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CPR Exam 2 > Pharm - Diuretics > Flashcards

Pharm - Diuretics Flashcards

1
Q

What are the 3 Thiazide Diuretics we discussed?

A

Hydrochlorothiazide
Metolazone
Chlorthalidone

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2
Q

What are the four Loop Diuretics we discussed?

A

Furosemide
Bumetadine
Torsemide
Ethacrynic Acid

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3
Q

What are the 2 K+ Sparing Diuretics we discussed that are Na+ Channel Blockers?

A

Amiloride

Triamterene

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4
Q

What are the 2 K+ Sparing Diuretics we discussed that are Aldosterone Antagonists

A

Spironolactone

Eplerenone

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5
Q

What is the one Carbonic Anhydrase Inhibitor we discussed?

A

Acetazolamide

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6
Q

What are the 2 Aquaretics we discussed?

A

Conivaptan

Tolvaptan

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7
Q

What is the 1 Osmotic Diuretic we discussed?

A

Mannitol

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8
Q

How does an Aquaretic differ from a Diuretic?

A

Aquaretic promote Free Water Clearance

Diuretics promote the Excretion of Urine

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9
Q

Which part of the Npehron functions to generate Countercurrent Flow in order to maintain a Hypertonic Renal Medullary Interstitium?

A

The Thick Ascending Limb of the Loop of Henle

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10
Q

Where in the Nprhon do K+ Sparing Diuretics work?

A

K+ Sparing Diuretics work in the Late DCT and the Collecting Duct

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11
Q

Where do the Loop Diruetics work?

A

Loop Diuretics work in the Thick Ascending Limb of the Loop of Henle

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12
Q

What effects will Hyperkalemia have on the Heart?

A 
Tall T Waves
Prolonged PR Interval
Widened QRS Complexes
Flattened P Waves
Arrhythmias including BRADYCARDIA, V-Tach, V-Fib
Sinus Arrest
Nodal Rhythm with possible asystole
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13
Q

What effects with Hypokalemia have on the heart?

A 
Flattened T Waves
ST Segment Depression
Prolonged QT Interval 
Tall U Waves
Atrial Arrhythmias
V-Tach or V-Fib
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14
Q

Which type of Diuretics produce the greatest amount of Diuresis?

A

Loop Diuretics produce the greatest amount of Diuresis

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15
Q

What is the significance of all but one of the Loop Diuretics being Sulfonamide Drugs?

A

Sulfonamide Drugs all pose a risk of Hypersensitivity Rxns in Pt’s

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16
Q

Which Loop Diuretic is not a Sulfonamide Drug?

A

Ethacrynic Acid is not a Sulfonamide

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17
Q

Where do Loop Diuretics exert their MOA?

What Channel/Transporter do they block?

A

Loop DIuretics work in the Thick Ascending Limb of the Loop of Henle

They Block the Action of the Na+/K+/2Cl- Channel

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18
Q

Unlike Thiazides, which drug works in Patients with HTN with Low GFR and RBF?

A

Furosemide

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19
Q

What are some of the side effects of Loop Diuretics?

A

Hypo: -natremia, -kalemia, -calcemia, -magnesemia,
Hypochloremic Metabolic Alkalosis
Hyperglycemia - increased cholesterol and TG’s
Hyperuricemia
Ototoxicity - Vertigo, Hearing impairments, Tinnitus (may or may not be reversible)

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20
Q

What are the uses of Furosemide (a Loop Diuretic)?

A

Furosemide may be used for:
Edema - associated with HF, Renal/Hepatic Disease
Acute Pulmonary Edema - rapid dyspnea relief due to PG-Mediated Venodilaton
HTN

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21
Q

What the difference between Furosemide ad Torsemide?

A

Torsemide and furosemide are both Sulfonamide Loop Diuretics. Torsemide has a longer half-life, better oral absorption, and there is some evidence it works better in Heart failure

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22
Q

What is the difference between Furosemide and Bumetanide?

A

Furosemide and Bumetanide are both Sulfonamide Loop Diuretics. Bumetanide has more predictable oral absorption though

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23
Q

What type of Patients is the Loop Diuretic, Ethacrynic Acid, used to treat?

A

Ethacrynic Acid is used to Treat patients with sensitivity to Sulfonamide Drugs

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24
Q

What effects will max doses of Loop Diuretics (Furosemide) have?

A

Dissipation of Medullary Interstitial Osmotic Gradient

Irrespective of Whether Urine was Dilute or Concentrated, you will get large volumes of Approximately Isotonic Urine

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25
Q

Describe the Pharmacokinetics of Loop Diuretics (Furosemide)?

