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Therapeutics > Potassium > Flashcards

Potassium Flashcards

1
Q

What is the most prevelant intracellular cation?

A

K

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2
Q

What is the intracellular concentration?

A

140

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3
Q

What is the normal serum level of K?

A

3.5-5

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4
Q

What is potassium required for?

A

cellular metabolism and growth, protein and glycogen synthesis

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5
Q

What does K determine?

A

the resting membrane potential across the cell membrane (cardiac conduction activity)

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6
Q

What determines the plasma potassium level?

A

relationship between K intake, GI and urinary excretion, hormones, acid base balance, and body fluid tonicity

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7
Q

What does insulin do to K?

How?

A

insulin increase uptake of K into the cell

it stimulates Na/K ATPase

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8
Q

What does NE do to K?

How?

A

increase uptake of K into the cell

stimulates Na/K ATPase

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9
Q

What does aldosterone do to K?

How?

A

promotes the excretion of K

through its effects on the Na/K ATPase in the collecting duct

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10
Q

What does an increase in K in the ECF do?

A

increases Angitensin II which stimulates Aldosterone

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11
Q

What role does PH play on K?

A

in metabolic acidosis, the cells uptake H, and push out K

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12
Q

Is the relationship between serum potassium and TBK linear?

How can you estimate?

A

no
a drop in 1 Meq/L (4-3) is equivalent to -200 to -400 in TBK, an increase in 1 Meq/L (3-4) is equivalent to 100-200 + in TBK

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13
Q

How is Hypokalemia defined?

A

decreased intake of K, increased movement into the cells, or most commonly increased losses from the urine, loss from GI or sweat

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14
Q

Give example of how hypokalemia can occur?

Give specific examples.

A

increase in extracellular Ph, icnreased insulin, , vomiting, diuretics, increased urinary loss in metabolic acidosis, polyuria

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15
Q

What are the most common causes of durg induced hypokalemia?

A

loop and thiazide

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16
Q

What are the 3 ways that drugs induce hypokalmia?

A

trancellular potassium shift, increased renal potassium loss, excess potassium loss in stool

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17
Q

Give examples of trancellular shifts?

A

B-adrenergic agonists, chlorquine, insulin overdose

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18
Q

Give examples of increased renal potassium loss?

A

diuretics, drugs associated with magnesium depletion

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19
Q

Give examples of potassium loss in stool?

A

phenolphthalein

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20
Q

What is the 2nd most common cause of hypokalemia?

A

GI loss of potassium rich fluids through vomiting and diarrhea

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21
Q

What percent of people also have hypomagnesia?

A

40%

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22
Q

What does hypokalemia do?

A

decreases intracellular potassium by impairing the function of the Na/K ATPase pump- promotes renal K wasting by unknown mechanism

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23
Q

When symptoms of hypokalemia occur how do they occur?

A

impairment of cardiovascular and/or muscular activity

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24
Q

What are 3 cardiac manifestations of hypokalemia?

A

hypertension, arrhythmias, ECG changes

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25
Q

What does hypertension lead to?

A

Na/H2O retention and IVF expansion

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26
Q

What are the 2 forms of oral potassium replacement?

What ist he best option?

A

tablet or liquid

encapsulated CR microencapsulated particles- (taste bad

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27
Q

When is potassium bicarbonate given?

A

in patients with hypokalemia and metabolic acidosis

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28
Q

When should you use potassium phosphate?

A

when there is a need for potassium and phosphate

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29
Q

What is generally preferred in the tx of hypokalemia?

Why?

A

potassium chloride

diarrhea and diuretics cause a loss of both potassium and chloride

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30
Q

Give examples of the oral potassium supplementation?

A

chloride, phosphate, and bicarbonate

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31
Q

Give examples of some of the neuromuscular manifestations.

A

muscle weakness, cramping, easy fatigability, myalgias

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32
Q

What are examples of the ECG changes?

A

ST-segment depression or flattening, T-wave inversion, and U-wave elevation

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33
Q

What arrhythmias are associated with hypokalemia?

A

bradycardia, heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, increased risk of digoxin toxicity

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34
Q

Who is at highest risk for Arrhythmias?

A

elderly patients with ischemic heart disease or CHF

35
Q

Which is more dangerous oral or IV K?

A

IV K

36
Q

When should IV be used?
What should it be mixed with?
It should not be mixed in what?

A

severe cases <2.5, patients exhibiting ECG changes, patients unalbe to tolerate oral therapy
0.9%, 0.45%
Dextrose

37
Q

How much K is added to each liter of fluid?

A

20-40 Meq

38
Q

What concentration can lead to pain and sclerosis of the peripheral vein?

A

60

39
Q

What should be done during K replacement?

A

monitor K rates and levels closely

40
Q

when is ECG monitoring required?

A

infusion rate exceeds 10 Meq/hour

41
Q

What concentrations should be given by a central line?

A

60 Meq/L

42
Q

give examples of good sources of K.

A

fruits, vegetables, and fruit juices

43
Q

Name 3 potassium sparing diuretics

What are they commonly given with?

A

amiloride, trimaterene, and spironolactone

K-wasting diuretics

44
Q

What type of diet leads to excessive K excretion?

