RAAS

Question 1

RAAS

Answer 1

Angiotensin II and aldosterone regulate fluid and BP

Question 2

Renin

Answer 2

Produced in the kidney, release can be triggered by multiple factors:
Decrease in BP
Decrease in blood volume
Decrease in plasma sodium content
Decrease in renal perfusion
Renin causes formation of angiotensin I from angiotensin (secreted by liver)

Question 3

Angiotensin system

Answer 3

Angiotensin I (inactive) has weak activity in the body, and precursor to II
Kinase II (found in blood) converts angiotensin I to II

Question 4

Angiotensin II

Answer 4

Vasoconstriction (more effect on arteries)
Stops nitric oxide to stop vasodilation
Stimulation of aldosterone

Question 5

Angiotensin II indirect actions

Answer 5

Sympathetic neurons to promote NE release
Adrenal medulla to promote Epi release
On adrenal cortex to promote secretion of aldosterone

Question 6

Aldosterone

Answer 6

Aldosterone acts on distal tubules in the kidney to cause sodium retention, and excretion of K+ and H+

Question 7

4 main drug families affect RAAS

Answer 7

ACE inhibitors
ARBs (angiotensin II receptor blockers)
Direct renin inhibitors (DRIs)
Aldosterone antagonists

Question 8

ACE inhibitors

Answer 8

Stop conversion of angiotensin I to II

Adverse effects include cough, angioedema, first dose hypotension, and hyperkalemia

Question 9

More ACE inhibitors sides

Answer 9

10% get dry, persistent cough
Stopping can cause potassium retention in kidney
HyperK+ rare, but pts shouldn’t be taking K+ supp

Question 10

ACE inhibitor MAO

Answer 10

Reduce level of angiotensin II
Increase levels of bradykinin (inhibits kinase II)
End result is non constricted blood vessels and stop release of aldosterone

Question 11

Ace inhibitor name

Answer 11

Pril
Benazepril
Captopril
Enalapril
Lisinopril
Ramipril

Question 12

ARBs

Answer 12

Block actions of angiotensin II
Lower risk of cough and hyperk+
Usually secondary to ace inhibitors which have better success in decreased cardiac morbidity and mortality

Question 13

ARBs

Answer 13

Block angiotensin II, also block release of aldosterone and so Na+ and H2O excretion is increased

Question 14

ARBs names

Answer 14

Sartan
Losartan
Valsartan
Olmesartan
Eprosartan
Candesartan

Question 15

DRIs

Answer 15

Direct Renin inhibitors
Act on renin to inhibit conversion of angiotensin to angiotensin I
Aliskiren is the only one, used for HTN

Question 16

Aldosterone antagonists

Answer 16

Block receptors for aldosterone for HTN and heart failure

2 drugs - eplerenone and spironolactone - K+ sparing diuretic

Question 17

Aldosterone receptors

Answer 17

In the kidney, activation of aldosterone receptors promotes excretion of K and retention of Na+ and H2O
Receptor blockade has opposite effect, retention of K+ and excretion of Na+ and H2O

Question 18

ACE inhibitors used in

Answer 18

HTN, CHF, diabetic neuropathy, MI and prevention of cardiovascular risks

Question 19

ARBS indications

Answer 19

HTN, CHF, diabetic neuropathy

Question 20

Aldosterone agonist indications

Answer 20

HTN, CHF also hypokalemia and hyperaldosteronism

Question 21

DRIs

Answer 21

Direct renin inhibitors, for HTN

Question 22

Angiotensions

Answer 22

I II and III
I is a precursor to II and isn’t very active
II is very active
III is from degradation of II and is moderately active

Question 23

Angiotensin II vasoconstriction

Answer 23

Direct vascular smooth muscle activation (more arterial than veins because of this) and also causes release of norepi, promotes medulla to release epi and CNS to increase sympa outflow to vessels

Question 24

Aldosterone

Answer 24

Released from angio II below vasoconstriction threshold.
From low Na+ or high K_
Acts on DISTAL tubules to retain sodium and excrete K+ and H+

