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CRNA Pharmacology > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Primary effect of diuretics is to?

A

increase Na+ excretion (natriuresis), increase free water excretion, and increase the rate of urine flow

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2
Q

Classification of Diuretics

A
  1. Thiazide and Thiazide-like diuretics
  2. Loop diuretics (also called High-Ceiling Diuretics)
  3. Potassium-sparing diuretics
    • Aldosterone Receptor Antagonists (aka: Mineralocorticoid
    Receptor Antagonists)
    • Renal Epithelial Na+ Channel Inhibitors
  4. Carbonic anhydrase inhibitors
  5. Osmotic diuretics
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3
Q

The term thiazide-like diuretics refers to?

A

diuretic drugs that are pharmacologically similar (i.e.: same mechanism of action) to thiazide diuretics but are not thiazides chemically

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4
Q

Site of action for Thizaide and Thiazide-Like diuretics?

A

DCT

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5
Q

Significance of ALL thiazide & thiazide-like diuretics being sulfonamide derivatives?

A

Use cautiously in patient’s allergic to sulfonamides as cross reaction can occur

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6
Q

Thiazide Diuretics

A 
1) Hydrochlorothiazide
(HydroDIURIL®)
2) Chlorothiazide (Diuril®) - The only IV agent from this class
3) Metolazone (Zaroxolyn®, Mykrox®)
4) Indapamide (Lozol®)
5) Chlorthalidone (Hygroton®)
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7
Q

Thiazide and Thiazide-Like Diuretics: Clinical Uses

A

1) hypertension
2) edema
3) Nephrogenic diabetes insipidus
4) kidney stones
5) hypocalcemia
6) Osteoporosis (very rarely done)

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8
Q

Thiazide and Thiazide-Like Diuretics are used to treat HTN either alone or in combination with ____?

A

other anti-hypertensive agents such as ACE-I’s, ARB’s, CCB’s, Beta-blockers, etc….

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9
Q

Thiazides effect on serum Calcium and Potassium levels?

A

1) increases calcium (hypercalcemia)

2) decreases K+ levels (hypokalemia)

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10
Q

Mechanism of Action of Thiazide Diuretics: work in the Distal Convoluted Tubule

A

1) freely filtered at the glomerulus AND actively secreted into the proximal tubule by the organic acid secretory pathway
2) these agents use both the processes of glomerular filtration AND active tubular secretion to gain access into the renal tubule
3) Thiazides bind to & inhibit the Na+-Cl- symporter in the distal convoluted tubule, thus inhibiting Na+ & Cl- reabsorption

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11
Q

With exception of ________, thiazide diuretics are ineffective in patients with severe renal insufficiency

A

Metolazone

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12
Q

Thiazide Diuretics Pharmacokinetics

A
  • Most are well absorbed, Onset of action typically within 1 hour
  • Dosages vary widely depending on potency of the individual agent
  • Large volume of distributions
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13
Q

major differences between the thiazides

A

The major differences between the thiazides is their serum t1/2 and duration of diuretic effect

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14
Q

Initial antihypertensive response of thiazide diuretics

A

The thiazide diuretics decrease blood pressure initially by decreasing extracellular fluid volume (decreasing blood volume, decreasing preload) with a subsequent decrease in cardiac output
• Long-term, cardiac output returns to baseline and extracellular volume returns almost to normal due to compensatory responses such as activation of renin-angiotensin-system

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15
Q

Sustained antihypertensive response of thiazide diuretics

A 
The sustained antihypertensive effects is due to a decrease in
vascular resistance (peripheral vasodilation)
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16
Q

Thiazide and Thiazide-Like Diuretics: Adverse Effects

A
  • Extracellular volume depletion (hypovolemia)
  • Hypotension, headache, dizziness
  • Metabolic alkalosis (Hypochloremic metabolic alkalosis) • Hyperglycemia (impaired glucose tolerance)
  • Hyperuricemia (increases uric acid in the body)
  • Photosensitivity and maculopapular skin rash
  • Can worsen renal function (not common) • Sexual dysfunction
  • Hyperlipidemia
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17
Q

Thiazide and Thiazide-Like Diuretics:Electrolyte abnormalities

A
  • 4:1
  • Hyponatremia, Hypokalemia, Hypochloremia, Hypomagnesemia,
    Hypercalcemia
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18
Q

