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Pharm 2 > Diuretic agents > Flashcards

Diuretic agents Flashcards

1
Q

What are the three carbonic anhydrase inhibitors? What is their mechanism of action?

A

Acetazolamide (diamox)
Dorzolamide (Azopt)
Brinzolamide (Trusopt)
Block H2CO3 production which drives H+ exchange, so with decreased H+ secretion, this leads to decreased Na+ reabsorption and increased loss of Na+ and water in the urine

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2
Q

What do CA inhibitors cause? What is this helpful in the treatment of?

A

a decrease in H+ secretion, treatment of acute mountain sickness (which results from a decrease in CO2 as ventilation increases, raising pH), prevents H+ secretion to try and lower pH.

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3
Q

What are some adverse effects of CA inhibitors?

A

Hyperchloremic metabolic acidosis (increased HCO3- in lumen increases Cl- reabsorption in collecting tubule)
Hypokalemia (increased Na+ in urine increased the Na/K+ exchanger in the distal tubule=more K+ excretion)
Hyperuricemia

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4
Q

A patient is taking acetazolamide and suffers a gouty attack. Why?

A

Due to hyperuricemia because these drugs are acids and their excretion competes with uric acid

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5
Q

What are some contraindications for CA (-amide) use?

A 
Sulfa hypersensitivity (major)
Hepatic cirrhosis (there will be an accumulation of NH4+)
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6
Q

What are the two effects of loop diuretics?

A 
#1 Blocks the NKCC2 transporter to reduce medullary concentration gradient to impair reabsorption of urine in collecting duct
#2 induces PG synthesis in the kidney which causes diminished salt transport, furthering diuretic action and causing renal and systemic vasodilation
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7
Q

What are the indications for loop diuretics?

A

CHF, pulmonary edema, and hypercalcemia (due to decreased K+ gradient which decreases reabsorption of Mg and Ca2+)

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8
Q

What are some major adverse effects of loop diuretics?

A

Hypochloremia, hypokalemic metabolic alkalosis (H+ follows K+ out), IRREVERSIBLE OTOTOXICITY, hyperuricemia

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9
Q

What are the loop diuretics? Which are sulfa derivatives and which are not?

A

Sulfa: Furosemide (lasix), bumetanide (bumex), torsemide (demadex)
Non-sulfa: ethacrynic acid

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10
Q

You have a patient with a sulfa allergy so you put them on ethacrynic acid. What should you be particularly concerned about? What other drug class should you not prescribe?

A

Ototoxicity, AMINOGLYCOSIDES

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11
Q

Contraindications for loop diuretics

A 
Sulfa sensitivity (except e.a.)
Drug interactions (COX inhibitors, AGs, Lithium (increased Na+ loss increases Li+ retention), Digoxin (loss of K+ protective effect))
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12
Q

What are THE thiazide diuretics?

A

Hydrochlorothiazide and Chlorothiazide

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13
Q

What are compounds related to thiazides?

A

Chlorothalidone, metolazone, quinethazone, indapamide

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14
Q

What is the MOA of thiazide action? What is this effect dependent on?

A

Inhibits the NCC transporter in the eartly distal tubule so the dilution of urine is blocked
Dependent on PG synthesis

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15
Q

What are the main clinical indications for thiazide diuretics?

A

HYPERTENSION, nephrolithiasis, nephrogenic DI

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16
Q

What is one beneficial and one harmful effect of the increase in ATP-dependent K+ channel opening?

A

Beneficial: Causes vasodilation due to hyperpolarization of VSMC membranes
Harmful: reduced insulin secretion from Beta cells

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17
Q

What is one beneficial effect of the increased luminal Na+ concentration on Ca2+ excretion?

A

In the treatment of renal calculus, this will increase Ca2+ reabsorption due to an increase in luminal Na+ concentration, thereby decreasing Ca2+ excretion

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18
Q

What is the only drug that is useful in renal insufficiency due to its liver excretion? What is it also useful for?

A

Indapamide; causes pronounced vasodilation due to calcium channel blocking effects and it does not increase plasma lipids as much as other thiazids

19
Q

What condition does loop and thiazide diuretics cause?

A

Hypokalemic metabolic alkalosis

20
Q

What condition does a CA inhibitor cause?

A

Hyperchloremic metabolic acidosis

21
Q

Which diuretics work at low GFR?

A

Loop diuretics and metolazone (thiazide type)

22
Q

What are the two classes of potassium sparing diuretics?

A

Aldosterone antagonists and direct inhibitors of Na+ flux

23
Q

What is the MOA for K+ sparing diuretics?

A

Blocks Na+ reabsorption but does not induce secretion of K+

24
Q

What is an indication for using K+ sparing diuretics?

A

Hypokalemia and minimizing alkalosis of other diuretics (due to H+ loss), used in combination with other drugs

25
Q

What are the aldosterone antagonists?

A

Spironolactone and eplerenone

26
Q

What are some other uses of potassium sparing diuretics?

A

Hyperaldosteronism, hirsutism

27
Q

What are some side effects of potassium sparing diuretics?

A

Gynecomastia (put on eplereone), hyperkalemia (usually with an ACE-I or an ARB)

28
Q

Contraindication for potassium sparing?

A

Hyperkalemia, chronic renal insufficiency (BUN/Cr), liver damage (watch for hyperchloremic acidosis)

29
Q

What is the one drug in the Selective aldosterone receptor antagonist class? Where is it metabolized?

A

Epelernone; liver by CYP3A4=many drug interactions

30
Q

How are Amilioride and Triamterene different from spiro and eplerenone?

A

They block the Na/K ion exchange mechanism independently of aldosterone, so they directly inhibit aldosterone-sensitive Na+ channel and leads to decreased K+ excretion

31
Q

What is the only diuretic class that is not an acid so does not invoke hyperuricemia?

A

K+ sparing (amiloride and triamterene)

32
Q

What is the DOC for Lithium induced diabetes insipidus?

A

Amiloride

33
Q

Why can you not use K+ sparing diuretics in burn patients?

A

Because they are already hyperkalemic and it leads to severe arrhythmias

34
Q

Why are osmotic diuretics given IV only?

A

If they were given orally, they would cause osmotic diarrhea. Filtered but not reabsorbed by kidneys and water follows!

35
Q

What are some indications for osmotic diuretic use?

A

For prophylaxis of acute renal failure, to decrease IOP and to decrease ICP

36
Q

What are adverse reactions of osmotic diuretics?

A

pulmonary edema in CHF, excessive cell dehydration

37
Q

What are the osmotic diuretics?

A

Mannitol, isosorbide, glycerin, urea

38
Q

What is the MOA for desmopressin?

A

Stimulates aquaporing insertion to promote water reabsorption to tx central diabetes insipidus to decrease water excretion. Can cause dilutional hyponatremia

39
Q

What is the treatment of euvolemic or hypovolemic hyponatremia? What class is it?

A

Conivaptan; ADH antagonist

40
Q

Use of what drug class will inhibit which diuretics (hence one of the most common causes of CHF exaccerbations):

A

NSAIDs; THIAZIDES more than loops (because loops cause PG synthesis)

41
Q

What aldosterone antagonist has many drug interactions but better for gynecomastia?

A

eplerenone

42
Q

What is the DOC for hyponatremia (prior to vaptans)?

A

lithium

43
Q

What is the DOC for SIADH (prior to vaptans)?

A

Demeclocycline (prior to vaptans)

Pharm 2 (11 decks)

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