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Hyponatremia or hyponatraemia is a low concentration of sodium in the blood. [4] It is generally defined as a sodium concentration of less than 135 mmol/L (135 mEq/L), with severe hyponatremia being below 120 mEq/L. [3] [8] Symptoms can be absent, mild or severe.
Hypoosmolar hyponatremia is a condition where hyponatremia is associated with a low plasma osmolality. [1] The term "hypotonic hyponatremia" is also sometimes used.[2]When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states: low volume, normal volume, or high volume.
“Zero dietary sodium intake may lead to clinically significant low blood sodium levels, which can cause severe muscle cramps, weakness, nausea and vomiting, seizures and coma, shock or even ...
Low is 0.3 g salt or less per 100 g (or 0.1 g sodium). If the amount of salt per 100 g is in between these figures, then that is a medium level of salt." In the UK, foods produced by some supermarkets and manufacturers have 'traffic light' colors on the front of the packet: red (high), amber (medium), or green (low).
These electrolytes must be replaced to keep the electrolyte concentrations of the body fluids constant. Hyponatremia, or low sodium, is the most commonly seen type of electrolyte imbalance. [12] [13] Treatment of electrolyte imbalance depends on the specific electrolyte involved and whether the levels are too high or too low. [3]
Hypotension, and hypovolemic shock, are the main symptoms of an adrenal crisis. Other symptoms include weakness, anorexia, nausea, vomiting, fever, fatigue, abnormal electrolytes, confusion, and coma. Laboratory testing may detect low sodium, high potassium, high lymphocyte count, high eosinophils, low blood sugar, and rarely high calcium. The ...
Hypoaldosteronism causes low sodium (hyponatremia), high potassium (hyperkalemia), and metabolic acidosis, a condition in which the body produces excess acid.These conditions are responsible for the symptoms of hypoaldosteronism, which include muscle weakness, nausea, palpitations, irregular heartbeat, and abnormal blood pressure.
All responded to sodium chloride administration but administering aldosterone precursor 11-deoxycorticosterone did not reverse renal sodium loss. The authors felt neither pituitary nor adrenal insufficiency was involved, but that direct neural control of renal proximal tubular reabsorption of sodium was disrupted. [25]