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
What does hypertension lead to?
Na/H2O retention and IVF expansion
26
What are the 2 forms of oral potassium replacement? | What ist he best option?
tablet or liquid | encapsulated CR microencapsulated particles- (taste bad
27
When is potassium bicarbonate given?
in patients with hypokalemia and metabolic acidosis
28
When should you use potassium phosphate?
when there is a need for potassium and phosphate
29
What is generally preferred in the tx of hypokalemia? | Why?
potassium chloride | diarrhea and diuretics cause a loss of both potassium and chloride
30
Give examples of the oral potassium supplementation?
chloride, phosphate, and bicarbonate
31
Give examples of some of the neuromuscular manifestations.
muscle weakness, cramping, easy fatigability, myalgias
32
What are examples of the ECG changes?
ST-segment depression or flattening, T-wave inversion, and U-wave elevation
33
What arrhythmias are associated with hypokalemia?
bradycardia, heart block, atrial flutter, paroxysmal atrial tachycardia, ventricular fibrillation, increased risk of digoxin toxicity
34
Who is at highest risk for Arrhythmias?
elderly patients with ischemic heart disease or CHF
35
Which is more dangerous oral or IV K?
IV K
36
When should IV be used? What should it be mixed with? It should not be mixed in what?
severe cases <2.5, patients exhibiting ECG changes, patients unalbe to tolerate oral therapy 0.9%, 0.45% Dextrose
37
How much K is added to each liter of fluid?
20-40 Meq
38
What concentration can lead to pain and sclerosis of the peripheral vein?
60
39
What should be done during K replacement?
monitor K rates and levels closely
40
when is ECG monitoring required?
infusion rate exceeds 10 Meq/hour
41
What concentrations should be given by a central line?
60 Meq/L
42
give examples of good sources of K.
fruits, vegetables, and fruit juices
43
Name 3 potassium sparing diuretics | What are they commonly given with?
amiloride, trimaterene, and spironolactone | K-wasting diuretics
44
What type of diet leads to excessive K excretion?
high sodium
45
How is K supplementation best administered orally?
divided doses, over several days
46
What is usually sufficient dose to prevent hypokalemia?
20 Meq/L
47
What is a sufficient dose of K to treat hypokalemia?
4-100 meq/l
48
What is a range of mild hyperkalemia?
5.5-6
49
What is a range of moderate hyperkalemia?
6.1-6.9
50
What is severe hyperkalmeia?
>7
51
When does hyperkalemia develop?
when K intake exceeds excretion or when the
52
When does increased K intake occur?
transcellular distribution of potassium is distributed | in renal insufficiency, these patients are non complient with dietary K restrictions
53
Who has decreased K excretion?
patients with acute or CKD who are unable to excrete potassium
54
What does digoxin do?
decreases the activity of na/K ATPase activity
55
Which medications can casue transcellular potassium shifts?
Beta Blockers
56
When does pseudohyperkalmeia occur?
in the setting of extravascular hemolysis of red blood cells
57
When does efflux of potassium into the ECF occur?
in metabolic acidosis
58
Which drugs interfere with tubular responsiveness to aldosterone?
K sparing diuretics, NSAIDs, ACE, ARB, trimethoprim, cyclosporine, heparin
59
how does Heparin work?
decreases aldosterone synthesis
60
How does Cyclosporine work?
decrease aldosterone synthesis, decrease Na/K ATPase, Decrease k channel activity
61
How does trimethoprim work?
blocks na channels in the principle cells
62
How do ACE and ARBs inhibit K excretion?
decrease aldosterone synthesis, decrease renal flow and renal GFR
63
How do NSAIDS inhibit K excretion?
they decrease aldosterone synthesis, decrease renal flow and renal GFR
64
How do K sparing diuretics prevent k excretion?
they block Na channels in the principle cells, aldosterone antagonism
65
which medications interfere with the kidneys ability to excrete potassium?
K sparing diuretics, NSAIDs, ACE, ARB, trimethoprim, cyclosporine, heparin
66
What do people with hyperkalemia often complain of? What can be signs of severe muscle weakness? What are example of ECG changes?
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
What is Kayexalate? | What is it in?
a cation exchange resin, each gram exchanges 1 Meq of sodium for 1 Meq of potassium. a sorbitol suspension which induces diarrhea
68
``` 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? ```
``` 15-60g q 4-6 hours the retention enema it must be retained for 30-60 minutes oral ```
69
Why are diuretics administered for hyperkalemia? What is the usual dose? what is the onset of action? What 2 things should be monitored?
to promote urinary excretion of K in patients with normal renal function 20-40 mg- titrate 4-6 hours electrolytes and volume
70
What is tx of hyperkalemia directed at?
antagonizing the membrane efects of k, drive K into the cells, remove excess potassium
71
What are your options for removing K from the body?
Kayexylate and diuretics
72
What can be used for antagonsim of membrane?
calcium gluconate
73
Which calcium has the most Meq?
calcium chloride---tissue necrosis
74
What should you monitor when you give calcium?
EC G findings
75
What are 3 options for driving potassium back into the cell?
insulin and dextrose, sodium bicarbonate, B2 adrenergic agonist
76
how does insulin drive K back into the cell?
insulin increases the activity of the Na/K ATPase pump in skeletal muscle
77
When do you not need to give dextrose with the insulin? | why do you have glucose if it less?
when glucose is above >250 | hypoglycemia
78
How much does insulin therapy decrease K? | How long does it take to see effects?
0.5-1.5 in plasma potassium | 15 min
79
Why is sodium bicarb used to drive K back into the cell?
raising the systemic pH with sodium bicarbonate results in hydrogen release from the cells--K moves into the cell
80
When is sodium bicarbonate preffered? | What is the dose of this?
in patients with metabolic acidosis | 50-100 meq over 2-5 minutes- rpt q 30 min
81
How does albuterol lower K? Why is it not first line? What is it reserved for?
stimulates na/K atp to promote intracellular uptake of K, and it stimulates B receptors to increase insulin secretion poor response, tachycardia
82
How is albuterol dosed? | when is the peak effect seen?
adjunctive therapy with insulin 10-20 mg in 4 ml of saline 90 min
83
What is wrong with the drugs that move K into the cell?
they are transient, additional therapy required to remove K from the body