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CPR EXAM 2 > Diuretics > Flashcards

Diuretics Flashcards

1
Q

Classes of diuretics and conditions they are used for

A

Thiazide diuretics (HTN, edema)

K+ sparing diuretics (HTN, edema)

Loop diuretics (HTN, edema)

Aquaretics (hyponatremia)

Carbonic anhydrase inhibitors (urinary alkalinization, mountain sickness, glaucoma)

Osmotic diuretics (maintain urine flow, pull water from cells for excretion)

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2
Q

3 drugs in thiazide diuretic class

A

Hydrochlorothiazide
Metolazone
Chlorthalidone

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3
Q

4 drugs in loop diuretic class

A

Furosemide
Torsemide
Bumetanide
Ethacrynic acid

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4
Q

Drugs in K+ sparing diuretic class

A

Na+ channel blockers:
Amiloride
Triamterene

Aldosterone antagonists (also used as antifibrotics in heart failure):
Spironolactone
Eplerenone
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5
Q

2 drugs in aquaretic diuretic class

A

Conivaptan

Tolvaptan

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6
Q

Carbonic anhydrase inhibitor diuretic used for urinary alkalinization, mountain sickness, and glaucoma

A

Acetazolamide

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7
Q

Osmotic diuretic used to maintain urine flow

A

Mannitol

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8
Q

Site of action of osmotic diuretics

A

Proximal tubule

Thin descending LoH

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9
Q

Site of action of carbonic anhydrase inhibitor diuretics

A

Proximal tubule

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10
Q

Site of action of loop diuretics

A

Thick ascending LoH

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11
Q

Site of action of thiazide diuretics

A

Distal convoluted tubule

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12
Q

Site of action of Na+-channel blocker Spironolactone

A

Cortical collecting duct

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13
Q

Site of action of the Vaptans (aquaretics)

A

Collecting duct [site of ADH-regulated water reabsorption]

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14
Q

K+ losing diuretics

A

NaCl cotransporter blockers = thiazides

Na+K+2Cl cotransporter blockers = loop diuretics

Carbonic anhydrase inhibitors (seldom used)

Nonreabsorbable solutes: osmotic diuretics

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15
Q

Effects of hyperkalemia on the heart

A 
Tall T waves
Prolonged PR interval 
Widened QRS
Arrhythmias including bradycardia, Vtach, fibrillation
Sinus arrest or nodal rhythm
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16
Q

Effects of hypokalemia on the heart

A 
Flattened T waves
ST depression
Prolonged QT
Tall U waves
Atrial arrhythmias
Vtach or Vfib
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17
Q

Which of the diuretics contain sulfa?

A

Furosemide
Torsemide
Bumetanide

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18
Q

MOA of furosemide

A

Directly inhibits reabsorption of Na and Cl in thick ascending LoH by blocking Na/K/2Cl cotransporter

Indirectly inhibits paracellular reabsorption of Ca and Mg by the TAL d/t loss of K+ backleak responsible for lumen+ transepithelial potential

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19
Q

Effects of furosemide (what gets excreted?)

A

Increased excretion of water, sodium, potassium, chloride, magnesium, and calcium

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20
Q

Clinical applications of furosemide

A

Management of edema associated with heart failure, hepatic disease, or renal disease

Acute pulmonary edema by decreasing preload (decreases EC volume, rapid dyspnea relief)

Tx of HTN (alone or combined with other hypertensives) — note that unlike thiazides, works in pts with low GFR

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21
Q

Potential toxicities associated with furosemide

A 
Hypokalemia
Hyponatremia
Hypocalcemia
Hypomagnesemia
Hypochloremic metabolic alkalosis
Hyperglycemia
Hyperuricemia (increased gout risk)
Increased cholesterol and triglycerides
Ototoxicity

Risk of sulfonamide hypersensitivity/allergy

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22
Q

Loop diuretic that works similarly to furosemide but with longer half-life, better oral absorption, and some evidence that it works better in heart failure

A

Torsemide

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23
Q

Loop diuretic that is a sulfonamide working similar to furosemide, but more predictable oral absorption

