Potassium Flashcards

0
Q

N/K ATPase

A

stimulated by insulin, aldosterone, and B agonists

pumps K into cells

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1
Q

where is K reabsorbed first

A

Ascending LOH by Na/K/2Cl

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2
Q

first line tx in hyperkalrmia

A

inject Ca2+

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3
Q

medications that cause hyperkalemia

A

k sparing diuretics
NSAIDs via 1) direct tubular damage (interstital nephritis)–>TG feedback–>dec renin production 2) blocks PG–>vascon on afferent arterial–>ischemia and dec tubular flow–>dec gradient
cyclosporine
bactrim

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4
Q

Na/K ATPase dec activity due to

A
ATP depletion (exercise, ischemia-reperfusion)
direct blockage via digitalis
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5
Q

how does hyperosmolarity affect K

A

ICF shifts to ECF and squeezes K out

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6
Q

ways to get hypoaldosteronism

A

PRIMARY
adrenal gland damage
congenital (21 alpha hydroxylase def)
heparin
SECONDARY
JGA Damage (diabetes, obstructibe uropathy)
ACEi/ARB- directly and via efferent dilation

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7
Q

acute hyperkalmia management

A

IV Ca
insulin/glucose
albuterol
bicarb

buy time but eventuallt need to remove k

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8
Q

how to get K out of body

A

Kayexalate

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9
Q

Familial Hyperkalemic HTN/Gordon’s Syndrome genes

A

WNK4 inact, WNK1 act

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10
Q

renal losses leading to hypokalemia

A

diuretic use
hyperaldo
anion excess
hypomagnesiemia (dysfunctioning Na/K ATPase)

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11
Q

GI losses leading to hypokalemia

A

massive diarrhea/laxative
gastric losses–>decrease H+–>alkalosis–>excrete HCO3- pulling K with it
*both of these have volume depletion aspect too

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12
Q

rapid cell growth

A

consumes a lot of K (tumors n stuff)

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13
Q

Bartter’s syndrome

A
defective Na/K/2Cl-- chronic look
hypokalemia
hypomag
volume dep
alkalosis
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14
Q

Gitelman’s

A

defective Na/Cl cotransporter at DCT–stimulates chronic thiazide
less severe than barterrs
hypokal/meta alk

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15
Q

liddles

A

constitutivelY ACTIVE enac–pseudohyperaldo

hypokal and htn

16
Q

patients with ___ are diuretic/vommiters until proven otherwise

A

low K
low urine K
meta acidosis

17
Q

refeeding syndrome

A

give food to starving person–>massive insulin–> all k goes insoide

18
Q

periodic paralysis

A

rare genetic disorder involving K channels that suddenly cause massive intracell k influx

19
Q

severe HTN and metabolic alkalosis

A

hyperaldosteronism until proven otherwise

20
Q

what do you use when treating hypokalemia

A

dextrose and glucose-free iv solutions to avoid insulin stimulations as it would increase itnracell shift