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Pharm II > Diuretic Agents > Flashcards

Diuretic Agents Flashcards

1
Q

Every nerve coming out of the CNS release ACh on what receptors?

A

N

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2
Q

What is the effect of all of the sympathetic pathways being “linked”?

A

Act cohesively (do not have sympathetic response in only part of the body)

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3
Q

Muscarinic M2 receptors:

  • Act via what G protein?
  • Phosphorylate or dephosphorylate Ca2+ channels?
  • Phosphorylate or dephosphorylate K+ channels?
  • Are all pre- or post- synaptic?
A

Gi, dephosphorylates Ca2+, phosphorylate K+, all pre

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4
Q

Beta1, 2, and 3 receptors:

  • Act via what G protein?
  • Phosphorylate or dephosphorylate Ca2+ channels?
  • Have what effect on Ca2+ channels?
A

Gs, phosphorylate Ca2+ channels

Then opens them, causes slight depolarization and releases insulin

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5
Q

Alpha receptor concentration is greatest where?

A

Large veins > resistance arteries (skin, elsewhere)

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6
Q

How does the baroreflex work?

A

Stretch receptors in carotid sinus and aortic arch → fire in response to ↑ stretch/BP to maintain homeostasis

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7
Q

Short-term regulation of BP via the baroreflex happens in how long?

A

~3-5 heart beats

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8
Q

Long-term regulation of BP happens when what?

A

MAP is high/ low for an extended time?

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9
Q

What is the drug response to a decrease in BP (immediate effect)?

A

Reflex tachycardia

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10
Q

What is the drug response to a decrease in BP (long-term effect)?

A

↑ renin release = ↑ Na+ and H2O retention

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11
Q

Altered blood circulation, altered blood composition, and inadequate lymphatic draining are conditions that promote the development of what?

A

Edema

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12
Q

What drugs are Carbonic Anhydrase Inhibitors

A

Acetazolamide, Dorzolamide, Brinzolamide

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13
Q

What drugs are Loop Diuretics?

A

Furosemide, Ethacrynic Acid

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14
Q

What drugs are Thiazide Diuretics?

A

Hydrochlorothiazide

Compounds related to Thiazides: Metolazone, Indapamide

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15
Q

What drugs are Potassium Sparing Diuretics?

A

Aldosterone Antagonist: Spironolactone, Eplerenone

Direct Inhibitors of Sodium Flux: Amiloride, TriamtereneE

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16
Q

What drugs are Osmotic Diuretics?

A

Mannitol, Isosorbide, GLycerin, Urea

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17
Q

What drugs are ADH Agonists and Antagonists?

A

Desmopressin, Conivaptan, Tolvaptan

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18
Q

Reabsorption in what part of the kidney cannot be influenced by drugs?

A

Proximal tubule

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19
Q

Exchange of Na+ with K+ in the DCT of the kidney can be modified by drugs that belong to which classes?

A

Aldosterone-antagonists and K+ sparing diuretics

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20
Q

Physiologically, what do thiazide diuretics do?

A

↑ Ca2+ reabsorption

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21
Q

Physiologically, what do loop diuretics do?

A

↑ Ca2+ and Mg2+ excretion

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22
Q

What do acidic drugs compete for? What can this lead to?

A

Uric acid excretion

Can lead to gouty attack

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23
Q

What drug class has the following MOA?

  1. Inhibits CA enzyme
  2. Blocks H2CO3 production
  3. ↓ H+ for exchange w Na+, resulting in ↑ Na+ (and H2O) loss
A

Carbonic anhydrase inhibitors

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24
Q

What are the indications for CA inhibitors? (3)

A

Glaucoma (↓ aqueous humor and CSF)
Alkalinization of the urine
Alkalosis (met and resp)

Acute mtn sickness = resp alkalosis

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25
Q

What important pharmokinetic property do CA inhibitors have?

A

Diuretic effectiveness decreases in several days

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26
Q

The following are the main adverse effects for what drug class?
Hyperchloremic metabolic acidosis
Hypokalemia
Hyperuricemia

A

CA inhibitors

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27
Q

What are the c/i’s and precautions for CA inhibitors? (2)

A

Hepatic cirrhosis

Sulfonamide hypersensitivity

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28
Q

The following is the MOA for which drug class?
Block the NaKCl2 co-transporter (impair concentrating/ diluting)
Induce kidney PGs (vasodilation)

A

Loop diuretics

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29
Q

What are the indications for loop duiretics? (4)

A

HF
Pulmonary edema (↑ systemic venous capacitance)
Hypercalcemia
Work well at low GFR

30
Q 
The following are adverse effects of which drug class? 
Hypokalemic metabolic alkalosis
Hypocalcemia/ hypomagnesemia
Hyperuricemia
Irreversible ototoxicity
A

Loop diuretics

31
Q

Sulfonamide hypersensitivity is a c/i/ precaution for which loop diuretic?

A

Furosemide

32
Q

What drug interactions may occur with loop diuretics?

A

Aminoglycosides and Digoxin

33
Q

What are the differences between Furosemide and Ethacrynic Acid?

A

Ethacrynic Acid is not a sulfonamide derivative and has the highest risk of ototoxicity

34
Q

What is the MOA for thiazide diuretics?

