Magnesium Flashcards

1
Q

What is the 4th most abundent cation in the body?

A

Magnesium

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2
Q

How often can you repeat doses of calcium?

A

every hour

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3
Q

What is the clinical effect like?

A

immediate, but transient

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4
Q

What does IV calcium do?

A

it directly antagonizes the NM and CV effects of hypermagnesemia

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5
Q

How do you treat a patient with severe hypermagnesemia?

A

with IV calcium

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6
Q

How can most cases of hypermagnesemia be anticipated?

A

renal failure patients should not be given mg meds, parenteral mg should be monitored

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7
Q

When do you see muscle paralysis, respiratory paralysis, cardiac arrest?

A

above 10

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8
Q

When do you see bradycardia, ecg changes, hypotension?

A

10-Jun

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9
Q

When do you see drowsiness, flushing and headache?

A

mg- 4-6

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10
Q

What 3 symptoms can be seen if potassium exceeeds 4 meq/L?

A

NM, CV, hypocalcemia

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11
Q

How can mild hypermagnesemia occur?

A

hyperparathyroidism, hypothyrodism, diabetic ketoacidosis, tumor lysis syndrome, theophylline intoxication, lithium ingestion, dead sea water poisoning

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12
Q

Where is the magnesium absorbed with magnesium enemas?

A

in the large bowel

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13
Q

Other than giving a massive dose, how else can mg be increased orally?
Give an example of these disorders

A

by a GI disorder that enhances magnesium absorption

ulcer disease, gastritis, colitis

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14
Q

What Is the 2nd most prevalent intracellular cation?

A

Magnesium

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15
Q

What are two ways patients can be given exogenous magnesium?

A

laxatives and antacids

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16
Q

What is the level for patient with end stage renal disease?

A

2.4-3.6

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17
Q

What is considered hypermagnesemia?

When is this usually seen?

A

> 2.1

impaired renal function, large doses of magnesium given iv, orally or as an enema

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18
Q

What can larger doses of mg precipitate?

A

diarrhea which exacerbates hypomagnesemia

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19
Q

When should IM be used?

How should they be diluted?

A

only if IV is limited access and severe hypomagnesemia

20% before injection to prevent venous sclerosis and pain

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20
Q

What is the IV bolus administration associated with?

A

flushing, sweating, and sensation of warmth

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21
Q

How much should you use for non life threatening?

A

1 Meq/kg

22
Q

How much should you use for life threatening symptoms?

A

2g MgSO4

23
Q

What does magnesium replacement depend on?

A

the severity of the clinical manifestation

24
Q

give examples of NM?

A

weakness, seizures, tetany, coma, depression, tremor, spasm

25
Q

Why is magnesium important?

A

it is a cofactor required for nearly all biochemical and enzyme systems

26
Q

What are the dominant organ systems involved in hypomagnesemia?

A

NM nad CV

27
Q

What is symptomatic hypomagnesemia often associated with?

A

multiple electrolyte abnormalitites including hypokalemia, hypocalcemia, and metabolic alkalosis

28
Q

What do nephrotoxins do?

Which medications are included in this?

A

produce urinary magnesium wasting

aminoglycosides, antibiotics, cisplatin, amphotericin B, cyclosporine, foscarnet, tacrolimus, and pentamidine

29
Q

What does hypovolemia do?

A

stimulates proximal sodium, water, and magnesium reabsorption

30
Q

What are examples of diuretics?

How do they do this?

A

loop and thiazide diuretics

inhibit mg reabsorption, produce mild hypomagnesemia

31
Q

Name two classes of drugs that can cause mg loss?

A

diuretics, and nephrotoxins

32
Q

What is one other way mg can be lost?

A

drugs

33
Q

What are examples of hormone induced renal loss?

A

hyperparathyroidism, hyperthyroidism, aldosteronism, hungry bone syndrome

34
Q

What are examples of tubular disorders?

A

postobstructive diuresis, renal tubular acidosis, Bartters syndome, primary renal magnesium wasting, glomeruloneprhitis

35
Q

What reactions is it involved in?

A

transfer of phophate groups, all reactions that require ATP, replication and transcription of DNA and the translation of mRNA

36
Q

How man Meq does a 70-kg adult have of Mg?

A

2000

37
Q

What are the two groups of renal losses?

A

primary tubule disorders, hormone induced renal losses

38
Q

give examples of GI losses?

A

prolonged nasogastric suctionling, acute and chronic diarrhea, malabsorption syndromes, extensive bowel resection, alcoholism, intestinal fistule, malabsorption,

39
Q

What are the 2 major mechanisms by which hypomagnesemia can be induced?

A

gastrointestinal or renal losses

40
Q

Where does hypomagnesemia occur commonly?

A

in inpatient settings

41
Q

What is classified as hypomagnesemia?

A

<1.4 Meq/L

42
Q

what does hypomagnesemia do?

A

stimulates transport

43
Q

How much is in the bone?

A

50-60%

44
Q

How much of extracellular magnesium accounts for the total body magnesium?

A

1%

45
Q

What does hypermagnesemia do

A

inhibits loop transport

46
Q

what is a major regulator of magnesium reabsorption?

A

the plasma concentration

47
Q

Where does 15-25% of magneisum get reabsorbed?

A

in the proximal tubule

48
Q

where does 60-70% of magnesium get absorbed?

A

in the thick ascending loop of henle

49
Q

Where is homeostasis regulated?

A

in the kidney through glomerular filtration and reabsorption

50
Q

How much of the ingested magnesium is absorbed in the small bowel?

A

30-40%

51
Q

What does magnesium balance depend on?

A

GI absorption and renal excretion

52
Q

What are the normal serum magnesium concentrations?

A

1.4-2.1 meq/L