A

high sodium

45
Q

How is K supplementation best administered orally?

A

divided doses, over several days

46
Q

What is usually sufficient dose to prevent hypokalemia?

A

20 Meq/L

47
Q

What is a sufficient dose of K to treat hypokalemia?

A

4-100 meq/l

48
Q

What is a range of mild hyperkalemia?

A

5.5-6

49
Q

What is a range of moderate hyperkalemia?

A

6.1-6.9

50
Q

What is severe hyperkalmeia?

A

> 7

51
Q

When does hyperkalemia develop?

A

when K intake exceeds excretion or when the

52
Q

When does increased K intake occur?

A

transcellular distribution of potassium is distributed

in renal insufficiency, these patients are non complient with dietary K restrictions

53
Q

Who has decreased K excretion?

A

patients with acute or CKD who are unable to excrete potassium

54
Q

What does digoxin do?

A

decreases the activity of na/K ATPase activity

55
Q

Which medications can casue transcellular potassium shifts?

A

Beta Blockers

56
Q

When does pseudohyperkalmeia occur?

A

in the setting of extravascular hemolysis of red blood cells

57
Q

When does efflux of potassium into the ECF occur?

A

in metabolic acidosis

58
Q

Which drugs interfere with tubular responsiveness to aldosterone?

A

K sparing diuretics, NSAIDs, ACE, ARB, trimethoprim, cyclosporine, heparin

59
Q

how does Heparin work?

A

decreases aldosterone synthesis

60
Q

How does Cyclosporine work?

A

decrease aldosterone synthesis, decrease Na/K ATPase, Decrease k channel activity

61
Q

How does trimethoprim work?

A

blocks na channels in the principle cells

62
Q

How do ACE and ARBs inhibit K excretion?

A

decrease aldosterone synthesis, decrease renal flow and renal GFR

63
Q

How do NSAIDS inhibit K excretion?

A

they decrease aldosterone synthesis, decrease renal flow and renal GFR

64
Q

How do K sparing diuretics prevent k excretion?

A

they block Na channels in the principle cells, aldosterone antagonism

65
Q

which medications interfere with the kidneys ability to excrete potassium?

A

K sparing diuretics, NSAIDs, ACE, ARB, trimethoprim, cyclosporine, heparin

66
Q

What do people with hyperkalemia often complain of?
What can be signs of severe muscle weakness?
What are example of ECG changes?

A

heart palpitations or skpped beats
electrocardiographic changes and severe muscle weakness
peaked T wave, widening of of the PR interval, loss of the P wave, widening of the QRS, and merging of the QRS with T wave

67
Q

What is Kayexalate?

What is it in?

A

a cation exchange resin, each gram exchanges 1 Meq of sodium for 1 Meq of potassium.
a sorbitol suspension which induces diarrhea

68
Q 
What is the usual dose of Kayexalate?
How often can it be repeated?
what is another option?
what is wrong with this?
which rout is preffered?
A 
15-60g
q 4-6 hours
the retention enema
it must be retained for 30-60 minutes
oral
69
Q

Why are diuretics administered for hyperkalemia?
What is the usual dose?
what is the onset of action?
What 2 things should be monitored?

A

to promote urinary excretion of K in patients with normal renal function
20-40 mg- titrate
4-6 hours
electrolytes and volume

70
Q

What is tx of hyperkalemia directed at?

A

antagonizing the membrane efects of k, drive K into the cells, remove excess potassium

71
Q

What are your options for removing K from the body?

A

Kayexylate and diuretics

72
Q

What can be used for antagonsim of membrane?

A

calcium gluconate

73
Q

Which calcium has the most Meq?

A

calcium chloride—tissue necrosis

74
Q

What should you monitor when you give calcium?

A

EC G findings

75
Q

What are 3 options for driving potassium back into the cell?

A

insulin and dextrose, sodium bicarbonate, B2 adrenergic agonist

76
Q

how does insulin drive K back into the cell?

A

insulin increases the activity of the Na/K ATPase pump in skeletal muscle

77
Q

When do you not need to give dextrose with the insulin?

why do you have glucose if it less?

A

when glucose is above >250

hypoglycemia

78
Q

How much does insulin therapy decrease K?

How long does it take to see effects?

A

0.5-1.5 in plasma potassium

15 min

79
Q

Why is sodium bicarb used to drive K back into the cell?

A

raising the systemic pH with sodium bicarbonate results in hydrogen release from the cells–K moves into the cell

80
Q

When is sodium bicarbonate preffered?

What is the dose of this?

A

in patients with metabolic acidosis

50-100 meq over 2-5 minutes- rpt q 30 min

81
Q

How does albuterol lower K?
Why is it not first line?
What is it reserved for?

A

stimulates na/K atp to promote intracellular uptake of K, and it stimulates B receptors to increase insulin secretion
poor response, tachycardia

82
Q

How is albuterol dosed?

when is the peak effect seen?

A

adjunctive therapy with insulin
10-20 mg in 4 ml of saline
90 min

83
Q

What is wrong with the drugs that move K into the cell?

A

they are transient, additional therapy required to remove K from the body

Therapeutics (8 decks)

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