A

Loop Diuretics (Furosemide)
IV - Onset 5 min, Duration 2 hours
Oral - Onset 30-60 min, Duration 8 hours
Eliminated Largely in Unchanged in Urine with very minor hepatic metabolism

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26
Q

What Drug Class would you want to use when HTN is unresponsive to other Diuretics?

A

Loop Diuretics still work in HTN unresponsive to other Diuretics as they work even when RBF and GFR are LOW

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27
Q

What drug class would you want to use when massive and rapid fluid removal is needed?

A

Loop Diuretics

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28
Q

Are Loop Diuretics Safe During pregnancy?

A

NO. Loop Diuretics are NOT safe during pregnancy, they cross the placenta

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29
Q

Why may Loop Diuretics increase the risk of Kidney Stones?

A

Loop Diuretics lead to decreased reabsorption of Calcium, leading to serum Hypocalcemia, and Subsequent increased concentration of Calcium in the Kindey tubules -> greater chance of Kidney Stones

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30
Q

Why might Loop Diuretics (Furosemide) increase risk of Gout?

A

Loop Diuretics (Furosemide) may cause an increased risk of Hyperuricemia -> worsening Gout

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31
Q

What Drug Interaction is important to remember between Loop Diuretics and Digoxin?

A

Loop Diuretics are NOT K+ sparing and thus can lead to Hypokalemia. Hypokalemia worsens Digoxin Toxicity.

32
Q

What drug interaction between Loop Diuretics and Ototoxic Drugs must be remembered?

A

There is increased risk of hearing loss when combining these drugs

33
Q

How significant is the Biacrbonate (HCO3-) loss caused by Loop Diuretics in comparison to Thiazides or K+ sparing Diuretics?

A

Loop Diuretics cause less Bicarbonate (HCO3-) loss than Thiazides or K+ Sparing Diuretics

34
Q

Where in the Nephron is the MOA of Thiazide Diuretics?

What Transporter/Channel do they block?

A

Thiazide Diuretics work on the DCT

They block the Na+/Cl- Cotransporter

35
Q

What effects do Thiazide Diuretics have Ca2+ and Mg2+?

A

Thiazide Diuretics lead to a greater excretion of Mg2+ than Loop Diuretics

Thiazides Diuretics lead to increased Ca2+ reabsorption in the PCT due to volume contraction

36
Q

Are Thiazide Diuretics useful in the treatment of Pt’s with HTN and a low GFR?

A

No they are not

37
Q

What are 2 of the off-label uses of Thiazide Diuretics?

A

Thiazide Diuretics may be used to treat:

  • Calcium Nephrolithiasis
  • Nephrogenic Diabetes Insipidus
38
Q

What are some of the adverse effects of Thiazide Diuretics?

A 
Orthostatic Hypotension
Hypo: -natremia, -kalemia, -magnesemia, 
Hypochloremic Metabolic Alkalosis
Hyper: -calcemia, -glycemia, -uricemia
Sulfonamide Hypersensitivity RXN
39
Q

What are the Pharmacokinetics of Hydrochlorothiazide?

A

Well absorbed Orally
Peak Action in 2hrs, Duration 6-12hrs
Eliminated in Urine, relatively unchanged, with half-life of 6-15hrs

40
Q

How does Chlorothiazide differ from Hydrochlorothiazide?

A

Chlorothiazide is similar to HCTZ but has poor Oral Absorption

41
Q

How does Chlorthalidone differ from HCTZ?

A

Chlorthalidone is similar to HCTZ, but has a half-life of 40-60 Hours. It is also more potent and has a greater volume of distribution than HCTZ.

Chlorthalidone has also been shown to reduce cardiovascular Morbidity and Mortality, and decrease BP more significantly

42
Q

What Thiazide Diuretic is Preferred by HTN specialists?

A

Chlorthalidone is preferred by HTN specialists over HCTZ due to its longer half-life, greater potency, ability to reduce CV morbidity and mortality, and exert a greater decrease in BP

43
Q

How does Metolazone differ from HCTZ?

A

Metolazone is another long-acting diuretic. It is preferred by Cardiologists for use as an adjunct diuretic in treatment of CHF

44
Q

Describe the Diuresis generated by Thiazide Diuretics in comparison to Loop Diuretics and K+ Sparing Diuretics?

A 
(Greatest Diuresis)
Loop Diuretics
Thiazide Diuretics
K+ Sparing Diuretics
(Least Diuresis)
45
Q

Which Diuretic drug class causes the greatest loss of Bicarbonate (HCO3-)?

