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