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Pharm > Nicole: Renal - Diuretics > Flashcards

Nicole: Renal - Diuretics Flashcards

1
Q

What are the different types of diuretics?

A
  1. Carbonic Anhydrous Inhibitors
  2. Thiazides and Thiazide-like
  3. Loop diuretics
  4. Potassium sparing diuretics
  5. Osmotic diuretics
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2
Q

How do the carbonic anhydrous inhibitors work?

A

Blocks carbonic anhydrase enzyme in lumen of PCT, inhibiting reabsorption of NaHCO3 resulting in diuresis

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3
Q

Where do the Carbonic anhydrous inhibitors work?

A

In the lumen of the PCT

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4
Q

What are the carbonic anhydrous inhibitors primarily used for?

A

Glaucoma
Acute mountain (altitude) sickness
CNS edema

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5
Q

What is the drug we will be using that is the carbonic anhydrous inhibitor?

A

Acetozolamide

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6
Q

What are the side effects that we should be aware of with acetozolamide?

A 
flushing
electrolyte imbalance
confusion
confusion
ataxia
SJS
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7
Q

Contraindications for acetozolamide are what?

A

Sulfa allergy

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8
Q

What are some drugs that you should avoid/be aware of with the use of acetozolamide?

A

Increases level of anti-hypertensives, anticonvulsants, alcohol

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9
Q

What is the site of action for acetozolamide?

A

tubular lumen of the PCT

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10
Q

What are the thiazide/thiazide-like diuretics?

A

Hydrochlorothiazide (HCTZ)
Clorthalidone
Metolazone
Indapamide

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11
Q

What are the loop diuretics

A

Furosemide
Bumetanide
Torsemide
Ethacrynic Acid

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12
Q

What is the MOA of the Thiazide Diuretics?

A

The inhibit NaCl simperer at the DCT, increasing Na and Cl excretion

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13
Q

What are some side effects of the thiazide diuretics?

A 
Hypokalemia
QT prolongation
photosensitivity
anorexia
nausea
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14
Q

What is an additional side effect of Indapamide?

A

Gout

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15
Q

what are drug drug interactions with thiazides?

A

NSAIDs
Beta Blockers increase risk of hyperglycemia
May decrease renal excretion of lithium

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16
Q

Why shouldn’t you use NSAIDs with diuretics?

A

They counteract the beneficial impact because the cause Na+ retention

17
Q

Bile acids should not be used with which two thiazide diuretics?

A

Metolazone

Indapamide

18
Q

Explain the action of Furosemide

A
  • loop diuretic
  • secreted into renal tubule via active transport PCT
  • Exert impact at the TAL:
    1. Induce prostaglandins-mediated increase of renal blood flow
    2. Increase sodium and water excretion via inhibition of Na-K-2Cl simper in TAL
19
Q

The oral bioavailability and IV dosing of Furosemide

A

50% oral bio

half the dose in IV use (1:2)

20
Q

The oral bioavailability and IV dosing of Bumetanide

A

89-90% oral bio

IV or oral

21
Q

The oral bioavailability and IV dosing of Torsemide

A

Oral Bioavailabilty 80-100%

Can be used in most settings as an oral drug and obtains same impact as IV (1:1)

22
Q

What is a ceiling dose?

A
  • Upper dose limit beyond which little additional impact is achieved
23
Q

Long term use of Loop diuretics results in what?

A

Compensatory increase in proximal and distal tubule Na resorption (Diuretic resistance

24
Q

How to you handle diuretic resistance?

A
  • Increase the dose
  • Increase the frequency of dosing
  • Continuous infusion
  • Add a thiazide diuretic (Metolazone) which impacts both the Loop of Henle and DCT
25
Q

What is the diuretic you should use when Furosemide absorption is poor in HF?

A

Torsemide

- 80-100% absorption, even with intestinal mucosal edema

26
Q

What are two things that should be known about Ethacrynic acid?

A
  1. Not a sulfonamide

2. Decreases serum uric acid concentration

27
Q

What are the K+ sparing diuretics?

A

Spironolactone
Eplenerone
Amiloride
Triameterene

28
Q

What is the physiology of Spironolactone?

A
  • Synthetic steroid that competitively antagonizes aldosterone (also androgen, progesterone receptors)
29
Q

What is the physiology of eplenerone?

A
  • Spironolactone analogue with much greater mineralcorticoid receptor selectivity (less interaction with androgen/progesterone receptors)
  • Will not cause gynecomastia
30
Q

The impact of both spironolactone and eplenerone are subject to the action of what?

A

NSAIDs - NSAIDs decrease prostaglandins (prostaglandins are vasodilators)

31
Q

What is the physiology of Amiloride?

A

Direct inhibitor of Na+ influx in cortical collecting tubule and ducts (doesn’t block aldosterone

(really exerts impact at K+ transport at CCT/ducts of nephrons)

32
Q

What is the physiology of Triameterene

A

Same MOA of Amiloride, but has shorter had life so must be dosed more frequently.

33
Q

Why are amilioride and triamterine usu dosed with a thiazide diuretic?

A

They counteract the K+ wasting effect

34
Q

What is the osmotic diuretic?

A

Mannitol

35
Q

Explain the physiology of Mannitol

A

It is not metabolized. Instead, it is filtered via the glomerulus.
Exerts osmotic forct in the PCT and DL of Loop of hence decreasing water reabsorption
Increased fluid flow partially decreases Na+ reabsorption also
(water loss > Na+ loss)

36
Q

Why do you use mannitol?

A
  • Reduction of intracranial or intraocular pressure

- Rhabdomyolysis

37
Q

What is important to know about the administration of Mannitol?

A

It is administered IV only

Not absorbed orally and oral use causes osmotic diarrhea

38
Q

What is the MOA of mannitol?

A

Osmosis producing increased water loss

Shifts fluid from intracellular to extracellular space

39
Q

When is mannitol contraindicated?

A

In renal failure and with lack of response to test dose

Pharm (12 decks)

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