Thiazides can INCREASE the effects of:

A

1) Nondepolarizing neuromuscular blocking agents (bro hypokalemia)
2) Skeletal muscle relaxants
3) Digoxin
4) Lithium
5) Lopp Diuretics

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19
Q

Thiazides DIMINISH the effects of:

A

1) Uricosuric agents used to treat gout •
2) Sulfonylureas
3) Insulin
* 4) NSAIDs

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20
Q

Thiazides and NSAIDs

A

NSAID’s – the administration of a non-steroidal anti-inflammatory agent can reduce the diuretic, natriuretic, and antihypertensive effects

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21
Q

Thiazides and inhaled anesthetics, barbiturates and narcotics

A

Hypotension may be observed during the administration of inhalation anesthetics, barbiturates, or narcotics

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22
Q

Thiazide and Thiazide-Like Diuretics: Disease State Concerns

A

1) Thiazides can cause/worsen hypovolemia
2) DM
3) Gout

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23
Q

Loop Diuretics Characteristics

A

1) cause greater diuresis than thiazide agents

2)

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24
Q

The efficacy of loop diuretics is due to a combination of TWO
factors:

A
  1. Approximately 25% of the filtered Na+ load normally is reabsorbed by the thick ascending limb of the loop of henle, and this is the region of the nephron where loop diuretics work
  2. Nephron segments past the thick ascending limb of the loop of henle DO NOT posses the reabsorptive capacity to rescue the flood of rejectate exiting the thick ascending limb
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25
Q

Why are Loop Diuretics called High Ceiling diuretics

A

due to their high diuretic potential

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26
Q

Loop diuretics enter the renal tubular lumen primarily by ____?

A

proximal tubular secretion by the organic acid transport system but glomerular filtration is also used to a minor degree

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27
Q

What is the reason why loop diuretics still have a diuretic effect in patients with severe renal insufficiency.

A

The responses to loop diuretics are maintained with GFR’s over a broad range, even in the presence of impaired renal function. However, higher doses are required in renal failure patients to obtain adequate delivery of the loop diuretic to its site of action

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28
Q

Why are Loop diuretics are less effective hypotensive agents than thiazide diuretics

A

Because the the antihypertensive effect is due to deceases in intravascular volume and salt elimination

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29
Q

Loop Diuretics: Currently Available Agents

A

1) Furosemide (Lasix®)
2) Bumetanide (Bumex®)
• Most potent loop diuretic
3) Torsemide (Demadex®)
• More potent than furosemide
4) Ethacrynic acid (Edecrin®)

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30
Q

What is the Only loop diuretic that can be given to a patient with a “true” sulfa or sulfonamide allergy?

A

Ethacrynic acid (Edecrin®)

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31
Q

Which Loop Diuretic is the least potent loop diuretic?

A

Ethacrynic acid (Edecrin®)

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32
Q

Loop Diuretics Chemistry

A
  • Furosemide, bumetanide, and torsemide all contain a sulfa moiety
  • Use these 3 agents cautiously in patient’s allergic to sulfa or sulfonamides
  • Ethacrynic acid is the only loop diuretic that DOES NOT contain a sulfa moiety
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33
Q

Loop Diuretics: Clinical Uses

A

• Treatment of acute pulmonary edema
• Treatment of edema associated with: CHF, liver disease, renal diseases
• Acute decompensated heart failure (Subset II or IV)
• Short-term management of ascites due to malignancy,
idiopathic edema, and lymphedema
• Treatment of increased ICP
• Treatment of hyperkalemia & acute hypercalcemia
• Loop diuretics have little use in the chronic treatment of essential hypertension but are sometimes used
• Differential diagnosis of acute oliguria
• Chemical intoxication (to increase renal elimination)

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34
Q

Effects of Loop Diuretics on ICP

A

decreases ICP

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35
Q

*Mechanism of Action: Loop Diuretics

A

Loop diuretics act by binding to and blocking the Na+-K+-2Cl- symport primarily in the *THICK ascending limb of the loop of Henle, which inhibits the reabsorption of Na+, K+, and Cl- from the tubule lumen.

