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Pharm block 4 hemostasis and cardiac > diuretics > Flashcards

diuretics Flashcards

1
Q

define diuretic

A

A substance or drug that tends to increase the discharge of urine.

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2
Q

Carbonic Anhydrase Inhibitors MOA

A

Acetazolamide, dorzolamide,
methazolamide, and dichlorphenamide inhibit CA in luminal membrane of proximal tubule, reducing proximal HCO3- reabsorption.

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3
Q

Osmotic Diuretics MOA

A

Freely filterable, non-reabsorbable osmotic agents like mannitol, glycerol, and urea act primarily on the proximal tubule to reduce the reabsorption of H2O and solutes including NaCl.

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4
Q

loop diuretics MOA

A

Furosemide, bumetanide, torsemide, and ethacrynic acid inhibit the Na+/ K+/2Cl- cotransport system in the thick
ascending limb of Henle’s loop (ALH).

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5
Q

Thiazide MOA

A

Chlorothiazide, hydrochlorothiazide, chlorthalidone, metolazone, indapamide inhibit NaCl cotransport in
early distal convoluted tubule (DCT).

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6
Q

K+ sparing diuretics MOA

A

Spironolactone & eplerenone competitively block the actions of aldosterone on the collecting tubules.

Amiloride and triamterene reduce Na+ entry across the luminal membrane of the principal cells of the collecting
tubules.

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7
Q

ADH antagonist MOA

A

Doxycycline, lithium, tolvaptan, conivaptan, mozavaptan, etc. prevent ADH induced water reabsorption in the
principal cells of the collecting tubule

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8
Q

what are the 6 classes of diuretics?

A 
Carbonic Anhydrase Inhibitors
Osmostic Diuretics
Loop Diuretics
Thiazide
K+ sparing Diuretics
ADH antagonists
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9
Q

acetazolamide is what type of diuretic and where does it primarily work

A

acts primarily in the PCT as a prototypical CA inhibitor. At its maximal effect, it can inhibit 85% of NaHCO3 reabsorption.

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10
Q

mannitol is what type of diuretic and where does it work

A

Mannitol is a prototypical osmotic diuretic, which limits water reabsorption in the water-permeable segments of the nephron (PCT, thin descending limb, and CT (with ADH)).

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11
Q

Furosemide is what type of diuretic and where does it work

A

Furosemide is a prototypical loop diuretic, which inhibits Na+/K+/2Cl- cotransport in the thick ascending limb of Henle’s loop.

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12
Q

where do thiazide diuretics work

A

inhibit NaCl co-transport in the DCT.

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13
Q

where do K+ sparing diuretics work

A

K+-sparing diuretics act on the CT by inhibition of aldosterone actions or directly blocking Na+ channels.

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14
Q

where do ADH antagonist work

A

ADH antagonists prevent the ADH-stimulated reabsorption of H2O in the CT.

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15
Q

what is the primary therapeutic goal of diuretic use

A

reduce edema (must have NaCl output greater than intake)

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16
Q

Most diuretics exert their effects from which side of the lumen? what are the exceptions?

A

Mostly from the luminal side of the nephron.

Exceptions are spironolactone and some ADH antagonist

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17
Q

how do diuretics enter the nephron and what is the consequence of this

A

Most are secreted across the proximal tubule via the organic acid/base secretory pathway
exception is Mannitol which is filtered

therefore decreased renal blood flow or renal failure reduces diuretic effectiveness as well as drugs that compete for the secretory pump

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18
Q

Na+ reabsorption is primarily driven by

A

the Na+/K+ ATPase on the basolateral (blood side) of the epithelial cells

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19
Q

where is bicarbonate reabsorbed

A

proximal convoluted tubule

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20
Q

ACETAZOLAMIDE belongs to which class and what is the mechanism of action?

