Diuretics

Front 1

Clinical use of Diurectics

Back 1

HTN, CHF, Edematous states, renal dysfunction, hypercalcemia, nephrolithiasis, glaucoma, mountain sickness, Increased intracranial pressure

Front 2

Na+ reabsorption in renal tubular segments (%)

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PCT >60%
TAL <25%
DCT <10%
CT <4%

Front 3

Mannitol

Back 3

Osmotic Diuretic IV only
Inhibits water reabsorption in PCT, thin descending loop of Henle and CT
Use: Hemolysis & rhabdo--increases urine volume/prevents anuria
W/ toxic drug therapy (Cisplatin)-facilitates elimination
Decreases intraocular & intracerebral pressure

SE: Nausea, vomiting, chills, electrolyte imbalance, hypovolemia, chest pain

Front 4

Carbonic Anhydrase Inhibitors

mechanism of action

Back 4

Inhibition of Carbonic Anhydrase (CA) on luminal membrane and in the PCT cell--decrased CO2 inside PCT cell--further decrease of CA formation--less intracellular HCO3- and H+ leading to decreases reabsoption of Na+ due to less H+ available for Na/H antiporter.
Na+ w/ H2O, K+ and HCO3- pissed out

Acetazolamide
dichlorphenamide
Methazolomide
(sulfonamide derivatives--chemo drug)

Front 5

Carbonic Anhydrase Inhibitors

Clinical Use

Back 5

Rarely used as a diuretic

Major use:open-angle glaucoma

correcting a metabolic alkalosis
elimination of acidic drugs--e.g ASA OD
altitude sickness
familial periodic paralysis
seizure disorders

Front 6

Acetozolomide

Back 6

Carbonic Anhydrase Inhibitor

open-angle glaucoma
correcting a metabolic alkalosis
edemas (pulmonary/cerebral)
altitude sickness
familial periodic paralysis

Front 7

Dichlorphenamide

Back 7

Carbonic Anhydrase Inhibitor

open-angle glaucoma
correcting a metabolic alkalosis

Front 8

Methazolomide

Back 8

Carbonic Anhydrase Inhibitor

open-angle glaucoma
correcting a metabolic alkalosis

Front 9

Side Effects of Carbonic Anhydrase Inhibitors

Back 9

Metabolic Acidosis
Urine alkaline--decreased solubility of Ca2+ salts--renal calculi
Potassium wasting may be severe

effects of carbonic anhydrase inhibitors on renal excretion are self-limiting probably because the resulting metabolic acidosis decreases the filtered load of HCO3– to the point that the uncatalyzed reaction between CO2 and water is sufficient to achieve HCO3– reabsorption

Front 10

Locations of Carbonic Anhydrase

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eye (decreases formation of aqeous humor--decreases IOP), gastric mucosa, pancreas, central nervous system (CNS), and erythrocytes

Front 11

Loop Diuretics

Back 11

"high ceiling diuretics"
Loop Diuretics inhibit the Na/K/2Cl cotransporter on the luminal membrane of the thick ascending loop of Henle (TAL)

Loop diuretics dump Na+, K+, Cl-, Ca2+ and Mg+ in the urine

They are absorbed in GI tract and eliminated by filtration and tubular secretion (also hepatic-biliary route)
oral or parenteral (diuresis happens in 30min (oral) to 5 min (IV)

Front 12

Loop diuretic (specific drugs)

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Furosemide (Lasix)
Piretanide
Bumetanide
Torsemide
Ethacrynic Acid

Front 13

Furosemide

additional-nondiuretic effects

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Acutely increase systemic venous capacitance and thereby decrease left ventricular filling pressure. This effect, which may be mediated by prostaglandins and requires intact kidneys, benefits patients with pulmonary edema even before diuresis ensues.

Front 14

)

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Ethacrynic Acid (Ethacrynate)> Furosemide

Front 15

Loop Diuretic

Side Effects

Back 15

Abnormalities of fluid and electrolyte balance
Allergies
Alkalosis
Ototoxicity-- manifests as tinnitus, hearing impairment, deafness, vertigo, and a sense of fullness in the ears (Ethacrynic Acid (Ethacrynate)> Furosemide--potentiated by aminoglycosides

hyperuricemia
hyperglycemia
increase LDL/decrease HDL
May decrease Lithium Clearance

Front 16

Contraindications to loop diuretics

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Contraindications to the use of loop diuretics include severe Na+ and volume depletion, hypersensitivity to sulfonamides (for sulfonamide-based loop diuretics), and anuria unresponsive to a trial dose of loop diuretic.