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36
Q

Loop Diuretics: Pharmacokinetics

A

• Well absorbed orally (60-100% bioavailability)
• Peak oral effect in 1-2 hours, IV onset is 5-20 minutes
t1/2 ranging from 0.8 - 3.5 hours (short t1/2)
• Duration of diuretic action: 2-8 hours
• Small volumes of distribution
• Highly protein bound agents
• Elimination is primarily via the kidneys

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37
Q

Loop Diuretics Exception TO Elimination is primarily via the kidneys

A

torsemide

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38
Q

Loop Diuretics EFFECT ON VENOUS SYSTEM

A

direct venodilating effect that increases venous capacitance and will ⇓ preload, which also leads to ⇓ left ventricular filling pressure

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39
Q

Loop Diuretics effect on renal prostaglandins

A

increase the production of renal prostaglandins and induce a prostaglandin mediated increase in renal blood flow which also contributes to their natriuretic effect

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40
Q

Loop Diuretics and NSAIDs

A

Giving NSAID’s such as indomethacin blocks this and decreases the diuretic effect of loop diuretics

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41
Q

Loop Diuretics effect on the frank Starling Curve

A

moves it up and to the left

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42
Q

Loop Diuretics effect on the intracranial pressure by inducing systemic diuresis

A

decrease intracranial pressure by inducing systemic diuresis, by decreasing CSF production via interfering with Na+ transport, and from resolving cerebral edema by improving cellular water transport

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43
Q

Can loop Diuretics be used in combo with Mannitol to treat increased ICP

A

Yes

44
Q

A combination of furosemide with mannitol is more efficacious in decreasing ICP than either drug alone, however, here is an increased risk of _____?

A

severe dehydration and electrolyte abnormalities with their combined use

45
Q

Loop Diuretics: Dose-Dependent Effect

A
  • Progressively increased diuresis is achieved at higher doses
  • A plateau is reached at which even higher doses produce no further diuresis; this dose is called the maximum effective dose
  • K+ excretion is also increased in a dose-related fashion
46
Q

Potency of Loop Diuretics

A

• Bumetanide is the most potent and is considered to be ~40 times more potent than furosemide. Thus, bumex 1 mg IV = furosemide 40 mg IV in terms of producing the same diuretic response

47
Q

*Loop Diuretics: Adverse Effects

A

• Extracellular volume depletion (hypovolemia), dehydration
• Hypotension
• Electrolyte imbalances
• Metabolic alkalosis (Hypochloremic metabolic alkalosis) • Muscle cramps
*• OTOTOXICITY (rare but serious)
• Hyperuricemia
• Hyperglycemia
• Far less of an incidence compared with thiazides • It is safe to give in diabetic patients
• Worsening renal function
• Dizziness, Lightheadedness • GI Disturbances

48
Q

Loop Diuretics Electrolyte Abnormalities

A

Hyponatremia, Hypokalemia, Hypochloremia, Hypomagnesemia,

Hypocalcemia

49
Q

Loop Diuretics: Ototoxicity

A

characterized by various degrees of hearing loss ranging from transient auditory disturbances, tinnitus, vertigo, and permanent hearing loss/deafness

50
Q

Loop Diuretics: Ototoxicity increased with?

A

• High peak concentrations – so avoid high/large IV bolus doses or
sustained high plasma concentrations
• Renal impairment
• Concomitant drug therapy with any other drug that can also cause ototoxicity
• Aminoglycosides, vancomycin, cisplatin

51
Q

Loop Diuretics Ototoxicity risk is worse/most common. ____?

A

with ethacrynic acid

52
Q

Loop Diuretics: Drug-Drug Interactions

A

1) Increases NMBs
2) Increases risk of lithium toxicity
3) ncreases warfarin’s anticoagulation effect
4) NSAID’s such as indomethacin blunt the diuretic effect of loop diuretics
5) synergistic effect with electrolyte abnormality development
increased nephrotoxcitity with Aminoglycosides, amphotericin B, cephalosporins, vancomycin

53
Q

Loop Diuretics: Disease State Concerns

A

1) hypovolemia
2) Diabetes Mellitus
3) Gout

54
Q

Hypokalemia increases the risk of Cardiac arrhythmias

A

Patient’s with underlying cardiac conditions at increased risk
• Hypokalemia as a result of chronic diuretic use may potentiate nondepolarizing neuromuscular blocking agents such as cisatracurium and increases the dose of neostigmine
• However, acute hypokalemia does not affect dose requirements for nondepolarizing neuromuscular blocking agents

