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33 Cards in this Set

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Site of action of Acetazolamide?
proximal convoluted tubule
Site of action of Osmotic diuretics (mannitol)? (3)
proximal convoluted tubule
loop of Henle
collecting duct
Site of action of Loop agents (furosemide)? (2)
distal convoluted tubule
thick ascending limb of loop of Henle
Site of action of K+ sparing diuretics?
distal convoluted tubule
Site of action of ADH antagonists?
collecting duct
MOA of Mannitol?
Osmotic diuretic, ↑ tubular fluid osmolarity, producing ↑ urine flow.
Clinical use of Mannitol?
-shock
-drug overdose
-↓ intracranial/intraocular pressure.
Toxicity of Mannitol? (2)

Who is it C/I in?
-pulmonary edema
-dehydration

Contraindicated in anuria, CHF.
MOA of Acetazolamide?

Where does it act?
Carbonic anhydrase inhibitor.

Causes self-limited NaHCO3 diuresis and reduction in total-body HCO3
– stores.

Acts at the proximal convoluted tubule.
Clinical use of Acetazolamide? (4)
Glaucoma
Urinary alkalinization
Metabolic alkalosis
Altitude sickness
Toxicity of Acetazolamide?
-hyperchloremic metabolic acidosis
-neuropathy
-NH3 toxicity
-sulfa allergy
does acetazolamide cause alkalosis or acidosis?
ACIDazolamide causes ACIDosis
MOA of Furosemide?

How do you remember what it does to calcium?
Sulfonamide loop diuretic.

Inhibits cotransport system (Na+, K+, 2 Cl−) of thick ascending limb
of loop of Henle.

Abolishes hypertonicity of medulla, preventing concentration of urine. ↑ Ca2+ excretion.

"Loops Lose calcium."
Clinical use of Furosemide? (3)
-Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), -hypertension
-hypercalcemia.
Toxicity of Furosemide?
-mnemonic?
"OH DANG"

Ototoxicity
Hypokalemia
Dehydration
Allergy (sulfa)
Nephritis (interstitial)
Gout
MOA of Ethacrynic acid?
Phenoxyacetic acid derivative (NOT a sulfonamide).

Essentially same action as furosemide.
Clinical use of Ethacrynic acid?
Diuresis in patients allergic to sulfa drugs.
Toxicity of Ethacrynic acid?

What should it never be used to treat?
Similar to furosemide; can be used in hyperuricemia, acute gout (never used to treat gout).
MOA of HCTZ?
Thiazide diuretic.

Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron.

↓ Ca2+ excretion.
Clinical use of HCTZ? (4)
Hypertension
CHF
Idiopathic hypercalciuria
Nephrogenic diabetes insipidus
Toxicity of HCTZ?
-mneumonic?
-allergy?
Hypokalemic metabolic alkalosis
hyponatremia
hyperGlycemia
hyperLipidemia
hyperUricemia
hyperCalcemia

"HyperGLUC"

Sulfa allergy
What drugs are K+-sparing diuretics? (4)
-mnemonic?
Spironolactone
Triamterene
Amiloride
eplereone

"The K+ STAys"
MOA of K+-sparing diuretics?
Spironolactone is a competitive aldosterone receptor antagonist in the cortical collecting tubule.

Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the CCT.
Clinical use of K+-sparing diuretics? (3)
Hyperaldosteronism
K+ depletion
CHF
Toxicity of K+-sparing diuretics? (2)
Hyperkalemia
Endocrine effects (e.g., spironolactone
causes gynecomastia, antiandrogen effects).
How does urine NaCl change with diuretics?
↑ (all diuretics––carbonic anhydrase inhibitors, loop diuretics, thiazides, K+-sparing diuretics).
How does urine K+ change with diuretics?
↑ (all except K+-sparing diuretics).
How does blood pH change with diuretics?
↓ (acidosis)––carbonic anhydrase inhibitors, K+-sparing diuretics

↑ (alkalosis)––loop diuretics, thiazides.
How does urine Ca+ change with diuretics?
↑ loop diuretics
↓ thiazides
What drugs are ACE inhibitors? (3)
Captopril
Enalapril
Lisinopril.
MOA of ACE inhibitors?
Inhibits angiotensin-converting enzyme, reducing levels of angotensin II and preventing inactivation of bradykinin, a potent vasodilator

Renin release is ↑ due to loss of feedback inhibition.
Clinical use of ACE inhibitors? (3)
Hypertension
CHF
Diabetic renal disease
Toxicity of ACE inhibitors?
-mnemonic?
"CAPTOPRIL"

Cough
Angioedema
Proteinuria
Taste changes
hypOtension
Pregnancy problems (fetal renal
damage)
Rash
Increased renin
Lower angiotensin II.

Also hyperkalemia.