Sodium metabolism, disorders

Gout. An inherited metabolic disorder occurring especially in men, characterized by a raised but variable blood uric acid level, recurrent acute arthritis of sudden onset, deposition of crystalline sodium urate in connective tissues and articular cartilage, and progressive chronic arthritis. 

The cyanide nitroprusside test determines the presence of free sulfhydryl or disulfide compounds in urine samples [1, 3,4]. During the first step of the assay, cyanide reduces any disulfides that are present to free sulfhydryl compounds. In the second step, a reddish color reaction results when the free sulfhydryl groups complex with nitroprusside. A positive result is most usually due to cystine in the urine. Familial cystinuria is among the most common aminoacidurias. Disulfides are also excreted in other metabolic disorders such as homo cystinuria and ji-m e reap lol ac la le - cy s lei ne disulfiduria. Both will also produce positive results according to the following reaction RSH + Na2Fe(CN)5NO (sodium nitroprusside) — chromophore + NO. 

The importance of maintaining precise concentration gradients is highlighted by the severe effects of metabolic disorders involving alkali metal cations. For example, high sodium intake is linked intimately with the development of high blood pressure on the other hand, aged... 

It has been recommended that caffeine and sodium benzoate injection should not be used in neonates however, sodium benzoate has been used by others in the treatment of some neonatal metabolic disorders. It has been suggested that there is a general adverse effect of benzoate preservatives on the behavior of 3-year-old children, which is detectable by parents, but not by a simple clinical assessment. ... 

Arieff Al, DeFronzo RA. Disorders of sodium metabolism— hyponatremia. In Arieff Al, DeFronza RA, eds. Huid, Electrolyte, and Acid-Base Disorders, 2nd ed. New York, Churchill Livingstone, 1995 255-303. 

Oh MS, Carroll HJ. Disorders of sodium metabolism Hypernatremia and hyponatremia. Crit Care Med 1992 20 94-103. 

Consequences of chronic renal failure include disordered water and sodium metabolism, hyperkalaemia, abnormal calcium and phosphate metabolism, and anaemia. 

Ans. Metabolic acidosis is a lowering of the blood pH as a result of a metabolic disorder as opposed to the failure of the H2CO3 — HCO3 buffer system. For example, there is a large and serious decrease in pH as a result of uncontrolled diabetes. The blood pH may fall from the normal 7.4 to as low as 6.8. The increased H concentration is due to the large amounts of ketone bodies produced in the liver. The products are acetoacetic acid and -hydroxybutyric acid. The bicarbonate buffer system attempts to compensate for the excess H", and the excess CO2 must be eliminated at the lungs. However, so much COj is lost by ventilation that the absolute concentration of the buffer system decreases, so the capacity of the buffer system is severely compromised and cannot reduce the metabolically produced excess H". In such cases, clinical treatment involves the intravenous administration of sodium bicarbonate to restore buffer capacity. 

Primary disturbances of plasma sodium cause a change in the plasma osmolality and this results in a redistribution of the body water. The opposite is true in that if there is a primary disturbance of water nietabolism, there is a subsequent disturbance of sodium metabolism. Thus water and sodium metabolism are closely linked. Nevertheless it is possible to identify certain conditions in which the primary disorder is one of sodium metabolism. 

Hypernatraemia is a feature of primary water depletion, although this must be distinguished from other causes of hypernatraemia due to disorders of sodium metabolism. 

Magnesium (Mg), the second intracellular cation after sodium, is a essential mineral. It is a critical cofactor in more than 300 enzymatic reactions. It may be required for substrate formation (Mg-ATP) and enzyme activation. It is critical for a great number of cellular functions, including oxidative phosphorylation, glycolysis, DNA transcription, and protein synthesis. It is involved in ion currents and membrane stabilization. Mg deficiency may be implicated in various metabolic disorders, including cardiovascular diseases, immune dysfunction and free radical damage. 

The metabolic component of mixed respiratory and metabolic alkalosis should be corrected by administering sodium and potassium chloride solutions. The respiratory component should be treated by readjusting the ventilator or by treating the underlying disorder causing hyperventilation. 

Pharmacology Lithium alters sodium transport in nerve and muscle cells, and effects a shift toward intraneuronal catecholamine metabolism. The specific mechanism in mania is unknown, but it affects neurotransmitters associated with affective disorders. Its antimanic effects may be the result of increases in norepinephrine reuptake and increased serotonin receptor sensitivity. Pharmacokinetics ... 

Several relatively common disorders result in aldosterone secretion abnormalities and aberrations of electrolyte status. In Addison s disease, the adrenal cortex is often destroyed through autoimmune processes. One of the effects is a lack of aldosterone secretion and decreased Na+ retention by the patient. In a typical Addison s disease patient, serum [Na+] and [CL] are 128 and 96 meq/L, respectively (see Table 16.2 for normal values). Potassium levels are elevated, 6 meq/L or higher, because the Na+ reabsorption system of the kidney, which is under aldosterone control, moves K+ into the urine just as it moves Na+ back into plasma. Thus, if more Na+ is excreted, more K+ is reabsorbed. Bicarbonate remains relatively normal. The opposite situation prevails in Cushing s disease, however, in which an overproduction of adrenocorticosteroids, especially cortisol, is present. Glucocorticoids have mild mineralocorticoid activities, but ACTH also increases aldosterone secretion. This may be caused by an oversecretion of ACTH by a tumor or by adrenal hyperplasia or tumors. Serum sodium in Cushing s disease is slightly elevated, [K+] is below normal (hypokalemia), and metabolic alkalosis is present. The patient is usually hypertensive. A more severe electrolyte abnormality is seen in Conn s syndrome or primary aldosteronism, usually caused by an adrenal tumor. Increased blood aldosterone levels result in the urinary loss of K+ and H+, retention of Na+ (hypernatremia), alkalosis, and profound hypertension. 

Cells throughout the gastrointestinal tract release somatostatin. Somatostatin inhibits acid secretion in the stomach and it promotes absorption of sodium, chloride and water in the small intestine and colon (Krejs 1986). The somatostatin analogs octreotide and lanreotide have been shown to decrease intestinal secretion in animal models (Botella et al 1993) and in humans with specific metabolic intestinal secretory disorders however, these drugs are not used widely in human medicine. In one study in horses, octreotide was shown to decrease gastric acidity (Sojka et al 1992) but its effects on intestinal or colonic secretion in horses have not been reported. 

Its U.SCS are the same as tho.se of levothyroxine sodium, including treatment of metabolic insufficiency, male infcnil-ity. and certain gynecological disorders. 

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