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?

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
What is the function of aldosterone?
Stimulates sodium retention (water follows) and potassium excretion, which increases blood pressure. Causes pathologic remodeling and hypertrophy of the myocardium
26
What enzyme activates angiotensinogen?
Renin
27
What substance activates angiotensin 1?
Angiotensinogen
28
What is the order of the RAAS?
renin-> Angiotensinogen-> Angiotensin 1-> Angiotensin 2 (ACE helped with the conversion) ->Aldosterone (allows sodium retention)
29
Function of ADH hormone
Allows water retention
30
What does ACE inhibitors do to the body?
Inhibits Angiotensin-converting enzyme, which causes: vasodilation, decreases the heart's workload, and lowers blood pressure
31
What effect does ACE inhibitors have on aldosterone?
It reduces aldosterone levels, causing sodium and water to excreted out of the body
32
What is a rare adverse effect of ACE inhibitors
Angioedema
33
What are the drug to drug interactions of ACE inhibitors and ARBs?
``` Diuretics (potential desirable and undesirable effects) Antihypertensive agents Drugs that raise potassium Lithium NSAIDs ```
34
What is the physiologic effects of ACE inhibitors, ARBs, and direct renin inhibitors?
Vasodilation Decrease production of aldosterone Reduce cardiac remodeling Dilation of renal blood vessels
35
What is the relationship between bradykinin and ACE inhibitors?
ACE inhibitors block kinase II from converting bradykinin into an inactive form (causes the dry cough adverse effect)
36
What ACE inhibitor is given through IV?
Enalaprilat
37
What drugs should not be given to pregnant women?
Angiotensin-converting enzyme inhibitors (ACE inhibitors) Angiotensin 2 receptor blockers (ARBs)
38
What rare adverse effect is found in both ACE inhibitors, Angiotensin 2 inhibitors, and Direct renin inhibitors?
Angioedema
39
What condition(s) could direct renin inhibitors treat?
Hypertension
40
Mechanism of direct renin inhibitors
Binds to renin and prevents it from cleaving angiotensinogen to angiotensin I
41
What are the adverse effects of direct renin inhibitors?
``` Diarrhea Angioedema (rare) Dry cough Hyperkalemia Fetal injury ```
42
Eplerenone is _______ for aldosterone receptors, while spironolactone is _______.
1. Selective | 2. Non-selective