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
What is the diuretic you should use when Furosemide absorption is poor in HF?
Torsemide | - 80-100% absorption, even with intestinal mucosal edema
26
What are two things that should be known about Ethacrynic acid?
1. Not a sulfonamide | 2. Decreases serum uric acid concentration
27
What are the K+ sparing diuretics?
Spironolactone Eplenerone Amiloride Triameterene
28
What is the physiology of Spironolactone?
- Synthetic steroid that competitively antagonizes aldosterone (also androgen, progesterone receptors)
29
What is the physiology of eplenerone?
- Spironolactone analogue with much greater mineralcorticoid receptor selectivity (less interaction with androgen/progesterone receptors) - Will not cause gynecomastia
30
The impact of both spironolactone and eplenerone are subject to the action of what?
NSAIDs - NSAIDs decrease prostaglandins (prostaglandins are vasodilators)
31
What is the physiology of Amiloride?
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
What is the physiology of Triameterene
Same MOA of Amiloride, but has shorter had life so must be dosed more frequently.
33
Why are amilioride and triamterine usu dosed with a thiazide diuretic?
They counteract the K+ wasting effect
34
What is the osmotic diuretic?
Mannitol
35
Explain the physiology of Mannitol
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
Why do you use mannitol?
- Reduction of intracranial or intraocular pressure | - Rhabdomyolysis
37
What is important to know about the administration of Mannitol?
It is administered IV only | Not absorbed orally and oral use causes osmotic diarrhea
38
What is the MOA of mannitol?
Osmosis producing increased water loss | Shifts fluid from intracellular to extracellular space
39
When is mannitol contraindicated?
In renal failure and with lack of response to test dose