Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Diuretics can result in various undesired biochemical changes, such as impotence, skin rashes, nausea, dizziness and lethargy as well as subjective side effects. The side effects are mostly predictable, their effects depending on both the circulatory blood volume and on the transport of water and solute in the renal tubules. Two of the commonest side effects are mild hypovolaemia, when any diuretic is used, and mild hypokalaemia when the non-potassium-sparing diuretics, such as thiazides and frusemide are used. Its occurrence is dose dependent and can be corrected by potassium supplements, but potassium-retaining diuretics, which also correct the often associated fall in serum magnesium, are preferable. Many reports link hypokalaemia with cardiac arrhythmias, but some dispute this association in the absence of the concomitant use of digoxin. Hyponatraemia rarely occurs, but can be life threatening. Calcium excretion is markedly reduced, but unlike other electrolyte disturbances from diuretics, this may be valuable: some suggest diuretics have an anti-osteoporotic action. Diuretics increase glucose and insulin resistance and should be used sparingly in diabetics. They rarely cause a non-ketotic hyperosmolar coma. Urate is raised, but clinical gout is not common. Cholesterol elevation has been reported in some studies, but long-term studies indicate that lipid changes are minor. Other rare side effects are not predictable from their pharmacological actions and these include the occurrence of skin rashes, thrombocytopenia, pancreatitis and interstitial nephritis; and ototoxicity from frusemide.
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PMID:Adverse reactions to diuretics. 148 14

A 73 year-old man experienced left monocular blindness and transient right hand clumsiness. A left carotid arteriogram was performed 4 days after admission. Immediately following arteriography, there was a right hemiparesia and dysphasia. After 24 hours, the abnormalities resolved. The patient was treated with heparin. During the following weeks, he became gradually drowsy and confused. Pseudo-bulbar palsy and astasia appeared after a fluctuating but progressive neurological course. The combination of systemic symptoms, high sedimentation rate, renal failure, livedo reticularis and purple toes suggested necrotizing angiitis. With corticosteroid treatment, there was a slight improvement of systemic symptoms. Cholesterol emboli were seen in both fundi. Cholesterol embolization was proved by identifying the biconcave cholesterol crystal clefts in muscle and skin biopsies. The subsequent course was marqued by continuous neurological deterioration. The patient became stuporous and died 7 months after admission. Despite the lack of central nervous system pathological study, the clinical picture was highly suggestive of cerebral cholesterol embolism. A few cases have been reported, with only eight well-documented clinical descriptions. Clinical signs and symptoms were closely similar to those of the present case. Anticoagulant therapy of cholesterol emboli has been unsuccessful. In the present case, the onset of embolization was temporally related to anticoagulation.
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PMID:[Retinal, muscular and cutaneous cholesterol emboli. Progressive encephalopathy]. 408 20