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Pharmacology > Diuretics, RAAS > Flashcards

Diuretics, RAAS Flashcards

1
Q

What are the two major applications of Diuretics?

A

-Hypertension
-Mobilization of edematous fluid to prevent renal failure

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2
Q

Diuretics
Mechanism of Action

A

Blockade of sodium and chloride

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3
Q

Diuretics
Adverse effects

A

Hypovolemia
Acid-base imbalance
Electrolyte imbalances

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4
Q

Thiazides and loop diuretics ____ K

A

decrease

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5
Q

Aldesterone blockers ______ K

A

increase

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6
Q

Furosemides (Lasix)
Mechanism of action

A

Acts on ascending loop of Henle to block reabsorption of sodium, chloride, potassium

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7
Q

Furosemide onset

A

IV - 5 mins
Oral - 60 mins

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8
Q

Furosemide
Therapeutic uses

A

Pulmonary edema
Edematous states
Hypertension

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9
Q

Signs of pulmonary embolism

A

SOB
Cough/wheeze/crackles
O2 low
RR elevated

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10
Q

Furosemide adverse effects

A

Hyponatremia (low sodium)
Hypochloremia
Hypokalemia
Hypotension
Hypocalcemia
Hypomagnesemia
Hyperuricemia (too much uric acid in the blood)

Ototoxicity
**May raise blood sugar and cholesterol **

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11
Q

In terms of adverse effects, how do you loops diuretics vs. thiazides differ?

A

Loop diuretics may cause ototoxicity, while thiazides do not

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12
Q

Furosemide
Drug interactions

A

Digoxin
Ototoxic drugs (like aminoglycoside abx “-micin”)
Lithium
Antihypertensive agents
NSAIDs

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13
Q

Bumetanide is a ____ diuretic

A

high-ceiling loop

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14
Q

Which causes more diuresis - thiazides or loop diuretics?

A

Loop diuretics

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15
Q

When are thiazides ineffective?

A

-Oliguria (reduced urine output)
-When GFR is low

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16
Q

Hydrochorothiazide
Therapeutics uses

A

Essential hypertension
Edema

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17
Q

What kind of diuretics do you use for pulmonary edema?

A

Loop diuretics - faster onset of action compared to thiazides (thiazides peak in 4-6 hours)

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18
Q

How do loop diuretics and hydrochlorothiazide differ in terms of drug interactions?

A

Hydrochlorothiazides do not cause ototoxity, so they can be combined with other drugs that are ototoxic like the mycin ABX (Gentamycin)

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19
Q

Spironolactone
Class

A

Potassium-sparing antidiuretic

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20
Q

Spironolactone
Mechanism of Action

A

Aldosterone antagonist
Retention of potassium
Increased excretion of sodium

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21
Q

Triamterene and Amiloride
Class

A

Potassium-sparing diuretics

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22
Q

Triamterene and Amiloride
Mechanism of action

A

-Block the exchange pump instead of the aldosterone receptor
-Decrease sodium reuptake

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23
Q

Spironolactone
Therapeutic uses

A

HEART FAILURE
-Hypertension (not first line)
-Edematous states
-Primary hyperaldosteronism
-PMS
-PCOS
-Acne in young women

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24
Q

Spironolactone
Adverse effects

A

Hyperkalemia
Benign and malignant tumors
Endocrine effects

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25
Q

Spironolactone
Drug interactions

A

-Thiazide and loop diuretics
-Agents that raise potassium levels

26
Q

Triamterene (Dyrenium) & Amiloride
Therapeutic uses

A

Hypertension
Edema
Counteract potassium loss caused by more powerful diuretic

27
Q

Triamterene (Dyrenium)
Adverse effects

A

-Hyperkalemia
-Leg cramps
-N/V, dizziness
-Blood dyscrasias (rare)

28
Q

Amiloride
Adverse effects

A

Hyperkalemia

29
Q

Amiloride
Drug interactions

A

-ACE inhibitors
-Other drugs that can cause hyperkalemia

30
Q

Mannitol (Osmitrol)
Mechanism of action

A

-Promotes diuresis by creating osmotic force within lumen of nephron

31
Q

Mannitol
Route of administration

A

IV

32
Q

Mannitol therapeutic uses

A

Prophylaxis of renal failure
Reduction of intracranial pressure/ intraocular pressure

33
Q

Mannitol
Adverse effects

A

-Edema- pulmonary edema
-Headache
-N/V

34
Q

What does RAAS stand for?

