Magnesium Flashcards

1
Q

What is the function of Magnesium Metabolism?

A

After K+ is most abundant intracellular cation.Within cells Mg is co-factor in over 300 enzymatic reactions

  • Energy metabolism
  • Calcium & potassium channels
  • Membrane stabilisation & neuromuscular excitability
  • Protein & nucleic acid synthesis
  • Oxidative phosphorylation
  • Particular importance in formation & utilisation of ATP
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2
Q

What is the ranges for Plasma Magnesium?

A

0.7 – 1.0 mmol / L

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3
Q

What are plasma magnesium levels with in the blood?

A
  • Less than 0.5% of total body Mg is in plasma
  • 60% ionized form
  • 15% complexed (phosphate, citrate or bicarbonate)
  • 25% protein bound

Various forms can be effected by protein concentration & pH

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4
Q

What is involved in Magnesium Homeostasis?

A
  • Daily intake ranges from 6-20 mmol/day
  • Green vegetables, hard water. Absorption in small bowel by active transport & passive diffusion
  • Between 3-5% of filtered Mg appears in the urine. Evidence that kidneys can conserve Mg excretion when Mg is low
  • Also intestinal adaptation when Mg is low
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5
Q

How is Magnesium managed by the kidneys?

A
  • Non–protein bound Mg2+ is filtered freely at the glomerulus, and the approximate percentages of filtered Mg2+ absorbed at different locations are shown.
  • Under most physiologic conditions, about 10% of filtered Mg2+ is excreted.
  • Final regulatory segment, the DCT, controls approximately 5% of filtered Mg2+, 25% in PCT and 60% in Loop of Henle
  • Mg2+ is transported by both the paracellular and transcellular pathways.
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6
Q

What are some congenital causes of magnesium disorders?

A
  • Mutations in paracellin-1 and claudin-19 are involved in familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC).
  • Mutations in TRPM6 are involved in HSH.
  • Mutations in NaCl cotransporter are involved in Gitelman syndrome,
  • Mutations in the γ subunit of Na,K-ATPase are involved in autosomal dominant renal hypomagnesemia with hypocalciuria (ADRHH).
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7
Q

How are Mg and PTH related?

A
  • Mg required for PTH release and action
  • Mg can regulate PTH secretion in a manner similar to calcium but much less potent.
  • PTH stimulated by modest hypoMg and suppressed by hyperMg
  • Profound hypoMg inhibits PTH release
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8
Q

What are symptoms of Hypomagnesaemia?

A
  • Neuromuscular excitability with tetany and seizures
  • Hypocalcaemic
  • Anorexia & nausea
  • Tremour
  • Apathy
  • Depression, agitation & confusion
  • Hypokalaemic
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9
Q

What cardiac effects of hypomagnesaemia?

A
  • Striking relationship between moderate hypomagnesaemia and dysrhythmias
  • Reduced levels of ATPase activity, loss of intracellular potassium and subsequent urinary loss
  • Ratio of intra to extracellular is reduced so increased electrical excitability
  • Some drug therapies for dysrhythmias are less responsive if patient hypomagnesaemic
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10
Q

What are causes of hypomagnesaemia?

A
  • Inadequate intake (Alcoholism, Protein Calorie Malnurition, Prologed Infusion or ingstion of low Mg diet)
  • Malabsorption (Inflammatory bowel disease, Gluten enteropathy, Intestinal bypass, Radiation enteritis, Familial primary hypomagnesaemia)
  • Intracellular shift (Post MI, Recovery from DKA, Refeeding syndrome, Acute pancreatitis)
  • Renal tubular dysfunction
  • Drugs (Proton Pump Inhibitors, Nephrotoxic drugs (amphotericin, cisplatin, laxatives), Diuretic (non-potassium sparing))
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11
Q

What are conditions that benefit from magnesium supplementation?

A
  • Acute myocardial infarction with: (recurrent ventricular fibrillation, recurrent ventricular tachycardia, complex ventricular tachycardia, supraventricular tachycardia)
  • Digoxin intoxication with arrhythmia
  • Torsades de pointes
  • Low K+ unresponsive to K+ supplementation
  • Low Ca++ unresponsive to Ca++ supplementation
  • Diuretic therapy
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12
Q

What types of patients do you expect to have hypomagnesaemia?

A
  • Alcoholics
  • Low Calcium
  • Low Potassium
  • Nutritionally Compromised
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13
Q

What is refeeding syndrome?

A
  • Chronic starvation leads to prolonged deficiency,
  • Upon Calorie provision on feeding there is Insulin secretion
  • This leads to synthesis of glycogen / fat / protein using Mg/ K/ PO4 and secretion drives Mg, K and PO4 in to cells
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14
Q

What are causes of Hypermagnesaemia?

A

Usually only a problem in patients with kidney failure.

Iatrogenic

  • Oral (generally + CRF) – i.e. laxatives, antacids
  • Rectal - purgation
  • Parenterally (Pre-eclampsia, Treatment of magnesium deficiency)

Renal failure

  • Chronic (& admin Mg) – antacids, cathartic, enema, infusion, dialysis
  • Acute - rhabdomyolysis
  • Cardiac surgery
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15
Q

What are symptoms of the Hypermagnesaemia?

A
  • Asymptomatic up to 1.5 -2.5 mmol/L
  • >2.5 mmol/L – areflexia, ECG changes (prolonged PR and QRS interval, peaked T waves)
  • Higher levels – respiratory paralysis & cardiac arrest
  • At very high levels Mg blocks acetylcholine release causing peripheral blockade
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16
Q

How is Hypermagnesaemia treated?

A
  • Stop I.V administration

  • I.V calcium gluconate
  • Dialysis
17
Q

How is Hypomagnesaemia treated?

A
  • Oral supplement Magnaspartate - Each 6.5g sachet of Magnaspartate® contains magnesium-L-aspartate 10 mmol of magnesium
  • Mg sulphate IV in a litre of 5% dextrose or saline 0.9% over 24 hours. May reduce the dose in renal impairment