A

Thiazide Diuretics cause the greatest Bicarbonate (HCO3-) loss among common classes of Diuretics

46
Q

Where in the Nephron is the MOA of ALL K+ Sparing Diuretics?

A

K+ Sparing Diuretics work in the Collecting Duct and the short region upstream of it known as the Collecting Tubule

47
Q

What is the Transporter/Channel blocked by the K+ Sparing Diuretics, Amiloride and Triamterene?

A

Amiloride and Triamterene function to block Luminal Na+ Channels in the Collecting Duct

48
Q

What is the Transported/Channel blocked by the K+ Sparing Diuretics Spironolactone and Eplerenone?

A

Spironolactone and Eplerenone functions to block the Aldosterone receptor in the Collecting Duct

49
Q

What are the effects of Na+ Channel Blocking, K+ Sparing Diuretics (Amiloride and Triamterene)?

A

Na+ Channel Blocking, K+ Sparing Diuretics (Amiloride and Triamterene) cause:

Small increases in Na+ Excretion
Decreased K+ excretion (i.e. loss)
Indirect decrease in H+, Ca2+, and Mg2+ Loss

50
Q

What is the clinical application of Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene)?

A

Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene) are used to counteract the K+ loss produced by other diuretics

51
Q

What are some of the side effects of Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene)?

A

Hyperkalemia
Hyperchloremic Metabolic Acidosis
Hypo: -natremia, -volemia,
Dizziness, fatigue, HA, Nausea, Vomitingm, Bloating, Diarrhea, constipation

52
Q

Describe the Pharmacokinetics of Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene)?

A

Administered Orally
Duration 6-9hrs, increased with low GFR
Excreted in urine (50%) and feces (40%) unchanged

53
Q

What are the off label uses for Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene)

A

Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene) may be used off label for Pediatric HTN and Ascites

54
Q

What are the Pharmacodynamics of Spironolactone and Eplerenone?

A

Spironolactone and Eplerenone function as Competitive Aldosterone Antagonists at Aldosterone receptors in the Collecting Duct

55
Q

How do Spironolactone and Eplerenone function to spare K+?

A

Spironolactone and Eplerenone function to spare K+ by decreasing Collecting Duct, Luminal ENaC Activity and decreasing basolateral Na+/K+ ATPase Activity, in order to decrease reabsorption of Na+ in exchange for K+

56
Q

What side effects might you get with Spironolactone that you won’t get with Eplerenone? Why?

So why do we use Spironolactone more often if it has greater incidence of side effects?

A

Spironolactone is also a partial agonist at Androgen Receptors, and thus can lead to Amenorrhea, Hirsutism, Gynecomastia, and Impotence.

Eplerenone is more selective for Aldosterone receptors than Spironolactone, and thus has less instances of these side effects. HOWEVER, Eplerenone is also far more expensive and thus is used less commonly

57
Q

What is the Chemical difference between Spironolactone and Eplerenone? Is it significant?

A

Spironolactone is a Sulfa drug, Eplerenone is not.

It’s not super significant as Sulfonamide Hypersensitivities to Spironolactone are rare

58
Q

Would you expect faster MOA from Na+ Channel Blocking, K+ Sparing Diuretiucs (Amiloride and Triamterene), or from Aldosterone Receptor Blocking, K+ Sparing Diuretics (Spironolactone and Eplerenone)?

A

Spironolactone and Eplerenone will take longer to achieve their MOA as they are interfering with thee action of Steroid Hormones, which have slightly delayed MOA anyhow

59
Q

What are the clinical applications of Aldosterone Receptor Blocking, K+ Sparing Diuretics (Spironolactone and Eplerenone)?

A

Reducing K+ loss alongside other Diuretics used to treat HTN, HF, Ascites

Used to Treat Primary Hyperaldosteronism

60
Q

What are some of the off-label applications of Aldosterone Receptor Blocking, K+ Sparing Diuretics (Spironolactone and Eplerenone)?

A

Off label uses include:

  • reducing Fibrosis in Post-MI Heart failure
  • to stimulate Hisutism to treat Androgenic Alopecia in Females
61
Q

What are the Pharmacokinetics of Aldosterone Receptor Blocking, K+ Sparing Diuretics (Spironolactone and Eplerenone)?

A

Both drugs have active metabolites
half-life of about 20hours
Steroid effects are slow-on and slow-off

62
Q

Where in the Nephron is the MOA of Aquaretics?

What do they function to block?

