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Antidiuretic hormone (ADH) is released from the posterior pituitary for a number of physiologic reasons. The majority of people with hyponatremia, other than those with excessive water intake or renal salt wasting, will have elevated ADH as the cause of their hyponatremia. However, not every person with hyponatremia and elevated ADH has SIADH.
The cornerstone of therapy for SIADH is reduction of water intake. If hyponatremia persists, then demeclocycline (an antibiotic with the side effect of inhibiting ADH) can be used. SIADH can also be treated with specific antagonists of the ADH receptors, such as conivaptan or tolvaptan. [citation needed] Another cause is psychogenic polydipsia. [3]
The treatment of hyponatremia depends on the underlying cause. [12] How quickly treatment is required depends on a person's symptoms. [12] Fluids are typically the cornerstone of initial management. [12] In those with severe disease an increase in sodium of about 5 mmol/L over one to four hours is recommended. [12]
Hyponatremia, an unusually low level of sodium in the blood that may cause confusion and seizures, is found in 40% of cases. This may be caused by low cortisol levels or by inappropriate release of antidiuretic hormone (ADH) from the posterior pituitary. [1]
V 2 R antagonists have become a mainstay of treatment for euvolemic (i.e., SIADH, postoperative hyponatremia) and hypervolemic hyponatremia (i.e., CHF and cirrhosis). [9] V 2 RAs predictably cause aquaresis leading to increased [Na +] in majority of patients with hyponatremia due to SIADH, CHF, and cirrhosis. The optimum use of VRAs has not yet ...
the physiologic response to a decrease in kidney perfusion is an increase in sodium reabsorption to control hyponatremia, often caused by volume depletion or decrease in effective circulating volume (e.g. low output heart failure). above 2% [citation needed] or 3% [2] acute tubular necrosis or other kidney damage (postrenal disease)
In 1953, Leaf et al., demonstrated that exogenous administration of the antidiuretic hormone vasopressin resulted in hyponatremia and a natriuresis dependent on water retention and weight gain. This was not "salt wasting"; it was a physiologic response to an expanded intravascular volume.
This means that psychogenic polydipsia may lead to test results (e.g. in a water restriction test) consistent with diabetes insipidus or SIADH, leading to misdiagnosis. [14] Dry mouth is often a side effect of medications used in the treatment of some mental disorders, rather than being caused by the underlying condition. [15]