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Pharmo for medic school > RAAS > Flashcards

RAAS Flashcards

1
Q

RAAS

A

Angiotensin II and aldosterone regulate fluid and BP

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2
Q

Renin

A

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)

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3
Q

Angiotensin system

A 
Angiotensin I (inactive) has weak activity in the body, and precursor to II
Kinase II (found in blood) converts angiotensin I to II
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4
Q

Angiotensin II

A

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

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5
Q

Angiotensin II indirect actions

A

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

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6
Q

Aldosterone

A

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

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7
Q

4 main drug families affect RAAS

A

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

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8
Q

ACE inhibitors

A

Stop conversion of angiotensin I to II

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

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9
Q

More ACE inhibitors sides

A

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

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10
Q

ACE inhibitor MAO

A

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

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11
Q

Ace inhibitor name

A 
Pril
Benazepril
Captopril
Enalapril
Lisinopril
Ramipril
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12
Q

ARBs

A

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

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13
Q

ARBs

A

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

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14
Q

ARBs names

A 
Sartan
Losartan
Valsartan
Olmesartan
Eprosartan
Candesartan
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15
Q

DRIs

A

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

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16
Q

Aldosterone antagonists

A

Block receptors for aldosterone for HTN and heart failure

2 drugs - eplerenone and spironolactone - K+ sparing diuretic

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17
Q

Aldosterone receptors

A

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

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18
Q

ACE inhibitors used in

A

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

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19
Q

ARBS indications

A

HTN, CHF, diabetic neuropathy

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20
Q

Aldosterone agonist indications

A

HTN, CHF also hypokalemia and hyperaldosteronism

21
Q

DRIs

A

Direct renin inhibitors, for HTN

22
Q

Angiotensions

A

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

23
Q

Angiotensin II vasoconstriction

A

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

24
Q

Aldosterone

A

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+

25
Q

Angio II formed through

A

Renin, ACE

26
Q

Renin

A

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

27
Q

Renin is released from

A

Drop in BP, volume, Na+ or renal perfusion

28
Q

ACE (kinase II)

A

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

29
Q

Angio II promoting renal water retention

A

Takes days weeks or even months

Constricts renal vessels to reduce GFR and stimulates release of aldosterone

30
Q

ACE inhibitors adverse effects

A

Cough, angioedema, first dose hypotension and hyperkalemia

31
Q

Kinase II (ACE) effects

A

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

32
Q

Effects of decreasing ACE (ace inhibitors)

A

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

33
Q

ACE inhibitors suffix

34
Q

ACE inhibitors renal failure

A

Renally excreted, therefore need reduced dose for renal failure pts

35
Q

Non BP effects on angio II

A

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)

36
Q

ACE inhibitors in heart failure

A

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)

37
Q

ACE inhibitors for post MI pts

A

Captopril, lisinopril, trandolapril

38
Q

ACE inhibitors kidneys

A

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

39
Q

Coversyl

A

Ace inhibitor, perindopril

40
Q

ACE in renal failures

A

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

41
Q

ACE inhibitors interactions

A

Can cause lithium to accumulate

NSAIDS reduce antihypertensive effects

42
Q

Indapamide

A

Thiazide like diuretic. Incombo with coversyl called coversyl plus

43
Q

Rampiril

A

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

44
Q

ARBS vs ACE inhibs

A

Biggest difference is no hyperK+ or cough with ARBS

ARBS aren’t proven to lower odds of MI/STROKE as well as ACE inhibitors

45
Q

ARBS suffix

A

Sartans

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

46
Q

Angioedema

A

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

47
Q

MOA aliskiren a DRI

A

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

48
Q

Aldosterone antagonists are

A

Spironolactone and eplerenone. Spironolactone is less selective

49
Q

MOA Aldosterone antagonists

A 
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

Pharmo for medic school (26 decks)

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