RAAS drugs Flashcards

1
Q

RAAS fxn

A

increase blood volume and blood pressure when it is low

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does blocking RAAS do?

A

reduce blood volume and pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

RAAS regulates

A

Blood pressure

Blood volume

Fluid and Electrolyte balance

  • also mediates changes associated with hypertension, heart failure and MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Where does RAAS exerts its effect through

A

angiotensin II and aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

aldosterone

A

increases Na+ reabsorption form the nrpgron tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

angiotensin II

A

increased release of vasopressin
= increased H2) reabsorption from kidneys
= increased blood volume and blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

actions of angiotensin II

A

vasoconstriction
- stimulates posterior pituitary to release vasopressin
- a) vasoconstriction
-b) increased H2) reabsorption from nephron

Stimulate aldosterone
- acts on adrenal cortex –> secrete aldosterone
- enhances Na+ reabsorption from nephron
Both raise BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Actions of Aldosterone

A

acts on distal nephron tubule
- increase Na+ reabsorption
–> h20 follows na
- increases BP/volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Renin

A

converts angiotensinogen into angiotensinogen I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Angiotensin - Converting Enzyme (ACE)

A

converts angiotensin I into active state angiotensin II.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

2 process of BP regulation by RAAS

A

1) Vasoconstriction- occurs within MINUTES

2) Renal retention of sodium - DAYS/ WEEKS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what are 2 ways angiotensin II promotes water retention

A

1) reducing glomerular filtration
- reduce urinary output (via vasoconstriction)

2) Aldosterone
- increase Na+ reabsorption and water follows na+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ACE inhibitor drug name

A

Catopril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ACE inhibitor fxn

A

prodrug treating hypertension, heart failure, and MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mechanism of ACE inhibitors

A

reduce angio II levels by inhibiting ACE
- decrease BV

Increase levels of Bradykinin
- natural body vasodilator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pharmakinetics of ACE inhibitors

A

A) PO with food

M) Prolonged half-life, administration 2x / day

Excretion: KIDNEYS = dangerous levels = kidney disease

17
Q

therapeutic use of ACE inhibitors

A

reduction of hypertension

Heart failure
- prevent/ reverse pathologic changes in cardiac structure

Prevention of MI and Stroke
- reduction BP/BV

Diabetic Nephropathy: leading cause of end stage renal disease
– slow progression of disease by lowering systemin BP= reducing glomerular filter pressure

18
Q

ACE inhibitor Adverse Effects

A

First Dose hypotension (wide-spread vasodilation

Hyperkalemia

Increased bradykinin
- cough
- angioedema: swelling like hives but underneath skin

Contradiction Renal failure in patients with renal artery stenosis (RAS)
- pt require greater pressure to overcome RAS
–> kidney secretes large amounts of renin
- ACE inhibitors stop this adaptation
- Contraindication for pt with RAS

19
Q

ACE inhibitor drug interactions

A

Diuretics
- may intensify first dose hypotension

Antihypertensive drugs
- may need to be reduced

NSAIDs
- reduce antihypertensive effects of ACE inhibitors

20
Q

Preparation and administration of anti ACE inhibitors

A

PO

available in combo with hydrochlorothiazide and perindopril

some combined with calcium channel blockers

21
Q

Angiotensin II Receptor Blocker drug name

A

Losartan

22
Q

ANG II receptor blockers work by

A

blocking action of ANG II

23
Q

Difference between ANG II receptor blockers and ACE inhib.

A

ace inhib- block production of ANG II

ang II recept. blockers = block action of ANG II
- less risk of cough and hyperkalemia

ACE inhib. preferred

24
Q

Direct Renin Inhibitors (DRI)

A

Aliskiren

25
Q

DRI mechanism

A

binds tightly with renin
-inhibits cleavage of ANG into ANG I

reduces influence of entire RAAS
- reduced BV/BP

26
Q

Therapeutic uses of DRI

A

Hypertension
- reduces BP to same level as ACE inhib

27
Q

Pharmacokinetics of DRI

A

OP with high fat meal

Half-life = 24 hours

28
Q

DRI adverse effects

A

Well tolerated

GI: dose dependent diarrhea, abd. pain, dyspepsia

Hyperkalemia if used with ACE inhib.

29
Q

dyspepsia

A

indigestion, upset stomach

30
Q

Prep, dosage, admin of DRI

A

Alone: 150 mg/day
- may increase to 300 mg
- above this diarrhea increased significantly

31
Q

Aldosterone Antagonist

A

Eplerenone
- first line

32
Q

Mech of Aldosterone Antagonist

A

Blocks aldosterone receptors

  • decreased Na+ reabsorption
    = water stays in kidney
    = reduced BP/BV
33
Q

Therapeutic uses of Aldosterone Antagonist

A

Hypertension
- max reduction takes 4 weeks

  • combination with ACE inhib or ARB produces further redicution in BP

Heart Failure

34
Q

Aldosterone Antagonist Pharmacokinetic

A

OP- not affected by food

35
Q

Adverse effects of Aldosterone Antagonist

A

Hyperkalemia (occurs secondary to sodium retention)
- don’t combine with sodium potassium supplements

  • contraindication for patients with high serum potassium (above 5.5 mEq/L)
36
Q

Aldosterone Antagonist drug interactions

A

P450 inhibitors
- increased levels eplerenone = toxicity

Drugs that raise potassium blood levels