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NURS 572 Ch 43

Pharm RAAS, ACE inhibitors, ARBs

Where should I review for this system see study guide for concept maps
what are both necesseray to stimulate renin release by JG cells of kidney *low glomerular pressure *low Na in PCT (macula densa cells)
what does renin act on converstion of angiotensiogen --> angiotensin-1
where is ACE and what does it act on Angiotensin converting enzyme from lungs. Its actions converts inactive angiotensin-1 to biolocially active angiotensin-2
angio-2 has 2 main actions, with a secondary action. what are they *potent vasoCON. when blocked --> vasoDIL *acts on adrenal cortex --> aldosterone *aldosterone --> retain Na/H20, excrete K
Upside of RAAS activation *maintains normal circulation *provides compensation when perfusion of vital organs is reduced
Downside of RAAS activation (counterproductive) *both angio-2 and aldosterone contribute to remodeling over time *fibrosis may result --> decrease fxn of myocardial and vascular smooth muscle cells
Can angio-2 come from any source besides RAAS *yes, can be produced bwo direct B-1 adrenergic stimulation
Is ACE known by any other names? also known as Kinase-II or Kinniase-II
so when ACE is called Kinase-II, what is its action it is also involved in the metabolisim of bradykinin, and other substances
when we block ACE, what are downstream effects on Angio-2 decreased angio-2 --> *vasoDIL *dec blood volume *dec cardiac and vascular remodeling *K retention *fetal injury
When we block ACE, what are downstream effects on bradykinin blocking ACE means that bradykinin IS NOT metabolized to inactive form. Result is bradykinin able to exert these effects *vasodilation (what we're looking for) *cough (SE) *angioedema (SE)
what do I need to fricking remember about blocking ACE blocking ACE essentially blocks TWO SYSTEMS *arteriole (--> vasoDIL) *aldosterone (-->Na/H20 reten, K wasting)
what activates RAAS *ANY volume depletion (dehydration, hemorrhage) *lowered Na levels in DCT
can true hyponatremia activate RAAS yes, it indirectly activates
ACE inhibitors are 'prils'. MOA please *prevents angio-2 from vasocon (result vasodil) *vasodil occurs in both arterial/venous --> *reduces afterload/arterial pressure *reduces preload/venous return *prevents heart/vessel remodeling *prevents aldosterone's Na/H20 save, K waste
Indications of ACE inhibitor -2 *HTN - decreases mortality *HF - dec sxs and remodeline
2 more indications of ACE inhibitors *AMI - dec mortality, progression to HF *nephropathy - dec. progression
What can ACE inhibitors help prevent prevention of AMI, CVA and death in pts at high risk of CV events
ADR of ACEIs - first two *first dose hypoTN like Alpha-1 blockers *cough due to bradykinin
ADR of ACEIs - second two *hyperkalemia - adlosterone shut down *renal failure - vasodil efferent > afferent. leads to dec intraglomerular pressure
ADRs of ACEIs - last two *angioedema - bwo bradykinin *fetal injury - Pregnancy category D
drug interactions with ACEI --> additive hypotensive effects *diuretics *antihypertensives
Drug interactions with ACEI-->hyperkalemia *K supplements, K sparing diuretics (spironaolactone, triamterene, amiloride) *NSAIDs
Drug interactions with ACEI --> increased lithium MOA ACEIs cause lithium levels to rise. anti-aldosterone means Na not being reabsorbed, so Lithium can't exchange with Na. Therefore, lithium levels increase
all ACEIs are 'prils', so tel me the first/shortest duration that is desired catopril
which 2 ACEIs are not prodrugs catopril, lisnopril
catopril dosing requirements BID/TID on empty stomach
which is the only ACEI not completely eliminated renally fosinopril
other ACEI taken on empty stomach moexipril
which ACEI is only avaiable as active IV form enalapril
other ACEIs for name recognition benaze - perindo - quina - rami - tranodola . . .all prils
what pregnancy category are ALL ACEIs pregnancy category D
ARBs = antgiotensin-2 Receptor Blockers MOA block action of Angio-2 at the receptor, therefore doesn't effect bradykinin accumulation
why would we give ABRs give to pt who can't tolerate SEs of ACEIs (cough, angioedema)
What ADRs DO WE excpect with ABRs same as ACEIs - first dose hypoTN, decreased renal function, hyperkalemia, fetal injury
ABRs indicated for *HTN *diabetic nephropathy *CHF
Sites of action ABRs *arteries - blocks vasocon-->vasodil *adrenal cortex - blocks aldosterone/vasopressin pathway
all ARBs are 'sartans' - name 4 cande - epro - irbe - lo ...sartans
Name other 3 'sartans' in ABR class olme - telmi - val . . .sartans
Renin Blocker MOA binds to renin to decrease the conversion of angiotensinogen --> angio-1 (rate limiting step in activating RAAS)
is there an increase in bradykinin associated with renin blockers nope, works further upstream
name 1 direct rening blocker aliskiren
aliskerin SEs *GI low incidence of cough/angioedema/hyperkalemia
Selective Aldosterone Receptor Blocker MOA selectively blocks aldosterone, so is K sparing. similar diuretic mechanism to spironolactone
name 1 selective receptor blocker eplerenone
does eplerenone have estrogenic SEs nope, differened chemical structure to spironolactone
what is the major SE of eplerenone hyperkalemia - watch for it
what are drug interactions of eplereonone any drugs that cause hyperkalemia or are CYP3A4 metabloism inhibitors
Created by: lorrelaws