A

CA inhibitor, reversible inhibition of CA (inhibiting reabsorption of HCO3- in the proximal tubule

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21
Q

Acetazolamide adverse effects

A

Metabolic acidosis
Hypokalemia
Calcium phosphate stones
Drowsiness, paresthesias & hypersensitivity rxns (sulfa drug)

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22
Q

Acetazolamide contraindicaitons

A

Cirrhosis (increased urine pH reduces NH3 secretion and thereby increases serum NH3)

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23
Q

Dichlorphenamide is what kind of drug

A

CA inhibitor - 30x more potent than acetazolamide

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24
Q

Methazolamide is what kind of drug

A

CA inhibitor - 5x more potent than acetazolamide

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25
Q

Dorzolamide is what kind of drug

A

CA inhibitor - topical preparation for ocular use (avoids systemic effects)

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26
Q

ACETAZOLAMIDE clinic uses

A

Diuretic agent: weak, but ok as backup

Glaucoma: reduction of intraocular pressure

Urinary alkalinization: drug overdose/some stones

Acute mountain sickness: buy’s some time only

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27
Q

Mannitol MOA

A

Osmotic diuretic
Major osmotic effects in proximal tubule and descending limb of the loop of Henle; collecting ducts too, if ADH is present

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28
Q

Can mannitol be given orally

A

No - not absorbed must be given via IV to reach the kidneys

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29
Q

how does Mannitol enter the nephron

A

via filtration in the glomerulous- adverse effects predominiate if filtration is impaired

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30
Q

Mannitol adverse effects

A 
Adverse effects
• Major toxicity due to increased plasma osmolality. With reduced glomerular filtration rate (CHF or renal failure) mannitol is retained in ECF. This moves water out of cells into ECF potentially worsening heart failure. In addition, Na+ follows water movement out of cells leading to hyponatremia. 
• Acute pulmonary edema
• Dehydration
• Headache, nausea & vomiting
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31
Q

Mannitol contraindications

A

Congestive heart failure
Renal failure
Pulmonary edema

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32
Q

Mannitol clinical indications

A

Maintain or increase urine volume
may be useful to treat or prevent acute renal failure
may promote renal excretion of toxic substances (eg., contrast dye or myoglobinemia)

Reduce intracranial pressure

Reduce intraocular pressure (glaucoma)

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33
Q

Does mannitol cross the BBB

A

NO- therefore it can draw fluid out of the intracranial compartment

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34
Q

Is the thick ascending limb permeable to water

A

NO

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35
Q

what is the most effective diuretic class

A

Loop diuretics - can cause excretion of up to 20% of the filtered Na+

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36
Q

how do loop diuretics work

A
  • Act primarily by blocking the Na+/K+/2Cl- co-transporter in the apical membrane of the thick ascending limb of Henle’s loop.
  • Reduce ability to concentrate ECF and to dilute lumenal fluid.
  • Increase urinary water, Na+, K+, Ca2+, and Mg2+ excretion. Most efficacious diuretic class; can cause excretion of up to 20% of the filtered Na+.
  • *Also cause dilation of the venous system and renal vasodilation – effects that may be mediated by prostaglandins. (unique to loop diuretics)
37
Q

FUROSEMIDE (Lasix® ) is what kind of diuretic

A

Loop diuretic - Reduces reabsorption of Na+, K+, Cl- as expected, but also Ca2+ & Mg2+ due to loss of (+) luminal charge

Renal vasodilation improves renal blood flow

38
Q

Furosemide pharmacokinetics

A

Oral absorption is rapid but variable for each patient
*Half-life is short (1-1.5 hrs) so duration is only 2-3 hrs
Renal secretion mechanism; organic acid transporter

39
Q

ferosemide adverse effects

A

mainly due to over diuresises of a pt bc they are so powerful

Hyponatremia, hypokalemia, hypomagnesemia
Dehydration
Metabolic alkalosis
Mild hyperglycemia
Ototoxicity
Hypersensitivity rxns
40
Q

clinical indications for ferosemide

A 
Acute pulmonary edema
Edema associated with congestive heart failure
Acute hypercalcemia
Acute hyperkalemia
Hypertension
41
Q

BUMETANIDE advantages/disadvantages over ferosemide

A

About 40X more potent than furosemide
Shorter half-life than furosemide: ~ 1 hr
50% metabolized by the liver

42
Q

TORSEMIDE advantages/disadvantages over ferosemide

A

Longer half-life than furosemide: ~ 3 hrs
Longer duration of action, too: ~ 5-6 hrs
Better oral absorption than furosemide
80% metabolized by the liver

