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Renal II Cumulative Final > 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
Q

Loop diuretics can be used for HTN that is unresponsive to other diuretics; unlike thiazides, they still work when ____ and ____ are low

A

RBF; GFR

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26
Q

MOA of HCTZ

A

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]

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27
Q

Clinical applications of HCTZ

A

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
Q

Toxicities associated with HCTZ

A 
Orthostatic hypotension
Hypokalemia
Hypomagnesemia
Hyponatremia
Hypochloremic metabolic alkalosis
Hypercalcemia
Hyperglycemia
Hyperuricemia

Risk of sulfonamide allergy

29
Q

Thiazide similar to HCTZ, but half-life of 40-60 hours allowing for prolonged/stable response with proven benefits

A

Chlorthalidone

30
Q

Long-acting thiazide diuretic that is favorite of cardiologists for use as an adjunct diuretic in the tx of CHF

A

Metolazone

31
Q

MOA of amiloride

A

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
Q

Clinical applications of amiloride

A

Counteracts K+ loss induced by other diuretics in the tx of HTN or heart failure

Off-label: ascites, pediatric hypertension

33
Q

Toxicities associated with amiloride

A 
Hyperkalemia (box warning)
Hyponatremia
Hypovolemia
Hyperchloremic metabolic acidosis
Dizziness, fatigue, headache
N/V, bloating, diarrhea, constipation
34
Q

_____ = used similar to amiloride for edema and off-label for HTN, rapidly absorbed, duration of action is 6-9 hours, eliminated as drug metabolites

A

Triamterene

35
Q

MOA of spironolactone

A

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
Q

Clinical applications of spironolactone

A

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
Q

Onset and duration of action of spironolactone

A

Has steroid-like effects, thus it is slow onset and long-duration of action

38
Q

Toxicities associated with spironolactone

A

Hyperkalemia

Amenorrhea, hirsutism, gynecomastia, impotence

Tumorigen in chronic animal toxicity studies — box warning states to avoid use unless necessary

39
Q

Similar to spironolactone but more selective aldosterone antagonist, approved for use in post-MI heart failure and alone or in combo for HTN

A

Eplerenone

40
Q

Drug interactions to be aware of with K+ sparing diuretics

A

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
Q

MOA of conivaptan

A

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
Q

Clinical applications for conivaptan

A

Tx of euvolemic and hypervolemic hyponatremia in patients who are hospitalized, symptomatic, or not responsive to fluid restriction

43
Q

Toxicities associated with conivaptan

A

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
Q

Selective V2 receptor antagonist admistered orally

A

Tolvaptan

45
Q

What are some important considerations when choosing to use Tolvaptan for diuresis?

A

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
Q

MOA of conivaptan (IV) and tolvaptan (PO)

A

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
Q

Adverse effects of the “vaptans”

A

Orthostatic hypotension

Fatigue

Thirst

Polyuria, bedwetting

Hypernatremia, hyperkalemia, hyperuricemia

48
Q

Drug interactions to consider with the “vaptans”

A

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
Q

Prototypical carbonic anhydrase inhibitor developed from a sulfonamide after it was discovered to cause metabolic acidosis and alkaline urine

A

Acetazolamide

50
Q

MOA of carbonic anhydrase inhibitors

A

Na+ bicarbonate diuresis

[bicarbonate ion remains in early proximal tubule, H+ cycling lost — inhibiting Na/H exchange]

51
Q

Carbonic anhydrase inhibitors are now rarely used for diuresis. What are some therapeutic uses still recognized?

A

Urinary alkalinization

Metabolic alkalosis

Glaucoma: acetazolamide, dorzalamide

Acute mountain sickness

52
Q

Adverse effects of carbonic anhydrase inhibitors

A

Hyperchloremic metabolic acidosis

Nephrolithiasis

Potassium wasting

53
Q

What type of diuretics can be used to help eliminate excess intracellular volume?

A

Osmotic diuretics

54
Q

Prototypical osmotic diuretic and its MOA

A

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
Q

Pharmacokinetics of mannitol

A

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
Q

Adverse effects of osmotic diuretics

A

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
Q

Therapeutic uses of mannitol

A

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
Q

What is important to remember about alternative medicines used for diuresis?

A

While some have been shown to be effective, active ingredients and MOAs are generally unknown — should not be mixed with conventional diuretics

59
Q

What’s the deal with European licorice?

A

European licorice contains glycyrrhizic acid which potentiates aldosterone effects in the kidney in dose-dependent manner, increasing systolic BP

60
Q

Diuretic therapy algorithm for edema caused by renal insufficiency or nephrotic syndrome

A

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
Q

Diuretic algorith for edema caused by cirrhosis

A

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
Q

Diuretic therapy algorithm for edema caused by cardiac disease (CHF)

A

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
Q

Common causes of diuretic resistance

A

Incorrect dx

Inappropriate NaCl or fluid intake

Inadequate drug reaching tubule lumen in active form

Inadequate renal response

64
Q

What are some causes of inadequate diuretic drug reaching tubule lumen in active form?

A

Nonadeherence

Dose inadequate or too infrequent

Poor absorption (uncompensated HF)

Decreased RBF (HF, cirrhosis, elderly)

Decreased functional renal mass (AKI, CKD, elderly)

Proteinuria

65
Q

What are some causes of inadequate renal response to diuretics?

A

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
Q

Tx of central diabetes insipidus

A

Exogenous ADH agonist (dDAVP)

Desmopressin

67
Q

Tx of nephrogenic diabetes insipidus

A

If NOT caused by Lithium —> tx with thiazide diuretics

Lithium therapy is MCC of nephrogenic DI, when lithium is the cause —> tx with amiloride

Renal II Cumulative Final (20 decks)

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