1
Third stage
Medicine
Lec-1
د
.
عبدالحق
1/1/2014
Hypomagnesemia
Etiology:
(NR of Mg :0.8-1.0 mmol/L)
Intake Starvation Malnutrition esp Alcoholism&vomiting
Shift to Cells Insulin administration , Pancreatitis
Excretion (Renal)
Diuretics loop, Thiazide,
Tubulotoxic drugs aminoglycosides, cisplatinum, amphotericin
Post-obstructive diuresis, Post ATN ,
primary hypoaldosteronism(w hyponatremia &hyperkalemia)
Post-renal transplant
Bartter’s/Gitelman’s syndromes
GIT Loss
Prolonged vomiting chronic Diarrhea ,laxative abuse GI malabsorption
Hypomagnesemia: ClinicalEffects
Simulate features of Hypocalcemia (Mg needed for secretion &action of PTH on the bone)
Cardiovascular
Arrhythmia (prolonged QT)
Vasocostriction &Hypertention
Metabolic
Hypocalcemia is frequently associated with Hypomag.
occasionally Hypokalemia & Hyponatremia associated
Neurological
Tetany
Seizures
2
Hypomagnesemia: Treatment
Treat underlying cause
if Diuretics Contribute..
Then use K sparing diuretic
Oral Mg Salts : Mg-containing antacids
absorption usually poor S/E Diarrhea
Mg sulfate : can be given IM..also used in treating Eclamptic convulsions
Mg Cl : Intravenous (rate not exceed 0.5mmol/Kg in the first 24 hr)
Hypermagnesemia :Etiology ..
nearly always Acute or Chronic renal failure
(Mg retention) is the underlying cause ,other causes
INTAKE
Mg-containing antacids/laxatives, enema
Iatrogenic IV magnesium replacement
SHIFT
DKA
Tissue injury
Clinical Consequences
According to severity
Vasodilatation..Hypotention
Inhibition of cardiac conduction Bradycardia, CHB
Inhibition of neuromuscular transmission
Respiratary muscle depression
muscle paralysis
Treatment
Loop diuretic which promote excretion
IV calcium gluconate to reverse cardiac ill effects
Dialysis in renal failure
3
Phosphorous
*Normal (0.8-1.4 mmol/L)
*Intracellular mineral
*Essential to tissue oxygenation& movement of glucose into cells.
*imp.for normal CNS function
* maintenance of acid-base balance
*Influenced by parathyroid hormone
* assists in regulation of Ca& has inverse relationship to Calcium
Causes
Shift into cells: refeeding after starvation, Alkalosis
Decrease Intake or absorption from gut: Malabsorption, chr diarrhea ,Antacids containing
phosphate binder
Increase renal loss: effect of PTH in Hyperparathyroidism(PTH incr Ca &decr PO4 tubular
reabsorption,
Diuresis , Osmotic diuresis proximal tubular transport defect(fanconi s syndrome&familial
Hypophosphatemic rickets' in which there is phosphaturia
Clinical manifestations of Hypophosphatemia
Skeletal Muscles: weakness resp failure
Cardiac Muscle: congestive heart failure
Smooth muscles :ileus
CNS: Convulsion ,coma
Treatment Hypophosphatemia.
high protein/dairy Dietary supplements
Oral phosphate salt supp
In sever cases IV Potassium phosphate
4
Hyperphosphatemia
Causes:
usaully Acute or chr renal failure
PTH defeciency in Hypoparathyroidism
Tumor lysis syndrome &Catabolic states
Inaproppriete Vit D therapy
Clinically features related to the usually associated Hypocalcemia &renal failure
Treatment by phosphate restriction & use of oral phosphate biders like Calcium Carbonate.