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Therapeutics II > Renal Pathophysiology and Diuretics > Flashcards

Renal Pathophysiology and Diuretics Flashcards

1
Q

Define diuretics

A

Agents that induce natriuresis (sodium excretion) and diuresis (water excretion)

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2
Q

Diuretics indications

A
  • edematous states
  • HTN
  • heart failure
  • acute renal failure
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3
Q

Common active ingredient in OTC diuretics

A

caffeine

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4
Q

Diuretic key principles

A
  • osmosis: water follows salt
  • when NA is excreted more than Na intake, BW and ECF decrease
  • When Na excretion is equal to na intake, BW and ECF stabilize at lower level due to braking effect
  • When Na excretion is less than Na intake, BW and ECF rise
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5
Q

Diuretic Braking Effect

A

The activation of the renin-angiotension-aldosterone system (RAAS) and symptomatic nervous system (SNS) when a new steady state is formed after Na excretion exceeds intake. There is a subsequent new steady state achieved where Na and excretion are equal but at a lower ECFV and body weight.

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6
Q

Classifications of diuretics (site of action, efficacy, structure, effect K+ excretion)

A
  • site of action = loop diuretics
  • efficacy = high-ceiling diuretics
  • structure = thiazides
  • effect K+ excretion = potassium-sparing
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7
Q

Site of diuretic drug action

A

in tubule

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8
Q

most diuretics have ____ protein binding —-> don’t filter through bowman’s capsule

A

high

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9
Q

most diuretics require transport/secretion in the _______ tubule

A

proximal

  • drug interactions with renal transporters
  • contrast many other drug classes (P450s)
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10
Q

T/F: Pharmacodynamic action doesn’t track with serum concentrations

A

TRUE

-correlates with renal excretion rates

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11
Q

Inhibitors of Carbonic anhydrase facts

A
  • CA-I inhibit both cytoplasmic CA and membrane-bound CA
  • CA-I essentially block reabsorption of NaHCO3
  • H2O chases Na
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12
Q

Carbonic anhydrase catalyzes

A

OH- + CO2 –> HCO3-

Since H2O –> OH- + H+, and HCO3- + H+ –> H2CO3, the net reaction is H2O + CO2 —> H2CO3

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13
Q

Sulfanilamide shown to produce mild _____

A

diuresis

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14
Q

inhibitors of carbonic anhydrase causes urine to become more

A

basic, acid is blocked from being formed. The antiporter is blocked

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15
Q

Carbonic anhydrase inhibitors POTENCY

A

dichlorphenamide (30) >

Methazolamide (>1, <10) >

acetazolamide (1)

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16
Q

Carbonic anhydrase inhibitor inhibitors ORAL BIOAVAILABILITY

A

acetazolamide = methazolamide = 100% bioavailability

dichlorphenamide = ID

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17
Q

Carbonic anhydrase inhibitor inhibitors HALF-LIFE

A

acetazolamide = 6 - 9 hours

methazolamide = ~14 hours

dichlorphenamide = ID

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18
Q

Carbonic anhydrase inhibitor inhibitors ROUTE OF ELIMINATION

A

acetazolamide = R

methazolamide = ~25%, ~75% M

dichlorphenamide = ID

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19
Q

Carbonic anhydrase inhibitor inhibitors CLINICAL USES

A
  • low efficacy
  • acute mountain sickness
  • metabolic alkalosis
  • glaucoma
  • urinary alkalinization
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20
Q

Carbonic anhydrase inhibitor inhibitors TOXICITIES

A

***hyperchloremic metabolic acidosis

  • renal stones
  • renal potassium wasting
  • drowsiness / paresthesia
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21
Q

Cross sensitivity with diuretics and sulfonamide antimicrobials

A
  • possibility but not contraindicated
  • most patients with purported drug allergy do not react upon exposure
  • rash is super rare
  • no study confirmed cross-sensitivity
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22
Q

