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Pharmacology B2 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Mannitol MOA

A

MOA: Osmotic diuretic. inhibits water reabsorption throughout the tubule. Increases urine volume.

Target: descending LOH and PCT

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2
Q

Carbonic Anhydrase Inhibitors and MOA

A

acetazolamide and dorzolamide

carbonic anhydrase inhibition in PCT

Urinary Electrolytes:
↑ Na+ ↑K+
↑↑ HCO3

Blood: Acidosis

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3
Q

Carbonic Anhydrase Inhibitors Uses

A 
Glaucoma, 
urinary alkalinization, 
metabolic alkalosis, 
altitude sickness, 
pseudotumor cerebri.
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4
Q

Mannitol Use

A

Use: Drug overdose, elevated intracranial/intraocular pressure.

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5
Q

Side effects and ADR of Mannitol

A

Side effects: acute hypovolemia

ADR: Pulmonary edema, dehydration. Contraindicated in anuria, HF.

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6
Q

Carbonic Anhydrase Inhibitors side effects:

A

Side effects:

  1. Hyperchloremic metabolic acidosis
  2. Renal stone: due to increase urine phosphate and calcium
  3. Hypokalemia
  4. Decreases urine NH4 + excretion, worsening hepatic coma
  5. Cross-allergy with sulfonamide
  6. Paresthesias
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7
Q

CA inhibitors contraindications

A

Contraindications:
Hepatic encephalopathy
Sulfonamide allergy

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8
Q

Loop diuretics and MOA

A

Furosemide, bumetanide, torsemide

Ethacrynic acid - no sulfonamide-like

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

Urine: 
↑↑ Na+
↑K+
↑ Ca2+
↑ Mg2+ ↑ Cl-

Blood: Alkalosis

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9
Q

Loop diuretics uses

A 
Uses: Edematous state
Hyperkalemia
Hypercalcemia (Loops Lose Ca2)
Acute renal failure
Acute heart failure
Hypertension emergency
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10
Q

Loop diuretics ADR: OHH DAANG

A 
Ototoxicity,
Hypokalemia, 
Hypomagnesemia, 
Dehydration, 
Allergy (sulfa),
metabolic Alkalosis, 
Nephritis (interstitial), 
Gout.
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11
Q

Loop diuretics drug interactions:

A

Drug interactions
– Aminoglycosides (enhanced ototoxicity)
– Lithium (chronic loop administration,↓clearance)
– Digoxin (↑ toxicity due to electrolyte disturbances)

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12
Q

Thiazides and MOA

A

Hydrochlorothiazide, chlorthalidone, metolazone.

Na+/Cl− transporter inhibition in early DCT

Urine:
↑ Na+ ↑K+
↑ Cl-
↓ Ca2+

Blood: Alkalosis

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13
Q

Thiazides Uses

A 
USES:
Hypertension
MOA: 
Short term is due to decrease of Blood Volume
Long term is due to direct decrease in vessel tension (possible by K+ channel opening)
Kidney stone or hypercalciuria
Nephrogenic diabetes insipidus
Chronic heart failure
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14
Q

Thiazides ADR (HyperGLUC)

A

HyperGLUC

Hypokalemic metabolic alkalosis, hyponatremia,

hyperGlycemia,
hyperLipidemia,
hyperUricemia,
hyperCalcemia.

Sulfa allergy.

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15
Q

K sparing diuretics MOA - The K+ STAys

A

Aldosterone antag: Spironolactone and eplerenone
ENaC direct inhibitors: Triamterene, and Amiloride

Spironolactone and eplerenone competitive aldosterone receptor antagonists in cortical collecting tubule.

Triamterene and amiloride act at the same part of the tubule by blocking Na+ channels in the cortical collecting tubule.

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16
Q

Combining K+-sparing diuretics with ________ may cause hyperkalemia.

A

ACEIs or ARBs

17
Q

Uses of K sparing diuretics:

A

Hyperaldosteronism, K+ depletion, HF, hepatic ascites (spironolactone), nephrogenic DI (amiloride), antiandrogen.

spironolactone and eplerenone decrease chronic heart failure (CHF) mortality- increase long term survival

18
Q

ADR of K sparing diuretics

A

Hyperkalemia (can lead to arrhythmias), endocrine effects with spironolactone (eg, gynecomastia, antiandrogen effects)

19
Q

How do B Blockers effect RAAS ?

A

BBs reduce renin, angio I, angio II, ald and do not affect bradykinin

20
Q

Aliskren MOA and effect on RAAS

A

inhibits renin

increase renin 
increase angio I 
decrease anio II 
decrease ald 
No effect on BradyK
21
Q

ACE inhibitors MOA and effect on RAAS

A

inhibit ACE

increase renin 
increase angio I 
decrease anio II 
decrease ald 
increase BradyK
22
Q

Angio II receptor 1 blocker (ARB) effect on RAAS

A 
increase renin 
increase angio I 
increase angio II 
decrease ald 
increase BradyK
23
Q

Angio II receptor 1 blocker (ARB) ADR - (CATCHH)

A

Captopril’s CATCHH.

Cough, 
Angioedema (due to  bradykinin; contraindicated in C1 esterase inhibitor deficiency), 
Teratogen (fetal renal malformations),
 Creatinine ( GFR), 
Hyperkalemia, and 
Hypotension.

No use in renal artery stenosis, will cause renal failure

24
Q

Uses of ACE inhibitors

A 
Hypertension, 
HF ( mortality), 
proteinuria, 
diabetic nephropathy.
Prevent unfavorable heart remodeling as a result of chronic hypertension.

Pharmacology B2 (10 decks)

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