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Therapeutics II > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Diuretics

A

-agents that help the body get rid of sodium and water
-natriuresis (sodium excretion)
-diuresis (water excretion)

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2
Q

Diuretics and blood pressure

A

-dec blood pressure by decreasing plasma volume
-less burden on cardiovasc disease

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3
Q

Diuretic indications

A

-edematous states
-HTN
-Heart failure
-Acute renal failure

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4
Q

Is caffeine a diuretic?

A

-doses in drinks don’t have diuretic action

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5
Q

Membrane transporters

A

-convective flow
-simple diffusion
-channel-mediated diffusion
-carrier-mediated diffusion
-ATP-mediated transport (active)
-Symport (active)
-Antiport (active)

-which are likely tarets of diuretics

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6
Q

Classification of Diuretics

A

-sites of action
-efficacy
-structure
-effect on potassium excretion
-MOA

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7
Q

Classification of diuretics based on MOA

A
  1. inhibitors of carbonic anhydrase
  2. Osmotic Diuretics
  3. Inhibitors of Na-K-2Cl symport
  4. Inhibitors of NaCl symport
  5. INhibitors of renal Na channels
    5b. Mineralcorticoid receptor antagonists
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8
Q

Transport of diuretics into proximal tubule

A

-high protein binding
-not filtered through Bowman’s (only unbound is filtered)
-transport/secretion into proximal tube

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9
Q

Active secretion in Proximal Tubule

A

-Organic Anion Transporter (OAT)
-Organic Cation Transporter (OCT)

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10
Q

Drugs secreted by Organic Anion Transport in proximal tubule

A

-Furosemide
-thiazides
-penicillin
-cephalosporin
-probenecid
-NSAIDs

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11
Q

Drugs secreted by Organic Cation Transport in proximal tubule

A

-Amiloride
-Cimetidine
-Digoxin
-Metformin
-Morphine
-Procainamide
-Quinidine
-Ranitidine
-Triamterene
-Trimethoprim
-Vancomycin

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12
Q

Active secretion in Prox tube mech (OAT and OCT)

A
  1. Diffusion out of capillary space into interstitial space
  2. Transport across basolateral membrane
  3. secretion across luminal membrane

-non-selective = competition

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13
Q

Active secretion depends on

A

-plasma protein binding
-rate of delivery of drug
-transporter saturation
-competing drugs

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14
Q

Probenecid

A

-secreted by OAT
-treats gout
-inc uric acid secretion
-competes w penicilin = slow excretion = prolong PCN activity (doubles blood concentration and exposure)

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15
Q

Penicillin

A

-secreted by OAT
-inhibit transpeptidase
-block crosslinking of peptidoglycans
-dec cell wall synthesis
-mostly cleared by kidneys unchanged
-was extracted and reused during WWII
-competition by probenecid at OAT to slow penicillin excretion and prolong activity

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16
Q

Inhibitors of Carbonic Anyhydrase

A

-inhibit cytoplasmic and membrane bound CA
-inhibit NaHCO3 reabsorption
=inc NaHCO3 excretion

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17
Q

Carbonic Anhydrase INhibitors SAR

A

-sulfanilamide derivatives
-high partition coefficient and lowest pKa have greater potency
-Sulfamoyl group essential
-sulfamoyl N unsubstituted to reatin activity

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18
Q

Carbonic Anhydrase Inhibitor Drugs

A

-Acetazolamide
-Dichlorphenamide
-Methazolamide

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19
Q

Carbonic Anhydrase Inhibitor Drug Uses

A

-low diuretic efficacy
-acute mountain sickness
-metabolic alkalosis
-glaucoma
-urinary alkalinization

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20
Q

Carbonic Anhydrase Inhibitor Drug Toxicities

A

-hypercloremic metabolic acidosis
-renal stones
-renal potassium wasting
-drowsiness/paresthesia

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21
Q

Acute Mountain sickness tx

A

-acetazolamide prophylactically several days before ascent above 10,000 feet
-metabolic acidosis produced by the drug counteracts the respiratory alkalosis that can result from hyperventilation