Osmotic diuretics facts

A
  • pharmacologically inert
  • non-reabsorbable substances that shift osmotic gradient/flow
  • major site = loop of henle + PCT
  • alternating renal medullary blood flow contributes to diuresis
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23
Q

Osmotic diuretics: Mannitol can cause

A
  • loss of water
  • reduced intracellular volume
  • hypernatremia risk
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24
Q

IV delivered osmotic diuretics

A

Mannitol, urea

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25
Q

Orally active osmotic diuretics

A

isosorbide, glycerin, glucose

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26
Q

Osomotic diuretics act in regions of _____ water permeability

A

high

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27
Q

Thick ascending limb =

A

high ceiling diuretics

28
Q

Inhibitors of Na+, -K+, -2Cl- Symport =

A

loop diuretics, high-ceiling diuretics

29
Q

Inhibitors of Na+, -K+, -2Cl- Symport (loop diuretics) facts

A
  • act on luminal surface symport –> must be in lumen for diuretic activity
  • rapid response after IV admin
  • most POTENT class (useful for edema)
  • some possess weak CA inhibitory activity (e.g. furosemide)
  • chronically reduce uric acid secretion
  • problems with K, Ca, Mg reuptake
30
Q

Most potent diuretic

A

inhibitors of Na+ -K+ -2Cl- Symport (loop diuretics)

31
Q

Inhibitors of Na+, -K+, -2Cl- Symport (loop diuretics) Problems with

A

K, Ca, Mg reuptake

32
Q

Inhibitors of Na+-K+-2Cl- Symport RELATIVE POTENCY

A

Bumetanide (40) > Torsemide (3) > Furosemide (1) > Ethacrynic Acid (0.7)

33
Q

Inhibitors of Na+-K+-2Cl- Symport ORAL BIOAVAILABILITY

A

Bumetanide = 80%

Torsemide = 80%

Furosemide = 60%

Ethacrynic Acid = 100%

34
Q

Inhibitors of Na+-K+-2Cl- Symport HALF-LIFE

A

Bumetanide = 0.8 hrs

Torsemide = 3.5 hrs

Furosemide = 1.5 hrs

Ethacrynic Acid = 3.5 hr

35
Q

Inhibitors of Na+-K+-2Cl- Symport ROUTE OF ELIMINATION

A

Bumetanide = 62% r, 38% m

Torsemide = 20% R, 80% M

Furosemide = 65% R, 35% m

Ethacrynic Acid = 67% R, 33% M

36
Q

Inhibitors of Na+-K+-2Cl- Symport CLINICAL USES

A
  • edematous conditions
  • acute pulmonary edema
  • acute hypercalcemia
  • hyperkalemia
  • acute renal failure
  • anion overdose
37
Q

Inhibitors of Na+-K+-2Cl- Symport TOXICITIES

A
  • dehydration (fluid intake important)
  • hypokalemic metabolic alkalosis
  • ototoxicity (rate of admin impt)
  • hyperuricemia (gout)
  • hypomagnesemia
38
Q

Inhibitors of Na+-Cl- Symport (thiazide) facts

A
  • predominantly increase NaCl excretion independent of CA
  • Act primarily on DCT, proximal tubule secondary
  • affects K+ reuptake
39
Q

Thiazides originally CA inhibitors

A

-optimization for diuretic efficacy revealed alternate target

(-Na-K+-2Cl- Symport –> Na+Cl- Symport)

  • work well but for the wrong reason
  • two subclasses: Thiazide + hydrothiazide
40
Q

Thiazide potency

A

Most potent = Polythiazide, Trichlormethiazide, Indapamide

Least potent = hydrochlorothiazide, hydroflumethiazide, chlorothiazide

41
Q

Thiazide Clinical uses

A
  • HTN
  • Heart failure
  • Nephrolithiasis due to idiopathic hypercalciuria
  • nephrogenic diabetes insipidus
42
Q

