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Pharm 6 > Diuretics > Flashcards

Diuretics Flashcards

0
Q

Na-K-2Cl symport inhibitor

A

Forosemide

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1
Q

Carbonic Anhydrase Inhibitor

A

Acetazolamide

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2
Q

NA-Cl Symport inhibitor

A

Chlorothiazide

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3
Q

Potassium sparring diuretic: Epithelial Na+ channel inhibitors

A

Amiloride, triamterene

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4
Q

Potassium sparing Diuretic: Aldosterone Antagonist

A

Spironolactone

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5
Q

Osmotic Diuretic

A

Mannitol

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6
Q

Vasopressin Receptor Antagonist

A

Demeclocycline

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7
Q

Na+/K+-ATPase- on the ______________ membrane of tubular epithelial cells maintains an intracellular ___ gradient that is the _________ __________ for tubular reabsorption of Na+

A

Basolateral,
Na+,
Driving force

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8
Q

Dodium transporters and channels- Exist on the ________ side of the tubular cells and are pathways for Na+ _______; they are the molecular targets for most diuretics (exception: aldosterone antagonists).

A

Apical (luminal),

entry

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9
Q

Compensation is when electrolyte (Na+) reabsorption at a particular site of nephron is blocked and then the nephron will attempt to “compensate” by reabsorbing downstream. What is a consequence of this?

A

Loss of K+: More Na+ in collecting duct=more K+ secreted

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10
Q

Site of action for Carbonic anhydrase Inhibitors (Acetazolamide)

A

Proximal tubule- compensation can occur to efficacy is moderate

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11
Q

MOA of Carbonic anhydrase inhibitors (Acetazolamide)

A

Competitive inhibitor of carbonic anhydrase (CA)

  • CA is responsible for Na HCO3 reabsorption and acid secretion
  • Inhibits both apical and membrane-bound (typeIV) and cytosolic (type II) CA
  • Blocks formation of CO2 at the luminal surface and protons in the cytosol
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12
Q

What drug is this: Therapeutic uses rarely as diuretic. Major use for open-angle glaucoma, altitude sickness, and epilepsy.

A

Carbonic anhydrase inhibitors (Acetazolamide)

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13
Q

Adverse effects for Carbonic anhydrase inhibitors (Acetazolamide)

A

Big ones: Urinary alkalinization and METABOLIC ACIDOSIS producing secondary effects: RENAL STONE FORMATION, hepatic encephalopathy, reduced excretion of weak bases.

  • Hypokalemia
  • Toxicities associated with sulfonamides
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14
Q

Site of action for: Na+-K+-2Cl- Symport Inhibitors: Loop diuretics (Furosemide)

A

Thick ascending limb, loop of henle- high efficacy

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15
Q

MOA for Na+-K+-2Cl- Symport Inhibitors: Loop diuretics (Furosemide)

A
  • Abolishes trans-epithelial potential difference that drives paracellular transport of Ca++ and Mg++
  • Marked increase in excretion of Ca++ and Mg++
  • Decreases Uric acid excretion (chronic effect)
  • Reduces ability of kidney to 1) concentrate urine in hydropenia and 2) dilute urine during water diuresis
16
Q

Therapeutic uses for Na+-K+-2Cl- Symport Inhibitors: Loop diuretics (Furosemide)

A

a) Acute pulmonary edema
b) CHF
3) Hypercalcemia
4) Hyponatremia
5) Edema for nephrotic syndrome

17
Q

Adverse effects for Na+-K+-2Cl- Symport Inhibitors: Loop diuretics (Furosemide)

A

Mostly caused by fluid and electrolyte imbalance.

a) OTOTOXICITY
b) HYPERGLYCEMIA
c) hyponatremia and hypokalemia
d) Hypocalcemia
e) Hyperuricemia
f) NSAIDS reduce diuretic efficacy

18
Q

Diuretic that acts at distal convoluted tubule

A

Na+-CL- Symport inhibitors- Thiazide and Thiazide-like diuretics (Chlorothiazide)
-Efficacy is moderate and dose response is shallow (compared to loops)

19
Q

MOA for Na+-CL- Symport inhibitors- Thiazide and Thiazide-like diuretics (Chlorothiazide)

A

a) Weak inhibitor of Carbonic anhydrase in PT as well.
b) In contrast to loop diuretics, efficacy is substantially REDUCED when GFR is low. Ex: In CHF
c) Decreases excretion on Ca++
d) Attenuates ability of kidney to dilute urine during diuresis; concentrating ability is unchanged.

20
Q

Therapeutic uses for Na+-CL- Symport inhibitors- Thiazide and Thiazide-like diuretics (Chlorothiazide)

A

a) HTN
b) Mild edema
c) Nephrogenic diabetes insipidus
d) Calcium nephrolithiasis and osteoporosis

21
Q

Adverse Effects of Na+-CL- Symport inhibitors- Thiazide and Thiazide-like diuretics (Chlorothiazide)

A

A) Hyperlipidemia and hyperglycemia
B) ERECTILE DYSFUNCTION
C) Hypokalemia, hyponatremia
D) Drug interactions: NSAIDS (reduce efficacy) and Quinidine (Hypokalemia increase torsades de pointes)

22
Q

What drugs site of action is at the late distal tubule and collecting duct?

A

Potassium Sparing Diuretics: Triamterene, Amiloride, Spirinolactone

23
Q

Triamterene and Amiloride are what type of inhibitors?

A

Renal epithelial Na+ channel (ENaC) inhibitors

24
Q

Spironlactone is what type of antagonist? MOA?

A

Aldosterone- block cytosolic mineralcorticoid receptors in principal cells

25
Q

Therapeutic uses for Potassium Sparing Diuretics: Triamterene, Amiloride, Spirinolactone

A

-Not for their diuretic effect
A) Both used with other (K-Wasting) diuretics to prevent hypokalemia- because they both abolish transepithelial potential that drives tubular secretion of K+.
B) ENaC inhibitors: Liddle syndrome and cystic fibrosis
C) Aldosterone Antag.: Primary hyperaldosteronism, hepatic cirrhosis, CHF (reduces mortality)

26
Q

Adverse effects of Potassium Sparing Diuretics: Triamterene, Amiloride, Spirinolactone

A

A) HYPERKALEMIA- Can be life threatening; use caution with NSAIDs and ACE Inhibitors.
B) Spironlactone- Affinity for steroid receptors can produce HYNECOMASTIA, IMPOTENCE, hirsutism, decreased libido

27
Q

What drugs site of action is at loop of henle (primary) and renal tubules (secondary)?

A

Osmotic diuretics: Mannitol

28
Q

MOA for Osmotic diuretics: Mannitol

A
  • Increases osmolality of tubular fluid (and plasma).
  • Reduces renal medullary tonicity, reducing passive reabsorption of NaCl in ascending loop of henle.
  • Expands extracellular fluid volume and inhibits release of renin.
29
Q

Effects on urinary excretion for Osmotic diuretics: Mannitol

A

Increases excretion of all electrolytes

30
Q

Therapeutic uses for Osmotic diuretics: Mannitol

A

Dialysis disequilibrium syndrome; reduces pre- and postoperative CSF and intraocular pressure

31
Q

Contraindications for Osmotic diuretics: Mannitol

A

Contraindicated in Heart failure (edema) and active cranial bleeding

Pharm 6 (9 decks)

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