55
Q

Other Hypokalemia increases the risk of

A
  • Quinidine-Induced Torsades de Pointes
  • Digoxin toxicity & digitalis induced cardiac arrhythmias
  • Skeletal muscle weakness, cramping, myalgia’s are all signs of hypokalemia
  • GI Ileus
  • Nephropathy
56
Q

Potassium Sparing Diuretics characteristics

A

1) Are “weak” diuretics due to their site of action in the lower portion of the nephron
2) • Used primarily when aldosterone is in excess or in combination with other diuretics to help maintain K+ balance
•3) Are ALL given via oral route of administration

57
Q

Potassium Sparing Diuretics: Classification

A
  • Renal Epithelial Na+ Channel Inhibitors • Amiloride (Midamor®)
  • Triamterene (Dyrenium®)
  • Aldosterone receptor antagonists (aka: Mineralocorticoid receptor antagonists)
  • Spironolactone (Aldactone®) • Eplerenone (Inspra®)
58
Q

Mechanism of action: Aldosterone receptor antagonists

A

1) Spironolactone & eplerenone are competitive antagonists of aldosterone at the cytoplasmic mineralocorticoid receptor (MR) and block the actions of aldosterone on gene expression
2) Aldosterone enters the epithelial cell from the basolateral membrane (from the plasma) and binds to the cytosolic MR and results in increased Na+ and H2O entry into cells (Na+ reabsorption) and increased K+ and H+ excretion

59
Q

Antagonism of aldosterone by spironolactone and eplerenone results in a decrease in ___?

A

Na+ entry into the epithelial cells causing decreased Na+ reabsorption (increased Na+ excretion) and decreased K+ excretion (increased K+ retention)

60
Q

Results of Spironolactone and eplerenone reaching the tubular cells from the plasma

A

they DO NOT require access to the tubular lumen in order to induce their diuretic effect. These are the only diuretics with this ability!

61
Q

Effects of Spironolactone and eplerenone being dependent upon endogenous aldosterone levels for their effects (which includes diuresis)

A

The higher the endogenous aldosterone level, the greater the diuretic effect of these agents

62
Q

Effect of Addison’s disease on Spironolactone and eplerenone

A

These agents are ineffective in the absence of circulating aldosterone (i.e.: Addison’s disease)

63
Q

Spironolactone (Aldactone®) MOA

A

1) Competitive antagonist of aldosterone at cytoplasmic mineralocorticoid receptors in the late distal tubule and collecting duct
2) Also has affinity toward progesterone and androgen receptors (anti-androgen agent) and antagonizes both these sex steroids receptors as well

64
Q

*Spironolactone (Aldactone®): Pharmacokinetics/Pharmacodynamics

A

• Rapid and extensive hepatic first-pass metabolism
• Has several active metabolites with long half-lives
*• Canrenone is the major active metabolite
• Protein binding: > 90% (high)

65
Q

Spironolactone: Clinical Uses

A
  • Management of congestive heart failure (EF<40%)
  • Left ventricular dysfunction immediately after an MI
  • Diagnosis and treatment of primary hyperaldosteronism
66
Q

Spironolactone (Aldactone®): Adverse Effects

A

HYPERKALEMIA

67
Q

Spironolactone also antagonizes progesterone and androgen

steroid receptors which can lead to ___?

A
  • Males – gynecomastia, impotence

* Females – breast tenderness, hirsutism (hair growth)

68
Q

Eplerenone (Inspra®) MOA

A

1) Is a selective, competitive aldosterone antagonist at mineralcorticoid receptors and is an analog of spironolactone
2) Eplerenone has VERY LOW affinity for androgen and progesterone receptors and results in far less anti-androgen and anti- progesterone side effects compared to spironolactone

69
Q

Eplerenone (Inspra®) Metabolization

A

Metabolized by CYP 3A4 to inactive metabolites

70
Q

Eplerenone (Inspra®) Adverse effects

A

HYPERKALEMIA

71
Q

Eplerenone (Inspra®) Clinical Uses

A
  • Essential hypertension

* Improve survival of stable patients with left ventricular dysfunction (EF < 40%) and CHF after an acute MI

