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Therapeutics I > Block 4: K+ and Mg2+ > Flashcards

Block 4: K+ and Mg2+ Flashcards

1
Q

What is the most abundant IC electrolyte?

A

Potassium

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2
Q

What are the functions of K+?

A
  1. Regulates osmolarity of ICF (balanced with H+)
  2. Maintains action potential
  3. Buffers blood pH
  4. Facilitates glycogen storage in liver and skeletal muscle cell
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3
Q

How does inulin affect K?

A
  1. Insulin shifts K into the cell
  2. Low K affects insulin production
  3. Insulin enable the cell to uptake glucose and glycogenesis
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4
Q

What does K/H exchanger do?

A

Shift H into the cell and K outward

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5
Q

What are the normal values of K?

A

3.5-5 mEq/L

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6
Q

What is the relationship between serum K and aldosterone?

A

Indirect, aldosterone increases K excretion and Na intracellularly

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7
Q

What should you check if serum K is low?

A

Mg2+

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8
Q

What causes hyperkalemia?

A
  1. Increased intake
  2. Decreased excretion
  3. Renal dysfunction
  4. Cellular shifts
  5. Insulin def
  6. Tissue catabolism
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9
Q

What kind of drugs cause hyperkalemia?

A
  1. K sparing
  2. ACEi/ARBs
  3. NSAIDs
  4. B blockers
  5. Digoxin
  6. Cyclosporine
  7. Tacrolimus
  8. Bactrim
  9. Heparin
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10
Q

What are the presentations of hyperK?

A
  1. EKG changes
  2. Cardiac arrhythmias
  3. Heart palpitations or skipped heartbeats
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11
Q

What are the levels of hyperkalemia?

A

Mild: 5.1-5.9 (asymptomatic)
Moderate: 6-7
Severe: >7 (palpitations)

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12
Q

What are the treatment for hyperkalemia?

A
  1. Dietary mod
  2. Adjustment of contributing med
  3. Furosemide 40-80 mg IV (↑ excretion)
  4. Potassium binders
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13
Q

What are the K binders?

A

SPS (Kayexalate)
Patiromer calcium (Veltassa)
Sodium zirconium cyclosillicate (Lokelma)

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14
Q

What K binders are used for emergency?

A

SPS and Sodium zirconium cyclosilicate (Lokelma)

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15
Q

What K binders exchange sodium for K+?

A

SPS and Lokelma

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16
Q

What are the MOA for K binders?

A

↑ fecal K elimination

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17
Q

What are the similarities of all K binders?

A

Treat chronic hyperK

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18
Q

What K binders must be separtared from other meds 3 hr before and after admin?

A

Veltassa and SPS

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19
Q

What are the ADRs of SPS? Indication?

A

Intestinal necrosis with rectal admin

For acute hyperK

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20
Q

How does patiromer differ from other K binders?

A

Exchanges Ca for K
Delayed onset of 48 hr

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21
Q

How should you take Lokelma?

A

Separate other meds by 2 hours pre and post

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22
Q

What are the steps of acute and symptomatic hyperK?

A
  1. Check if EKG is abnormal
  2. Redistribution and intracellular K+ shift
  3. Eliminate K+ from body
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23
Q

What do you do about the ECG in hyperK?

A

Abnormal: 1g IV calcium gluconate

If normal don’t give IV calcium

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24
Q

How do you redistribute K?

A
  1. Regular insulin 10 u IV + 25 g dextrose unless BG >250
  2. 50-100mEq IV sodium bicarbonate if pH <7.3
  3. Albuterol nebulizer 10-20 mg over 10 min if no IV access
  4. Just use insulin if hyperglycemic
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25
Q

How should you eliminate K from the body?

A
  1. SPS 15-30 g PO
  2. IV loop diuretic if making urine
  3. Hemodialysis for CKD or life-threatening
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26
Q

When would albuterol be used for hyperkalemia?

A
  1. Tachycardia present
  2. Not effective
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27
Q

What is hypokalemia?

A

<3,5

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28
Q

What causes hypoK?

A
  1. GI/renal losses
  2. Intracellular shifts (metabolic alkalosis)
  3. Hypomagnesemia
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29
Q

What drugs cause hypokalemia?

A
  1. Loops
  2. Thiazides
  3. Beta blockers
  4. Laxatives
  5. Insulin
  6. Sodium bicard
  7. K binders
30
Q

What are the presentations and tx of mild hypoK?

A

3.1-3.5
Asymptomatic

↑ dietary intake

31
Q

What are the presentations and tx of moderate hypoK?

A

2.5-3

Cramping, weakness, malaise, myalgia

PO K

32
Q

What are the presentations and tx of severe hypoK?

A

<2.5

ECG changes and arrhythmias

33
Q

When do you start chronic supplementation of hypoK?

A
  1. underlying conditions
  2. Arrhythmia risk
  3. Concomitant meds
34
Q

What is the treatment goalsof hypoK?

A

K<3 mEq/L requires treatment with goal K 4-4.5 mEq/L

35
Q

What are the IV K salts?

