1/67. Clinics in diagnostic imaging (39). Conn's syndrome due to adrenocortical adenoma (Conn's tumour).A 33-year-old man presenting with muscle weakness and hypertension was found to have hypokalaemia and metabolic alkalosis. Computed tomography (CT) showed an adrenal mass. Conn's syndrome due to an adrenocortical adenoma was confirmed at surgery. hypertension-related adrenal disorders such as Cushing's syndrome, carcinoma and phaeochromocytoma are discussed. CT is currently the single most useful imaging method for identifying adrenal masses.- - - - - - - - - - ranking = 1keywords = alkalosis (Clic here for more details about this article) |
2/67. Peritoneal carcinomatosis following laparoscopic resection of an adrenocortical tumor causing primary hyperaldosteronism.A clinical syndrome combining hypertension and hypokalemic alkalosis led to the diagnosis of primary hyperaldosteronism, caused by a right-sided, 2 cm large, apparently benign aldosterone-producing adenoma. The adrenal tumor was completely resected by laparoscopic adrenalectomy. Six months after surgery, the patient exhibited a severe relapse of hyperaldosteronism. Extensive peritoneal metastases of a mixed aldosterone- and cortisol-secreting adrenocortical carcinoma were found at abdominal laparotomy. In the light of this case report, we discuss the possibility that laparoscopic resection of adrenocortical tumors might contribute to their subsequent peritoneal dissemination.- - - - - - - - - - ranking = 103.48884023798keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
3/67. hypokalemia and metabolic alkalosis: algorithms for combined clinical problem solving.This article reviews an approach to patients with hypokalemia and metabolic alkalosis using the information obtained from spot urine chloride values, blood pressure determinations, and renin and aldosterone measurements in order to simplify clinical problem solving.- - - - - - - - - - ranking = 5keywords = alkalosis (Clic here for more details about this article) |
4/67. Bartter's syndrome. New insights into pathogenesis and treatment.Discussed here is a patient with normotension, hypokalemic alkalosis, hyperreninemia, hyperaldosteronism, juxtaglomerular cell hyperplasia and insensitivity to the pressor effects of angiotensin (Bartter's syndrome). The hyperreninemia and hyperaldosteronism were both suppressible with volume expansion. hypokalemia was correctible both short-term with potassium chloride infusions and long-term with spironolactone. Nevertheless, the abnormal pressor response to infused angiotensin could not be corrected by these maeuvers, suggesting that this defect is likely to be of primary pathophysiologic significance. We found that potassium loading markedly stimulated aldosterone excretion. This may explain the inadequacy of potassium supplementation alone to correct the hypokalemia and the observed "escape" from the potassium conserving effects of spironolactone seen in patients with Bartter's syndrome. The administration of propranolol in large doses only partially suppressed the marked hyperreniemia of our patient and failed to prevent a subsequent rise in the renin level which was associated with spironolactone therapy. In contrast, suppression of the renin level to normal was demonstrated by sodium loading. It is suggested that patients with Bartter's syndrome be treated simultaneously with large doses of spironolactone and a high sodium intake.- - - - - - - - - - ranking = 103.48884023798keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
5/67. bartter syndrome. Typical facies and normal plasma volume.Two girls with hypokalemic and hypochloremic metabolic alkalosis and failure to thrive were found to have bartter syndrome at ages 9 and 6 months. Both had normal blood pressures despite substantial elevation of plasma renin activity and evidence of secondary hyperaldosteronism. A similarity in facial features, including prominent forhead, a large head, triangular facies with drooping mouth, and large eyes and pinnae, was noted in these two infants and in published pictures of other infants with the syndrome. Although the normotension associated with substanital elevation of plasma renin activity and hyperaldosteronism in bartter syndrome has been considered the effect of hypovolemia, a normal or slightly elevated plasma volume was found in these infants, suggesting that in certain cases an alternate mechanism for the depressed response to renin may be present.- - - - - - - - - - ranking = 2.4899618862748keywords = hypokalemic, alkalosis (Clic here for more details about this article) |