A

Aquaretics function in thee Collecting Duct

Aquaretics function to block the ADH Receptor in the collecting duct

63
Q

What is the difference in target selectivity between the 2 Aquaretics, Conivaptan and Tolvaptan?

A

Conivapatn is a non-peptide antagonist with affinity for V1a and V2 AVP (ADH) Receptor subtypes

Tolvaptan is a V2 AVP (ADH) Selective Antagonist

64
Q

What is the effect of Aquaretics’ (Conivaptan and Tolvaptan) MOA?

A

Conivaptan and Tolvaptan lead to decreased uptake of H2O via Aquaporin 2, leading to increased excretion of free water (without electrolytes)

65
Q

How are the 2 Aquaretics, Conivaptan and Tolvaptan, administered?

A

Conivaptan is administered IV

Tolvaptan is administered Orally

66
Q

What are the clinical applications of Aquaretics, Conivaptan and Tolvaptan?

A

Aquaretics, Conivaptan and Tolvaptan, are used:
- to treat Euvolemic and Hypervolemic Hyponatremia in Hospitalized and Symptomatic Pt’s who are not responsive to fluid restriction

67
Q

Why must the use of Aquaretics, Conivaptan and Tolvaptan, be monitored closely?

A

Aquaretics, Conivaptan and Tolvaptan, administration must be subsequently monitored closely for serum Sodium levels. Too rapid serum sodium correction (>12mEq/L/24hrs) may lead to seizures, osmotic demyelination, coma, or death

68
Q

Besides Euvollemic and Hypervolemic Hyponatremia, what condition may Tolvaptan be used to help treat?

A

Tolvaptan may be used to help treat AD Polycystic Kidney Disease by slowing its progression. Though this does require liver monitoring.

69
Q

What are some of the adverse effects of Aquaretics, Conivaptan and Tolvaptan?

A

Orthostatic Hypotension
Fatigue
Thirst
Polyuria, Bedwetting

70
Q

What drug interactions must be taken into consideration when giving a patient an Aquaretic (Conivaptan and Tolvaptan)?

A

Aquaretics, Conivaptan and Tolvaptan, are metabolized by CYP3A4, and thus anything that induces or inhibits these enzymes must be taken into consideration

71
Q

Where in the Npehron is the MOA of Carbonic Anhydrase Inhibitors (Acetazolamide)?
What is its MOA?

A

Carbonic Anhydrase Inhibitors (Acetazolamide) exert their effects in the PCT.

They function to decrease Na+/H+ Cycling, thus decreasing the absorption of Bicarbonate (HCO3-) and Na+

72
Q

What are the (Quite Limited) therapeutic uses of Carbonic Anhydrase Inhibitors (Acetazolamide)?

A

Carbonic Anhydrase Inhibitors are used for:

  • increasing Urinary Alkalinization
  • treating Metabolic Alkalosis
  • Glaucoma
  • Acute Mountain Sickness
73
Q

What are some of the adverse effects of Carbonic Anhydrase Inhibitors (Acetazolamide)?

A

Carbonic Anhydrase Inhibitors (Acetazolamide) may cause:

  • Hyperchloremic Metabolic Acidosis
  • Nephrolithiasis
  • Potassium Wasting
74
Q

Where in the Nephron do Osmotic Diuretics (Mannitol) exert their effects?
What is their MOA?

A

Osmotic Diuretics (Mannitol) exert their effects in the PCT and the Thin Descending Limb of the Loop of Henle.

They exert their effects by being freely filtered by the glomerulus with minimal reabsorption, keeping water in the PCT and delivering it to the distal Nephron where it will ultimately be excreted. Their NET EFFECT is excretion of TBW in excess of Plasma Electrolytes

75
Q

Describe the Pharmacokinetics of Osmotic Diuretics (Mannitol)?

A

Must be Given IV
Distributes in ECF
Effects noticeable within 30-60min
Eliminated in the Urine unchanged over a period of 6-8hrs

76
Q

What are some of the Adverse effects of Osmotic Diuretics (Mannitol)?

A 
ECF Volume is acutely increased because Mannitol sucks H2O from ICF in cells, can exacerbate Heart failure 
HA
Nausea
Vomiting
Fluid and Electrolyte Imbalances
77
Q

What are the therapeutic uses of Osmotic Diuretics (Mannitol)?

A

Osmotic Diuretics (Mannitol) may be used for:

  • Prophylaxis of Renal failure - keeps some fluid volume in tubules to prevent them from collapsing if GFR is low
  • Reduction of Intracranial Pressure
  • reduction of Intracranial Pressure - Glaucoma, if Pt’s haven’t responded to other treatments

CPR Exam 2 (4 decks)

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