Question 25

Angio II formed through

Answer 25

Renin, ACE

Question 26

Renin

Answer 26

Catalyzes angio I from angiotensin It is the rate limiting step in I and II formation (II needs I) Produced by juxtaglomerular cells of kindey

Question 27

Renin is released from

Answer 27

Drop in BP, volume, Na+ or renal perfusion

Question 28

ACE (kinase II)

Answer 28

Converts I to II On luminal surface of all blood vessels, lungs are especially rich Called Kinase II when acting on bradykinin

Question 29

Angio II promoting renal water retention

Answer 29

Takes days weeks or even months | Constricts renal vessels to reduce GFR and stimulates release of aldosterone

Question 30

ACE inhibitors adverse effects

Answer 30

Cough, angioedema, first dose hypotension and hyperkalemia

Question 31

Kinase II (ACE) effects

Answer 31

If ACE is blocked, angio II goes down but bradykinin goes up (can't be converted to inactive) Vasodilation (secondary to increase prostaglandins and nitric oxide), cough and rarely angio edema occur

Question 32

Effects of decreasing ACE (ace inhibitors)

Answer 32

Vasodilation, decreased volume and cardiac remodeling, potassium retention, fetal injury

Question 33

ACE inhibitors suffix

Answer 33

PRIL

Question 34

ACE inhibitors renal failure

Answer 34

Renally excreted, therefore need reduced dose for renal failure pts

Question 35

Non BP effects on angio II

Answer 35

Increased migration, proliferation and hypertrophy of vasc smooth muscle cells Increased ECM in VSM cells Hypertrophy of cardiac myocytes Increased ECG matrix by cardiac fibroblasts (this means it contributes to atherosclerosis and blocking lowers risk of MI and stroke)

Question 36

ACE inhibitors in heart failure

Answer 36

Lower arterial tone to improve blood flow Reduce afterload to increase CO Venos dilation improves pulmonary congestion and edema Dilate kidney vessels to improve flow Excrete Na+ and volume which reduces edema and preload (drops right sided strain)

Question 37

ACE inhibitors for post MI pts

Answer 37

Captopril, lisinopril, trandolapril

Question 38

ACE inhibitors kidneys

Answer 38

Reduce glomerular filtration pressure to prevent damage. When renal efferent arterial pressure is increased it increases back pressure in glomerulus Slows progression of established nephropathy but does not protect against kidney damage

Question 39

Coversyl

Answer 39

Ace inhibitor, perindopril

Question 40

ACE in renal failures

Answer 40

If renal stenosis is present, angio II is good as it maintains renal perfusion

Question 41

ACE inhibitors interactions

Answer 41

Can cause lithium to accumulate | NSAIDS reduce antihypertensive effects

Question 42

Indapamide

Answer 42

Thiazide like diuretic. Incombo with coversyl called coversyl plus

Question 43

Rampiril

Answer 43

On its on. Altace is combine with HCT (hydrochlorothiazide)

Question 44

ARBS vs ACE inhibs

Answer 44

Biggest difference is no hyperK+ or cough with ARBS | ARBS aren't proven to lower odds of MI/STROKE as well as ACE inhibitors

Question 45

ARBS suffix

Answer 45

Sartans | ARBS are reserved for pts who can't tolerate ACE inhibs as mortality benefits aren't proven with ARBS

Question 46

Angioedema

Answer 46

More common in ACE inhibitors but both may cause it and is an absolute contraindication

Question 47

MOA aliskiren a DRI

Answer 47

Binds to renin tightly and inhibits its ability to clean angio into angio I and therefore reduces both angio II and aldosterone Only approved for HTN

Question 48

Aldosterone antagonists are

Answer 48

Spironolactone and eplerenone. Spironolactone is less selective

Question 49

MOA Aldosterone antagonists

Answer 49

``` Blocks aldosterone (selectively so no effect on glucocorticoids, progresterone, androgens) blocking aldosterone and so increases K+ and decreases Na+ Metabolized by CYP3A4 and inhibtors of 3A4 have a very strong effect on drug concentration ```