key factor with diuretics

What is reabsorbed and where is it re-absorbed?

"pumps"

organic acids and organic bases

manitol osmotic diuretic

carbonic anyhydrase inhibitor

used for: mountain climbers - high altitude - swelling of the brain

Potasium sparing diuretics/aldosterone antagonist

(spironolactone, aldactone)

primarily used for HTN that doesn't respond to other drugs

commonly used for pulmonary and generalized edema

used with heart, kidney and liver failure ( only diurectic that works even with kidney failure)

keeps sodium in lumen of tubule

last around six hours

PO: diuresis w/in 60 min

IV: diuresis within 5-10 min

Fluid volume deficit (hypotension)

arterio/venous dilation

inc. resistance over time

ototoxicity (problem with large IV dosing)

hypokalemia

hyponatremia (as well as all other electrolytes)

leg cramps

Digoxin (potentiates toxicity due to low K⁺ levels)

aminoglycosides (also produce ototoxicity)

cephalosporins (compete in gut with lasix for transfer into body, Tx inc. lasix)

NSAIDS (dec. effectiveness of lasix, Tx change pain med)

take in morning

leg cramps are not RLS

K⁺ supplement

watch BP

hyponatremia

drug interactions

hyperglycemia

inc. LDL and HDL (watch lipid profile)

inc. uric acid (gouty attacks)

initial HTN Tx (mild - moderate)

Vasodilation (diuretic effect dwindles but this stays)

Ca⁺⁺ spilling in urine (helps reabsorb higher rates of calcium)

slows osteoporotic process

digoxin

NSAIDS

FVD

Hypokalemia (not as severe as lasix)

all electrolyte deficit (except Ca⁺⁺)

inc. CBG's

lipid changes

ototoxicity

hypercalcemia

HF, MI (aldosterone antagonist properties)

used with lasix?

monitor serum and sodium levels

no K⁺ salts or substitutes

steroid structure (inc. testosterone like effect)

profound hyperkalemia