Exam 1 - RAAS, ACEIs, ARBs, and Renin Inhibitors Flashcards
Explain the RAAS pathway
Decreased renal blood flow stimulates receptors in juxtaglomerular apparatus of kidney to secrete renin (hormone/enzyme)
Renin converts angiotensinogen (produced by liver) to angiotensin I
ACE (from the lungs) converts angiotensin I to angiotensin II
Angiotensin II (potent vasoconstrictor) increases BP and glomerular secretion
Angiotensin II stimulates aldosterone secretion
Aldosterone increases Na+ and water retention, which increases blood volume, which increases BP
what mediates the BP increase from RAAS?
stimulation of angiotensin II type 1 receptors
What effects can result from a chronic elevation of angiotensin II?
Volume overload + increased SVR
Renal damage
Risk of increased CV related morbidity and mortality
What can be seen with the volume overload and increased SVR resulting from a chronic elevation of angiotensin II?
Cardiac hypertrophy and remodeling
Coronary vascular damage and remodeling
Hypovolemia (low blood volume) and dehydration stimulate the ___ in the ___ to release ___ from the the ___ gland
- Osmoreceptors
- Hypothalamus
- ADH
- Posterior pituitary gland
What does ADH cause? What does this lead to?
Causes water reabsorption at kidney tubules
Leads to increased blood volume and BP
what is the main regulator of Na+ retention?
NB (can’t find what this stands for - coming back to it)
What else is produced when ACE converts angiotensin I to angiotensin II? What is it and what does it do?
Bradykinins
Potent vasodilator
Decreases BP
what drugs are ACE inhibitors?
Lisinopril (zestril, prinivil)
Enalapril (vasotec)
Enalaprilat (IV vasotec)
Captopril (Capoten)
Ramipril (altace)
Benazepril (lotensin)
Quinapril (accupril)
Trandolapril (mavik)
Perindopril (aceon)
(Just know they end in -pril but don’t forget enalaprilat)
(ACEi pharmacological effects): how do ACE inhibitors dilate arteries and veins? What does this do?
Dilation by blocking angiotensin II formation and inhibiting bradykinin metabolism
Vasodilation reduces:
- Arterial pressure
- Preload
- Afterload
What are the pharmacological effects of ACE inhibitors?
Dilate arteries
Down regulate sympathetic adrenergic activity
Promote renal excretion of sodium and water (natriuretic and diuretic effects)
Inhibit cardiac and vascular remodeling
(ACEi pharmacological effects): how do they down regulate sympathetic adrenergic activity?
Blocking the effects of angiotensin II on sympathetic nerve release and reuptake of NE
(ACEi pharmacological effects): how do they promote renal excretion of Na+ and water? What does this do?
Blocking effects of angiotensin II in kidney
Blocking angiotensin II stimulation of aldosterone secretion
This reduces blood volume, venous pressure, and arterial pressure
Why can ACEIs cause a dry cough?
increase in bradykinin
(ACEi pharmacological effects): Inhibit cardiac and vascular remodeling associated with ___
HTN
Heart failure
MI
What are the AEs of ACE inhibitors?
Dry cough in ~ 10% of pts
Hypotension
Angioedema (life threatening airway swelling and obstruction; 0.1 - 0.2% of pts)
Hyperkalemia
Pts w/ bilateral renal artery stenosis may experience renal failure
(Playing Hay Day At Home)
ACEI use can cause hypotension, especially in ___ pts
heart failure
Why can hyperkalemia occur as a SE of ACEI?
reduced aldosterone formation
What is a contraindication for ACEI? Why?
Pregnancy
Can induce fetal malformations (teratogenic)
ACEI may cause hyperkalemia in what patients?
CKD
Those taking:
- K+ sparing diuretic
- Aldosterone antagonists
- ARB
- Direct renin inhibitor
What is an ARB?
angiotensin II receptor blocker
The starting dose of an ACEI should be reduced by ___ in pts who are ___, ___, or ___. Why?
Reduced by 50%
On a thiazide
Volume depleted
Very elderly
Risk of hypotension
what drugs are ARBs?
Candesartan (atacand)
Valsartan (diovan)
Losartan (cozaar)
Olmesartan (benicar)
Irbesartan (avapro)
Telmisartan (micardis)
Eprosartan (teveten)
(Just remember -sartan)
What is the MOA of ARBs?
Block angiotensin receptors on blood vessels and other tissues
Decreases the activation of angiotensin I receptors by angiotensin II
Vasodilation
Blocked aldosterone secretion
Lowers BP