72
Q

Mechanism of action: Renal Epithelial Na+

Channel Inhibitors

A

1) These agents “spare” K+ by interfering with this renal epithelial Na+ channel
2) Renal epithelial Na+ channel inhibitors BLOCK the epithelial Na+ channel in principle cells in the late distal tubule and collecting ducts decreasing the electrical chemical gradient across the cell and enhance Na+ excretion and decrease K+ excretion

73
Q

Are Renal Epithelial Na+

Channel Inhibitors dependent on the presence of circulating aldosterone levels to produce their diuretic effect?

A

NO

74
Q

Renal Epithelial Na+

Channel Inhibitors is dependent on the amount of Na+ ____?

A

amount of Na+ delivered to the late distal tubule and collecting ducts

75
Q

Renal Epithelial Na+

Channel Inhibitors Adverse effects

A

Hyperkalemia

76
Q

Renal Epithelial Na+ Channel Inhibitors: Clinical Uses

A

1) reatment of edema or essential hypertension

2) Amiloride

77
Q

Carbonic Anhydrase Inhibitors

A
  • Acetazolamide (Diamox®)
  • Methazolamide (Glauctabs®, Neptazane®)
  • Dorzolamide (Trusopt®)
  • only available in an eye drop dosage form
  • Brinzolamide (Azopt®)
  • only available in an eye drop dosage form
78
Q

Carbonic Anhydrase Inhibitors: Mechanism of action

A

1) CAI’s potently inhibit, via noncompetitive inhibition, BOTH membrane-bound and cytoplasmic carbonic anhydrase in the PCT.
2) also inhibit carbonic anhydrase that is located in the collecting duct system but this is a secondary site of action of the CAI’s

79
Q

Carbonic anhydrase inhibition results _____?

A

1) decrease in the reabsorption of HCO3-

2) Na+ & water from the proximal convoluted tubule lumen

80
Q

Carbonic Anhydrase Inhibitors: Effect on Urinary Excretion

A

1) Increase in urinary excretion of HCO3- and a decrease in urinary excretion of H+ (body retains H+)
2) l- is retained by the kidneys in the loop of Henle to offset the loss of HCO3-
3) Increase in urinary excretion of water, K+, and slight increase in Na+ excretion

81
Q

The net effect of all CAIs urinary changes is ____?

A

an alkaline urine (increase in urinary pH ~8) and development of metabolic acidosis (hyperchloremic metabolic acidosis)

82
Q

Carbonic Anhydrase Inhibitors: Clinical Uses

A
  • Glaucoma
  • This is the major indication of topical CAI’s
  • Metabolic alkalosis (i.e.: Hypercapnic COPD patients)
  • Acute mountain sickness (aka: High-Altitude Sickness)
  • Central sleep apnea
  • Suppression of some forms of epilepsy (rare)
  • Idiopathic intracranial hypertension
  • CAI’s are not generally used for diuresis since they are not potent diuretics
83
Q

Acetazolamide (Diamox®) MOA

A

A sulfonamide derivative type drug that is the prototype for the carbonic anhydrase inhibitor drug class

84
Q

Acetazolamide (Diamox®) Dosage forms?

A

IV and oral

85
Q

Acetazolamide (Diamox®) Pharmacokinetics

A
  • Readily absorbed from the GI tract (PO)
  • Bioavailability: ~100%
  • Peak effect: IV = 15 minutes, PO = 2-4 hours • Excretion: Urine (70-100% unchanged drug)
86
Q

Acetazolamide (Diamox®) ,most adverse effects contraindications, and drug interactions for acetazolamide are secondary ____?

A

secondary to urinary alkalinization or metabolic acidosis adverse effect from the drug

87
Q

cetazolamide (Diamox®): Adverse Effects

A
  • Metabolic hyperchloremic acidosis
  • Electrolyte abnormalities (hypokalemia)
  • CNS effects
  • Dermatologic
  • Hematologic (rare)
88
Q

Osmotic Diuretics Characteristics

A
  • Are pharmacologically inert substances
  • Are FREELY filtered at the glomerulus
  • Are not secreted by renal tubular cells
  • Undergo limited reabsorption from the renal tubule after glomerular filtration
  • Resist metabolism – these agents do not undergo metabolism after administration
89
Q

Osmotic diuretics are administered to increase the osmolarity of ____?

