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NURS615 Pharmacology > Exam 3- Cardiovascular Drugs > Flashcards

Exam 3- Cardiovascular Drugs Flashcards

1
Q

What would be the best choice of Beta blockers based on pharmacokinetics?

A

–One with a long enough half-life to permit once daily dosing
–Consistent bioavailability
–Limited CNS penetration
–An excretion mechanism that does not require dosage adjustments

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2
Q

Combined alpha and beta blockers

A

Carvedilol (Coreg), labetolol (Normodyne)
•The alpha1 and beta blockade decreases blood pressure and peripheral resistance by peripheral vasodilation
–Standing BP is more affected than supine

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3
Q

ACEIs (-pril)

A

Effective for all types and stages of HTN
•Their action on the renin-angiotensin-aldosterone system (RAAS) makes them popular drugs
Elevate bradykinin which causes cough.

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4
Q

ARBs (-sartan)

A
  • Same indications as ACEIs
  • Several are pro drugs
  • Do not elevate levels of bradykinin → therefore, incidence of cough is rare
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5
Q

CCBs

A

Dihydropyridines – amlodipiine, felodipine, isradipine, nifedipine
•Nondihydropyridines – diltiazem, verapamil
•Used as first line therapy – especially in black patients and patients with ischemic heart disease
•Also used in older adults with isolated systolic hypertension

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6
Q

Alpha 1 blockers

A

•Block postsynaptic alpha1 receptors in the vasculature resulting in a decrease in both arterial and venous vasoconstriction
•Also relax bladder neck and prostate gland
•Side effects – significant orthostatic
Ex: Doxazosin (Cardura), prazosin (Minipress), terazosin (Hytrin)

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7
Q

Central Alpha2 agonists

A

•Stimulate alpha2 receptors in the brainstem which decreases sympathetic stimulation to the heart and PVS
–Reduces BP and pulse; also decreases renin production in kidneys
•Not used as monotherapy – side effects
Ex: Clonidine (Catapres), methyldopa (Aldomet)

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8
Q

Direct-acting peripheral vasodilators (PVDs)

A

•Act by direct relaxation and dilation of arteriolar smooth muscle – decreasing PVR
•Used for severe HTN
•Side effects – rebound HTN, dizziness
Ex: Hydralazine (Apresoline), minoxidil (Loniten)

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9
Q

Antilipidemic drugs

A 
Types:
HMG-CoA Reductase Inhibitors
•Cholesterol Absorption Inhibitor
•Bile Acid Resins
•Fibric Acid Derivatives
•Niacin
•Omega 3 and Omega 6 Fatty Acids
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10
Q

Statins

A

Block HMG-CoA reductase, an enzyme required in the initial step in cholesterol synthesis

Lowers LDL

•Adverse effects – small elevations in LFTs, myopathy

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11
Q

Cholesterol absorption inhibitors

A

Ezetimibe (Zetia) zebra entering studio with diarrhea

  • blocks absorption of cholesterol.
  • Used as adjunct to diet and statin in reducing total cholesterol, LDL, and TG levels, and increasing HDL levels

•Side effects - Diarrhea

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12
Q

Bile acid resins

A

Block intestinal reabsorption of bile. Used to lower LDL levels when triglycerides are well-controlled.

Can increase triglycerides, N/V, gallstones.

Cholestyramine (Questran), Colesevelam (WelChol)

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13
Q

Fibric Acid Derivatives

A
  • Fenofibrate (Tricor), gemfibrozil (Lopid)
  • Act by increasing lipolysis of triglycerides by lipoprotein lipase
  • Used for treatment of high triglycerides.
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14
Q

Niacin

A

Inhibits VLDL secretion → decreases production of LDL
–Reduces TG, total cholesterol, LDL levels; increases HDL levels
•Side effects – intense flushing and pruritis, N/V, diarrhea

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15
Q

Omega-3 and Omega-6 Fatty Acids

A
  • (Lovaza), Fish oil
  • Reduce TG by inhibiting VLDL and apo-B-100 synthesis; also decrease postprandial lipemia
  • Side effects – interfere with coagulation at high doses, GI upset
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16
Q

Nitrates

A

•Used for immediate relief of acute angina, and prevention of anginal attacks
•Reduce afterload and preload
–Preload reduction is most important
•Nitroglycerin has short half-life
•Adverse reactions – orthostatic hypotension, syncope, headache

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17
Q

Beta Blockers

A

•Reduce oxygen requirements of myocardium by preventing stimulation of SNS receptors
–Reduces contractility
–Decreases sinus node rate
–Decreases atrioventricular conduction velocity
•Side effects – hypotension, bradycardia, bronchospasm