A

Inhibition of sodium resorption at the early DCT

35
Q

What are the main clinical indications for thiazide diuretics?

A

HTN, HF

36
Q

Thiazide diuretics increase ATP-dependent K+ channel opening. This results in relaxation of smooth muscle cells and vasodilation (beneficial effect). What is an adverse effect of this?

A

Reduced insulin secretion

37
Q

Besides increasing ATP-dependent K+ channel opening, what other therapeutic effects do thiazide diuretics have?

A

↓ Ca2+ excretion

↓ systemic BP and enhance anti-HTN action of other drugs

38
Q

With respect to pharmokinetics, how is Indapamide different?

A

Excreted by the biliary system (vs organic acid secreting system) therefore useful in pts w renal insufficiency

39
Q

Besides dizziness, weakness, fatigue and leg cramps, which are common adverse effects of thiazide diuretics… what are the 2 more concerning ones?

A

Hypokalemic metabolic alkalosis

Hyperuricemia

40
Q

The following are the main adverse effects of which drug class?
Magnesium loss
Hyperglycemia
Elevated serum lipid levels

A

Thiazide diuretics

41
Q

Which drug belonging to the thiazide diuretic class does not elevate serum lipid levels?

A

Indapamide

42
Q

The following are the c/i’s and precautions of which drug class?
Hypokalemia can precipitate digitalis toxicity
Hyperglycemia and carbohydrate intolerance may occur
C/i in diabetics
Hyperuricemia = acute gouty attacks

A

Thiazide diuretics

43
Q

What toxicity is aggravated by thiazides?

A

Lithium toxicity

44
Q

Thiazide diuretics can cause what adverse effect in elderly patients?

A

Necrotizing vasculitis of skin and kidney

45
Q

Which drug in the thiazide class is able to produce diuresis in patients with a reduced GFR?

A

Metolazone

46
Q

What 3 major differences does Indapamide have from all other thiazide drugs?

A

Pronounced vasodilation
Does not increase plasma lipids
Metabolized in the liver and kidney

47
Q

Are K+ sparing diuretics strong or weak compared to thiazides and loop?

A

Weak

48
Q

What is the primary MOA for aldosterone antagonists that leads to the following?
Less Na+ channels
Blocked Na+ conductance
↓ Na+K+ATPase activity

A

Competitive inhibitor of aldosterone

49
Q

What is the most effective drug for treating hyperaldosteronism?

A

Spironolactone

50
Q

What is an occasional adverse effect seen with Spironolactone?

A

Hyperkalemia

51
Q

What is the primary c/i for Spironolactone?

A

Hyperkalemia (burn pts)

52
Q

Which diuretic is a selective aldosterone receptor antagonist (SARA)?

A

Eplerenone

53
Q

Pt taking Eplerenone will experience decreased incidence of what?

A

Endocrine related SE’s

54
Q

What is a precaution for Eplerenone?

A

Drug interactions (CYP3A4)

55
Q

What is the primary MOA for potassium sparing diuretics that leads to the following?
Directly inhibits aldosterone-sensitive Na+ channel
Leads to a ↓ K+ excretion

A

Inhibits Na+K+ ion exchange mech independently of aldosterone

56
Q

What is the main use of potassium sparing diuretics?

A

Combination with K+ losing diuretics

57
Q

Why do pts taking potassium sparing diuretics do not experience urate retention/ hyperuricemia?

A

They are not acids

58
Q

What is the only serious toxicity and only c/i for potassium sparing diuretics?

A

Hyperkalemia

59
Q

How are osmotic diuretics given?

A

IV only (not absorbed orally)

60
Q

The following are the indications for which drug class?
Prophylaxis of acute renal failure
↓ intraocular/ intracranial pressure
Protect kidney against nephrotoxic substance

A

Osmotic diuretics

61
Q

Excessive administration of osmotic diuretics can lead to what adverse effect? Therefore c/i in what populations?

A

EC volume expansion/ pulmonary edema

C/i in HF

62
Q

What drug treats sxs of central DI?

A

Desmopressin (ADH agonist)

63
Q

What is the indication for Conivaptan (ADH antagonist)?

A

Tx of eu/hypervolemic hyponatremia in hospitalized pts

64
Q

How is Conivaptan given?

A

IV only

65
Q

What is the main adverse effect associated with Conivaptan?

A

Hypokalemia

66
Q

What is the main precaution associated with Conivaptan?

A

Hyponatremia associated w hypovolemia

67
Q

The following is the MOA for which ADH antagonist?

Non-peptide V1a and V2 receptor antagonist

A

Conivaptan

68
Q

The following is the MOA for which ADH antagonist?

Non-peptide V2 vasopressin receptor antagonist

A

Tolvaptan

69
Q

How is Tolvaptan given?

A

Orally

70
Q

Which ADH antagonist is initiated and re-initiated in a hospital and then continued on an outpt basis?

A

Tolvaptan

71
Q

What is the order of the expected max diuretic effect?

A

Loops + thiazides&raquo_space; loop&raquo_space; thiazides&raquo_space; CA inhibitors > K+ sparing

72
Q

Which type of diuretics produce a dose-depdendent diuresis throughout their therapeutic dosage range?

A

Loop

Thizides have relatively flat dose-response curve and limited max response

Pharm II (13 decks)

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