A

Bumetanide

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24
Q

Non-sulfonamide loop diuretic reserved for those with sulfa allergy

A

Ethacrynic acid

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25
Loop diuretics can be used for HTN that is unresponsive to other diuretics; unlike thiazides, they still work when ____ and ____ are low
RBF; GFR
26
MOA of HCTZ
Inhibits sodium reabsorption in the distal tubules via blockade of Na/Cl cotransporter Results in increased urine excretion of Na and H2O as well as K+ and Mg++ [potassium-losing diuretics]
27
Clinical applications of HCTZ
Management of mild-to-moderate HTN alone or in combo with other hypertensives (note: not effective in those with low GFR) Treatment of edema (adjunct role) Off-label: calcium nephrolithiasis, nephrogenic diabetes insipidus
28
Toxicities associated with HCTZ
``` Orthostatic hypotension Hypokalemia Hypomagnesemia Hyponatremia Hypochloremic metabolic alkalosis Hypercalcemia Hyperglycemia Hyperuricemia ``` Risk of sulfonamide allergy
29
Thiazide similar to HCTZ, but half-life of 40-60 hours allowing for prolonged/stable response with proven benefits
Chlorthalidone
30
Long-acting thiazide diuretic that is favorite of cardiologists for use as an adjunct diuretic in the tx of CHF
Metolazone
31
MOA of amiloride
Blocks epithelial sodium channels (ENaC) in the CDs responsible for Na/K exchange Causes small increase in Na excretion, blocks major pathway for K elimination so K+ is retained H, Mg, and Ca excretion are also indirectly decreased
32
Clinical applications of amiloride
Counteracts K+ loss induced by other diuretics in the tx of HTN or heart failure Off-label: ascites, pediatric hypertension
33
Toxicities associated with amiloride
``` Hyperkalemia (box warning) Hyponatremia Hypovolemia Hyperchloremic metabolic acidosis Dizziness, fatigue, headache N/V, bloating, diarrhea, constipation ```
34
_____ = used similar to amiloride for edema and off-label for HTN, rapidly absorbed, duration of action is 6-9 hours, eliminated as drug metabolites
Triamterene
35
MOA of spironolactone
Competitive antagonist of aldosterone receptors, decreases aldosterone stimulated gene expression Side effects due in part to it being a partial agonist at androgen receptors It is a K+ sparing diuretic that blunts ability of aldosterone to promote Na/K exchange in the CDs
36
Clinical applications of spironolactone
Counteracts K+ loss induced by other diuretics in tx of HTN, heart failure, and ascites Tx of primary hyperaldosteronism Off-label: reduce fibrosis post-MI heart failure, hirsutism, tx of androgenic alopecia in females
37
Onset and duration of action of spironolactone
Has steroid-like effects, thus it is slow onset and long-duration of action
38
Toxicities associated with spironolactone
Hyperkalemia Amenorrhea, hirsutism, gynecomastia, impotence Tumorigen in chronic animal toxicity studies — box warning states to avoid use unless necessary
39
Similar to spironolactone but more selective aldosterone antagonist, approved for use in post-MI heart failure and alone or in combo for HTN
Eplerenone
40
Drug interactions to be aware of with K+ sparing diuretics
Should “never” be given with drugs that increase plasma potassium levels....but note that they may be used cautiously with ACE inhibitors in heart failure
41
MOA of conivaptan
Non-peptide arginine vasopressin receptor antagonist (AVP aka ADH antagonist); has affinity for ADH receptor subtypes V1A and V2 Promotes excretion of free water (decreased Uosm, increased Posm)
42
Clinical applications for conivaptan
Tx of euvolemic and hypervolemic hyponatremia in patients who are hospitalized, symptomatic, or not responsive to fluid restriction
43
Toxicities associated with conivaptan
Orthostatic hypotension Fatigue Thirst Polyuria, bedwetting Monitor plasma sodium and neurologic status closely because too rapid serum sodium correction can lead to seizures, osmotic demyelination, coma, or death
44
Selective V2 receptor antagonist admistered orally
Tolvaptan
45
What are some important considerations when choosing to use Tolvaptan for diuresis?
Used ONLY in hospital setting where plasma sodium can be closely monitored Must use for less than 30 days for hyponatremia — longer use can lead to potentially fatal hepatotoxicity (used to slow progression of adult polycystic kidney dz but must monitor liver tests)
46
MOA of conivaptan (IV) and tolvaptan (PO)
Increase free water clearance by preventing ADH-mediated insertion of aquaporins into luminal membrane of principal cells in collecting duct [prevents reabsorption of water, therefore increasing water excretion —> decreased plasma volume and increased plasma osmolality, primarily d/t increase in plasma sodium concentration]
