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CH 43: Renin-Angio
Drugs acting on the Renin-angiotensin-aldosterone system
| Question | Answer |
|---|---|
| Describe the renin-angiotensin-aldosterone system | Renin is excreted by the kidneys. in the presence of Angiotensinogen it is converted into Angiotensin I(inactive) which is converted by ACE into Angiotensin II(active) |
| Once Angiotensin II is created, what happens? | (1) systemic vasoconstriction of veins and arteries (2) renal constriction -> decreased renal blood flow -> decreased glomerular filtration (3) promotes release of aldosterone both (2) and (3) cause the retention of NA+/loss K+ ALL CAUSE INCREASED BP |
| What is the PRO of angiotensin II? | increased BP/perfusion when hypotension has occured |
| What are the CONs for Angiotensin II? | Angiotensin II can cause HYPERTROPHY in the heart = BAD! It can also cause cardiovascular remodeling (changing the shape and fucntion of teh cells in the left ventricle) |
| Aldosterone is stimulated by _____: | Angiotensin II |
| What 3 things does Aldosterone do? | (1) increase Blood Volume by increasing retention of Na+ (2) Excretes K+ (3) Activates SNS -> increased HR -> dysrhythmias |
| what releases aldosterone? | The Adrenal Cortex |
| What are the 4 classes of Renin-AngiotensinII-Aldosterone system? | ACE inhibitors ARBs (Angiotension II Receptor Blockers) Direct Renin Inhibitors Aldosterone Antagonists |
| What are the indications for ACE inhibitors? | PRIMARY = HTN CHF Diabetes nephropathy Post MI |
| Why do ACE inhibitors work for HTN? | ACE inhibitors block the conversion of Angiotensin I into Angiotensin II. By blocking Angiotenin II, there is a decrease in vasoconstriction -> decreased BP |
| Why do ACE inhibitors work for CHF? | ACE inhibitors inhibit Angiotensin I from becoming Angiotensin II. This reduces afterload which makes the job of the L ventricle easier |
| Why do ACE inhibitors work for Diabetic nephropathy? | ACE inhibitors decrease the glomerlular filtration pressure on the kidneys which delays kidney dysfunction. DIABETIC PATIENTS SHOULD ALWAYS BE ON AN ACE INHIBITOR |
| Why do ACE inhibitors work for Post MI patients? | one downside to the angiotensin II system is hypertrophy and remodeling of the heart. Ace inhibitors block Angiotensin I from becoming Angiotensin II which eliminates the risk for these side effects. |
| how long should a post MI patient be on an ACE inhibitor? | at least 6 weeks |
| What is the goal of an ACE inhibitor? | reducing angiotensin II |
| what is the mechanism of action of an ACE inhibitor? | Inhibiting Angiotensin Converting Enzyme as a result, a decreased stimulation of aldosterone production will occur which will lead to decreased water retention ALSO, ACE inhibitors increase levels of bradykinin (which causes vasodilation) |
| Which drugs end in -pril? | ACE inhibitors |
| How can you identify an ACE inhibitor by name? | they end in -pril |
| administration route of ACE inhibitors: | MOSTLY oral, some IV |
| can you administer ACE inhibitors with food? | you can administer ACE inhibitors with or without food |
| T/F: Almost all ACE inhibitors are in their active forms | F: Almost all ACE inhibitors are converted to their active form after metabolism |
| Where does metabolism of ACE inhibitors occur? | For most ACE inhibitors, metabolism occurs in the small intestine |
| How often do you administer ACE inhibitors? why? | Most ACE inhibitors have long half lives and therefore are able to be administered once or twice per day |
| How well are ACE inhibitors tolerated? | they are well tolerated |
| How safe are ACE inhibitors during pregnancy? | NOT SAFE! |
| What are the characteristic side effects of ACE inhibitors? | (1) first dose hypotension (2) Dry cough (3) Angioedema (4) Hyperkalemia (4) Renal Failure (ONLY if pt has bilateral renal artery stenosis) (5) Neutropenia |
| Why might a dry cough develop in someone on an ACE inhibitor? | his is related to the production of bradykinin which is secondary to the inhibition of ACE |
| What is angioedema? what must be done if this develops? | angioedema is edema of the face, the drug must be DC IMMEDIATELY!!! |
| Why might hyperkalemia occur in patients on ACE inhibitors? | Hyperkalemia might occur dt decreased aldosterone. Aldosterone is responsible for conserving sodium and water and excreting potassium. if it is not excreting potassium, there can be a build up. |
| When might renal failure occur in a patient on an ACE inhibitor? | renal failure will only occur in a patient on an ACE inhibitor who has bilateral renal arterial stenosis. |
| ACE inhibitors can cause neutropenia, what should you do as a nurse in response to this fact? | you should monitor your pts CBCs |
| What are the drug interactions you should pay attention to when your patient is on an ACE inhibitor? | Other hypertensive drugs (this could lead to too much of a drop in BP) Drugs/foods that raise K+ NSAIDS (they cann suppress the effects of ACE inhibitors) |
| Angiotensin II receptor blockers (ARBs) can be identified by name, How? | Angiotensin II receptor blockers will end in -sartan. |
| What is mechanism of action of ARBs? | ARBs block the binding of Angiotensin II which causes the same effects as ACE inhibitors. |
| which is preferred, ACE inhibitors or ARBs? Why? | ACE inhibitors are preferred because there is evidence that proves that ACE inhibitors decrease cardiovascular morbidity and mortality. |
| What are the indications for Angiotensin II receptor blockers? | Same as ACE inhibitors: HTN CHF Diabetic Nephropathy Post MI |
| What are the side effects of ARBs? | Same as ACE inhibitors: well tolerated angioedema renal failure (in pts with bilateral renal arterial stenosis) hyperkalemia neutropenia |
| Are ARBs safe for pregnancy? | no |
| What are ARBs often combined with? when should they be administered? why? | ARBs are often combined with HCTZ diuretics and should be taken in the morning to avoid nocturea |
| What is the mechanism of action for Direct Renin Inhibitors? | Direct Renin Inhibitors block the entire Renin-angiotensin-aldosterone system by blocking Renin itself. |
| What Drugs are available in the class of Direct Renin Inhibitors? | Just one. Tekturna. |
| What kind of drug is Tekurna? What is it approved for? | Tekturna is a Direct Renin Inhibitor. It works to stop the entire Renin-Angiotensin II-Aldosterone system. Tekturna is approved ONLY for hypertension. It is used as a last stitch effort because there are many other better HTN drugs out there. |
| what are the adverse effects of Tekturna? | Cough Angioedema DIARRHEA (this is the different one) Hyperkalemia |
| Is Tekurna safe during pregnancy? | NO |
| Tell me the name of the Aldosterone Agonist drug: | Inspra |
| What class of drug is Inspra? What is the mechanism of action? | Inspra is an aldosterone Antagonist. It blunts aldosterone which leads to the retention of K+. It is also a last resort when other HTN drugs are not working. |
| What is Inspra indicated for? | Inspra is an aldosterone antagonist. It blunts aldosterone. It is indicated for HTN and HEART FAILURE |
| by what route is Inspra administered? | Orally with or without food |
| What are the side effects of Inspra? | Inspra is an aldosterone Antagonist. It has these side effects: Hyperkalemia, Diarrhea, Abdominal pain and fatigue |
| What is a major difference between ACE inhibitors and ARBs? | ACE inhibitors produce elevated levels of bradykinin which leads to a dry cough. ARBs do not increase bradykinin, therefore NO COUGH |
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