A

plasma, glomerular filtrate, and renal tubular fluid resulting in osmotic diuresis

90
Q

Osmotic diuretics primary site of action

A

Loop of Henle

91
Q

Osmotic Diuretics Drugs

A
  • Mannitol (Osmitrol®)
  • Only IV osmotic diuretic used clinically and the most studied
  • Glycerin (Osmoglyn®) • only given orally
  • Isosorbide (Ismotic®) • only given orally
  • Urea (Ureaphil®)
  • not available IV in the United States
92
Q

Why should you ALWAYS use a filter needle when administering mannitol IV?

A

In case crystals for as you are administering it because it’s cold in the OR

93
Q

Mannitol: Mechanism of action Renal Effect

A

1) When administered IV, mannitol is completely filtered at the glomerulus and increases the osmolarity of the glomerular filtrate and prevents the reabsorption of water in the proximal convoluted tubule, loop of Henle, and collecting duct
2) also extracts water from intracellular compartments which expands extracellular fluid volume, decreases blood viscosity, and inhibits renin release.

94
Q

Primary site of action for Mannitol

A

Loop of Henle

95
Q

How does Mannitol decrease ICP and Intracarnial edema effects

A

increases plasma osmolarity which will induce the movement of intracellular water to the extracellular and vascular spaces along as osmotic gradient. Mannitol reduces blood viscosity which in turn reduces cerebral blood volume. This redistribution of fluid from intracellular spaces decreases brain bulk, reduces intracranial pressure and intracranial edema

96
Q

Effect of The administration of 50 grams of IV mannitol

A

can pull 1 liter of fluid from the intracellular to the extracellular compartment

97
Q

Mannitol is also a scavenger of oxygen-free radicals (aka: free radical scavenger), which may prevent _____?

A

cellular injury, may limit cellular edema and protect tissues from damage

98
Q

Mannitol: Pharmacokinetics

A

1) not absorbed from the GI tract and is not given orally
2) Does not cross BBB
3) Does not undergo significant metabolism
4) Excretion - Clearance from plasma is solely by glomerular filtration

99
Q

Mannitol: Clinical Uses

A
  • Treatment of increased intracranial pressure
  • Severe traumatic brain injury
  • Reduce cerebral edema and brain mass before and after neurosurgery
  • Reduce intraocular pressure (Treatment of glaucoma)
  • Prophylaxis against acute renal failure/acute kidney injury
  • Cardiovascular surgery, transplantation surgery, extensive trauma, nephrotoxic conditions (hemolytic transfusion reactions)
  • There is very little clinical evidence to support this clinical use
  • Differential diagnosis of acute oliguria
  • Promotion of urinary excretion of toxic materials
100
Q

Mannitol: Most common Adverse Effects

A

Headache, nausea, and vomiting

101
Q

Mannitol: less common Adverse Effects

A

1) Pulmonary edema/congestion
2) Volume expansion
3) Metabolic acidosis, edema, and hypotension

102
Q

Mannitol Prolonged use may cause ____?

A

electrolyte imbalances with hypokalemic hypochloremic alkalosis, hyponatremia or hypernatremia can occur, and plasma hyperosmolarity due to excessive Na+ and water excretion

103
Q

Mannitol: Complications

A

1) Volume depletion and hypernatremia
2) Volume expansion, hyponatremia, and metabolic acidosis caused by mannitol
3) Increased ICP
4) Acute renal failure
5) Extravasation

104
Q

Mannitol:

Treatment of Increased ICP

A

Dose: 0.25 - 2 g/kg/dose IV over 30 - 60 minutes

105
Q

Mannitol Onset of Action

A

10 - 15 minutes, peak effect of 30-45 minutes and

duration of effect up to 6 hours. The effect on ICP is dose-depedent

106
Q

An intact BBB is necessary to prevent mannitol’s entrance into the CNS. If the BBB is disrupted, mannitol may enter the brain leading to a ____?

A

drawing fluid with it, leading to rebound cerebral edema and increase ICP!

CRNA Pharmacology (8 decks)

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