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32 Cards in this Set

  • Front
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Acetazolamide
Dorzolamide
Diuretic
CA Inhibitor (everywhere)
- Decrease bicarbonate reabsorption
- Less Na+ recovery (diuresis)
- Produce alkaline urine
- Produce acidotic blood
1) What are the CA Inhibitor diuretics?

2) Where do they work?

3) What are they indicated for?

4) What are adverse effects?
1) Acetazolamide and Dorzolamide

2) PT

3) Glaucoma, urine alkalization for elimination of toxic/lipid soluble weak acids

4) Metabolic acidosis, elevated renal pH, renal stones

Also used for Altitude sickness (stimulates hyperventilation from metabolic acidosis)
Furosemide (Lasix)
Diuretic
Loop Diuretic
- Sulfonamide

- Used when rapid volume depletion needed (e.g. acute pulmonary edema)

- Major side effects (e.g. Hypo- magnesium, calcium, kalemia, chloride)
Bumetanide
Diuretic
Loop Diuretic
- Sulfonamide
Torsemide
Diuretic
Loop Diuretic
- Sulfonamide
Ethacrynic Acid
Diuretic
Loop Diuretic
- NOT Sulfonamide
1) What is the MOA of Loop Diuretics?

2) Where specifically do they work?

3) What are Loop Diuretics indicated in?

4) What are the side effects of Loop Diuretics?
1) Inhibit Na,K,Cl cotransporter (this site is responsible for recovering 30% of filtered Na+)
Also lose Ca, Mg, HOH

2) TAL - thick ascending limb

3) Acute pulmonary edema, CHF, HTN, refractory edemas, Hypercalcemia <---**

4) Hypokalemia (Alkalosis)
Hypovolumia-->thirst-->hyponatremia
HYPERuricemia
HYPERglycemia
Ototoxicity (Ethacrynic acid)
Sulfa Sensitivity (Other 3)

High-Ceiling Diuretics (POWERFUL)
Chlorothiazide (Diuril)
Diuretic
Thiazide
Hydrochlorothiazide (HCTZ)
Diuretic
Thiazide
Polythiazide
Diuretic
Thiazide (DCT)
Indapamide
Diuretic
Thiazide
PLUS vasodilator
(HCTZ is not also vasodilator)
Chlorthalidone
Diuretic
Thiazide
Metolazone
Diuretic
Thiazide
Spironolactone
Diuretic
Potassium-Sparing
- Also aldosterone ANT
Eplerenone
Diuretic
Potassium-Sparing
Triamterene
Diuretic
Potassium-Sparing
Amiloride
Diuretic
Potassium-Sparing
Mannitol
Diuretic
Osmotic
Vasopressin (ADH)
Diuretic
ADH Agonist
V1 and V2
Desmopressin
Diuretic
ADH Agonist
V2 only
Lithium Ion
Anti-Diuretic
ADH Inhibitors
- Blocks V2 mechanism
- Li-induced DB insipidus is treated w/ desmopression
1) What drug class / loop diuretic combination can enhance ototoxicity?

2) What drug can enhance hypokalemia if taken w/ Loop Diuretics?
1) Aminoglycosides and the non-sulfa loop diuretic, ethacrynic acid

2) Digoxin - hypokalemia
1) What are the sulfonamides?

2) What Sulfa antibiotics can these drugs cross-react with?

3) What class of diuretic can cross react with the sulfonamide drugs?
1) Furosemide, bumetanide, torsemide (loop diuretics)

2) Sulfamethoxazole

3) Thiazides (DCT): HCTZ, Indapamide
1) What are symptoms of sulfonamide hypersensitivity?
1) Skin Reactions: hive, photo sensitivity, Stevens-Johnson syndrome (painful rash on mucuous membranes and all over body)

- Hepatitis, kidney failure

- Reduced WBC, RBC, Platelets
1) What are the thiazides?

2) What is the MOA?

3) What is retained (vs. other diuretics)?
1) Thiazides: HCTZ, Indapamide, others

2) They work on the DCT.
- Inhibit the Na+Cl- cotransporter

3) Ca2+ is retained
1) What are thiazides indicated in?

2) What are side effects of thiazides?
1) CHF, HTN, Nephrogenic DB insipidus (direct stimulus of ADH site)
- Reduces Ca2+ stone formation

2) Hypokalemia / Alkalosis
Hyperuricemia
Hypercalcemia (<-- ONLY DIFF IN SIDE EFFECTS FROM LOOPS)
Hyperglycemia
Sulfa Sensitivity
1) What drug is used when RAA is high? What class of diuretic is it?

2) What are other classes of K+ sparring diuretics?
1) Spironolactone: CT, K+ sparing (is an aldosterone ANT)

2) Amiloride and Triamterene
1) Describe why loop and thiazide (DCT) may result in hyperuricemia?

2) Describe why some loop diuretics result in hyperglycemia?

3) How does the hypovolemia and hyponatremia occur?
1) Loop Diuretics / Thiazides are weak acids --> compete for oraganic acid excretion sites in PT --> uric acid buildup

(uric has to compete w/ diuretics, lactate, etc)

2) Hypokalemia -->less K+ for beta cell K+ current -->steeper gradient (faster current)-->less insulin release

3) During Na+ and water loss, compensatory mechanisms kick in (ADH, etc); pt wants water-->unrestricted water intake leads to acute dilutional hyponatremia (CNS, ventricular arrhythmias, convulsions)
1) Which K+ sparring diuretic is used specifically against high aldosterone?

2) How does it do this?

3) What are some possible side effects?
1) Spironolactone

2) Aldosterone receptor competitive ANT (Anti-HTN, Anti-CHF)

3) Hyperkalemia, acidosis (DIFFERENT FROM OTHERS)
1) What K+ sparring diuretics are Na+ transport blockers?
1) Amiloride, Tramterene

Usually combined w/ thiazides or loops to neutralize K+ loss
1) What is the major osmotic diuretic?

2) How does it work?

3) What is it indicated in?
1) Mannitol

2) filtered, not reabsorbed

3) edema, glaucoma, to make nephrotoxic drugs readily excretable
1) Why is desmopressin and not vasopressin indicated in neurogenic diabetes insipidus?
1) Vasopressin acts at V1 AND V2 receptors, producing vasoconstriction and increased BP (V1) and water retention (V2); Desmopressin only works at V2