RAAS Flashcards

1
Q

What enzyme starts the RAAS?

A

Renin

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2
Q

What is the function of renin?

A

cleaves angiotensinogen into angiotensin I

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3
Q

What is the function of ACE?

A

converts Ang I to Ang II

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4
Q

What is the function of Ang II?

A

Powerful vasoconstrictor

Stimulates the release of aldosterone (increases blood pressure)

Causes remodeling and hypertrophy of the myocardium

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5
Q

_____ _______ reflects angiotensinogen levels and renin activity.

A

Blood pressure

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6
Q

Ang II is a potent ________.

A

vasoconstrictor

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7
Q

Ang II stimulates _____ release.

A

ADH

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8
Q

Ang II promotes Na _______ in the ________ tubule.

A

reabsorption

proximal

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9
Q

Ang II increases _________ synthesis and secretion.

A

aldosterone

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10
Q

What is the only direct renin inhibitor agent?

A

Aliskiren

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11
Q

What are the adverse effects of Aliskiren?

A
Angioedema
Dry cough
Diarrhea
Hyperkalemia
Fetal injury
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12
Q

In what groups is Aliskiren contraindicated?

A

pregnancy

those who have experienced angioedema

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13
Q

Which ACE inhibitor(s) is(are) the most therapeutically effective?

A

none; they are all equally effective

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14
Q

What are the clinical uses of ACE inhibitors?

A

Hypertension
Heart Failure (ripped hearts)
Diabetic nephropathy (delay renal injury by decreasing pressure in the glomerulus)
Myocardial infarction
Prevention of MI, stroke, and death in high risk patients

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15
Q

What are the major adverse effects of ACE inhibitors?

A

First-dose hypotension

Dry cough (due to the stimulation of bradykninen)

Hyperkalemia (opponent has a lot of banana clips)

Renal failure in patients with bilateral renal artery stenosis

Fetal injury

Very rare cases of Angioedema (swollen face since the opponent was angry)

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16
Q

What is the ending for ACE inhibitors?

A

-pril

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17
Q

What is the MOA of ARBs?

A

block Ang II from binding to its receptor

18
Q

What conditions could be treated with ARBs and ACE inhibitors?

A
Hypertension
heart failure
diabetic nephropathy
Myocardial infarction
Prevention of MI, stroke, and death in high risk patients
19
Q

What are the adverse effects of ARBs?

A

Angioedema
Fetal harm
Renal failure

20
Q

What is the ending for ARBs?

A

-sartan

21
Q

What is the purpose of the RAAS?

A

It regulates our blood pressure, blood volume, fluids, and electrolytes (specifically when it happens to drop from normal levels).

It wants to activate Angiotensin 2 to help cause vasoconstriction (increase blood pressure)

22
Q

How does the RAAS work?

A

It converts Angiotensin 1 into Angiotensin 2 by using angiotensin-converting enzyme (ACE)

23
Q

When is renin produced by kidney?

A

In response to:

Low blood pressure
Low blood volume
Low sodium concentration

24
Q

When does renin production stop?

A

When the body’s blood pressure, blood volume, and sodium concentration becomes normal again

25
Q

What is the function of aldosterone?

A

Stimulates sodium retention (water follows) and potassium excretion, which increases blood pressure.

Causes pathologic remodeling and hypertrophy of the myocardium

26
Q

What enzyme activates angiotensinogen?

A

Renin

27
Q

What substance activates angiotensin 1?

A

Angiotensinogen

28
Q

What is the order of the RAAS?

A

renin-> Angiotensinogen-> Angiotensin 1-> Angiotensin 2 (ACE helped with the conversion) ->Aldosterone (allows sodium retention)

29
Q

Function of ADH hormone

A

Allows water retention

30
Q

What does ACE inhibitors do to the body?

A

Inhibits Angiotensin-converting enzyme, which causes: vasodilation, decreases the heart’s workload, and lowers blood pressure

31
Q

What effect does ACE inhibitors have on aldosterone?

A

It reduces aldosterone levels, causing sodium and water to excreted out of the body

32
Q

What is a rare adverse effect of ACE inhibitors

A

Angioedema

33
Q

What are the drug to drug interactions of ACE inhibitors and ARBs?

A
Diuretics (potential desirable and undesirable effects)
Antihypertensive agents
Drugs that raise potassium
Lithium
NSAIDs
34
Q

What is the physiologic effects of ACE inhibitors, ARBs, and direct renin inhibitors?

A

Vasodilation

Decrease production of aldosterone

Reduce cardiac remodeling

Dilation of renal blood vessels

35
Q

What is the relationship between bradykinin and ACE inhibitors?

A

ACE inhibitors block kinase II from converting bradykinin into an inactive form (causes the dry cough adverse effect)

36
Q

What ACE inhibitor is given through IV?

A

Enalaprilat

37
Q

What drugs should not be given to pregnant women?

A

Angiotensin-converting enzyme inhibitors (ACE inhibitors)

Angiotensin 2 receptor blockers (ARBs)

38
Q

What rare adverse effect is found in both ACE inhibitors, Angiotensin 2 inhibitors, and Direct renin inhibitors?

A

Angioedema

39
Q

What condition(s) could direct renin inhibitors treat?

A

Hypertension

40
Q

Mechanism of direct renin inhibitors

A

Binds to renin and prevents it from cleaving angiotensinogen to angiotensin I

41
Q

What are the adverse effects of direct renin inhibitors?

A
Diarrhea
Angioedema (rare)
Dry cough
Hyperkalemia
Fetal injury
42
Q

Eplerenone is _______ for aldosterone receptors, while spironolactone is _______.

A
  1. Selective

2. Non-selective