RAAS Flashcards

(45 cards)

1
Q

What stimulates the release of renin from the JGA?

A

decreased afferent blood pressure

decreased tubular NaCl (urine)

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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

constricts the efferent arteriole to increase GFR

stimulates the release of aldosterone from adrenal

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5
Q

Where/how is angiotensinogen released?

A

continuously from the liver

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6
Q

Plasma levels of angiotensinogen are increased by what?

A
glucocorticoids
thyroid hormone
estrogen (pregnancy)
Ang II
inflammation
insulin
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7
Q

_____ _______ reflects angiotensinogen levels and renin activity.

A

Blood pressure

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8
Q

Ang II is a potent vaso________.

A

vasoconstrictor

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9
Q

Ang II stimulates _____ release.

A

ADH

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10
Q

Ang II promotes Na _______ in the ________ tubule.

A

reabsorption

proximal

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11
Q

Ang II increases _________ synthesis and secretion.

A

aldosterone

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12
Q

Renin is secreted as _______.

A

prorenin

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13
Q

Pregnant women and diabetics have ________ levels of prorenin.

A

elevated

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14
Q

The newest hypertensive on the market is of what class?

A

renin inhibitor

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15
Q

What is the renin inhibitor agent?

A

Aliskiren

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16
Q

Aliskiren decreases plasma renin activity by __-__%

A

50 - 80%

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17
Q

Aliskiren ______ Ang I and Ang II levels.

A

decreases

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18
Q

Aliskiren decreases BP by __-__ mm Hg.

A

10-15

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19
Q

Aliskiren _____ plasma renin concentration.

20
Q

Aliskiren is dosed how often?

21
Q

What are the adverse effects of Aliskiren?

A

mild diarrhea
suppression of hematopoiesis
hyperkalemia

22
Q

In what groups is Aliskiren contraindicated?

A

pregnancy

those who have experienced angioedema

23
Q

ACE ______ bradykinin.

24
Q

Bradykinin is a vaso______ that promotes ___ and ____ loss.

A

vasodilator
Na
water

25
Inhibition of ACE creates what effects?
decrease in Ang II increase in bradykinin vasodilation and diuresis
26
Where is ACE located?
on the luminal surface of the endothelial and kidney epithelial cells
27
ACE inhibitors ______ plasma renin levels.
increase
28
ACE inhibitors ______ plasma Ang I levels.
increase
29
ACE inhibitors ______ bradykinin degradation.
decrease
30
What are the 3 classes of ACE inhibitors?
sulfhydryls dicarboxylates phosphonates
31
Which ACE inhibitor(s) is(are) the most therapeutically effective?
none; they are all equal
32
What are the clinical uses of ACE inhibitors?
``` HTN CHF left ventricular dysfunction post MI diabetic and nondiabetic neuropathy ```
33
What are the major adverse effects of ACE inhibitors?
``` hypotension cough angioedema skin rash dysgeusia neutropenia hyperkalemia ```
34
In what groups are ACE inhibitors contraindicated?
pregnancy bilateral renal stenosis severe CHF
35
What is the ending for ACE inhibitors?
-pril
36
The affinity of ARBs is so much ______ than Ang II that it is essentially ________.
greater | insurmountable
37
ARBs are not effective in _______ HTN.
low-renin
38
What is the MOA of ARBs?
block the activity of Ang II on the Ang II receptor and thus decreasing aldosterone and ADH secretion
39
What are the therapeutic uses of ARBs?
HTN heart failure diabetic neuropathy
40
What are the adverse effects of ARBs?
not different than placebo
41
Combining ACE inhibitors with ARBs can lead to what?
hyperkalemia | kidney injury
42
What groups are ARBs contraindicated in?
pregnancy | careful use in renally compromised patients
43
What is the ending for ARBs?
-artan
44
What is Entresto?
A combination of ARB with sacubitril (a neprilysin inhibitor)
45
In what population is Entresto recommended?
heart failure