A

Renin-Angiotensin-Aldosterone System

35
Q

What does ACE inhibitor stand for?

A

Angiotensin-converting enzyme inhibitors

36
Q

Which type of angiotensin is responsible for much of the damage in CV disease?

A

Angiotensin II

37
Q

What are the actions of angiotensin II?

A

-Vasoconstriction
-Release of aldosterone > BP increases
-Cardiac remodeling

38
Q

What are the actions of aldosterone?

A

-Regulation of blood volume and BP
-Cardiac remodeling

39
Q

What ending do the ACE inhibitors have?

A

-pril

40
Q

ACE inhibitors mechanism of action

A

-Reduce levels of angiotensin II
-Increase levels of bradykinin

41
Q

ACE inhibitors
therapeutic uses

A

-Hypertension
-Heart failure
-Prevention of MI, stroke death
-Nephropathy (diabetic & non-diabetic)

42
Q

ACE inhibitors reduce levels of angiotensin II. What effect does this have?

A

-Vasodilation
-Reduced blood volume
-Reduced remodeling
-Potassium retention
-Fetal injury

43
Q

ACE inhibitors raise levels of Bradykinin. What major Therapeutic effect does this have? Name 2 adverse effects.

A

-Vasodilation
-Cough
-Angioedema (rare)

44
Q

Aldosterone effect on sodium

A

More sodium absorbed into the blood (sodium reabsorption)

45
Q

ACE inhibitors
Adverse effects

A

-First-dose hypotension
-Fetal injury
-Cough
-Angioedema
-Hyperkalemia
-Renal failure

46
Q

ACE inhibitors
Drug interactions

A

-Diuretics
-Antihypertensive agents
-Drugs that raise K levels
-NSAIDs

47
Q

Salt substitutes can _____ K

A

elevate

48
Q

Angiotensin II Receptor Blockers end in _____

A

-sartan

49
Q

Angiotensin II Receptor Blockers (-sartan) cause _____ of blood vessels

A

dilation

50
Q

Angiotensin II Receptor Blockers (-sartan)
Pharmacologic effects

A

Same as ACE inhibitors
-Prevent cardiac remodeling
-Reduce excretion of potassium
-Decrease release of aldosterone
-Increase excretion of sodium and water

EXCEPT:
-Do NOT inhibit kinase I (means less cough)

51
Q

How do ACE inhibitors and Angiotensin II Receptor Blockers differ in terms of adverse effects?

A

The only difference is that Angiotensin II Receptor Blockers (-sartans) do not inhibit kinase, and therefore do not produce cough

52
Q

A very rare but serious side effect of ARBs and ACE inhibitors. It involves swelling of the face, lips, tongue, throat, or extremities and can potentially lead to airway obstruction, requiring immediate medical attention

A

Angioedema

53
Q

Aliskiren (Tekturna)
Class

A

Direct Renin Inhibitor - binds tightly with renin and inhibits the conversion angiotensinogen to angiotensin I

54
Q

Aliskiren (Tekturna)
Adverse effects

A

Same as ACE Inhibitors - angioedema, cough, hyperkalemia, fetal injury

55
Q

Eplerenone (Inspra)
Mechanism of action

A

Aldosterone antagonist

56
Q

Aldosterone Antagonist (Eplerenone)
Therapeutic uses

A

Hypertension
Heart failure

57
Q

Aldosterone Antagonist (Eplerenone)
Adverse effect

A

Hyperkalemia

58
Q

Aldosterone Antagonist (Eplerenone)
Drug interactions

A

Drugs that raise potassium levels

59
Q

Spironolactone (Aldacton)
Adverse effects

A

Hyperkalemia

Hormonal effects:
Gynecomastia
Menstrual irregularities
Impotence
Hirsutism
Deepening of the voice

60
Q

Spironolactone vs Eplerenone
How do they differ in terms of selectivity

A

Spironolactone is less selective, it binds with receptors for other steroid hormones as well - which results in some unusual adverse effects

61
Q

A medical condition characterized by excessive hair growth in women in areas where hair is typically more common in males.

A

Hirsutism

Pharmacology (21 decks)

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