ACE Inhibitors Flashcards
Drugs that blocks angiotensin-converting enzyme that activates angiotensin II, therefore decreasing PVR and causing little absorption of aldosterone (cause Na+ to spread)
- Tx for mild-severe HTN, CHF, after MI to improve weakened myocradium, renal failure in people with DM.
- DRUG AGENTS END WITH “PRIL”
- doesnt interfere with cardiovascular system
- interfere with RAAS
- well absorbed orally, produce effect in 1 hr and last for 24 hrs
ACE-Inhibitors
ACE-Inhibitor agent that is used for Tx of HTN, HF, Diabetic nephropathy, left ventricular dystfunction after MI.
- PO; Onset 15 min. Peak 30-90 min, T1/2 2 hrs.
- Excreted in urine
- Adverse effects include tachycardia, MI, rash, pruritus, GI, peptic ulcer, bone marrow suppression, ACE cough
- 25 mg PO bid for HTN; 50-100mg PO TID for HF.
Captopril (p) Capoten
ACE inhibitor agents that is used to treat HTN and adjunct theraphy for CHF-safety. Has parenteral use if oral dosing is not possible or rapid onset is required. Not established for children. Low dose for elderly.
enalapril (Vasotec, Apo-enapril)
Quinapril (Accupril)
ACE inhibitor agents that are used for Tx of HTN, CHF, and MI.
Ramipril (Altace)
Lisinopril (Prinivil)
Trandolapril (Mavik)
Contraindications for ACE inhibitors
Hypersensitivity, Renal artery stenosis, renal dysfunction, hyperkalemia, pregnancy (adverse effects of fetus and during lactation bc of potential decrease in milk production and effects on the neonate)
- SO CHECK RENAL FUNCTION BEFORE TX AND 2WKS INTO TX.
True or False.
The PaSNS has no effect on BP and sweatglands.
TRUE
Drugs that decreases ACE inhibitor absorption
Antacids, NSAID, rifamin, food (so tkae 1hr before meal or 2 hrs after meal)
Adverse effects of ACE inhibitors
Bc it occurs in the lungs, it can cause ACE cough or dry hacking cough, rash, itching, GI probs, headache, dizziness, tachycardia, OH, Hyperkalemia in diabetic clients, renal impairment, pts taking NSAIDs and K-supplements
Why can’t we give cough medications to pts in ACE inhibitors?
Bc it increase BP and blocks binding site of ACE.
Drugs that selectively binds to angiotensin receptors in vascular smooth muscle and adrenal cortex to block contraction of smooth muscle and release of aldosterone. NO ALDOSTERONE IS MADE. AGENTS END IN SARTAN.
- Tx HTN and HF in pts who cant tolerate ACE inhibitors, slow regression of renal disease in pts with HTN and DM2
- ORAL. MEtabolized in the liver P450 system, excreted in urine, feces, breast milk.
- Contraindicated by allergy and pregnancy. Use with caution in pts with liver and renal impairment.
ARBs (Angiotensin II Receptor Blockers)
Decrease antihypertensive effect off ARBs if taken with ____, _____, ____, _____.
Ketoconazole
Fluconazole
Antifungal drugs
Calcium channel blocker dilitazem
Angiotensin II Receptor Blocker agents
candesartan (Atacand) eprosartan Mesylate (Teveten) Irbesartan (Avapro) lorasartan (Cozaar) olmesartan (Olmetec) telmisartan (micadis) valsartan (diovan)
How is Angiotensin II (weak vasoconstrictor) produced?
Renin (kidney) + Angiotensinogen (Liver)
Enzyme in the lung that converts angiotensin I to angiotensin II. It is a potent vasoconstrictor that causes smooth muscle to constrict thus resulting in increases BP, increase reabsorption of Na+, and increased vol of blood.
Angiotensin-Converting Enzyme