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PCM Exam 2 Pharm > Antianginal Drugs > Flashcards

Antianginal Drugs Flashcards

1
Q

What are the risk factors for CAD

A
  • Advanced age (> 55 y for men; > 65 y for women) • Family history of premature cardiovascular disease • Hypertension • Cigarette Smoking
  • Diabetes Mellitus • Dyslipidemia • Kidney disease • Obesity • Physical inactivity
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2
Q

What are the common features in Angina Pectoris?

A
  • Angina pectoris is the principal clinical manifestation of CAD
  • Characterized by pre-cordial pressure-like discomfort resulting from myocardial ischemia
  • Transient episodes that don’t cause cellular death (MI) & last 15 to 15 min)
  • Immediate cause of angina pectoris = imbalance between myocardial O2 supply and demand
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3
Q

What is the Pathophysiology of Angina?

A
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4
Q

Features of Chronic Stable Angina?

A
  • Relative ischemia occurs when oxygen demand increases.
  • Pain is usually associated with a predictable threshold of physical activity
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5
Q

What are the common features of Unstable Angina?

A

Clots often form in response to plaque rupture in atherosclerotic coronary arteries; however can also form because diseased coronary artery endothelium is unable to produce NO and prostacyclin that inhibit platelet aggregation and clot formation

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6
Q

What are the common features of variant Angina?

A
  • Enhanced sympathetic activity (eg, emotional stress) especially when coupled with a dysfunctional coronary vascular endothelium (reduced NO) can precipitate vasospastic angina
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7
Q

What are the treatment rational when treating Angina?

A

• Increase oxygen delivery
• Coronary vasodilators

• Anti-thrombotic drugs

• Decrease oxygen demand

  • Vasodilators (reduce afterload & preload)
  • Cardiac depressants (reduce heart rate & contractility)
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8
Q

What is the Nitrates Mechanism of Action?

A

Nitrates mimic the actions of endogenous NO

Rapid reduction in myocardial O2 demand (systemic vasodilatation) & relief of symptoms

• In CV system, nitrous oxide (NO) is primarily produced by vascular endothelial cells

• NO functions: • vasodilation • anti-thrombotic • anti-inflammatory
(all involve NO-stimulated formation of cGMP)

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9
Q

Nitrates Mechanism of Action MAP?

A
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10
Q

What is the Cardiovascular Action of Nitrates?

A

Systemic Vasculature

• Vasodilation (venous dilation > arterial dilation)

  • Decreased venous pressure
  • Decreased arterial pressure (small effect)

Cardiac

  • Reduced preload & afterload (decreased wall stress)
  • Decreased oxygen demand

Coronary

  • Prevents/reverses vasospasm
  • Vasodilation
  • Improves subendocardial perfusion

• Increased oxygen delivery

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11
Q

Nitrates - Clinical Application?

A
  • IV nitroglycerin = unstable angina & acute heart failure
  • Nitroglycerin (sublingual or spray) = first-line therapy for treatment of acute anginal symptoms
  • Isosorbide mononitrate = orally for prophylaxis (sustained release preps available)
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12
Q

Why use Isosorbide Mononitrate?

A
  • Longer onset of action & duration of action than nitroglycerin (more useful for long-term prophylaxis)
  • Isosorbide mononitrate = >1 h (time to onset of action) & nearly 100 % oral bioavailability
  • Metabolites have longer t1/2’s and significant activity
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13
Q

What are the adverse effects of Nitrates?

A
  • Headache (cerebral vasodilation)
  • High doses = postural hypotension, facial flushing, reflex tachycardia

Contraindications • Sildenafil

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14
Q

Common features of Sodium Nitroprusside?

A
  • Direct NO donor = very effective, immediate vasodilator
  • Clinical Applications • ICU & emergency settings • Used to treat severe hypertensive emergencies &severe heart failure
  • Pharmacokinetics • IV only (t1/2 < 3min) • Continuous infusion is required
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15
Q

Sodium Nitroprusside Adverse effects?

A

• Severe nausea

  • Vomiting
  • Headache etc

• High doses = cyanide intoxification (nitroprusside releases cyanide along with NO)

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16
Q

B-Blockers Mechanism of action?

A
  • Block b1 receptors
  • Reduce both heart rate & contractility
  • O2 demand is reduced during exercise and at rest

• Reduce frequency and severity of angina attacks

Drugs

  • Propranolol = non-selective
  • Metoprolol & atenolol = b1 selective
17
Q

What are the Clinical Application of B-Blockers?

