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33 Cards in this Set
- Front
- Back
Site of action of Acetazolamide?
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proximal convoluted tubule
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Site of action of Osmotic diuretics (mannitol)? (3)
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proximal convoluted tubule
loop of Henle collecting duct |
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Site of action of Loop agents (furosemide)? (2)
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distal convoluted tubule
thick ascending limb of loop of Henle |
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Site of action of K+ sparing diuretics?
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distal convoluted tubule
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Site of action of ADH antagonists?
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collecting duct
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MOA of Mannitol?
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Osmotic diuretic, ↑ tubular fluid osmolarity, producing ↑ urine flow.
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Clinical use of Mannitol?
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-shock
-drug overdose -↓ intracranial/intraocular pressure. |
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Toxicity of Mannitol? (2)
Who is it C/I in? |
-pulmonary edema
-dehydration Contraindicated in anuria, CHF. |
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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. |
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Clinical use of Acetazolamide? (4)
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Glaucoma
Urinary alkalinization Metabolic alkalosis Altitude sickness |
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Toxicity of Acetazolamide?
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-hyperchloremic metabolic acidosis
-neuropathy -NH3 toxicity -sulfa allergy |
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does acetazolamide cause alkalosis or acidosis?
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ACIDazolamide causes ACIDosis
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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." |
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Clinical use of Furosemide? (3)
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-Edematous states (CHF, cirrhosis, nephrotic syndrome, pulmonary edema), -hypertension
-hypercalcemia. |
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Toxicity of Furosemide?
-mnemonic? |
"OH DANG"
Ototoxicity Hypokalemia Dehydration Allergy (sulfa) Nephritis (interstitial) Gout |
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MOA of Ethacrynic acid?
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Phenoxyacetic acid derivative (NOT a sulfonamide).
Essentially same action as furosemide. |
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Clinical use of Ethacrynic acid?
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Diuresis in patients allergic to sulfa drugs.
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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).
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MOA of HCTZ?
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Thiazide diuretic.
Inhibits NaCl reabsorption in early distal tubule, reducing diluting capacity of the nephron. ↓ Ca2+ excretion. |
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Clinical use of HCTZ? (4)
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Hypertension
CHF Idiopathic hypercalciuria Nephrogenic diabetes insipidus |
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Toxicity of HCTZ?
-mneumonic? -allergy? |
Hypokalemic metabolic alkalosis
hyponatremia hyperGlycemia hyperLipidemia hyperUricemia hyperCalcemia "HyperGLUC" Sulfa allergy |
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What drugs are K+-sparing diuretics? (4)
-mnemonic? |
Spironolactone
Triamterene Amiloride eplereone "The K+ STAys" |
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MOA of K+-sparing diuretics?
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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. |
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Clinical use of K+-sparing diuretics? (3)
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Hyperaldosteronism
K+ depletion CHF |
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Toxicity of K+-sparing diuretics? (2)
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Hyperkalemia
Endocrine effects (e.g., spironolactone causes gynecomastia, antiandrogen effects). |
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How does urine NaCl change with diuretics?
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↑ (all diuretics––carbonic anhydrase inhibitors, loop diuretics, thiazides, K+-sparing diuretics).
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How does urine K+ change with diuretics?
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↑ (all except K+-sparing diuretics).
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How does blood pH change with diuretics?
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↓ (acidosis)––carbonic anhydrase inhibitors, K+-sparing diuretics
↑ (alkalosis)––loop diuretics, thiazides. |
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How does urine Ca+ change with diuretics?
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↑ loop diuretics
↓ thiazides |
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What drugs are ACE inhibitors? (3)
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Captopril
Enalapril Lisinopril. |
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MOA of ACE inhibitors?
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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. |
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Clinical use of ACE inhibitors? (3)
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Hypertension
CHF Diabetic renal disease |
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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. |