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32 Cards in this Set

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Clinical use of Diurectics
HTN, CHF, Edematous states, renal dysfunction, hypercalcemia, nephrolithiasis, glaucoma, mountain sickness, Increased intracranial pressure
Na+ reabsorption in renal tubular segments (%)
PCT >60%
TAL <25%
DCT <10%
CT <4%
Mannitol
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
Carbonic Anhydrase Inhibitors

mechanism of action
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)
Carbonic Anhydrase Inhibitors

Clinical Use
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
Acetozolomide
Carbonic Anhydrase Inhibitor

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

open-angle glaucoma
correcting a metabolic alkalosis
Methazolomide
Carbonic Anhydrase Inhibitor

open-angle glaucoma
correcting a metabolic alkalosis
Side Effects of Carbonic Anhydrase Inhibitors
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
Locations of Carbonic Anhydrase
eye (decreases formation of aqeous humor--decreases IOP), gastric mucosa, pancreas, central nervous system (CNS), and erythrocytes
Loop Diuretics
"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)
Loop diuretic (specific drugs)
Furosemide (Lasix)
Piretanide
Bumetanide
Torsemide
Ethacrynic Acid
Furosemide

additional-nondiuretic effects
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.
)
Ethacrynic Acid (Ethacrynate)> Furosemide
Loop Diuretic

Side Effects
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
Contraindications to loop diuretics
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.
Thiazides
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
Thiazide Diuretics
Specific Drugs
Hydrochlorothiazide
Chlorothiazide (parenteral)
Methylothiazide
Polythiazide
Metalazone
Quinazolinone family (Thiazide like)

Can be used in pt's with renal impairment

Other quinazolinone:
Metolazone
Chlorhalidone
Indapamide
Indoline family (thiazide like diuretic)
Can be used in pt's with renal impairment
Therapeutic use of Thiazides
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
Thiazides
Side effects:
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
Potassium Sparing Diuretics
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
Spironolactone
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)
Amiloride
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)
Triamterene
Potassium Sparing Diuretics (independent of Aldosterone)
Mechanism: Block Na+/K+(H+) exchange
K+ Sparing Diuretics
Side Effects
Hyperkalemia--ventricular arrhytmias (decrease K+ in diet)
Acidosis
Nausea, vomiting

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

Triamterene:
Nephrolithiasis
Therapeutic indications for Urea as a diuretic
Osmotic Diuretic--IV

reduction of intracranial & intraocular pressure
Therapeutic indications for Glycerin as a diuretic
Osmotic Diuretic--PO

used in opthalmic procedures

topically--for corneal edema
Desmopressin
Anti-diuretic (Vasopressin/ADH analogue)
Use: diabetes insipidus, noctural enuresis

Also, to maintain BP in pt's with Septic Shock
Drugs that enhance the action of ADH
Mechanism: reduce kidney's prostaglandin production
Chlopropamide (sulfanourea)
Acetaminophen
Indomethasin

Clofibrate increases the release of ADH centrally
ADH Antagonists
Use: SIADH (e.g. ADH secreting lung cancer)

Demeclocycline
Lithium Carbonate