apnea due to incomplete paralysis of the bilateral vocal cords. Sleep apnea due to vocal cord paralysis is sometimes found to be complicated in patients with multiple system atrophy (MSA) including Shy-Drager syndrome, and is known as Gerhardt syndrome. This is the first report on a case of Shy-Drager syndrome complicated with SIADH and bilateral vocal cord paralysis. In this case, SIADH is caused by impaired afferent pathways from baroreceptors to the hypothalamus, which transfer inhibitory stimuli on ADH secretion. It is suggested that Shy-Drager syndrome should be considered one of the causes of SIADH.
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PMID:[A case of Shy-Drager syndrome complicated with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) and incomplete paralysis of bilateral vocal cords]. 795 87