43
Q

ETHACRYNIC ACID advantages/disadvantages over ferosemide

A

Last resort; used only when others exhibit hypersensitivity
No CA inhibition
Nephrotoxic and ototoxic

44
Q

Thiazide diuretics MOA

A

Inhibition of Na+/Cl- cotransporter in distal tubule
Produces relatively mild diuresis
**Results in increased Ca2+ reabsorption (opposite loop diuretics)

45
Q

Hydochlorothiazide pharmacokinetics

A

Good oral absorption and renal elimination

Half-life of 2.5 hrs

46
Q

HYDROCHLOROTHIAZIDE adverse effects

A 
Adverse Effects
Hyponatremia & **hypokalemia
Dehydration
*Metabolic alkalosis
Hyperuricemia
**Hyperglycemia
**Hyperlipidemia (increased LDL)
Weakness, fatigue, paresthesias & hypersensitivity
47
Q

HYDROCHLOROTHIAZIDE clinical uses

A

Hypertension* main use
Congestive heart failure
Reduce Ca2+ excretion to prevent kidney stones

48
Q

CHLOROTHIAZIDE compared to hydrochlorothiazide

A

1/10th the potency of Hydrochlorothiazide

Half-life of 1.5 hrs (shorter)

49
Q

Metolazone compared to hydrochlorothiazide

A

10X more potent than Hydrochlorothiazide
Half-life of 4-5 hrs (longer)
not a sulfa drug

50
Q

Indapamide compared to hydrochlorothiazide

A

20X more potent than Hydrochlorothiazide

*Half-life of 10-22 hrs; metabolized extensively by the liver

51
Q

Chlorthalidone compared to hydrochlorothiazide

A

Same potency as Hydrochlorothiazide

Half-life of 44 hrs** (much much longer)

52
Q

how do CA inhibitors cause hypokalemia?

A

K+ moves with its concentration gradient in the collecting tubule (principal cells). The CA inhibitors increase the amount of HCO3- in the lumen increasing its negative potential which increases the efflux of K+ out of the cells.

53
Q

how do thiazide and loop diuretics cause hypokalemia?

A

thiazide and loop diuretics increase the amount of Cl- in the lumen which makes the lumenal potential more negative. This increases K+ efflux in the collecting ducts.

54
Q

how do thiazide and loop diuretics cause metabolic ALKalosis

A

by increasing the luminal negative potential (higher concentrations of Na+ and Cl-) more H+ is secreted from the intercalculated cells of the collecting ducts

55
Q

how are potassium sparing diuretics used

A

These agents are often given to avoid the hypokalemia that accompanies the agents previously described.

56
Q

when should you NEVER give a K+ sparing diuretic

A

They should never be given in the setting of hyperkalemia or in patients on drugs or with disease states likely to cause hyperkalemia. These include diabetes mellitus, multiple myeloma, tubulointerstitial renal disease, and renal insufficiency.

or with drugs that can cause hyperkalemia potassium supplements and ACE inhibitors are common.

57
Q

SPIRONOLACTONE MOA

A

Competitive inhibition of the aldosterone receptor
Anti-androgenic effects
- Decrease testosterone synthesis
- Competitive inhibition of DHT receptor

58
Q

SPIRONOLACTONE effects

A

Mild diuresis due to decreased Na+ reabsorption secondary to aldosterone inhibition

“Sparing” of K+ & H+ also secondary to aldosterone inhibition

59
Q

Spironolactone pharmacodynamics

A

Slow onset of action; days to take effect

Liver metabolism to several active metabolites

60
Q

spironolactone adverse effects

A

Hyperkalemia
Metabolic acidosis
Gynecomastia, amenorrhea, impotence, decreased libido (due to also binding the mineralocorticoid receptor)
GI upset, including association with peptic ulcers
CNS effects: headache, fatigue, confusion, etc.

61
Q

EPLERENONE MOA and advantages

A

competitive antagonist of aldosterone binding to mineralocorticoid receptor.

Eplerenone is considerably more expensive than spironolactone, but it does not inhibit testosterone binding and therefore it does not induce gynecomastia or other related anti-androgenic side effects.

