Search results
Results from the WOW.Com Content Network
Hypernatremia due to diabetes insipidus as a result of a brain disorder, may be treated with the medication desmopressin. [1] If the diabetes insipidus is due to kidney problems the medication causing the problem may need to be stopped or the underlying electrolyte disturbance corrected. [1] [7] Hypernatremia affects 0.3–1% of people in ...
High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). Metabolic acidosis occurs when the body produces too much acid , or when the kidneys are not removing enough acid from the body.
This keeps serum sodium concentration – a proxy for solute concentration – at normal levels, prevents hypernatremia and turns off the osmoreceptors. [7] Specifically, when the serum sodium rises above 142 mEq/L, ADH secretion is maximal (and thirst is stimulated as well); when it is below 135 mEq/L, there is no secretion. [8]
Type A (essential hypernatremia syndrome) involves an increase of the level in which solvent molecules can pass through cell membranes (osmotic threshold) for vasopressin release and the activation of the feeling of thirst. This is the most characterized sub-type of adipsia, however there is no known cause for Type A adipsia.
In summary, hyperaldosteronism causes hypernatremia, hypokalemia, and metabolic alkalosis. [ 13 ] Finer notes on aldosterone include the fact that it stimulates sodium-potassium ATPase in muscle cells , increasing intracellular potassium and also increases sodium reabsorption all along the intestine and nephron , possibly due to widespread ...
Hypernatremia is not common in individuals with no other health concerns. [3] Most individuals with this disorder have either experienced loss of water from diarrhea, altered sense of thirst, inability to consume water, inability of kidneys to make concentrated urine, or increased salt intake.
Furosemide is primarily used for the treatment of edema, but also in some cases of hypertension (where there is also kidney or heart impairment). [14] It is often viewed as a first-line agent in most people with edema caused by congestive heart failure because of its anti-vasoconstrictor and diuretic effects.
Apparent mineralocorticoid excess is a rare form of monogenic hypertension that is transmitted as an autosomal recessive trait. The clinical symptoms of AME were first reported in 1974 by a Professor from Switzerland; Edmond A Werder in a 3-year-old girl with low birth weight, delayed growth, polydipsia, polyuria, and hypertension.