DIURETICS

CA Inhibitors

Acetazolamide & Dorzolamide (topical eye drop)

MoA: Inhibits NaHCO3 reabsorptionLocation: PROXIMAL TUBULE

Sulfonamides = avoid in gout Actions:

Causes metabolic acidosis (limits H+ excretion)

Decreases aqueous humor & CSF production

CA Inhibitors Adverse

Nephrolithiasis since CaPO4 precipitates in alkaline urine

Hypokalemia (adverse effect of all diuretics except for K-sparring ones)

Contra-indicated in gout and COPD (because of effects of CA in lungs)

Therapeutic UsesOpen angle glaucomaIn combo with other diuretics to counter alkalosis

effectsEdema from heart failure

Thiazides Hydrochlorothiazide & Indapamide MoA: blocks the Na/Cl symport

Location: Acts in early DCT (diluting capacity is decreased)

Also are sulfonamides (contra for gout) Metabolic alkalosis (opposite of CA

Inhibitors) Calcium is retained HYPERCALCEMIA Only effective when GFR > 30 mL/min

Thiazides Adverse

Hypokalemia (more Na reaching collecting tubule causes high K secretion)

Hypercalcemia (lower intracellular Na limits Ca exchange; also limits Li excretion)

Metabolic alkalosisSexual dysfunction, postural hypotensionNot for pregnancy

Therapeutic Use1st choice for hypertensionUsed when there is any edemaCa Nephrolithiasis

Loop Diuretics Furosemide & Ethacrynic acid (not a sulfonamide) MoA: Blocks Na/K/Cl in the TAL of loop of henle

Decreased lumen positive potential = dilution ability is affected (Ca loss)

Decreased hypertonicity of medulla = decreased concentrating ability

Inhibition of macula densa sensitivity (work even with low GFR)

Osmolality is same as plasma due to loss of concentration and dilution ability!!

Metabolic alkalosis; increased Ca and Mg excretion

Loop Diuretics Only diuretics which work with low GFR!!

(due to inhibition of macula densa sensitivity) ADVERSE

Hypocalcemia, hypokalemia, hypochloremiaTinnitus (due to alteration of endolymph)Hyperglycemia in DM ptsHypokalemia can increase digoxin and Li toxicity

Therapeutic UsePulmonary edema, Heart failureHypertension – only if renal insufficiency (allows

to work with low GFR)

K+ Sparring Diuretics Triamterene; Amiloride; Spironolactone MoA:

Triamterene and Amiloride block Na channels directly Spironolactone blocks aldosterone receptors (which

prevents Na channels from even being produced) Location: late DCT & Cortical Collecting Tube

ONLY diuretics which do not cause increased K excretion

Spironolactone takes 1-3 days to take effect (blocks protein synthesis) and is metabolized to its active metabolite – canrenone

Amiloride is excreted unchanged

K+ Sparring Diuretics Adverse

Hyperkalemia (may cause asystole)Sexual dysfunction (spironolactone)Mixing with b-blockers, ACE inhibitors, NSAIDS

(renin-angiotensin system blunters) may increase hyperkalemia

Therapeutic UsesPrevention of hypokalemic statesSpironolactone for primary hyperaldosteronism

(Conn syndrome), secondary hyperaldosteronism (Cushing’s), and hypertension with heart failure

Amiloride for Li-Induced nephrogenic DI

Osmotic Diuretics Mannitol MoA: Increase the osmolarity of tubular fluid

Location: proximal tubule & thick descending limb of loop of Henle

Increases excretion of all ions Urine becomes acidic (but body is normal) Causes EXTRACELLULAR VOLUME EXPANSION initially

but then diuresis causes EXTRACELLULAR VOLUME REDUCTION !!!!!!!○ Can cause PULMONARY EDEMA

Therapeutic Use Reduces cerebral edema (neurosurgery) Reduces intraocular pressure in acute closed-angle

glaucoma

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