A
  1. Chloride (for alkalosis)
    2, Acetate (for acidosis)
  2. Phosphate (for low P)
36
Q

What are PO K salts?

A
  1. Chloride (for alkalosis)
  2. Phosphate (for low P)
  3. Bicarbonate (for acidosis)
37
Q

What are the the K-sparing diuretics?

A
  1. Spironolacotone
  2. Triamterene
  3. Amiloride

Use add on with loops or thiazides

38
Q

How do you dose IV/PO K?

A

1.Each 10 mEq od K will ↑ Serum K bu 0.1
2. ((4-K)/sCr)x100

Round to the nearest 10 mEq

39
Q

How should IV K be given?

A

Diluted in NS is preferred

Administer via central line if >20mEq/100mL

Cardiac monitoring is admin >10 mEq/hr

40
Q

What are the infusion rate of IV K?

A

Peripheral: 10 mEq/hr
Central: 20 mEq/hr

41
Q

ADRs of IV K?

A

Burning (reduce rate)

42
Q

What is the reasons for poor adherence of PO K?

A

Large tablets and GI intolerance

43
Q

How do you administer PO K?

A

Lower and more frequent doses

Microencapsulated tablets

44
Q

What are the KCl dosage forms?

A
  1. CR microencapsulated tabs (Kdur)
  2. Elixer
  3. Effervescent tabs
  4. Wax-matrix ER tabs (Klor-Con)
45
Q

What KCl has the best GI tolerability?

A

CR microencapsulated tabs (Kdur)

46
Q

What Kcl is rapid acting?

A

Elixer

47
Q

What KCl is easy to swallow however cause more GI erosion?

A

Wax-matrix ER tabs (Klor-Con)

48
Q

What KCl is more expensive?

A

Effervescent tabs

49
Q

What are K bicarb and citrate used for?

A

Acid/base disorders

50
Q

How do you manage K when taking other drugs?

A

Daily supplant for thiazides and loops to prevent hypokalemia

K-sparing can be added to counteract depletion

51
Q

What is the most common K formulation?

A

Chloride

52
Q

What is the 2nd most abundant electrolyte in ICF?

A

Mg

53
Q

What is most Mg found? How is it eliminated?

A

bone

Renal

54
Q

What are the functions of Mg?

A
  1. Mg helps K absorption
  2. Helps Ca absorption, however, Ca inhibits Mg absorption
  3. Cofactor in reactions dependent on ATP
  4. Regulate PTH
  5. Regulates glucose metabolism
55
Q

What is hypermagnesiem?

A

> 2.4 mg/dL

56
Q

What causes hyperMg?

A
  1. Renal failure
  2. Drugs (Mg citrate and supplements)
57
Q

What are the presentations of hyperMg?

A
  1. Muscle weakness
  2. Shallow respirations
  3. Arrhythmias
  4. Symptoms rare when <4.9
58
Q

What are primary treatments for hyperMg?

A
  1. Reduce intake
  2. Enhance elimination
  3. Antagonize physiologic effects
59
Q

What are the treatment options for hyperK?

A
  1. IV potassium
  2. PO potassium
  3. K sparing diuretics
60
Q

What do we use to treat hyperMg?

A
  1. Calcium gluconate 2g IVP until symptoms abate
  2. 0.45% NaCl + Loop diuretic
  3. hemodialysis
61
Q

What are the characteristic of calcium gluconate with hyperMg?

A
  1. May repeat Q1H prn
  2. Antagonizes effects
  3. PO calcium has porr F and slow onset
62
Q

Why is 0.45% NaCl + Loop diuretic used as a combo for hyperMg?

A
  1. Enhances elimination
  2. In patients with normal renal function or CKD 1-3
  3. Onset 6-12H
63
Q

When is hemodialysis used for hyperMg?

A
  1. Enhances elimination
  2. Onset 4H
64
Q

What are the causes of hypomagnesemia?

A
  1. Impaired absorption
  2. Increased excretion
  3. Alcoholism
  4. Diuretics, laxatives, PPIs
65
Q

What are the presentations of hypoMg?

A

<1.5
1. Muscle weakness, paralysis
2. QT prolongation/arrhythmias
3. Hypokalemia
4. Hypocalcemia

Symptoms until <1 mg/dL

66
Q

How and when do you dose IV Mg sulfate?

A

If Mg <1.2 mg/dL OR s/s present
Diluted in IVF
Dosing: 4-6 grams in 2-3 divided doses (Max infusion rate < 150 mg/min )

1g=8mEq

67
Q

ADRs of IV mag?

A

Hypocalcemia

68
Q

How and when do you dose PO Mg sulfate?

A

If Mg >1.2 mg/dL and asymptomatic

1-2 tabs PO BID-TID

69
Q

What are the salt forms of PO mg?

A

Oxide, gluconate, chloride

70
Q

ADR of PO Mg?

A

Diarrhea

SR products improve compliance and reduce GI effects

71
Q

Describe PO Mg replacements?

A
72
Q
A

Therapeutics I (32 decks)

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