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22
Q

diuretic and sulfonaimde antimicrobials cross-sensitivity

A

-most pt do with drug allergy don’t react
-Sulfa rash in 5-10% of pt (rare in diuretics)
-withholding sulfamoyl containing diuretics from pt with hx of sulfonamide allergy is not justified

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23
Q

Osmotic Diuretics

A

-inc H2O excretion
-renal prox tubule
-descending limb of loop of henle
-pharmacologically inert
-non-reabsorbable substances shifting osmotic flow
-alter renal blood flow

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24
Q

Osmotic diuretic drugs

A

-Mannitol (IV)
-Urea (IV)
-Glucose
-Isosorbide
-Glycerine

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25
Q

Mannitol side effects?

A

-loss of water
-reduced intracellular volume
-hypernatremia risk

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26
Q

Osmotic SAR and MOA

A
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27
Q

Na-K-2Cl symport Inhibitors

A

-inc Na, K, Cl
-loop diuretics and high ceiling diuretics
-thick ascending limb

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28
Q

Na-K-2Cl inhibitors

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 have weak CA inhibitory activity
-Chronically reduce uric acid secretion
-problems w K, Ca, Mg reuptake

29
Q

Na-K-2Cl symport inhibitor SAR

A

-1 position must have acidic substitent (carboxyl best, tetrazole)
-sulfamoyl group at 5 is essential
-activating group at 4 (Cl, CF3, phenoxy, alkoxy, anilino, benzyl, benzoyl group

30
Q

Na-K-2Cl symport inhibitor drugs

A

-Furosemide
-Bumetanide
-Ethacrynic acid
-Torsemide

31
Q

Na-K-2Cl symport inhibitor drug use

A

-edema
-acute pulmonary edema
-HTN, HF
-acute hypercalcemia
-hyperkalemia
-acute renal failure
-anion overdose

32
Q

Na-K-2Cl symport inhibitor drug toxicities

A

-dehydration
-hypokalemic metabolic alkalosis*
-Ototoxicity*
-hyperuricemia
-hypomagnesmia

33
Q

Ethacrynic Acid (Edecrin)

A

-Na-K-2Cl symport inhibitor
=not derived from sulfonamides
-alkylates thiols to give the sulfhydryl-containing conjugates that are diuretics
-prodrug?
-structure?

34
Q

NaCl symport inhibitors

A

-inc NaCl excretion
-thiazides
-DCT, PCT secondary
-enhance potency of CA-I
-reduce K reuptake

35
Q

SAR of thiazides (NaCl inhibitor)

A

-slide 30
-sulfaniliamide to acetazolamide to dichlorphenamide to chlorothiazide
-2 rings

36
Q

NaCl inhibitor drug classes

A

-Thiazide (acylating agent)
-Hydrothiazide (aldehyde or ketones)

37
Q

NaCl inhibitor drugs

A

-Chlorothiazide
-Hydrochlorothiazide
-Chlorothalidone
-Metolazone

38
Q

NaCl inhibitor drug use

A

-HTN
-HF
-nephrolithiasis due to hypercalciuria
-nephrogenic diabetes insipidus

39
Q

NaCl inhibitor drug toxicities

A

-Hypokalemic metabolic acidosis
-hyperuricemia
-hyperglycemia
-impaired carbohydrate tolerance
-hyperlipidemia
-hyponatremia

40
Q

The post-discharge therapy included a substitution of hydrochlorothiazide
with furosemide. Which of the following statements best explains why loop
diuretics are far more effective than thiazide diuretics?

A

More sodium is physiologically reabsorbed at the loop of Henle than at the
distal convolute tubule.

41
Q

Renal Epithelial Na channel inhibitors

A

-potassium-sparing diuretics
-late DCT and collecting duct
-weak diuretics
-used in combo w other diuretics

42
Q

Renal Epithelial Na channel inhibitor drugs

A

-Amiloride
-Triamterene

43
Q

Renal Epithelial Na channel inhibitor drug use

A

-adjunctive tx w thiazide or loop diuretic in HF or HTN

44
Q

Renal Epithelial Na channel inhibitor drug toxicities

A

-Hyperkalemia*
-Hyperchloremic metabolic acidosis

45
Q

Renal Epithelial Na channel inhibitor drug contraindications

A

-K+ supplements
-ACE inhibitors

46
Q

Mineralcorticoid Receptor Antagonists (MRA)

A

-aldosterone antagonists
-potassium-sparing diuretics
-inc Na excretion
-inc K retention
-bind to MR but don’t stimulate AIP production
-only diuretics that do not act within the tubular lumen!

