Pharmacology of Renal System

osmotic diuretics moa

osmotic diuretics moa

on proximal tubule, increases urinary excretion of almost all electrolytes

Cli osmotic diuretics

narrow → acute RF, brain + eye edema

Mannitol

osmotic diuretic

SE osmotic diuretics

hyponatremia + pul edema OR hypernatremia + dehydration

furosemide

loop diuretic

what is the strongest diuretic?

loop diuretics (furosemide)

Moa loop diuretics

on loop of henle → blocks reabsorption Na + K + H20, Mg + Ca excreted, increases renal flow + venodilation

Cli loop diuretics

emergency, HTN + edema in RF, pul edema in HF

loop diuretics are used w/

K+ sparing diuretics

SE loop diuretics

cramps, ion imbalances (hypokalemia, hypomagnesemia, hyperuricemia), hypotension, ototoxicity

DDI loop diuretics

aminoglycosides, lithium, digoxin, ACE-i

hydrochlorothiazide (HCht) + Indapamide

thiazide diuretics

Moa thiazides

on distal tubule → increases salt + water loss

Cli thiazides

wide → HTN, HF (arrhythmias, post-MI), diabetes insipidus

SE thiazides

hypercalcemia, gout, dizziness, cramps, hypokalemia

DDI thiazides

lithium, digoxin, ACE-i

SE of thiazides are hypokalemia which is remedied by administering what

K+ sparing diuretics

Amiloride

K+ sparing diuretics (weak)

moa k+ sparing diuretics

on distal tubule

K+ sparing diuretics SE

hyperkalemia, GIT symptoms

moa spironolactone

ALD regulated → resembles steroid, antagonist mineralocorticoid r in distal tubules + collecting duct, natriuretic + k+ sparing

SE spirinolactone

hyperkalemia, mimics steroids (gynecomastia, impotence, menstrual disturbances)

Cli spirinolactone

cardiac edema + HTN, cirrhosis

Th urge incontinence (overactivity detrusor)

parasympatholytics (oxybutinin) + alpha-agonist

moa psly (oxybutinin)

inhibition detrusor contractions, extends time of urgency to urinate

moa alpha-agonists

increases intraurethral p → increased sphincter tone → bladder closure

th for stress incontinence (defective closure)

a-agonists

most common cause of drug induced incontinence

diuretics, alcohol, anticholinergics

Th BPH

a1-antagonists (tamsulosin) + 5a-reductase i (finasteride)

moa a1 antagonist

causes m in prostate to relax

5a-reductase i (finasteride) moa

competes w/ testosterone for enzyme (DHT inhibited) → prostate volume reduction