Drugs to treat hypo- hyperkalemia Flashcards
How much K+ is eliminated
the same amount that is taken in
what is considered hyperkalemia?
> 5 mEq/L
what is considered hypokalemia?
<3.7 mEq/L
what does insulin, beta catechol, alkalosis, and hyperosmolality do to K+?
increases K+ uptake by cells
what does alpha catecholamines, and acidosis do to K+?
decrease the cell uptake of K+
what do thyroid, adrenal steroids, exercise and growth do to ATP pump density?
increase ATP pump density
what does diabetes, K+ deficiency, chronic renal failure do to ATP pump density+
decreases ATP pump density
where is most of K+ secreted
Distal tubule
increase flow rate and increase Na+ do what to K+
Increase K+ secretion
Hyperkalemia does what to the membrane initially and chronic?
initially increase excitability but chronic will cause paralysis due to Na+ channel inactivation
What happens to membranes during hypokalemia
more negative RMP, hyperpolarized membranes
triamterene, amiloride
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
Spironolactone
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
thiazides
NaCl cotransporter blocker (NCCT) in distal convoluted tubule
furosemide
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
torsemide
longer half life than furosemide
better oral absorption, works better in HF
loop diuretic
Bumetanide
more predictable oral absorption than furosemide
loop diuretic
ethacrynic acid
non sulfonamide loop diuretic
HCTZ
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-
licorice
contains sweet glycyrrhizic acid
potentiates aldosterone effects in kidney and dose dependently increases systolic BP
symptoms of hypokalemia
lethargic low respirations lethal cardiac disarrhythmias lots of urine leg cramps limp muscles low BP
symptoms of Hyperkalemia
abnormal heart rhythm, bradycardia peaked T wave widened QRS numbness weakness flaccid paralysis little urine output decreased contractility of heart twitches early
convivaptan
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
tolvaptan
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
vaptans MOA
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+
Uses of vaptans
hypervolemic or euvolemic hyponatremia
autosomal dominant Polycystic kidney dz
adverse effects of Vaptans
orthostatic hypotension
fatigue
thirst
polyuria and bedwetting
drug interactions of vaptans
metabolized by cyp3a4
selective water loss means possibility of hypovolemia, other electrolytes
DDAV
desmopressin
V2 selective agonist
used for central diabetes insipidus and primary nocturnal enuresis
can cause hyponatremia
Diabetes insipidus
increased urine
imbalances in fluids in body
what are the 2 types of diabetes insipidus
central - lack of ADK and you treat with exogenous ADH (DDAVP)
nephrogenic - unresponsive to ADH , treat with drinking water and thiazides
what is a common cause of nephrogenic type of Diabetes insipidus
Li therapy - used for bipolar disorder
Thiazide diuretics are CI in Li induced DI
what is the treatment for Li induced DI
amiloride - blocks influx of Li into CD cells allowing ADH to work
