Jan9 M2-Potassium Pathophysiology Flashcards

1
Q

hyperK and hypoK effect on resting potential

A

hyperK: depol (resting potential more positive)
hypoK: hyperpol (resting potential more negative)

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2
Q

electrical effects of hyperK on the heart + ultimate effect (less or more excitable)

A
  • sustained gradual depolarization
  • inactivation of Na channels
  • *less excitable even though closer to threshold bc Na channels inactivated
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3
Q

hyperK on ECG (step by step)

A

peaked T wave, widened QRS, loss of P wave, sine wave, V fib

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4
Q

3 causes of hyperkalemia

A

impaired cell entry, increased cell release, reduced urinary excretion

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5
Q

key points in hyperK

A

almost all cases involve decreased GFR and are multifactorial

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6
Q

why can have hyperK in heart failure

A

volume contraction with decreased GFR

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7
Q

hormonal problem that can cause hyperK and 3 causes to that

A

hypoaldosteronism (1. primary adrenal insufficiency 2. ACEi 3. NSAIDs bc inhibit PGs’ effect on renin release)

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8
Q

drug that can cause hyperK

A

K sparing diuretics

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9
Q

can high K diet cause hyperK? yes no and why

A

no bc aldo turned on and K excreted normally

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10
Q

why does high K diet not cause high Na reabso

A

when euvolemic, RAAS is off (aldo is on because detects K but renin and therefore AT2 are off so AT2 doesn’t promote Na reabso at PCT)

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11
Q

hyperK cause related to not enough cell entry

A

insulin deficiency in hyperglycemia or uncontrolled diabetes

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12
Q

hyperK cause related to too much excretion from cells

A

rhabdomyolysis (muscle breakdown so K from these cells is released)

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13
Q

why can have false positive hyperK

A

when blood sample is hemolyzed (cells in it lysed)

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14
Q

history of patient with hyperK

A
  • ask for CKD!!! (GFR!!), diabetes, adrenal insufficiency

- drugs taken (ACEi, ARB, K-sparing like spironolactone)

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15
Q

labs in hyperK patient

A

Cr, urea (GFR!!), glucose, electrolytes, bicarb

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16
Q

important test to do in hyperK patient

A

ECG

17
Q

drugs that contribute to hyperK (4 types)

A
  • ACEi and ARBs
  • NSAIDs
  • cyclosporine (reduce renin release)
  • all K sparing (ENac blockers or MRAs)
18
Q

how diabetes affects renin release

A

reduced renin release

19
Q

symptoms of hyperK + what kind of arrhythmia

A

weakness, feeling faint, arrhythmia (brady)

20
Q

summary of 3 causes to hyperK

A
low GFR
low aldo (drug, adrenals)
K shift out (insulin, rhabdo)
21
Q

3 parts of hyperK treatment

A
  • protect the heart
  • shift the K in the cells
  • excrete the K
22
Q

hyperK treatment: how to protect the heart and when

A

if peaked T waves, give IV Ca gluconate. Ca increases AP threshold

23
Q

hyperK treatment: how to shift K in the cells (2)

A
  • IV D5W + insulin

- inhaled beta-2 agonist (salbutamol)

24
Q

hyperK treatment: how to excrete the K + this part of the treatment depends on what

A

oral K exchange resin (exchanges K with Ca)
loop diuretic if volume overloaded
NS if volume deplete

25
Q

other considerations in hyperK treatment (think of causes)

A

dietary review
control diabetes
stop the meds (ACEi, K-sparing diuretics, NSAIDs, etc.)

26
Q

does IV bicarb decrease K levels? what’s the basis for that

A

no. (but would think yes because H (out) K (in) exchanger in alpha intercalated cells would work less and keep more K out)

27
Q

if you’re on ACEi or ARB or NSAID, how much aldo secretion after K intake

A

some secretion bc adrenals react to K level

28
Q

channels stimulated by aldo (or synthesized to its effects)

A
  • ENac, ROMK and Na-K ATPase of principal

- H (out) K (in) ATPase exchanger in alpha int.

29
Q

ECG changes in hypoK

A

U wave formation, T wave flattening, arrhythmia but less than hyperK

30
Q

effect of hypoK on muscles

A

muscle weakness, cramping and pain (myalgias)

rhabdomyolysis and paralysis if severe

31
Q

most common cause of hypoK + other causes

A
  • diuretics (distal flow of Na increases K secretion)
  • high aldo
  • chemo (Fanconi Syndrome: less PCT reabso)
  • GI losses
  • black licorice (acts like aldo)
32
Q

hypoK symptoms

A

weakness or brady arrhythmia

33
Q

3 conditions or states where hypoK is caused by urinary loss (and increased distal Na flow)

A
  • primary hyperaldo
  • RAS
  • diuretics
34
Q

most common GI tract loss cause of hypoK and why

A

diarrhea (bc GI secretion with highest K)

35
Q

does alkalosis cause hypoK. (this question is different from ‘‘does bicarb reduce K’’) if yes how

A

yes. alkalosis: bicarbonaturia. bicarb enters the CCD cells and H (out) K (in) ATPase works less so that H stays inside with bicarb

36
Q

history in hypoK

A

hyperaldo? diuretics? diarrhea?

37
Q

how to differentiate between renal vs extra-renal K loss

A
  • if renal (urine K spot>15 and 24hr>30)

- if extra-renal (diarrhea): low urine K

38
Q

hypoK treatment

A

IV or oral replacement

39
Q

very important rule in K administration

A

for a serum deficit of 1 mM, there is a K deficit of 100-150 mM (in the body). (K conc in the ICW is 140 mM)