Magnesium Disorders Flashcards

1
Q

What are causes of decreased magnesium reabsorption

A

Volume expansion, hypercalcemia, hypophosphatemia, metabolic acidosis

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2
Q

What are causes of increased magnesium reabsorption

A

Volume depletion, hypocalcemia, metabolic alkalosis

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3
Q

Who is at high risk for hypomagnesemia

A

Malnutrition, alcoholism, CHF

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4
Q

Causes of hypomagnesemia d/t deficient intake, GI losses, renal losses, and redistribution

A

Deficient intake: ETOH, TPN
GI loss: Diarrhea, celiac, IBD, small bowel resection, PPI
Renal loss: loop diuretics, volume expansion, osmotic dieresis, tubular dysfunction
Redistribution: acute pancreatitis, hungry bone syndrome

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5
Q

Cardiovascular, neuro, and metabolic clinical manifestations of hypomagnesemia

A

Cards: torsades
Neuro: muscle weakness, tetany, seizures
Metabolic: hypokalemia, hypocalcemia

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6
Q

Management of hypomagnesemia including torsades

A

Torsades or v fib: 2g mag IV push with STAT CMP
Less urgent: Mag sulfate 1-4 grams, check K, po mag oxide 240-1600 QD-QID

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7
Q

Hypermagnesemia causes

A

Compromised renal function, enteral or TPN, massive mag intake, hypothyroidism, hyperparathyroidism, Addison’s disease, lithium treatment

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8
Q

Cardiovascular, GI, and neuro clinical manifestations of hypermagnesemia

A

Cards: hypotension, bradycardia, HB, asystole
GI: N/V, ileus
Neuro: hyperreflexia, flaccidity, skeletal muscle paralysis, respiratory muscle weakness/paralysis, lethargy, coma, urinary retention

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9
Q

Treatment plan of hypermagnesemia (asymptomatic, symptomatic, vs chronic RF)

A

Asymptomatic: no treatment, remove exogenous source, saline added, loop diuretics
Symptomatic: calcium gluconate 1g IV over 5 mins
Chronic RF: HD

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10
Q

Role of Phosphate in normal physiology

A

Skeletal integrity, energy economy, formation of high energy phosphate bonds, structure of nucleic acid, lipids, and proteins

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11
Q

Regulators of phosphate levels

A

Parathyroid hormone: increases excretion
Fibroblast growth factor: Increases excretion
Extracellular volume expansion
Acute hypercalcemia
Common diuretics

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12
Q

Redistribution causes of hypophosphatemia

A

Respiratory alkalosis, Sepsis, Rapid refeeding, leukemia, DKA, anorexia, alcoholism

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13
Q

Causes of increased excretion of hypophosphatemia

A

Primary hyperparathyroidism, extracellular volume expansion, diuretics

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14
Q

Causes of decreased absorption hypophosphatemia

A

Hyperparathyroidism, ethanol, glycosuria, phosphate binders, antacids, chronic diarrhea, chronic alcoholism

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15
Q

Hypophosphatemia clinical manifestations

A

Hemolysis
Rhabdo
Seizure
Coma

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16
Q

Treatment plan for hypophosphatemia including Prevention, Mild-mod, and Severe cases

A

Prevention: recognition and correction
Mild-mod (1.5): oral replacement via skim milk or sodium phosphate tabs
Severe (<1.5): IV phos replacement 2.5-5mg/kg over 6 hours, monitor ionized calcium

17
Q

What level is considered hyperphosphatemia

A

> 5.0

18
Q

What is hyperphosphatemia most commonly associated with

A

Renal dysfunction

19
Q

Redistribution causes of hyperphosphatemia

A

Tumor lysis syndrome, rhabdo, acute on chronic respiratory acidosis, acute pancreatitis, DKA, Lactic acidosis

20
Q

Increased intake causes of hyperphosphatemia

A

Laxatives in elderly
Parenteral phosphorous supplementation
Increased interstitial uptake of vitamin D with decreased PTH

21
Q

Clinical manifestations of hyperphostphatemia

A

Hypocalcemia
Ectopy
Increased anion gap

22
Q

Hyperphosphatemia treatment plan

A

Reduce phosphate intake <800mg/dl
Phosphate binders
Diamox
HD