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Renal Pharm > Drugs to treat hypo- hyperkalemia > Flashcards

Drugs to treat hypo- hyperkalemia Flashcards

1
Q

How much K+ is eliminated

A

the same amount that is taken in

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2
Q

what is considered hyperkalemia?

A

> 5 mEq/L

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3
Q

what is considered hypokalemia?

A

<3.7 mEq/L

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4
Q

what does insulin, beta catechol, alkalosis, and hyperosmolality do to K+?

A

increases K+ uptake by cells

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5
Q

what does alpha catecholamines, and acidosis do to K+?

A

decrease the cell uptake of K+

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6
Q

what do thyroid, adrenal steroids, exercise and growth do to ATP pump density?

A

increase ATP pump density

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7
Q

what does diabetes, K+ deficiency, chronic renal failure do to ATP pump density+

A

decreases ATP pump density

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8
Q

where is most of K+ secreted

A

Distal tubule

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9
Q

increase flow rate and increase Na+ do what to K+

A

Increase K+ secretion

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10
Q

Hyperkalemia does what to the membrane initially and chronic?

A

initially increase excitability but chronic will cause paralysis due to Na+ channel inactivation

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11
Q

What happens to membranes during hypokalemia

A

more negative RMP, hyperpolarized membranes

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12
Q

triamterene, amiloride

A 
ENaC blocker in CD
H+, Mg+, Ca2+ excretion increased 
counters K+ loss
hyperkalemia is a risk 
duration of triamterene is 6-9 hours and it is eliminated as a drug metabolite
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13
Q

Spironolactone

A 
competitive antagonist of aldosterone receptors in CD 
Partial agonist at androgen receptors 
K+ sparing diuretic 
reduces fibrosis post MI, HF
steroid effects are slow on and off 
can cause hyperkalemia
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14
Q

thiazides

A

NaCl cotransporter blocker (NCCT) in distal convoluted tubule

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15
Q

furosemide

A

loop diuretic

blocks the Na K Cl cotransporter (NKCC2) in thick ascending limb
used for edema management, decrease preload, decreasing EC volume, rapid dyspnea, HTN

can cause Hypo K+, Na+, Ca2+, Mg2+, Cl-
can cause hyper glycemia and uricemia
can cause ototoxicity, vertigo and hearing impairment

sulfonamide containing

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16
Q

torsemide

A

longer half life than furosemide
better oral absorption, works better in HF

loop diuretic

17
Q

Bumetanide

A

more predictable oral absorption than furosemide

loop diuretic

18
Q

ethacrynic acid

A

non sulfonamide loop diuretic

19
Q

HCTZ

A

blocks NaCl cotransporter
K+ losing
for HTN, not effective in pts with low GFR
off label use for calcium nephrolithiasis
can cause hypo K+, Mg2+, Na+, Cl-, metabolic alkalosis
increased loss of HCO3-

20
Q

licorice

A

contains sweet glycyrrhizic acid

potentiates aldosterone effects in kidney and dose dependently increases systolic BP

21
Q

symptoms of hypokalemia

A 
lethargic
low respirations
lethal cardiac disarrhythmias 
lots of urine 
leg cramps 
limp muscles 
low BP
22
Q

symptoms of Hyperkalemia

A 
abnormal heart rhythm, bradycardia
peaked T wave
widened QRS
numbness
weakness
flaccid paralysis 
little urine output 
decreased contractility of heart
twitches early
23
Q

convivaptan

A

nonpeptide arginine vasopressin receptor antagonist
promotes the excretion of free water

tx of euvolemic and hypervolemic hyponatremia in pt who are hospitalized, symptomatic or not responsive to fluid restriction

too rapid serum Na+ correction can lead to seizures, osmotic demyelination, coma, or death

24
Q

tolvaptan

A

selective V2 receptor antagonist given orally
only give in pt in a hospital where you can monitor Na+ levels

must use <30 days for hyponatremia, longer use can potentially be hepatotoxic

slows progression of adult polycystic kidney dz

effects increase to peak at 4 hrs, effects 4-8 hrs

25
Q

vaptans MOA

A

MOA: prevents ADH mediated insertion of the aquaporin water channels into luminal membrane of principal cells in CD

prevents the reabsorption of water, therefore increase water excretion

decrease plasma volume and increase plasma osmolality primarily due to an increase in plasma Na+

26
Q

Uses of vaptans

A

hypervolemic or euvolemic hyponatremia

autosomal dominant Polycystic kidney dz

27
Q

adverse effects of Vaptans

A

orthostatic hypotension
fatigue
thirst
polyuria and bedwetting

28
Q

drug interactions of vaptans

A

metabolized by cyp3a4

selective water loss means possibility of hypovolemia, other electrolytes

29
Q

DDAV

A

desmopressin
V2 selective agonist
used for central diabetes insipidus and primary nocturnal enuresis
can cause hyponatremia

30
Q

Diabetes insipidus

A

increased urine

imbalances in fluids in body

31
Q

what are the 2 types of diabetes insipidus

A

central - lack of ADK and you treat with exogenous ADH (DDAVP)

nephrogenic - unresponsive to ADH , treat with drinking water and thiazides

32
Q

what is a common cause of nephrogenic type of Diabetes insipidus

A

Li therapy - used for bipolar disorder

Thiazide diuretics are CI in Li induced DI

33
Q

what is the treatment for Li induced DI

A

amiloride - blocks influx of Li into CD cells allowing ADH to work

Renal Pharm (1 decks)

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