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18
Q

Calcium Channel Blockers

A

All CCBs relax arterial smooth muscle, but have little effect on venous beds
–Significant reduction in afterload with limited effect on preload
•Act via two types of receptors
–Dihydropyridine
–Nondihydorpyridine
•The two classes of CCBs have different effects on AV nodal conduction

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19
Q

Use of CCBs in Angina

A
  • Nifedipine (Procardia), amlodipine (Norvasc), felodipine (Plendil)
  • Considerable variation in oral absorption
  • Highly protein bound
  • Side effects – headache, dizziness, hypotension
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20
Q

Class I Antiarrhythmics

A
  • Sodium channel blockers

* Similar in structure and action to local anesthetics

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21
Q

Class IA antiarrhythmics

A
  • Block fast Na channels → slows action potential depolarization
  • Also block PNS discharge → increased conduction rate at the AV node
  • Side effects – N/V, increased heart rate, widened QRS complex, prolongation of PR and QT intervals
  • Procainamide, quinidine
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22
Q

Class IB Antiarrhythmics

A
  • Lidocaine
  • Block both activated and inactivated Na channels
  • Most effective in treating acute ventricular arrhythmias associated with MI, cardiac surgery and catheterization, cardioversion, and digoxin toxicity
Extensive first-pass metabolism
•Widely distributed through the body
–Concentrated in adipose tissue
–Crosses blood-brain barrier
•Adverse effects – drowsiness, confusion, CV depression
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23
Q

Class IC Antiarrhythmics

A
  • Flecainide (Tambacor), Propafenone (Rhythmol)
  • Block the Na fast channel during phase zero of the action potential
  • Used to manage severe refractory ventricular arrhythmias because of their propensity to exacerbate arrhythmias
  • Well absorbed orally
  • Side effects – malignant arrhythmias, dizziness, fatigue
  • Drug interactions – cimetidine, propanolol, digoxin
24
Q

Class II Antiarrhythmics

A
  • Acebutolol (Sectral), esmolol (Brevibloc), propanolol
  • Cause a significant increase in the effective refractory period of the AV node
  • Also exert significant negative inotropic effects
  • Side effects – bradycardia, dizziness, fatigue
25
Q

Class III Antiarrhythmics

A

•Amiodarone, sotalol (Betapace)
Considered second- or third-line drugs because of their adverse effects
•Amiodarone exhibits electrophysilogic activity of each of the classes
–Causes potent blocade of Na and Ca channels

26
Q

Class IV Antiarrhythmics

A
  • Diltiazem and verapamil
  • Inhibition of Ca movement slows the conduction rate between atria and ventricles
  • Adverse effects – peripheral edema, facial flushing, dizziness
27
Q

Adenosine

A

Atypical antiarrhythmic
•Used for converting supraventricular tachycardia to sinus rhythm
•Activates K channels, and by increasing K outflow, hyperpolarizes the membrane potential, decreasing spontaneous SA nodal depolarization

28
Q

Adenosine

A
  • Half-life - < 10 seconds

* Adverse events – new arrhythmias, headache, facial flushing, chest discomfort

29
Q

What assessments should be made before prescribing any antihypertensive agent?

A

Baseline BP and a pulse reading should be taken before initiating therapy and with each change in dosage. Weight and other indicators of fluid status should also be monitored.

30
Q

Why are ACE inhibitors the drug of choice in diabetic patients with hypertension?

A

To prevent diabetic nephropathy or slow its progression. In patients with type 1 diabetes, with or without HTN, ACEIs have been demonstrated to significantly delay the progression of diabetic nephropathy. In patients with type 2 diabetes, HTN, and microalbuminuria, ACEIs and ARBs have been shown to delay the progression to macroalbuminuria. In diabetic patients with macroalbuminuria and renal insufficiency, ARBs have been shown to delay the progression to nephropathy.

31
Q

What is the most common adverse effect of an ACE inhibitor?

A

What is the most common adverse effect of an ACE inhibitor?

32
Q

What is the mechanism of action of ACE inhibitors?

A

inhibition of ACE activity (ACEIs) results in decreased production of both angiotensin II (AT II) and aldosterone. AT II has multiple roles in the cardiovascular system. It increases vasomotor tone by direct stimulation of vascular smooth muscle contraction and through the inhibition of endothelial nitric oxide and prostaglandin release, raising BP and decreasing blood flow through arteries, including the coronary arteries. AT II increases intravascular volume through its stimulation of sodium and water retention (with aldosterone), shifting of the pressure-natriuresis relationship, and altering glomerular hemodynamics. stimulation of smooth muscle cell and fibroblast proliferation with thickening of the vessel wall (remodeling). promotes intravascular inflammation and clotting and contributes to the atherosclerotic process. Finally, in the heart, AT II also causes remodeling, resulting in hypertrophy and fibrosis of myocardial tissue after ischemic injury or in response to persistent afterload. This is a primary mechanism in HF.

