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0. Step Ia > Renal Pharm from FA > Flashcards

Renal Pharm from FA Flashcards

1
Q

Mannitol

Mechanism?

A

Osmotic diuretic

Incr tubular fluid osmolarity producing increased urine flow

decreases intracranial/ontraocular pressure

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2
Q

Mannitol

Clinical Use?

A

Drug OD

increased intracranial or intraocular pressure

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3
Q

Mannitol

Tox?

A

Pulmonary edema

Dehydration

Contraindicated in anuria, CHF

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4
Q

Acetazolamide

Mechanism?

A

Carbonic anhydrase inhibitor

Cuases self-limited NaHCO3 diuresis and decreased total-body HCO3- stores

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5
Q

Acetazolamide

Clinical Use?

A
  • Glaucoma
  • Urinary alkalization
  • Metabolic alkalosis
  • Altitude sickness
  • Pseudotumor cerebri (hydrocephalus, occurs w young obese women, decreased CSF outflow at arachnoid villi)
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6
Q

Acetazolamide

Tox?

A

Hypercloremic metabolic acidosis

Paresthesias

NH3 toxicity

Sulfa allergies

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7
Q

Acetazolamide

site of action?

A

Prox convoluted tubule

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8
Q

Mannitol

site of action?

A

Descending tubule

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9
Q

Loop Diuretics: name 2

A
  • Furosemide
  • Ethacrynic acid
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10
Q

Furosemide

site of action?

A

Loop - thick ascending limb

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11
Q

Ethacrynic acid

site of action?

A

Loop - thick ascending limb

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12
Q

Furosemide

Mech?

effect on Ca excretion?

A

Sulfonamide loop diuretic

Inhibits cotransport system (Na/K/2Cl) of thick ascending limb of LOH

abolishes hypertonicity of medulla, preventing concentration of urine.

Stimulates PGE release (vasodilatory effect on afferent arteriole)

Increases Ca excretion

“Loops Lose calcium”

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13
Q

Furosemide

what inhibits it?

A

NSAIDs

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14
Q

Furosemide

Use?

A
  • Edematous states (CHF, cirrhosis, nephrotic syndrome, pulm edema)
  • Hypertension
  • Hypercalcemia
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15
Q

Furosemide

Tox?

A

Ototoxicity

Hypokalemia

Dehydration

Allergy (sulfa)

Nephritis (interstitial)

Gout

“OH DANG”

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16
Q

Ethacrynic Acid

Mech?

effect on Ca excretion?

A

Phenoxyacetic acid derivative (NOT a sulfanamide!)

Same action as Furosemide (inhibits cotransport (Na/K/2Cl).

-> Prevents urine concentration.

Increases Ca excretion

“Loops Lose Ca”

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17
Q

Ethacrynic Acid

Use?

A

Diuresis in patients allergic to sulfa drugs

18
Q

Ethacrynic Acid

Tox?

A

similar to Furosemide (OH DANG)

Can cause hyperuricemia

Never use to treat gout

19
Q

Thiazides

site of action?

A

Distal convoluted tubule

20
Q

Hydrochlorothiazide

Mech?

Effect on Ca excretion?

A

Thiazide diuretic

Inhibts NaCl reabsorption in early distal tubule, decreasing the diluting capacity of the nephron.

Decreases Ca excretion (Ca-sparing)

21
Q

Hydrochlorothiazide

Use?

A

HTN

CHF

Idiopathic hypercalciuria

nephrogenic diabetes insipidus

osteoporosis

22
Q

Hydrochlorothiazide

Tox?

A

Hypokalemic metabolic alkalosis

Hyponatremia

HyperGlycemia

HyperLipidemia

HyperUricemia

HyperCalcemia

Sulfa drug -> allergies

“HyperGLUC”

23
Q

K+ sparing diuretics

Name 4

A

Spironolactone (& Eplerenone)

Triamterene

Amiloride

“The K+ STAyEs”

24
Q

K+ sparing diuretics/Spironolactone and Eplerenone

Mech?

Site of action?

A

Competitive aldosterone receptor antagonists

Cortical collecting tubule

25
Q

K+ sparing diuretics/Trimterene, Amiloride

Mech?

Site of action?

A

Cortical collecting tubule

Block Na+ channels

26
Q

K+ sparing diuretics

Use?

A

Hyperaldosteronism

K+ depletion

CHF

27
Q

K+ sparing diuretics

Tox?

A

Hyperkalemia (can lead to arrhythmias)

Spironolactone: Endocrine effects (gynecomastia, andiandrogen)

28
Q

Diuretics in general

Effect on Urine NaCl?

A

All increase Urine NaCl except Acetazolamide

Serum NaCl may decrease as a result.

29
Q

Diuretics in general

Effect on Urine K?

A

Loop and Thiazide diuretics: Urine K increases

Serum K may decrease

30
Q

Loop diuretics: effect on Urine Ca2+?

A

Urine Ca2+ increases with Loop Diuretics

Mech: decreased paracellular Ca2+ absorption -> hypocalcemia

31
Q

Thiazide diuretics: effect on Urine Ca2+?

A

Urine Ca2+ decreases with Thiazides

Mech: enhanced paracellular Ca2+ reabsorbtion in the distal tubule

32
Q

Which diuretics cause acidemia? mech?

A

Carbonic anhydrase inhibitors (acetazolamide)

Mech: **decreases HCO3- absorption. **

  • > K+ sparing aldosterone blockade prevents K+ secretion and H+ secretion.
  • > Hyperkalemia leads to K+ entering all cells (via H/K exchanger) in exchange for H+ exiting cells
33
Q

What diuretics cause alkalemia?

mech?

A

Loop diuretics and thiazides.

Mech 1: Volume contraction -> incr AT II -> incr Na/H exchange in prox tubule -> incr HCO3- reabsorption (contraction alkalosis)

Mech 2: K+ loss leads to K+ exiting all cells in exchange for H+ entering cells

Mech 3: in low K+ state, H+ is exchanged for Na+ (rather than K+) in cortical collecting tubule -> alkalosis and “paradoxical aciduria”

34
Q

ACE inhibitors

name 3

A

Captopril

Enalapril

Lisinopril

35
Q

ACE inhibitors

mech?

A

inhibit ACE -> decr At II -> decr GFR by preventing constriction of efferent arterioles.

Renin increases due to loss of feedback inhibition.

ACE inhibition also prevents inactivation of bradykinin (vasodilator)

36
Q

AT II blockers (-sartans)

effect?

A

similar to ACE inhibitors

do not increase bradykinin so there is decr risk of cough or angioedema

37
Q

ACE inhibitors

use?

A

HTN

CHF

proteinuria

diabetic nephropathy

Prevent heart remodeling as a result of chronic HTN

38
Q

ACE inhibitors

Tox?

A

Cough

Angioedema

Teratogen

incr Creatinine (decr GFR)

HyperKalemia

Hypotension

“Captoprils CATCHH”

39
Q

ACE inhibitors

teratogenic effect?

A

fetal renal malformations

40
Q

ACE inhibitors

contraindications?

A
  • C1 esterase inhbitor deficiency
  • Bilateral renal artery stenosis (because ACE inh will further decr GFR -> renal failure)

0. Step Ia (28 decks)

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