Magnesium Flashcards

1
Q

How abundant is Mg?

A
  • 4th most abundant in body

- 2nd most abundant intracellular

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2
Q

How is Mg distributed in the body?

A
  • 53% in bone
  • 46% in muscle and soft tissue
  • <1% in serum and RBC’s
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3
Q

Mg ions in the serum

A
  • 33% bound to protein (mostly albumin)
  • 61% free (ionized- physiologically active)
  • 5% complexed w/ free ions
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4
Q

Name some roles of Mg

A
  • Essential cofactor for >300 enzymes
  • Transcellular ion transport
  • Synth of carbs, proteins, lipids and nucleic acids
  • Release of/response to hormones
  • Neuromuscular transmission, muscle contration, metabolic function
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5
Q

How is Mg obtained?

A

Dietary:
- Rich; raw nuts, dry cereal, “hard” water
- Other: beggies, meat, fish, fruit
NOTE: processed foods are low

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6
Q

Which organ is responsible for Mg regulation?

A
  • By kidneys
  • Renal threshold; 0.60-0.85
  • Non-protein bound is filtered by glomerulus (25-30% reabsorbed in PCT, 2-5% in DCT, 50-60% reabsorbed in loop of henle
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7
Q

What hormones play a part in regulation of Mg?

A

(Related to Ca+Na regulation)

  • PTH (increases renal absorption along with Ca; enhances absorption in the intestines
  • Aldosterone and thyroxine (increase renal excretion)
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8
Q

When is hypomagnesemia most common?

A

In hospitalized patients (ICU, diuretic therapy, digitalis therapy(heart conditions))

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9
Q

Name symptoms of hypomagnesemia

A

< 0.5mmol/L:
- Cardiovascular and neuromuscular (faulty ATPase pump)
- Neuromuscular (Ca uptake after muscle contraction and reg of acetylcholine impaired-weakness, tremors, tetany, paralysis, coma)
- Psychiatric (depression, psychosis)
- Metabolic (impairs PTH release/target tissue response)
NOTE: strong association w/ hypokalemia, hyponatremia, hypophosphatemia

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10
Q

How is hypomagnesemia treated?

A
Usually orally (Mg lactate, Mg oxide, MgCl2 Mg-containing antacid
- Severely ill: parenteral (npo) MgSO4 solution

Mg treatment alone may fix other hypos.

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11
Q

When is hypermagnesemia seen?

A

Most common in renal failure
Most severe: decreased renal func + increased intake of antacids, enemas or cathartics
Pseudo- due to dehydration

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12
Q

When is MgSO4 used theraputically?

A
  • Cardiac arrhythmia and myocardial infarction
  • Antacids, enemas, cathartics
  • Preeclampsia; decreases hyperactivity, increases uterine blood flow, neonatal hypermagnesemia may occur due to immature kidneys
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13
Q

Name symptoms of mild to moderate/ critical hypermagnesemia

A

MM- hypotension, bradycardia, skin flushing, nausea

Crit- ECG cahnges, aystole (flat line), coma, respiratory depression/arrest, paralysis

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14
Q

Other symptoms of hypermagnesemia

A
  • May inhibit PTH release (hypocalcemia, hypercalcuria)

- Hemostasis inhibited due to competition b/w increased MG and Ca

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15
Q

Treatment of hypermagnesemia

A
  • Discontinue source of Mg (increased intake)
  • Immediate supportive therapy for severe
  • Diuretics and IV fluid if normal renal func
  • Hemodialysis with renal failure
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16
Q

What specimen is required?

A
  • Serum/lithium heparin plasma

- Urine: 24hr (diurnal variation) w/ HCl to avoid precipitation.

17
Q

Why do we avoid hemolysis with Mg testing?

A

Intracellular [ ] is 10x extracellular, separate ASAP

18
Q

Method for Mg measurement?

A
  • Reference method: AAS
  • Colorimetric:
    1. Calmagite (reddish violet, 532nm)
    2. Formazen (blue-green, 660nm)
    3. Methylthymol blue (colour
    Note: use chelator (calcium shelter) to prevent interference
19
Q

Which method do we use?

A

Calmagite at 520nm

20
Q

Measuring total Mg what do we miss out on?

A
  • Intracellular
  • The physiologically active Mg (free ionized Mg)
    Note: Serum [ ] cannot reflect status of intracellular Mg
21
Q

Mg reference ranges

A

Serum: 0.63-1.00
24hr urine: 3.0-4.3

Critical: <0.50 >2.00
(possible exception for preeclampsia)