Front 17

Thiazides

Back 17

Organic acids--are both filtered and secreted

Inhibit Na/Cl cotransporter on the luminal membrane of DCT (bind to Cl site)

Dump Na+, Cl-, K+ and at high doses HCO3- (may also inhibit Carbonic Anhydrase), into the urine
Reduce Ca2+ excretion

Hydrochlorithiazide
Chlorothiazide
Chlorthalidone
Metalazone

Front 18

Thiazide Diuretics
Specific Drugs

Back 18

Hydrochlorothiazide
Chlorothiazide (parenteral)
Methylothiazide
Polythiazide

Front 19

Metalazone

Back 19

Quinazolinone family (Thiazide like)

Can be used in pt's with renal impairment

Other quinazolinone:
Metolazone
Chlorhalidone

Front 20

Indapamide

Back 20

Indoline family (thiazide like diuretic)
Can be used in pt's with renal impairment

Front 21

Therapeutic use of Thiazides

Back 21

Hypertension (when normal renal function)
In combination with other antihypertensives (e.g w/ K+ sparing diuretics)
Reduce formation of new Calcium stones in (idiopathic hypercalciuria)
Meniere's disease

Front 22

Thiazides
Side effects:

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Caution if pt has renal or liver disease
Hypokalemia
Hyponatremia
Hypochloremic Alkalosis
Hyperglycemia
Hypersensitivity reactions
Elevated serum Urate--competes for elimination--gout like symphtoms
increased cholesterol and TG's

Front 23

Potassium Sparing Diuretics

Back 23

Reduce Na+ reabsorption and reduce K+ & H+ secretion in distal nephron (Collecting Tubule)

Contraindicated in Renal insufficiency (especially DM)

Weak diuretics--most filtered Na+ is reabsorbed before reaching CT

Front 24

Spironolactone

Back 24

K+ Sparing diuretic

Use: in hyperaldosteronic states as adjunctive w/ other diuretics in HTN and CHF. Improves survival when used w/ ACEI

Aldosterone receptor antagonist (works only when endogenous Aldesterone is present)
Blocks formation of Na+ channels--prevents Na+ absorption (minor effect to total Na+ reabsorption but major effect on K+ & H+ retention)

Front 25

Amiloride

Back 25

Potassium Sparing Diuretics (independent of Aldosterone)

Mechanism: Block Na+/K+(H+) exchange
(epithelial Na+ channels called ENaC, in the luminal membrane of principal cells in the late distal tubule and collecting duct)

Front 26

Triamterene

Back 26

Potassium Sparing Diuretics (independent of Aldosterone)
Mechanism: Block Na+/K+(H+) exchange

Front 27

K+ Sparing Diuretics
Side Effects

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Hyperkalemia--ventricular arrhytmias (decrease K+ in diet)
Acidosis
Nausea, vomiting

Spironolactone: gynegomastia--antiandrogenic effects (can also tx hirsutism), libido changes

Triamterene:
Nephrolithiasis

Front 28

Therapeutic indications for Urea as a diuretic

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Osmotic Diuretic--IV

reduction of intracranial & intraocular pressure

Front 29

Therapeutic indications for Glycerin as a diuretic

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Osmotic Diuretic--PO

used in opthalmic procedures

topically--for corneal edema

Front 30

Desmopressin

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Anti-diuretic (Vasopressin/ADH analogue)
Use: diabetes insipidus, noctural enuresis

Also, to maintain BP in pt's with Septic Shock

Front 31

Drugs that enhance the action of ADH

Back 31

Mechanism: reduce kidney's prostaglandin production
Chlopropamide (sulfanourea)
Acetaminophen
Indomethasin

Clofibrate increases the release of ADH centrally

Front 32

ADH Antagonists

Back 32

Use: SIADH (e.g. ADH secreting lung cancer)

Demeclocycline
Lithium Carbonate