47
Adverse effects of the “vaptans”
Orthostatic hypotension Fatigue Thirst Polyuria, bedwetting Hypernatremia, hyperkalemia, hyperuricemia
48
Drug interactions to consider with the “vaptans”
Metabolized by CYP3A4, so inhibitors and inducers of this enzyme can alter its half-life and potential for toxicity Selective water loss means possibility of hypovolemia which may increase concentration of drugs leading to toxic levels
49
Prototypical carbonic anhydrase inhibitor developed from a sulfonamide after it was discovered to cause metabolic acidosis and alkaline urine
Acetazolamide
50
MOA of carbonic anhydrase inhibitors
Na+ bicarbonate diuresis [bicarbonate ion remains in early proximal tubule, H+ cycling lost — inhibiting Na/H exchange]
51
Carbonic anhydrase inhibitors are now rarely used for diuresis. What are some therapeutic uses still recognized?
Urinary alkalinization Metabolic alkalosis Glaucoma: acetazolamide, dorzalamide Acute mountain sickness
52
Adverse effects of carbonic anhydrase inhibitors
Hyperchloremic metabolic acidosis Nephrolithiasis Potassium wasting
53
What type of diuretics can be used to help eliminate excess intracellular volume?
Osmotic diuretics
54
Prototypical osmotic diuretic and its MOA
Mannitol (can also use urea, glycerin, and isosorbide) MOA: the inability to reabsorb mannitol keeps water in the PT lumen; this water is delivered to the distal portions of the nephron where much of it is excreted Mannitol acts throughout the body to pull water out of the cells with net effect of TBW excretion in excess of plasma electrolytes
55
Pharmacokinetics of mannitol
Distributes in ECF, must give IV in large amounts sufficient to raise its osmolality (e.g., 50-200g over 24 hours) Effects noticable w/i 30-60 mins, and is fully eliminated unchanged in urine over period of 6-8 hours
56
Adverse effects of osmotic diuretics
ECV is acutely increased because mannitol sucks water out of cells, which can exacerbate heart failure HA, nausea, vomiting, and fluid/electrolyte imbalances also occur
57
Therapeutic uses of mannitol
Prophylaxis of renal failure (keeps some fluid volume in tubules to prevent them from collapsing when glomerular filtration rate is very low) Reduction of intracranial pressure Reduction of intraocular pressure when no response to other therapies
58
What is important to remember about alternative medicines used for diuresis?
While some have been shown to be effective, active ingredients and MOAs are generally unknown — should not be mixed with conventional diuretics
59
What’s the deal with European licorice?
European licorice contains glycyrrhizic acid which potentiates aldosterone effects in the kidney in dose-dependent manner, increasing systolic BP
60
Diuretic therapy algorithm for edema caused by renal insufficiency or nephrotic syndrome
Start with loop diuretic Add thiazide if needed Add distal diuretic drug if ClCr > 75 mL/min, for K+ homeostasis, or for added natriuresis (if urinary excretion of sodium is decreased and urinary excretion of potassium is increased)
61
Diuretic algorith for edema caused by cirrhosis
Start with spironolactone If ClCr > 50 mL/min, add HCTZ If ClCr is < 50 mL/min, add a loop diuretic (can subsequently add thiazide then distal diuretic drug)
62
Diuretic therapy algorithm for edema caused by cardiac disease (CHF)
If mild disease, with ClCr > 50 mL/min, start with HCTZ If more severe disease, start with loop diuretic, then add thiazide, then distal diuretic
63
Common causes of diuretic resistance
Incorrect dx Inappropriate NaCl or fluid intake Inadequate drug reaching tubule lumen in active form Inadequate renal response
64
What are some causes of inadequate diuretic drug reaching tubule lumen in active form?
Nonadeherence Dose inadequate or too infrequent Poor absorption (uncompensated HF) Decreased RBF (HF, cirrhosis, elderly) Decreased functional renal mass (AKI, CKD, elderly) Proteinuria
65
What are some causes of inadequate renal response to diuretics?
Low GFR (AKI, CKD) Decreased effective arterial volume (edematous conditions) Activation of RAAS (edematous conditions) Nephron adaptation (prolonged therapy) NSAIDs (e.g., Indomethacin, ASA)
66
Tx of central diabetes insipidus
Exogenous ADH agonist (dDAVP) Desmopressin
67
Tx of nephrogenic diabetes insipidus
If NOT caused by Lithium —> tx with thiazide diuretics Lithium therapy is MCC of nephrogenic DI, when lithium is the cause —> tx with amiloride

CPR EXAM 2 (52 decks)

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