33
Q

What is the mechanism of action angiotensin receptor blockers?

A

ARBs do not affect ACE activity but rather act by blocking the AT II receptor. They have similar action to ACEIs on vasoconstriction and aldosterone secretion, but no activity related to bradykinin. ACEIs and ARBs do not affect cardiac output and so do not produce reflex tachycardia.

34
Q

What is the mechanism of action of calcium channel blockers?

A

contraction of smooth muscles is triggered by an influx of calcium through transmembrane calcium channels. CCBs directly block the influx of calcium at the onset of the cycle, like the sodium channel blockade in local anesthetics. The drugs act from the inner side of the membrane and bind to channels in depolarized membranes, converting the mode of operation of the channel from frequent openings to rare openings. The result is a marked decrease in transmembrane calcium content and prolonged vascular smooth muscle relaxation. The blocking action of CCBs occurs via three different receptors: diphenylalkylamine-based and benzothiazepinebased (both type 1 receptors) and dihydropyridine-based (type 2 receptors). The physiological response in the calcium channel is different for these two receptor types, and these differences are important in the clinical choice of CCB.

35
Q

What are the adverse effects of dihydropyridine-type calcium channel blockers?

A

Their strong peripheral vasodilating effects result in peripheral pooling of blood and may lead to reflex tachycardia. Can also cause flushing, headache, excessive hypotension, and edema.

36
Q

What are the side effects of the calcium channel blockers?

A

The more common adverse reactions of CCBs are extensions of their actions. Reduction in BP secondary to vasodilation may result in dizziness, headache, hypotension, and syncope. These lead to HF with congestion, shortness of breath, cough, and palpitations; though a potential class effect, HF is worse with verapamil, diltiazem, and nifedipine. Gastrointestinal (GI) symptoms can include dry mouth, nausea, vomiting, reflux, and constipation.

37
Q

What are the adverse effects of statins.

A

Active liver disease is a contraindication for all antilipidemics except the bile-acid sequestrants. The FDA has required that all reductase inhibitors carry a warning about possible blood sugar increases along with concentration and memory issues. There is a small risk of developing more than glucose intolerance. The risk of a major CV event is far greater, so the use of statins should continue. The reductase inhibitors all have mild headache as a common adverse reaction. Rhabdomyolysis with renal dysfunction secondary to myoglobinuria has occurred with reductase inhibitors.

38
Q

What patient education will you provide for a client in which you have prescribed a statin?

A

Reductase inhibitors are traditionally taken in the evening because of their action on cholesterol synthesis; however, this is not clinically significant except for lovastatin. For all reductase inhibitors, muscle tenderness or pain may indicate a serious problem that may require discontinuance of the drug.

39
Q

What lipid disorder(s) do fibric acid derivatives treat?

A

Elevated Very-Low-Density Lipoproteins and Elevated Triglycerides

40
Q

What lipid disorder(s) do bile acid sequestrants treat?

A

High LDL, low HDL.

41
Q

What would you recommend to a patient who is experiencing flushing with niacin therapy.

A

Don’t take with hot fluids. Take with meals to decrease incidence of this reaction.

42
Q

Digoxin

A

Cardiac glycoside

used in management of heart failure and also atrial fibrillation

Toxic if >2 ng/ml

43
Q

Phosphodiasterase Inhibitors

A
  • Inamrinone (Inocor), milrinone (Primicor)
  • Inhibits phosphodiasterase resulting in the accumulation of intracellular cyclic AMP – decreasing peripheral and pulmonary vascular resistance and dilating coronary vessels.
  • IV form only
  • Adverse effects – arrhythmias, thrombocytopenia
  • Drug interactions
44
Q

Amiodarone

A

Antiarrhythmic

45
Q

Digoxin drug interactions

A

Any drug that may cause hypokalemia, hypercalcemia, or hypomagnesemia increases the risk of toxicity. Several antiarrhythmic drugs (quinidine, amiodarone, verapamil, diltiazem, and propafenone) increase serum CG levels and toxicity risk. Drugs that induce bradycardia can exhibit additive bradycardia when given with CGs. This is especially a concern with BBs.

