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Cardio Drugs 3
Advanced Pharm for Nursing Practice 3
| Question | Answer |
|---|---|
| Meds used for erectile dysfunction are also used for pulm HTN | Meds used for erectile dysfunction are also used for pulm HTN |
| What is the trade name of the vasodilator sildenafil when used for Erectile Dysfunction? Pulmonary HTN? | sildenafil is Viagra for erectile dysfunction & Revatio for pulmonary HTN |
| Vasodilators/Erectile dysfunction generic drugs end with? | Vasodilators/Erectile dysfunction generic drugs end with –AFIL |
| What’s the use of tadalafil (Cialis)? | Cialis is an erectile dysfunction drug that has also been approved for tx of pullm arterial HTN |
| What are SE/ADR of –AFIL vasodilator/erectile dysfunction drugs? | HA, flushing, nasal congestion, abnormal vision (blue-green vision); WARNING: LOSS OF VISION |
| What’s a contraindication for vasodilators/erectile dysfunction drugs? | contraindicated with Nitrates |
| What are the 2 groups of CCBs and what are their prototypes? | the 2 Ca+ channel blocker groups are dihydropyridine [nifedipine (Procardia)] and non-dihydropyridine [verapamil] |
| Verapamil is what type of drug? It has the greatest affect on what? And the least effect on what? | Verapamil is a non-dihydropyridine Ca+ channel blocker; it has the greatest affect on heart and the least affect on bld vessels |
| Diltiazem* is what type of drug? It has the greatest affect on what? And the least affect on what? | Diltiazem is a non-dihydropyridine Ca+ channel blocker; it has EQUAL affect on the heart and bld vessels |
| What is Nifedipine (Procardia)? | nifedipine the prototype dihydropyridine Ca+ channel blocker and it has LITTLE effect on the heart and its greatest affect on bld vessels |
| How does verapamil work? | verapamil decr contractility (inotropic contraction strength) |
| How does diltiazem* work? | diltiazem slows conduction through the AV node |
| Which CCB has the greatest effect on the heart? | verapamil has the greatest affect on the heart |
| Which CCB has the greatest effect on the blood vessels? | nifedipine has the greatest affect on bld vessels |
| What is relationship between Ca+ channel blockers and action potential? | leakage of Ca+ causes action potential, and when it reaches Na+ potential, there’s a spike causing action potential to go down the neuron. Blocking Ca+ channels slows the heart bc of the blocked Ca+ leakage |
| How do Ca+ channel blockers work? | CCBs block channels in cardiac and smooth muscle (CALCIUM IS NECESSARY TO ACTIVATE CONTRACTION OF ACTIN AND MYOSIN) |
| How does Calcium work in contraction? | Calcium removes the “blindfolds” of troponin & calmodulin, activating myosin contraction |
| How do CCBs work in the heart? In the smooth muscles? | CCBs slow the SA node, blocking AV conduction; this more so decreases contractility (how strong it beats) more so than how fast it beats; smooth muscle is relaxed by CCBs, this lowers BP bc of vasodilation |
| What are indications for CCBs? | indications for CCBs are supraventricular tachyarrythmias, Verapamil can be given IV or PO; all CCBs are useful for coronary artery vasospasm and angina; amlodipine (Norvasc) is drug most commonly used to treat primary HTN & vasospastic angina |
| Which CCB would a pt prefer between nifedipine (Procardia) vs amlodipine (Norvasc)? Why? | a pt would prefer amlodipine over nifedipine because amlodipine is a 1x/day drug, but nifedipine must be taken 3x./day |
| What are drug interactions with Verapamil? | verapamil is a cardiac depressant & can cause additive cardiac depression /c other depressants; ex: Digoxin and verapamil both slow the heart; beta-blockers and verapamil slow the heart and decr contractility |
| Can verapamil be added to anti-arrythmics? | yes, verapamil can be added to anti-arrythmic drugs |
| Verapamil and diltiazem of the CCB group are specifically in the what group? What types of enzymes are they? | verapamil and diltiazem are of the dihyropyridine group, they are ENZYME INHIBITORS (toxicity with other drugs more likely) |
| What is the relationship between grapefruit, CCBs, and cytochrome 3A4? | grapefruit is an enzyme inhibitor; grapefruit interferes /c cytochrome 3A4, this would cause drugs that ordinarily have a low bioavailability will now have increased concentrations |
| Why is amlodipine (Norvasc) such a popular drug? | Amlodipine is so popular because of its high bioavailability; it’s not affected by 1st pass effect or grapefruit juice |
