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Pharm Spring Exam 1 > Exam I - Diuretics > Flashcards

Exam I - Diuretics Flashcards

1
Q

Drug List

Carbonic Anhydrase Inhibs

A

Acetazolamide

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2
Q

Drug List

Osmotic Diuretics

A

Mannitol

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3
Q

Drug List

Loop Diuretics

A

Furosemide

inhibit TAL Na/K/2Cl

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4
Q

Drug List

Thiazides

A

Hydrochlorathiazide

inhib DCT Na/Cl

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5
Q

Drug List

K-Sparing

A

Amiloride

inhib late DCT ENaC

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6
Q

Drug List

ARB/K-sparing

A

Spironolactone
(block Aldosterone by
inhib DCT Na/K)

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7
Q

Drug List

ADH antags

A

Tolvaptan

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8
Q

Diuretic Braking

A

-Physiological compensation
for lost Na
-^symp, ^RAAS, ^ADH
-new steady state reached

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9
Q

ECFV Body Fluid

A
  • 44% interstitium
  • 17% plasma
  • 17% bone
  • 17% dens conn tiss
  • 5% transcellular
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10
Q

Diuretics target what ECFV?

A

-plasma
-interstitial
(these compartments equilibrate)

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11
Q

Edematous Indications

A
  • CHF
  • Pulm Edema
  • Nephrotic Dz
  • Hepatic Cirrhosis
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12
Q

Hypertensive Indications

A
  • Essential
  • Renovasc HTN (hypoperfusion)
  • Renal HTN (poor excretion)
  • Hyperaldosteronism
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13
Q

Right-sided HF

Pathophysiology/Clin

A
  • systemic edema
  • ascites
  • nocturia
  • hepatomegaly
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14
Q

Left-sided HF

Pathophysiology/Clin

A
  • pulm edema
  • SOB
  • Wheezing
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15
Q

Renal Handling Na+
Nephron Reabsorption
Percentages

A
  • 67% PCT
  • 25% TAL
  • 4% early DCT
  • 3% late DCT
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16
Q

Renal Handling Na+
Nephron Reabsorption
Channels

A
  • PCT: glc/AA/phosph symport
  • PCT: H+ antiport
  • TAL: Na/K/2Cl symport
  • DCT: Na/Cl symport
  • DCT: Na/K antiport
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17
Q

Carbonic Anhydrase

Function

A
  • drives HCO3->H2CO3-> H2O/CO2
  • intracellularly and in PCT
  • increases intracellular H+ for H+/Na+ antiport
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18
Q

Carbonic Anhydrase Inhibitors

Mechanism

A

-CAIs secreted into PCT
-inhibs CA both
intra/extracellularly
-reduces available H+ for Na+/H+ antiport
-Na+ therefore left in PCT lumen

19
Q

Carbonic Anhydrase Inhibitors

Systemic Effects

A
  • Alkalinized urine
  • Activates TGF
  • decr. Plasma HCO3 (decr. pH), Cl
20
Q

Carbonic Andydrase Inhibitors

Indications

A
  • decr intraocular pressure
  • metabolic alkalosis
  • acute mountain sickness
  • resp alkalosis prophylaxis
21
Q

Carbonic Anhydrase Inhibitors

Adverse

A
  • hyperchloremic metabolic acidosis

- renal stones

22
Q

Loop Diuretics

Mechanism

A
  • secreted into PCT
  • Blocks TAL Na/K/2Cl symport
  • Abolishes corticomedullary gradient
23
Q

Loop Diuretics

Adverse

A
  • abolish osmotic gradient
  • increase renal blood flow
  • increased excretion of all ions
  • hypokalemia (arrhythmias)
  • HoTN
  • Hyperuricemia
  • Ototoxicity
24
Q

Loop Diuretics

Indications

A

-Edema of renal/pulm/cardiac/hepatic origin

25
Q

Thiazides

Mechanism

A
  • Secreted into PCT (anion transporter)
  • Inhibit Na/Cl contransporter in DCT
  • Do NOT abolish corticomedullary gradient
  • Ca2+ sparing
26
Q

Thiazides

Adverse

A
  • hypokalemia (combat with ACEI co-rx)
  • metablolic alkalosis
  • hypovolemia (and further hypokalemic exacerbation)
  • hypercalcemia/glycemia (DM)/lipidemia/uricemia
  • HoTN
27
Q

Thiazides

Indications

A
  • hypercalciuria
  • Nephrogenic diabetes insipidus
  • HTN, CHF
28
Q

Loop/Thiazide
K+ loss
Cells responsible

A
  • CD principle cells

- via apical K+ channels

29
Q

Loop/Thiazide
H+ loss
Cells responsible

A
  • CD intercalated cells

- via H+/K+ exchange

30
Q

K-sparing ARBs

Mechanism

A
  • do NOT need to be secreted; act on basolateral membrane
  • canrenone is active metabolite
  • complexes with and inactivates mineralocorticoid receptor in DCT
  • inhibits Na/K antiporter in CD
31
Q

K-sparing ENaC blockers

Mechanism

A
  • secreted into PCT by cation transporter
  • block luminal ENaC Na+ reabsorption in late DCT/CD
  • downregs complimentary K+ secretion/excretion
  • effects are independent from aldosterone
32
Q

K-Sparing ENaC blockers

Adverse

A

-hyperkalemia (esp w/ renal dz)

33
Q

K-Sparing ENaC blockers

indications

A

-adjunct to loop/thiazide tx to preserve K+

34
Q

K-Sparing ARBs

adverse

A
  • hyperkalemia (contra’d in chronic renal insufficiency)
  • gynecomastia :( (antiandrogenic)
  • menstrual irregularities
35
Q

Osmotic Diuretics

Mechanism

A
  • freely filtered at glomerulus
  • osmotic gradient favors water in tubules
  • acts on water permeable segments (PT, TDLH, CD)
  • incr renal blood flow
36
Q

Osmotic Diuretics

Adverse

A
  • Mg2+ wasting

- Hyperkalemia

37
Q

Osmotic Diuretics

Indications

A

-reduce intracranial/intraocular P before/after surgery

38
Q

ADH antagonists

Mechanism

A

-binds V2 ADH receptor on CD basolateral membrane

39
Q

ADH antagonists

Adverse

A

-hypernatremia

40
Q

ADH antagonists

Indications

A

-SIADH

41
Q

Is EtOH diuretic?

A
  • Yes!

- Why? Interferes with Aquaporins in CD

42
Q

Diuresis not optimal?

What shoud you do?

A
  • synergistic additive effects of co-rx loop + thiazide

- co-rx should be given with close hemodynamic monitoring

43
Q

Diuresis causing hypokalemia?

What should you do?

A

-co-rx with K-sparing diuretic

44
Q

Is caffeine diuretic?

A
  • Yes!

- Why? it’s a methylxanthine; blocks PCT Na reabsorption

Pharm Spring Exam 1 (8 decks)

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