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NURS 572 Ch 43
Pharm RAAS, ACE inhibitors, ARBs
| Question | Answer |
|---|---|
| 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
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