46
Q

How is amlodipine metabolized?

A

All CCBs are extensively metabolized by the liver via the CYP 3A4 channel.

47
Q

What are the side effects of amlodipine?

A

Pulmonary fibrosis, thyroid dysfunction. The more common adverse reactions of CCBs are extensions of their actions. Reduction in BP secondary to vasodilation may result in dizziness, headache, hypotension, and syncope. These lead to HF with congestion, shortness of breath, cough, and palpitations;

48
Q

What patient teaching will you provide when prescribing amiodarone?

A

if a dose is missed at its usual time, it should not be taken at all that day; the patient should simply take the next day’s dose. Its very long half-life maintains a stable level. Dizziness is the most common adverse response. Changing position slowly, especially when arising from a lying position, decreases this reaction. Monitoring of pulse rate and rhythm and BP provides early indications of efficacy and toxicity. Patients should learn to take their own pulse and BP and check them whenever symptoms occur. Hypotension and slow, rapid, or irregular heart rates should be reported promptly. With amiodarone, a bluish discoloration of the skin in areas exposed to sunlight may occur. It is usually reversible and fades over several months. This drug is also associated with epididymitis and pulmonary fibrosis. Patients should report scrotal pain or swelling and decreased exercise tolerance.

49
Q

What is the purpose of a thyroid panel with amiodarone?

A

Amiodarone is a potent antiarrhythmic drug associated with thyroid dysfunction. Its high iodine content causes inhibition of 5′-deiodinase activity. Most patients remain euthyroid. Amiodarone-induced thyrotoxicosis (AIT) or amiodarone-induced hypothyroidism (AIH) may occur depending on the iodine status of individuals and prior thyroid disease.

50
Q

What is nitrate tolerance?

A

With continuous exposure, smooth muscle develops clinically significant tolerance (tachyphylaxis). In well-controlled clinical trials, nitrates were no more effective than placebo after 18 to 24 hours of continuous therapy, particularly for long-acting/ sustained-release preparations. The mechanisms by which this occurs are not fully understood. Only after nitrates have been absent from the body for 10 to 12 hours does their effectiveness return.

51
Q

What are the contraindications to therapy with Coumadin?

A

All anticoagulants are contraindicated for patients who are hypersensitive to the drug or actively bleeding or who have hemophilia, thrombocytopenia, severe hypertension (HTN), intracranial hemorrhage, infective endocarditis, active tuberculosis, or ulcerative lesions of the GI tract. Hepatic dysfunction potentiates the response to warfarin through impaired synthesis of coagulation factors. Hypermetabolic states produced by fever or hyperthyroidism also increase responsiveness to warfarin, probably by increasing the catabolism of vitamin K–dependent coagulation factors.

52
Q

What classes of medications are used in the treatment of congestive heart failure?

A

ACEIs and ARBs are useful in treating heart failure related to CAD, primarily for their role in reducing remodeling. Another underlying cause for HF is chronic HTN. ACEIs and ARBs are also effective in treating this underlying cause. ACEIs are a cornerstone of therapy for HF and are recommended for patients with a history of atherosclerotic vascular disease, diabetes mellitus, or HTN. They have been shown to improve symptoms, decrease morbidity, and increase life expectancy. Because they are the only drugs that address all of the pathological mechanisms that produce HF, they are appropriate for all subsets of patients unless these patients have an absolute contraindication. Although no longer the first-line drug for treatment of HF, digoxin is still central to treatment for patients with severe systolic dysfunction. Hydralazine, a peripheral vasodilator (PAD), with concurrent administration of isosorbide dinitrate, has been used to treat HF. The role of diuretics is supplemental and only part of a treatment regimen. The most effective class for this indication is the loop diuretics.

53
Q

Positive inotropic actions

A

increase the contractile forces of the heart
–Cause the ventricles to empty more completely
–Improve cardiac output
•Digoxin, Dobutamine, Dopamine, Epinephrine

53
Q

Negative inotropic actions

A

weaken or decrease the force of myocardial contraction

–Lidocaine, Propanolol

53
Q

Cardiac Glycosides (CG)

A

•Among the oldest known drugs
•Strong and highly selective inhibitors of the Na-K-ATPase system (the sodium pump)
–Result in mild positive inotropic action
•Well absorbed from GI tract
•Wide area of distribution
–Crosses placenta and blood-brain barrier
•Contraindicated in patients with AV blocks and renal impairment
•Side effects – GI, visual disturbances (toxicity)
•Drug interactions
•Patient education
Ex: Digoxin
Antidote: Digibind

NURS615 Pharmacology (16 decks)

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