Diuretic agents Flashcards

(43 cards)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A
Sulfa hypersensitivity (major)
Hepatic cirrhosis (there will be an accumulation of NH4+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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+)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some major adverse effects of loop diuretics?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are THE thiazide diuretics?

A

Hydrochlorothiazide and Chlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are compounds related to thiazides?

A

Chlorothalidone, metolazone, quinethazone, indapamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the main clinical indications for thiazide diuretics?

A

HYPERTENSION, nephrolithiasis, nephrogenic DI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
What are the aldosterone antagonists?
Spironolactone and eplerenone
26
What are some other uses of potassium sparing diuretics?
Hyperaldosteronism, hirsutism
27
What are some side effects of potassium sparing diuretics?
Gynecomastia (put on eplereone), hyperkalemia (usually with an ACE-I or an ARB)
28
Contraindication for potassium sparing?
Hyperkalemia, chronic renal insufficiency (BUN/Cr), liver damage (watch for hyperchloremic acidosis)
29
What is the one drug in the Selective aldosterone receptor antagonist class? Where is it metabolized?
Epelernone; liver by CYP3A4=many drug interactions
30
How are Amilioride and Triamterene different from spiro and eplerenone?
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
What is the only diuretic class that is not an acid so does not invoke hyperuricemia?
K+ sparing (amiloride and triamterene)
32
What is the DOC for Lithium induced diabetes insipidus?
Amiloride
33
Why can you not use K+ sparing diuretics in burn patients?
Because they are already hyperkalemic and it leads to severe arrhythmias
34
Why are osmotic diuretics given IV only?
If they were given orally, they would cause osmotic diarrhea. Filtered but not reabsorbed by kidneys and water follows!
35
What are some indications for osmotic diuretic use?
For prophylaxis of acute renal failure, to decrease IOP and to decrease ICP
36
What are adverse reactions of osmotic diuretics?
pulmonary edema in CHF, excessive cell dehydration
37
What are the osmotic diuretics?
Mannitol, isosorbide, glycerin, urea
38
What is the MOA for desmopressin?
Stimulates aquaporing insertion to promote water reabsorption to tx central diabetes insipidus to decrease water excretion. Can cause dilutional hyponatremia
39
What is the treatment of euvolemic or hypovolemic hyponatremia? What class is it?
Conivaptan; ADH antagonist
40
Use of what drug class will inhibit which diuretics (hence one of the most common causes of CHF exaccerbations):
NSAIDs; THIAZIDES more than loops (because loops cause PG synthesis)
41
What aldosterone antagonist has many drug interactions but better for gynecomastia?
eplerenone
42
What is the DOC for hyponatremia (prior to vaptans)?
lithium
43
What is the DOC for SIADH (prior to vaptans)?
Demeclocycline (prior to vaptans)