A

• Recommended in all patients (unless contraindicated) with stable angina who have had an ACS or who have left ventricular dysfunction

18
Q

What are the adverse effects of B-Blockers?

A
  • Bradycardia
  • Conduction disturbances
  • Bronchoconstriction
  • Worsening of symptoms of peripheral vascular disease • Fatigue,
  • CNS effects
  • Impotence etc.
19
Q

Contraindications of B-Blockers?

A
  • Variant angina (treated by Ca2+ channel blockers or nitrates)
  • Use with caution in patients with obstructive airway disease or peripheral vascular disease and, initially at very low doses in patients with heart failure
  • NEVER discontinue abruptly (can cause rebound hypertension or angina)
20
Q

What is the mechanism of actin of Ca2+ Channel Blocker?

A
  • Ca2+ is essential for muscular contraction
  • Ca2+ is increased in ischemia due to hypoxia-induced membrane depolarization
  • L-type Ca2+ channel is dominant in cardiac & smooth muscle

Ca2+ channel blockers improve angina symptoms by: • Coronary & peripheral vasodilatation • Reducing contractility

21
Q

WHat is the Clinical Application of Ca2+ Channel Blocker?

A
  • Used in combination with b-blockers when initial treatment with b-blocker is not successful or, as a b- blocker substitute when b-blockers are contraindicated
  • Relieve symptoms of variant angina
22
Q

What is Nifedipine and Amlodipine Mechanism of Action, adverse effects and Class?

A

Ca2+ Channel blocker

  • Minimal effect on cardiac conduction or HR
  • Short-acting dihydropyridines should be avoided unless combined with b-blocker (increased mortality)

Adverse Effects
• Flushing • Headache • Hypotension • Peripheral edema (eg, pedal edema) • Constipation

23
Q

What is Verapamil Mechanism of Action, Adverse effects, contrainidications and Class?

A

Ca2+ Channel Blocker

  • Slows AV conduction directly à HR, contractility, BP & O2 demand
  • Has greater inotropic effects than dihydropyridines (weaker vasodilator)

Adverse Effects- Same as other Ca2+ channel blockers • Constipation

Contraindications: • Preexisting depressed cardiac function or AV conduction abnormalities, • Use with caution in patients taking digoxin (increases digoxin levels)

24
Q

What is Diltiazem Mechanism of Action, Adverse effects, contrainidications and Class?

A

Ca2+ Channel Blocker

• Similar effects to verapamil (slow AV conduction) • HR (lesser extent than verapamil) & BP

Adverse Effects • Same as other Ca2+ channel blockers but incidence is low

Contraindications • Same as verapamil

25
Q

What is Ranolazine Mechanism of Action and Class?

A

Na+ Channel Blocker

  • Blockade of Na+ current that facilitates Ca2+ entry via Na+/Ca2+ exchanger
  • Decreased intracellular Ca2+ reduces ventricular tension & myocardial O2 demand
  • Thought to also produce myocardial relaxation
  • May modify fatty acid oxidation
26
Q

What is the clinical applications, PK, and Adverse effects of Na+ Channel Blocker?

A

• Option for patients who have failed all other antianginal therapies

Pharmacokinetics - Metabolized by CYP 3A4

Adverse Effects - QT interval prolongation (main concern with this new drug), Nausea ,Constipation , Dizziness

27
Q

Stable Angina Treatment?

A

• Acute attacks: promptly relieved by rest or nitroglycerin

  • Maintenance therapy: long-acting nitrates & b- blockers are preferred
  • Ca2+ channel blockers: when b-blockers are not successful or are contraindicated

• Ranolazine: when nitrates, b-blockers & Ca2+-blockers are unsuccessful

28
Q

Unstable Angina Treatment?

A
  • The link between stable angina & MI. Chest pains occur more frequently & precipitated more easily.
  • Symptoms relieved by rest or nitroglycerin
  • In addition, therapy with nitroglycerin & b-blockers should be considered
29
Q

Variant Angina Treatment?

A

Episodic angina due to coronary artery spasm. Unrelated to activity, HR or BP.

Symptoms respond to nitroglycerin & Ca2+ channel blockers

All available Ca2+ channel blockers appear to be equally effective.

• Choice of drug is based on each individual patient

30
Q
A

PCM Exam 2 Pharm (14 decks)

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