Thiazide Toxicities

A
  • hypokalemic metabolic alkalosis
  • hyperuricemia (secretion)
  • impaired carbohydrate tolerance
  • hyperlipidemia
  • hyponatremia
43
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics)

A
  • act at late distal tubule and collecting duct
  • agents are relatively weak diuretics

***primarily used in combination with other diuretics

-K sparing

44
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) RELATIVE POTENCY

A

Amiloride (1) > triamterene (0.1)

45
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) ORAL BIOAVAILABILITY

A

Amiloride = 15 - 25%

triamterene = 50%

46
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) HALF LIFE

A

Amiloride = 21 hours

triamterene = 4 hours

47
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) ROUTE OF ELIMINATION

A

Amiloride = r

triamterene = m (transformed into an active metabolite that is excreted in the urine)

48
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) CLINICAL USES

A

adjunctive treatment with thiazide or loop diuretic in heart failure or HTN

49
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) TOXICITIES

A
  • hyperkalemia

- hyperchloremic metabolic acidosis

50
Q

Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) CONTRAINDICATIONS

A
  • k+ supplements

- ACE inhibitors

51
Q

Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) FACTS

A
  • MRA bind to MR and block AIP production
  • only diuretics that do not act within the tubular lumen
  • Drugs need to be lipophillic to enter cells
  • DRUGS LOOK LIKE STEROIDS!!!
52
Q

Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) ORAL BIOAVAILABILITY

A

Spironolactone = 65%

other 3, ID

53
Q

Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) HALF LIFE

A
  • Spironolactone = 1.6 hrs
  • Canrenone = 16.5 hrs
  • Potassium = ID
  • Eplerenone = 5 hrs
54
Q

Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics)

A
  • Spironolactone = M
  • Canrenone = M
  • Potassium = M
  • Eplerenone = M
55
Q

Mineralocorticoid Receptor Antagonists (MRA) CLINICAL USES

A
  • HTN
  • Mineralocorticoid excess
  • Aldosteronism (primary or secondary from HF, hepatic cirrhosis or nephrotic syndrome)
56
Q

Mineralocorticoid Receptor Antagonists (MRA) TOXICITIES

A
  • hyperkalemia
  • hyperchloremic metabolic acidosis
  • gynecomastia (due to blocking P450, blocks androgen)
  • impotence
  • BPH
57
Q

Mineralocorticoid Receptor Antagonists (MRA) CONTRAINDICATIONS

A
  • k+ supplements, ACE inhibitors

- chronic renal insufficiency

58
Q

Non-specific Cation Channel Inhibitors (Nesiritide Natrecor)

A
  • recombinant form of the 32 AA human B-type natriuretic peptide
  • inhibits cGMP-gated cation channel
  • therapeutic role in HF debated

(large peptide that interferes with ion channels)

59
Q

Vasopressin Antagonists Facts

A

V1 = blood vessels constrict = increased systemic vascular resistance = increased arterial pressure

V2 = kidneys cause fluid reabsorption = increased blood bolume = increased arterial pressure

H2O REABSORPTION IS STOPPED

60
Q

Vasopressin Antagonists are ______ potent diuretics

A

not very

61
Q

Diuretic response: Action ______ correlate with serum/plasma concentrations

A

does not

62
Q

Diuretic response: site of action is __________

A

luminal

63
Q

CA inhibitors, furosemide and thiazide diuretics highly bound to plasma protein —> _________ not __________

A

secreted not filtered

64
Q

Secretion (transporters) is saturable —> _________

Increased doses will not ______ urine

Consider changing ________ to increase response

Secretion of diuretics decreases with progressive renal failure —> _______ their effectiveness (drug doesn’t reach site of action)

A

DOSE DEPENDENT

increase

frequency

reduces

65
Q

Sensitivity to diuretics is _______ due to homeostatic responses in CRF (including hyperaldosteronism)

A

reduced

Therapeutics II (12 decks)

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