6/67. Severe hypomagnesaemia-induced hypocalcaemia in a patient with Gitelman's syndrome.Gitelman's syndrome (GS) is characterized by hyperreninaemic hyperaldosteronism, hypokalaemia, metabolic alkalosis, hypomagnesaemia and hypocalciuria and is due to a defect of the Na-Cl cotransporter at the distal tubule, which may appear in a sporadic or in a familial form. It is an autosomal recessive disorder associated with normal or reduced blood pressure. We report a case of severe hypomagnesaemia-induced hypocalcaemia in a 39-year-old Caucasian woman with GS. The patient had impaired parathormone (PTH) responsiveness to peripheral stimuli, as proved by the marked PTH increase and normalization of plasma calcium levels after acute and chronic administration of magnesium salts. Secondary normotensive hyperreninaemic hyperaldosteronism with hypokalaemia and metabolic alkalosis was also present. Normal plasma renin activity (PRA) and aldosterone levels were restored by administration of an inhibitor of prostaglandin synthesis. The electrolyte imbalance was successfully corrected with chronic treatment with magnesium and potassium salts. Genetic analysis identified a compound heterozygous mutation in the Na-Cl cotransporter gene (NCCT), confirming the diagnosis of GS. The striking feature of this case of GS was impaired PTH responsiveness to peripheral stimuli determined by hypomagnesaemia and the resulting severe hypocalcaemia, which had not previously been described in this syndrome.- - - - - - - - - - ranking = 2keywords = alkalosis (Clic here for more details about this article) |
7/67. Successful treatment by cyclooxyenase-2 inhibitor of refractory hypokalemia in a patient with Gitelman's syndrome.Gitelman's syndrome is manifested by hypokalemic alkalosis, hypomagnesemia, hypocalciuria, normotensive hyperreninemia and hyperaldosteronism. hypokalemia can at times be refractory to treatment. We present a patient refractory to a variety of drugs including indomethacin, the nonspecific COX inhibitor. Rofecoxib, a specific COX 2 inhibitor, promptly elevated serum potassium concentration with normalization of plasma aldosterone and near normalization of renin without a change in serum magnesium. Our patient also had rhabdomyolysis, a rarely reported complication, which was also ameliorated by COX 2 inhibition.- - - - - - - - - - ranking = 103.48884023798keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
8/67. Twenty-four year spironolactone therapy in an aged patient with aldosterone-producing adenoma.A case of primary aldosteronism treated with spironolactone therapy has been followed up for 24 years. This is probably the longest case of spironolactone therapy for primary aldosteronism that has ever been reported. Long-term treatment with spironolactone controlled the hypertension and prevented hypokalemic alkalosis in this patient, without any deleterious effects on steroid biosynthesis. Based on data obtained during dose reduction and subsequent withdrawal of spironolactone, it is suggested that the suppressed plasma renin activity associated with adenoma-induced aldosteronism develops prior to hypokalemia and hypertension.- - - - - - - - - - ranking = 103.48884023798keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
9/67. Hyperreninemia and secondary hyperaldosteronism in a patient with pheochromocytoma and von hippel-lindau disease.In a 21-year-old Caucasian women with von hippel-lindau disease, norepinephrine-producing adrenal pheochromocytoma was identified as the underlying cause of severe hypertension. She was found to have extremely elevated levels of circulating renin and aldosterone, and she was markedly hypokalemic. Administration of captopril further enhanced renin secretion, while her blood pressure improved. The patient became normokalemic following tumor removal, and her blood pressure decreased to normal levels with reestablishment of normal circadian blood pressure rhythm. This case demonstrates that, in the absence of renovascular or malignant hypertension, pheochromocytoma can be the underlying cause for the clinical syndrome of hypertension associated with severe hypokalemia and hyperreninemic hyperaldosteronism.- - - - - - - - - - ranking = 1.4899618862748keywords = hypokalemic (Clic here for more details about this article) |
10/67. Cardiomyopathy in an adult with Bartter's syndrome and hypokalemia. Hemodynamic, angiographic and metabolic studies.A case of an adult with Bartter's syndrome (hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis) is described; the patient had the unusual manifestation of cardiomyopathy, probably secondary to severe hypokalemia. Results of metabolic studies and kidney biopsy were consistent with Bartter's syndrome; angiographic and hemodynamic findings were abnormal. The cardiomyopathy was confirmed at autopsy after the patient's sudden death. Conclusions from this case are that severe hypokalemia can pose a serious threat both immediately in the form of dangerous arrhythmias and in the long term in the form of cardiomyopathy.- - - - - - - - - - ranking = 103.48884023798keywords = hypokalemic alkalosis, hypokalemic, alkalosis (Clic here for more details about this article) |
| | Next -> |