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Therapeutics II > Renal Pathophysiology and Diuretics > Flashcards

Renal Pathophysiology and Diuretics Flashcards

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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
Orally active osmotic diuretics
isosorbide, glycerin, glucose
26
Osomotic diuretics act in regions of _____ water permeability
high
27
Thick ascending limb =
high ceiling diuretics
28
Inhibitors of Na+, -K+, -2Cl- Symport =
loop diuretics, high-ceiling diuretics
29
Inhibitors of Na+, -K+, -2Cl- Symport (loop diuretics) facts
- 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
Most potent diuretic
inhibitors of Na+ -K+ -2Cl- Symport (loop diuretics)
31
Inhibitors of Na+, -K+, -2Cl- Symport (loop diuretics) Problems with
K, Ca, Mg reuptake
32
Inhibitors of Na+-K+-2Cl- Symport RELATIVE POTENCY
Bumetanide (40) > Torsemide (3) > Furosemide (1) > Ethacrynic Acid (0.7)
33
Inhibitors of Na+-K+-2Cl- Symport ORAL BIOAVAILABILITY
Bumetanide = 80% Torsemide = 80% Furosemide = 60% Ethacrynic Acid = 100%
34
Inhibitors of Na+-K+-2Cl- Symport HALF-LIFE
Bumetanide = 0.8 hrs Torsemide = 3.5 hrs Furosemide = 1.5 hrs Ethacrynic Acid = 3.5 hr
35
Inhibitors of Na+-K+-2Cl- Symport ROUTE OF ELIMINATION
Bumetanide = 62% r, 38% m Torsemide = 20% R, 80% M Furosemide = 65% R, 35% m Ethacrynic Acid = 67% R, 33% M
36
Inhibitors of Na+-K+-2Cl- Symport CLINICAL USES
- edematous conditions - acute pulmonary edema - acute hypercalcemia - hyperkalemia - acute renal failure - anion overdose
37
Inhibitors of Na+-K+-2Cl- Symport TOXICITIES
- dehydration (fluid intake important) - hypokalemic metabolic alkalosis - ototoxicity (rate of admin impt) - hyperuricemia (gout) - hypomagnesemia
38
Inhibitors of Na+-Cl- Symport (thiazide) facts
- predominantly increase NaCl excretion independent of CA - Act primarily on DCT, proximal tubule secondary - affects K+ reuptake
39
Thiazides originally CA inhibitors
-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
Thiazide potency
Most potent = Polythiazide, Trichlormethiazide, Indapamide Least potent = hydrochlorothiazide, hydroflumethiazide, chlorothiazide
41
Thiazide Clinical uses
- HTN - Heart failure - Nephrolithiasis due to idiopathic hypercalciuria - nephrogenic diabetes insipidus
42
Thiazide Toxicities
- hypokalemic metabolic alkalosis - hyperuricemia (secretion) - impaired carbohydrate tolerance - hyperlipidemia - hyponatremia
43
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics)
- act at late distal tubule and collecting duct - agents are relatively weak diuretics ***primarily used in combination with other diuretics -K sparing
44
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) RELATIVE POTENCY
Amiloride (1) > triamterene (0.1)
45
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) ORAL BIOAVAILABILITY
Amiloride = 15 - 25% triamterene = 50%
46
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) HALF LIFE
Amiloride = 21 hours triamterene = 4 hours
47
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) ROUTE OF ELIMINATION
Amiloride = r triamterene = m (transformed into an active metabolite that is excreted in the urine)
48
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) CLINICAL USES
adjunctive treatment with thiazide or loop diuretic in heart failure or HTN
49
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) TOXICITIES
- hyperkalemia | - hyperchloremic metabolic acidosis
50
Inhibitors of Renal Epithelial Na+ channels (aka K-sparing diuretics) CONTRAINDICATIONS
- k+ supplements | - ACE inhibitors
51
Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) FACTS
- 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
Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) ORAL BIOAVAILABILITY
Spironolactone = 65% | other 3, ID
53
Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics) HALF LIFE
- Spironolactone = 1.6 hrs - Canrenone = 16.5 hrs - Potassium = ID - Eplerenone = 5 hrs
54
Mineralocorticoid Receptor Antagonists (MRA) - (aka aldosterone antagonists, K-sparing diuretics)
- Spironolactone = M - Canrenone = M - Potassium = M - Eplerenone = M
55
Mineralocorticoid Receptor Antagonists (MRA) CLINICAL USES
- HTN - Mineralocorticoid excess - Aldosteronism (primary or secondary from HF, hepatic cirrhosis or nephrotic syndrome)
56
Mineralocorticoid Receptor Antagonists (MRA) TOXICITIES
- hyperkalemia - hyperchloremic metabolic acidosis - gynecomastia (due to blocking P450, blocks androgen) - impotence - BPH
57
Mineralocorticoid Receptor Antagonists (MRA) CONTRAINDICATIONS
- k+ supplements, ACE inhibitors | - chronic renal insufficiency
58
Non-specific Cation Channel Inhibitors (Nesiritide Natrecor)
- 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
Vasopressin Antagonists Facts
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
Vasopressin Antagonists are ______ potent diuretics
not very
61
Diuretic response: Action ______ correlate with serum/plasma concentrations
does not
62
Diuretic response: site of action is __________
luminal
63
CA inhibitors, furosemide and thiazide diuretics highly bound to plasma protein ---> _________ not __________
secreted not filtered
64
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)
DOSE DEPENDENT increase frequency reduces
65
Sensitivity to diuretics is _______ due to homeostatic responses in CRF (including hyperaldosteronism)
reduced

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