47
Q

MRA drugs

A

-spironolactone
-canrenone
-potassium canrenoate
-eplerenone

48
Q

MRA toxicities

A

-Hyperkalemia
-Hyperchloremic metabolic acidosis
-Gynecomastia
-impotence
-benign prostatic hyperplasia

48
Q

MRA drug use

A

-HTN or HF w other diuretics
-excess mineralcorticoids
-Aldosteronism

49
Q

MRA drug contraindications

A

-K supplements
-ACE inhibitors
-Chronic renal insufficiency

50
Q

PK and PD determinants of diuretic response

A

-luminal (not MRAs)
-CA-I, furosemide and thiazide are highly bound to plasma protein (secreted not filtered)
-secretion is saturable (dose-dependent)
-secretion decreases with renal failure (reduced efficacy)
-sensitivity to diuretics reduced bc homeostatic responses in CRF (inc hyperaldosteronism)

51
Q

Diuretic site of action

A

-luminal
-except MRAs

52
Q

Diuretic secretion

A

-CA-I, furosemide, thiazide (not filtered bc bound to plasma protein)
-saturable (dose-dependent)
-dec with renal failure

53
Q

Braking Phenomenon

A

-Osmosis (water follows salts)
-when Na excretion > Na intake, BW and ECF decrease
-activation of RAAS and SNS
-BW and ECF stabilize at output=input
-BW and ECF rise when output<input

54
Q

Diuretic responsiveness in HF

A

-reduced
-diuretics can;t manage pt well as HF progresses

55
Q

Diuretic responsiveness in CRF

A

-potency shifts
-efficacy can be obtained w increased dose

56
Q

Combining diuretics w different MOAs

A

-more effective than dose inc of single agent

57
Q

Slide 44

A

Slide 44

58
Q

CA I Drugs to know

A

Acetazolamide

59
Q

Osmotic diuretics to know

A

Mannitol

60
Q

Loop diuretics to know

A

-Furosemide
-Bumetanide
-Torsemide
-Ethacrynic acid

61
Q

Distal tubule diuretics to know

A

-Hydrochlorothiazide
-chlorthalidone
-metolazone

62
Q

K-sparing diuretics to know

A

-NaCl I: amiloride and triamterine
-Aldosterone Antagonists (MRA): spirinolactone and eplerenone

63
Q

chart on slide 45

A

chart on slife 45

64
Q

A 55-year-old male with kidney stones has been placed on a
diuretic to decrease calcium excretion. However, after a few weeks,
he develops an attack of gout. Which diuretic was he taking?

A

-thiazides associated w elevated SUA levels

65
Q

Question: An 83-year-old man has been effectively treated with
hydrochlorothiazide to control his elevated blood pressure. He has
had a recent onset of weakness. Blood chemistry analysis reveals
hypokalemia. Another drug is added, and 1 month later his serum
K+ is normal. Which of the following drugs most likely helped
normalize his serum potassium levels?

A

Amiloride

66
Q

Question: A patient taking an oral diuretic for about 6 months
presents with elevated fasting and postprandial blood glucose
levels. You suspect the glycemic problems are diuretic-induced.
Which of the following was the most likely cause?

A

Hydrochlorothiazide

67
Q

Question: A patient with severe infectious disease is being treated
with an aminoglycoside antibiotic. Which of the following diuretics
should be avoided, if possible, because of the risk of a serious
common and additive adverse effect?

A

-Furosemide

68
Q

aminoglycoside antibiotic

A

-gentamicin
-protein synthesis inhibitor
-avoid with loop diuretics
-ototoxic and nephrotoxic

Therapeutics II (38 decks)

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