Magnesium disorders Magnesium is an intracellular cation Plays

Magnesium disorders

�Magnesium is an intracellular cation �Plays an important role in the function of many enzymes, including the Na, K-ATPase �Regulates both potassium and calcium channels �It is to stabiliser of excitable cell membranes

�One-half of the 25 g (1000 mmol) of total body magnesium is located in bone �Almost all extraskeletal magnesium is present within cells �Because only 1% of body magnesium resides in the ECF, measurements of serum magnesium levels may not accurately reflect the level of total body magnesium stores

�Dietary magnesium content normally ranges from 6 to 15 mmol/d, of which 30– 40% is absorbed, mainly in the jejunum and ileum �Intestinal magnesium absorptive efficiency is stimulated by 1, 25(OH)2 D and can reach 70% during magnesium deprivation

�Plasma magnesium is freely filtered in the kidneys �About 70% is reabsorbed in the loop of Henle, & remaining in the proximal and distal tubules �Reabsorption is enhanced by parathyroid hormone (PTH)

Hypomagnesaemia �Plasma magnesium concentration below 1. 5 – 2. 0 meq/L Causes �Inadequate intake: Starvation, malnutrition (esp. alcoholism)

Excessive losses Gastrointestinal losses �Prolonged vomiting �Nasogastric aspiration �Chronic diarrhoea/laxative abuse �Malabsorption

Urinary losses �Diuretic therapy �Alcohol �Tubulotoxic drugs (gentamicin, cisplatin) �Volume expansion (Primary hyperaldosteronism) �Diabetic ketoacidosis �Post-obstructive diuresis �Recovery from acute tubular necrosis

Miscellaneous � Acute pancreatitis �Diabetes mellitus

�Hypomagnesaemia is frequently associated with hypocalcaemia �Magnesium is required for the normal secretion of PTH in response to a fall in serum calcium �Hypomagnesaemia induces resistance to PTH in bone

Clinical Manifestations �Mild to moderate magnesium deficiency is frequently asymptomatic �Manifestations of increased neuronal excitability are the most common symptoms, including paresthesias, tetany, and seizures �Coexistent hypokalemia is very common

�Cardiac disturbances may also occur and range in severity from mild electrocardiographic abnormalities (nonspecific T wave changes, U waves, prolonged QT interval, and repolarization alternans) to ventricular tachycardia, torsades de pointes, and ventricular fibrillation

Management �Treatment involves identification and correction of the cause where possible �Oral magnesium salts have limited effectiveness due to poor absorption and may cause diarrhoea

�When symptoms are present, treatment should be with intravenous magnesium chloride at a rate not exceeding 0. 5 mmol/kg in the first 24 hours �When intravenous access is not available, magnesium sulphate can be given intramuscularly

�If hypomagnesaemia is due to diuretic treatment, adjunctive use of a potassiumsparing agent will also reduce magnesium loss into the urine

Hypermagnesaemia �This is a much less common abnormality than hypomagnesaemia �The cause nearly always involves acute or chronic renal failure �Adrenocortical insufficiency also predisposes to magnesium retention

Clinical features �Bradycardia �Hypotension �Reduced consciousness �Respiratory depression

Management �Stop all magnesium intake �Improve renal function if possible �Promote urinary magnesium excretion using a loop diuretic with intravenous hydration �Calcium gluconate may be given intravenously to reverse overt cardiac effects

Phosphate disorders �Phosphorus has many critical roles �It is a major component of bone mineral, of phospholipids in cell membranes, and of nucleic acids �It forms high-energy phosphate bonds in compounds such as adenosine triphosphate (ATP) �Acts as a major p. H buffer in serum and urine

�Of the total body phosphorus content, 85% is in bone, 14% is in intracellular compartments, and only 1% is in extracellular fluid �The normal concentration of phosphorus in plasma is 3 to 4. 5 mg/d. L

�Phosphorus is present in many foods, including dairy products, meat, and grains, and is absorbed in the small intestine �The kidneys excrete excess phosphorus �Ninety percent of serum phosphate is filtered at the glomerulus, of which 80 to 97% is reabsorbed along the nephron, primarily in the proximal tubule

�Parathyroid hormone increases renal phosphate excretion whereas vitamin D enhances intestinal phosphate absorption

Hypophosphataemia Causes Redistribution into cells �Refeeding after starvation �Respiratory alkalosis �Treatment of diabetic ketoacidosis

Inadequate intake or absorption �Malnutrition, malabsorption �Chronic diarrhoea �Phosphate binders (antacids) �Vitamin D deficiency or resistance

Increased renal excretion �Hyperparathyroidism �ECF volume expansion with diuresis �Osmotic diuresis

Clinical manifestations �Phosphate depletion has widespread effects in tissue metabolism �Blood : impaires function and survival of all cell lines �Skeletal muscle : weakness, respiratory failure

�Cardiac muscle : congestive cardiac failure �Smooth muscle : ileus �CNS : decreased consciousness, seizures and coma �Bone : osteomalacia

Management �Oral phosphate supplements and highprotein/high-dairy dietary supplements which are rich in naturally occurring phosphate

Hyperphosphataemia Occures due to Phosphate accumulation Causes �Reduced excretion in acute or chronic renal failure & in hypoparathyroidism �Redistribution of phosphate from cells into the plasma in the ‘tumour lysis’ syndrome and in catabolic states

�The clinical features relate to hypocalcaemia and metastatic calcification, particularly in chronic renal failure �Management involves volume expansion with intravenous normal saline which promotes phosphate excretion if renal function is normal

�In the presence of renal failure, dietary phosphate restriction and the use of oral phosphate binders (such as calcium carbonate) are used

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