62
Q

How does Spironolactone cause metabolic acidosis

A

Decreased lumen negative potential
Reduced driving force for H+
Decreased expression of H+ pumps

therefore less H+ is excreted and more is left in the blood

63
Q

Spironolactone clinical uses

A

Primary hyperaldosteronism
Secondary hyperaldosteronism
Liver cirrhosis* (drug of choice for edema w/liver cirrhosis)
Hypertension

64
Q

Amiloride MOA and class

A

K+ sparing diuretic

Mechanism of Action
Blocks Na+ channels in the principal cell
Blocking Na+ influx decreases the driving force for K+ efflux so K+ is “spared” (less negative outside the cell)

65
Q

amiloride adverse effects

A

Hyperkalemia (NSAIDs can exacerbate this)
GI upset: nausea, vomiting, diarrhea
Muscle cramps
CNS effects: headache, dizziness, etc.

66
Q

how does amiloride’s cause hyperkalemia

A

by blocking the Na+ channel in the principle cells there is more Na+ in the lumen which makes the lumenal potential more positive therefore decreasing the force driving K+ out of the principal cells

67
Q

AMILORIDE clinical indications

A

Edema
Hypertension
Usually used in combination with other diuretics to reduce K+ loss

68
Q

Triamterene MOA and pharmacodynamics

A

Blocks Na+ channels in the principal cells
Pharmacodynamics
Blocking Na+ influx decreases the driving force for K+ efflux so K+ is “spared”
Active form can precipitate in the tubules and obstruct flow

69
Q

which is more potent amiloride or triamterene

A

amiloride (triamterene is 10x less potent)

70
Q

ADH antagonists that are no longer used

A

Demeclocycline and lithium both are nephrotoxic

71
Q

TOLVAPTAN MOA

A

is a selective antagonist of the vasopressin V2 receptor.
Induces increased, dose-dependent production of dilute urine.
Does not alter serum electrolyte balance.
Tolvaptan is orally available and has a half-life of 6 to 8 hours.

72
Q

what are the V2 receptor antagonists

A

tolvaptan, moxavaptan, and lixivaptan

73
Q

what are the V1a and V2 antagonists

A

conivaptan

74
Q

adverse affects of ADH receptor antagonists

A

hypernatremia, thirst, dry mouth, hypotension, dizziness.

75
Q

indications for use of ADH receptors antagonist

A

SIADH, euvolemic or hypervolemic hyponatremia; congestive heart failure.

76
Q

which ADH receptor antagonist can be used for euvolemic hyponatremia

A

conivaptam

77
Q

with CA inhibitors what is the main electrolytes in the urine

A

NaHCO3

78
Q

with thiazide diuretics what is the main electrolyte in the urine

A

NaCl

79
Q

with loop diuretics what is the main electrolyte in the urine

A

NaCl

80
Q

how does diabetic nephropathy affect potassium balance and which diuretics should be used

A

often associated with hyperkalemia- can use thiazide or loop diuretics

81
Q

best drug for HEPATIC CIRRHOSIS

A

Spironolactone - resistant to loop diuretics

82
Q

drug use for heart failure

A

Loop diuretics (IV for acute left sided failure, oral for chronic right sided)

83
Q

Tolvaptan is what kind of drug and is useful in what disease process

A

vasopressin antagonist and is shown to be useful in pts with CHF in addition to standard therapy including diuretics

84
Q

symptoms of hyponatriemia

A 
Headache/disorientation
Fatigue
Hallucinations
Respiratory arrest
Seizures
Coma
Death
85
Q

what drug should be used for uncomplicated hypertension

A

thiazide diurteic either alone or with another drug

86
Q

what is the effect of using a thiazide diuretic in pts with diabetes insipidus

A

reduced polyuria and increase urine osmolarity (the opposit of what was though)

87
Q

how are thiazide diuretics helpful to pts with kidney stones

A

decreases Ca concentrations in the urine

88
Q

what kind of diuretic may be helpful to pts with hypercalcemia

A

loop diuretics - increase Ca excretion (avoid thiazide diuretics)

Pharm block 4 hemostasis and cardiac (12 decks)

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