الفهرس 
SODIUM PHYSIOLOGYOnly 14 pages are availabe for public view
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Abstract
Sodium (Na) is a major mineral which was first-isolated by sir Humphry Davy in 1807. Sodium has great importance in nature and human body. Sodium is the primary cation in extracellular fluid. To understand effect of sodium disturbances we must understand water homeostasis and sodium physiology. Water constitute 55 to 65 percent of human body weight which distributed between extracellular fluid (ECF) and intracellular fluid (ICF).The two main effectors responsiple for regulating the balance between water intake and excretion are thirst and pituitary secretion of arginine vasopressin (AVP).
Sodium is a positively charged electrolyte that helps to balance fluid levels in the body and facilitates neuromuscular functioning. Sodium is the main extracellular cation and the major contributor to the osmolality of me extracellular fluid (ECF).
Sodium play a major role in assessment of acid base status through calculation of anion gap and strong ion difference.
In normal individuals the kidneys strive to achieve sodium balance that is to have sodium excretion equal to sodium ingestion. The vast majority of sodium that is filtered by the kidney is reabsorbed in the proximal tubule and loop of henle. Some hormones increase sodium reabsorption such as rennin, Angiotensin II, aldosterone and AVP. Others increase sodium excretion such as atrial natriutic peptide (ANP) and brain natriutic peptide (BNP).
Disturbances of sodium levels are pathognomonic to many clinical problematic situations in ICU such as hypernatraemia which occur when serum sodium concentration exceeds 145mmol/l. It is much less common than hyponatraemia which occur when serum sodium concentration is below 135 mmol/L.
Hypernatraemia is rarely due to excess administration of sodium and more commonly occurs as a result of inadequate administration of free water to a critically ill patient with excessive insensible losses of water from diarrhoea, vomiting , sweating or diuresis. The massive renal loss of free water that characterizes diabetes insipidus causes rapid onset of hypernatraemia. Initially euvolaemia is maintained but uncorrected water loss leads to severe dehydration and hypovolaemia. Diabetes insipidus may follow head injury and is diagnosed when polyuria (>400 ml/ hour) occurs in the presence of raised serum osmolality (>300 mosmol/ litre) together with an inappropriately low urine osmolality (<150 mosmol/litre).
Clinical features include lethargy, irritability, nausea and vomiting. In severe cases muscle twitching, hyper-reflexia, spasticity, seizures and coma may occur.
Management: free water is administered as intravenous 5% dextrose or as water added to enteral feed. If the patient is haemodynamically unstable then intravascular volume should be restored rapidly with normal saline. Free water is then administered (0.5-2 ml/kg/hour). A rapid fall in sodium may cause cerebral oedema and seizures.
Diabetes insipidus is treated with the vasopressin analogue desmopressin. Sodium also is very important in cirrhotic patients with ascites and sodium retention. Sodium levels in HF have prognostic significance as well.
Plasma sodium levels have been observed to parallel HF severity. This relationship is prognostically significant, as patient survival is adversely affected once the plasma sodium concentration falls below 137 meq/L. Additionally, plasma sodium concentration below 125 meq/L usually represents patients with end-stage HF.