Pharmacology: Diuretics Flashcards

(50 cards)

1
Q

What are the 4 classes of natriuretic diuretics?

A
  1. Carbonic anydrase inhibitors
  2. Loop Diuretics
  3. Thiazide Diuretics
  4. K+ Sparing Diuretics
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2
Q

What are osmotic diuretics?

A

Aquaretics

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3
Q

Where do carbonic anydrase inhibitors act?

A

Proximal tubule

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4
Q

Where do osmotic diuretics act?

A

Proximal tubule and thin descending limb of henle

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5
Q

Where do loop diuretics act?

A

Thick ascending limb of henle

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6
Q

Where to thiazide diuretics act?

A

Distal convoluted tubule

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7
Q

Wherre do K sparing diuretics act?

A

Collecting duct

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8
Q

What is acetazolamide?

A

Carbonic anhydrase inhibitor

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9
Q

What type of transporters excrete acetazolamide and where?

A

Organic acid transporters

S2 segment of the proximal tubule

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10
Q

What does acetazolamide inhibit?

A

Lumenal and intracellular carbonic anhydrases

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11
Q

What is the efficacy of acetazolamide and why?

A

It has limited efficacy (2-3 days) because of bicarb depletion and eventual increased reabsorption distal to the proximal tubule

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12
Q

What are the 6 features cellularly associated with acetazolamide?

A
  1. Bicarbonaturia
  2. Natriuresis
  3. Diuresis
  4. Metabolic acidosis
  5. Hyperchloremia
  6. Hypokalemia
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13
Q

What are the 5 adverse effects of acetazolamide?

A
  1. Hyperchloremic metabolic acidosis
  2. Hypokalemia
  3. Alkalinization of urine
  4. Allergic reactions
  5. Paresthesia, nervous system toxicity
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14
Q

What causes hypokalemia associated with acetazolamide?

A

The upregulation of Na reabsorption (and thus K excretion) in the distal convoluted tubules

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15
Q

With acetazolamide, the AE of urine alkalinization can lead to what 2 things?

A
  1. Calcium stone pecipitation

2. Hyperammonemia

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16
Q

What can hperammonemia lead to in patients with cirrhosis?

A

Hepatic encephalopathy (AKA be careful giving acetazolamide to patients with cirrhosis)

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17
Q

What component of acetazolamide can cause allergic reactions?

A

The sulfonamide moiety

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18
Q

What are the 4 clinical indications for acetazolamide?

A
  1. Glaucoma
  2. Prophylactic for altitude sickness
  3. Urinary alkalinaztion
  4. Metabolic alkalosis
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19
Q

Why is acetazolamide used in glaucoma?

A

It reduces aqueous humor formation

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20
Q

How does acetazolamide work to reduce altitude sickness?

A

It reduces CSF formation and decreases pH of CSF and brain, which leads to increased ventilation and reduced ICP at high altitudes

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21
Q

What is the osmotic diuretic we discussed?

22
Q

When referring to the primary mechanism of action for mannitol, how is the drug given?

A

IV, it is poorly absorbed by GI and not metabolized

23
Q

What are the 4 actions mannitol has orimarily?

A
  1. Increases extracellular osmolarity
  2. Expands ECF volume
  3. Decreases renin release
  4. Increases renal blood flow
24
Q

Is renal medullary tonicity increased or reduced due to the primary effects of mannitol?

25
What does mannitol do primarily in the thin descending limb of Henle and what is the result of this?
It reduces the gradient for water reabsorption and reduces NaCl concentration
26
Because of the effect that mannitol has of reducing NaCl concentration in the thin descending limb of Henle, what happens in the thick ascending limb of henle?
The thick ascending limb detects less NaCl and feeds back to inhibit proximal tubular reabsorption of Na
27
If the proximal tubular reabsorption of Na is blocked by mannitol, what else is a consequence of this?
The loss of ability to reabsorb water in the proximal tubule
28
When referring to the secondary MOA of mannitol, what route is the drug given by?
IV, because it is poorly absorbed by GI and not metabolized and freely filtered
29
What are the 2 features of the secondary MOA of mannitol?
1. Increases lumenal osmolality in the proximal tubule and descending limb of Henle 2. Reduce water reabsorption in the proximal tubule and thin descending limb of Henle
30
What is the major AE of mannitol?
Extracellular volume expansion...results in hyponatremia
31
What can result if you don't give water replacement for patients taking mannitol?
Dehydration, hyperkalemia, and hypernatremia
32
What are the clinical indications for mannitol?
1. Reduce ICP in neurologic conditions 2. Reduce intraocular pressure before opthalmologic surgery 3. Increase urine volume
33
What are the 3 ADH antagonists we discussed?
1. Conivaptan 2. Tolvaptan 3. Demeclocycline
34
Where do ADH antagonists act?
In the collecting ducts
35
What type of ADH receptors to conivaptan and tolvaptan act at?
V2 receptors
36
How is conivaptan given?
IV
37
Is tolvaptan given IV?
No, tolvaptan is orally bioavailable
38
Which V2 receptor antagonist is selective for V2?
Tolvaptan
39
What other receptor can conivaptan bind besides V2?
V1a
40
What is the adverse effect of V2 receptor antagonists?
Nephrogenic diabetes insipidus
41
What are the clinical indications for V2 receptor antagonists?
Hyponatremia associated with syndrome of inappropriate ADH secretion (SIADH)
42
What is demeclocycline?
A post-receptor ADH antagonist
43
How is demeclocycline given?
It is orally bioavailable
44
How does demeclocycline
It blocks the insertion of aquaporin 2 into the collecting duct by an unknown mechanism
45
What is the propsed mechanism of how demeclocycline blocks insertion of AQP-2 into the collecting duct?
Interferes with adenylate cyclase bloccking the formation of cAMP
46
What adverse effects are associated the demeclocycline?
1. Nephrogenic diabetes insipidus | 2. Acute renal failure
47
What are the clinical indications for demeclocycline?
Persistent chronic SIADH
48
How do osmotic diuretics initially work?
They expand extracelular fluid volume
49
What can the expansion of extracellular fluid volume due to osmotic diuretics result in?
Exacerbation of heart failure | -Osmotic diuretics are contraindicated in patients with heart failure
50
What other condition do you have to be careful with in giving osmotic diuretics to due to the inability to handle the expansion of extracellular fluid volume?
Impaired renal function