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Hypertension > RAAS > Flashcards

RAAS Flashcards

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.

A

increases

20
Q

Aliskiren is dosed how often?

A

daily

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.

A

decreases

24
Q

Bradykinin is a vaso______ that promotes ___ and ____ loss.

A

vasodilator
Na
water

25
Q

Inhibition of ACE creates what effects?

A

decrease in Ang II
increase in bradykinin
vasodilation and diuresis

26
Q

Where is ACE located?

A

on the luminal surface of the endothelial and kidney epithelial cells

27
Q

ACE inhibitors ______ plasma renin levels.

A

increase

28
Q

ACE inhibitors ______ plasma Ang I levels.

A

increase

29
Q

ACE inhibitors ______ bradykinin degradation.

A

decrease

30
Q

What are the 3 classes of ACE inhibitors?

A

sulfhydryls
dicarboxylates
phosphonates

31
Q

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

A

none; they are all equal

32
Q

What are the clinical uses of ACE inhibitors?

A 
HTN
CHF
left ventricular dysfunction
post MI
diabetic and nondiabetic neuropathy
33
Q

What are the major adverse effects of ACE inhibitors?

A 
hypotension
cough
angioedema
skin rash
dysgeusia
neutropenia
hyperkalemia
34
Q

In what groups are ACE inhibitors contraindicated?

A

pregnancy
bilateral renal stenosis
severe CHF

35
Q

What is the ending for ACE inhibitors?

A

-pril

36
Q

The affinity of ARBs is so much ______ than Ang II that it is essentially ________.

A

greater

insurmountable

37
Q

ARBs are not effective in _______ HTN.

A

low-renin

38
Q

What is the MOA of ARBs?

A

block the activity of Ang II on the Ang II receptor and thus decreasing aldosterone and ADH secretion

39
Q

What are the therapeutic uses of ARBs?

A

HTN
heart failure
diabetic neuropathy

40
Q

What are the adverse effects of ARBs?

A

not different than placebo

41
Q

Combining ACE inhibitors with ARBs can lead to what?

A

hyperkalemia

kidney injury

42
Q

What groups are ARBs contraindicated in?

A

pregnancy

careful use in renally compromised patients

43
Q

What is the ending for ARBs?

A

-artan

44
Q

What is Entresto?

A

A combination of ARB with sacubitril (a neprilysin inhibitor)

45
Q

In what population is Entresto recommended?

A

heart failure

Hypertension (8 decks)

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