Cardio Pharm- RAAS inhibitors (ACEis, ARBS, ARAs, renin inhhibitors)

lisinopril, captopril, fosinopril, enalapril, benazepril

are __________

angiotensin converting enzyme inhibitors

angiotensin receptor blockers

aldosterone receptor blockers

renin inhibitors

angiotensin converting enzyme (ACE) inhibitors

this class of meds decrease conversion of angiotensin I to angiotensin II, thus decreasing vasoconstriction; this class also inhibits bradykinin breakdown

ACE inhibitors

lisinopril, captopril, etc. ______ bradykinin breakdown

increase

decrease

decrease!! by decreasing the breakdown of bradykinin, the BRADYKININ LEVELS GO UP, LEADING TO INCREASED NO AND PGI2 AKA VASODILATING EFFECT

which ace inhibitor has decreased absorption with food

lisinopril

captopril

benazepril

enalapril

CAPTOPRIL!!

dont take CAPTopril with CAPTAIN crunch bc itll decrease absorption aka it wont be as effective

which ace inhibitor is not excreted in the urine

Fosinopril, excreted in Feces

which class of HTN meds is first line for AN UNCOMPLICATED pt with diabetes with proteinuria or pts w CKD

ACEs/ARBs

ARBs

thiazides

loop diuretics

alpha-1 blockers

calcium channel blockers

ACEs/ARBs, note: if the person has CAD, HTN, and diabetes, although ACEs/ARBs are renoprotective and great for diabetes, they may need a stronger med due to the CAD, so even though in the pharm slides it says beta blockers are contraindicated for diabetes bc risk of masking hypoglycemia symptoms, IF THE PT HAS CORONARY ARTERY DISEASE U TREAT THAT ASAPPPPPP

ACEs have a renal protective effect and are used in pts with proteinuric chronic kidney disease because of vasodilation of ________ arteriole, leading to DECREASED GFR and thus DECREASED proteinuria

efferent

afferent

efferent

*VERY IMPORTANT*

ACE inhibitors (and ARBs) ______ glomerular filtration rate (GFR) AND WHY IS THIS IMPORTANT

increase

decrease

DECREASE- why is this good? bc in someone with proteinuric kidney disease or diabetes, decreasing the GFR REDUCES PRESSURE WITHIN THE KIDNEYS, ALLOWING THE GLOMERULI (tiny fitlers) TO REST/SLOW DOWN, THUS SLOWING THE PROGRESSION OF KIDNEY DAMAGE

THIS IS WHY ACEs (and ARBs) are the preferred HTN med for diabetics/those w CKD

can ACE inhibitors/ARBs be used in pregnancy

NOOOOOOOOOOO

persistent dry cough/angiodema is a risk for

ACEs

ARBs

both

ACEinhibitors - its bc of the increased bradykinin levels since were inhibiting bradykinin breakdown

if someone has AEs with ACEinhibitor, switch to ARB

ACEs/ARBs increase risk for _____kalemia

hypo

hyper

HYPER

so increased risk for too much potassium

T/F: ACEis/ARBs have a BOXED WARNING for fetal hypotension, oligohydraminios, and renal injury if taken during pregnancy

T- DO NOT EVER EVER EVER GIVE AN ACE/ARB DURING PREGNANCY

T/F: ACEs/ARBs have renal protective function and are preferred for diabetics/CKD HOWEVER, not good in someone with BILATERAL RENAL ARTERY STENOSIS

T

how is that possible

well, in CKD the kidney are damaged bc of TOO MUCH PRESSURE IN THE KIDNEYS, and ACEis/ARBs DECREASE that pressure by decreasing GFR, so thats a great thing, aka the renal protective effect of ACEs/ARBs (protecting the kidneys from pressure overload)

HOWEVER

in renal artery stenosis, this is a completely different issue- the artery providing blood to the kidney is STENOSED AKA NARROWED, we DO NOT want to further reduce that blood flow by decreasing pressure that would not be good

losartan, valsartan, candesartan, telimisartan are:

thiazides

loop diuretics

non dihydropyridines

dihydropyridines

angiotensin II receptor blockers

angiotensin II receptor blockers (ARBs)

losartan, valsartan, etc work by:

inhibiting the actions of angiotensin II by blocking their receptors

decrease conversion of angiotensin I to angiotensin II

inhibit renin activity

inhibiting the actions of angiotensin II by blocking their receptors

they are angiotensin II RECEPTOR blockers, so angiotensin II is still formed, but it cant exert its actions bc ITS RECEPTORS ARE BLOCKED!!!!!

ACEs and ARBs decrease water and _____ retention

K+

Na+

Ca2+

Mg2+

Na+

________ inhibits activation of angiotensinogen into angiotensin I

angiotensin converting enzyme inhibitors

angiotensin receptor blockers

renin inhibitors

renin inhibitors (ex: Aliskiren)

REN in akiskiren, RENin inhibitor

remember, in general "ogen" means precursor, so we're preventing the conversion of angiotensinogen (precursor) into its active form, angiotensin I

raas pathway is:

AngiotensINOGEN

Angiotensin I

Angiotensin II

Aldosterone

eplerenone blocks aldosterone receptors and _____ K+ excretion

increases

decreases

DECREASES

its similar to spironolactone; they are both ARAs meaning aldosterone receptor ANTAGONISTs, and they RETAIN K+!!!! meaning if we retain K+ in body, so were not peeing out as much K+ aka decreased K+ excretion

think about spiro working at a derm office, whenever we prescribed it for acne we told pts to avoid high potassium foods bc it can increase ur K+ retention, same idea w eplerenone, these are K+ sparing diuretics meaning we keep our K+

does Eplerenone have gynecomastia side effects like spironolactone

no