| What are SE/ADR of CCBs? | verapamil causes bradycardia & constipation; dihydropyridines (like nifedipine) can cause reflex tachycardia bc of extreme decr in BP [rembr. sinus/carotid stimulation]; other SE of nifedipine are: lower bld pressure, dizziness, peripheral edema, & HA |
| Why can you get reflex tachycardia with nifedipine? | nifedipine, which is a dihydropyridine will lower BP bc of its function has a CCB, & often /c XS decr of BP, reflex tachycardia is triggered; in this case, bld vessels are what’s affected most, NOT t/ heart (so heart keeps vasoconstricting) |
| Which CCB has the least negative side effects? | Diltiazem |
| How does the juxtaglomerular apparatus work in the kidneys?? When the juxtaglomerular apparatus senses a decr in the amount of bld and Na+ going through it, it will release RENIN; | renin acts on the protein ANGIOTENSINOGEN (that floats around in the bld and causes the stimulation & release of ANGIOTENSIN). |
| How does angiotensin converting enzyme convert angiotensinogen to angiotensin? | ANGIOTENSIN is a potent vasoconstrictor. ANGIOTENSIN acts on the adrenal medulla to cause release of ALDOSTERONE which is a potent Na+ RETENTION SUBSTANCE. ANGIOTENSIN is formed from angiotensinogen by ANGIOTENSIN CONVERTING ENZYME |
| How does Angiotensin converting enzyme inhibitors work? | angiotensin converting enzyme inhibitors prevent the conversion of angiotensin from angiotensinogen |
| What is the ACEI prototype? | Captopril (Capoten) |
| What do ACEI generic drugs end in? | ACEI generic drugs end in –PRIL |
| How do angiotensin converting enzyme inhibitors work? | ACEIs inhibit angiotensin converting enzyme; it decreases the availability of angiotensin II, resulting in VASODILATION & DECR ALDOSTERONE RELEASE |
| What does angiotensin do to blood vessels? | angiotensin is a powerful vasoconstrictor |
| What is bradykinin? | bradykinin is a vasodilator mostly found in the lungs |
| What is the relationship between ACEIs and bradykinin? | ACEI inhibit the metabolism of bradykinin, enhancing vasodilation |
| What are the actions of ACEIs? | ACEIs enhance vasdodilation through inhibition of metabolism of bradykinin; may activate prostaglandins; may reverse cardiac hypertrophy, primarily by blocking effect of aldosterone; may cause a mild naturesis (diuresis of much Na+), & prevent loss of K+ |
| What’s the indications for ACEIs? | tx of HTN (step 1 drug); coronary artery dz (step 1); heart failure (step 1); nephropathy treatment |
| Even though Captopril is the prototype for ACEIs, what is the | 1 ACEI drug and why? |
| What’s a negative and annoying side effect of ACEIs that often causes a change in what med? | ACEIs cause a cough (bc of the bradykinin irritating the lungs); the only way to stop the cough is to change to an angiotensin receptor blocker |
| What are general SE/ADR of ACEIs? | skin rash and dysgeusia (bad taste) (more common w/ Captopril), cough; 1st dose hypotension (start lowest dose at night in bed and titrate up); this is only a prob for hypovolemic pts |
| What are contraindications/cautions of ACEIs? | pregnancy cat D., very rarely cause angioedema with face and tongue swelling. STOP ACEIs IMMEDIATELY & GIVE EPINEPHRINE AND change do diff drug; renal artery stenosis can occur if you dilate that artery and stop the blood flow to the kidney |
| What are ACEIs interactions? | NSAIDS interfere /c prostaglandins; Lithium bc ACEI change Na+ availability & Na+ availability can change Lithium toxicity; K+supplments bc ACEIs cause hypokalemia; diuretics cause hypovolemia |
| When would you put a pt on an angiotensin receptor blocker? | you’d put a pt on an angiotensin receptor blocker if they began coughing from the ACEIs; ARBs are an alternative (that may be better) |
| What is the prototype for angiotensin receptor blockers? | the ARB prototype is LOSARTAN* (Cozaar) |
| What do generic ARB’s end with? | generic ARBs end with –SARTAN |
| The SARTAN sisters Are Real B’s [ARBs] | The SARTAN sisters Are Real B’s [ARBs] |
| What is most commonly prescribed Angiotensin Receptor Blocker? | VALSARTAN is the most commonly prescribed angiotensin receptor blocker |
| How do angiotensin receptor blockers work? | angiotensin receptor blockers selectively block angiotensin I receptor sites in the adrenal medulla & prevent the release of aldosterone. |
| What are the indications for Angiotensin Receptor blocker? | ARBs are indicated #1 for HTN and heart failure, & also to tyr and prevent diabetic nephropathy |
| What are contraindications/warnings about angiotensin receptor blockers? | angiotensin receptor blockers are pregnancy category D (just like ACEIs); renal failure, and hypovolemia |
Created by:
Fukanwa
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