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Cardiovascular II Exam 3 > Pharm Anti-Anginal Agents Linger > Flashcards

Pharm Anti-Anginal Agents Linger Flashcards

(55 cards)

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1
Q

4 common β-Adrenergic Antagonists (β-Blockers) from the list

A

Atenolol Metoprolol Propranolol Timolol

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2
Q

Name the 3 Organic Nitrates

A

Nitroglycerin Isosorbide dinitrate Isosorbide mononitrate

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3
Q

Name the 2 sub-classes of Calcium Channel Blockers (CCBs)

A

Dihydropyridines (DHPs) Non-dihydropyridines

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4
Q

Name the Dihydropyridines (DHPs)

A

Amlodipine Felodipine Nicardipine

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5
Q

Name the Non-dihydropyridines

A

Diltiazem Verapamil

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6
Q

What is the primary symptom of ischemic heart disease?

A

Angina Pectoris

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7
Q

What are the types of Angina?

A

Effort angina Variant angina Unstable angina

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8
Q

What is effort angina?

A

Increased myocardial O2 demand (exercise) exceeds coronary flow abilities

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9
Q

What is variant angina?

A

Pain due to coronary artery vaso spasm (Prinzmetal’s angina)

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10
Q

What is unstable angina?

A

Chest pain at rest, typically a progression from effort angina.

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11
Q

Agents that decrease O2 demand

A

ß adrenergic antagonist, Ca entry blockers, organic nitrates,

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12
Q

Agents that increase O2 supply

A

Vasodilators, statins, anti-thrombotics

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13
Q

Nitrates and nitrites MOA

A

metabolized to NO which Increase cGMP

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14
Q

Which Ca blockers are cardio specific

A

Non-DHPs (Verapamil > diltiazem > DHPs)

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15
Q

Non-DHPs physiologic effect

A

decrease rate and contractility in cardiac myocytes

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16
Q

Organic nitrates prototype?

A

nitroglycerin (NTG)

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17
Q

NTG formulation?

A
  1. Sublingual tablet
  2. spray
  3. Sustained release oral capsules
  4. Buccal tablets
  5. gel Ointment
  6. Transdermal patch
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18
Q

NTG preferentially dilates which vessels?

A

Large veins

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19
Q

How does NTG relieve angina?

A

Primary antiischemic effect is to decrease myocardial O2 demand by producing systemic vasodilation (more so than coronary vasodilation)

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20
Q

First-line therapy for an acute anginal attack?

A

NTG typically sublingual administration, spray equally effective

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21
Q

NTG formulations that improve exercise tolerance and time to onset of angina?

A

Long-acting oral and transdermal formulations

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22
Q

NTG improves antianginal and antiischemic effects of?

A

beta blockers and calcium channels blockers

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23
Q

NTG Long-term utility is limited by?

24
Q

NTG tolerance is not a problem with which formulation?

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A

Generally not a problem with sublingual nitroglycerin

25
How to prevent nitrate tolerance?
Intermittent therapy with a nitrate-free interval of at least 8 hours may prevent tolerance
26
Nitrates: Adverse Effects
Common: orthostatic hypotension, syncope, throbbing headache, flushing
27
NTG Drug-drug interaction?
synergistic hypotension with phosphodiesterase type 5 (PDE5) inhibitors (e.g., sildenafil, tadalafil, vardenafil) Think viagra. Can lead to myocardial infarction and death
28
ß blockers list the non-selective
Propranolol Carteolol Nadolol Penbutolol Timolol Pindolol
29
Cardioselective ß blocker
Metoprolol Acebutolol Atenolol Nebivolol Esmolol Bisoprolol Betaxolol
30
Combined alpha beta blockers
Labetalol Carvedilol
31
Beta Blockers: Pharmacodynamics
Reduce cardiac work (i.e., O2 consumption) by decreasing heart rate and contractility Most are not vasodilators; no effect on O2 supply
32
Beta Blocker Use in Angina prototype
Propranolol
33
First-line therapy to reduce frequency of angina (i.e., prophylaxis) and improve exercise tolerance
Propranolol
34
Propranolol Reduce O2 requirement by?
reducing heart rate and contractility
35
ß blocker NOT effective in\_\_\_\_\_ angina.
variant
36
All types of ß blockers are equally effective in _______ angina; _______ often preferred
exertional cardioselective (β1-selective)
37
Beta Blockers that Prolong Survival After MI
**Timolol, propranolol, and metoprolol** have been specifically studied in large-scale clinical trials Use of other beta-blockers for this indication is less compelling
38
Why are ß blockers used in conjunction with ACE inhibitors for Tx of CHF
Combined effect on mortality is increased over using either alone
39
Beta Blockers Adverse Effects?
Most common: bradycardia and fatigue
40
ß blocker Relative contraindications
Asthma/COPD Diabetes Variant angina Acute decompensated heart failure
41
ß blocker Can cause heart block, especially if combined with
other negative inotropes (e.g., verapamil, diltiazem)
42
Calcium Channel Blockers (CCBs) bind to?
L-type Ca++ channels But the two classes bind to different sites, resulting in different effects on vascular versus cardiac tissue. Non-dihydropyridines: Prominent cardiac effects, but also act at vascular tissues **Verapamil \> Diltiazem** Dihydropyridines (DHPs): Predominantly arteriolar vasodilation effects **Amlodipine**, Clevidipine, **Felodipine**, Isradipine, Nicardipine, Nifedipine, Nisoldipine
43
Pharmacokinetic Properties of CCBs
Good oral absorption but high 1st pass effect Amlodipine, felodipine, isradipine slowly absorbed, long t1/2 is advantage **DHPs with long plasma half-lives preferred to minimize reflex cardiac effects; extended release preparations available** Nifedipine, clevidipine, verapamil, and diltiazem sometimes used IV
44
CCBs: Pharmacodynamics
Relaxation of vascular smooth muscle causes peripheral vasodilation Arterioles are more sensitive than veins Reduce afterload and decrease O2 demand Little effect on preload Also increase O2 supply due to dilation of coronaries
45
vasodilator that is most effective on 1. large veins 2. arterioles
1. organic nitrates 2. Ca channel blockers
46
Calcium Channel Blocker Use in Angina
**Preferred agents**: diltiazem, verapamil, amlodopine, or felodipine Added to or substituted for beta blockers in chronic stable angina Also effective in vasospastic angina Reduce O2 requirement by reducing heart rate and contractility Increase O2 delivery by vasodilation and reversal of vasospasm
47
CCBs: Adverse Effects & Toxicity
Generally very well tolerated Excessive vasodilation – dizziness, hypotension, headache, flushing, nausea; diminished by long-acting formulations and long half-life agents Constipation (esp., verapamil), peripheral edema, coughing, wheezing, pulmonary edema Use of verapamil/diltiazem with a β-blocker is contraindicated because of the potential for AV block Verapamil/diltiazem should not be used in patients with ventricular dysfunction, SA or AV nodal conduction defects and systolic BP\< 90 mmHg Short-acting dihydropyridines can cause reflex tachycardia
48
According to board exams constipation is always caused by?
verapamil
49
Relatively newer antianginal drug with a MOA: late sodium channel blocker
Ranolazine Typically reserved for angina that is refractory to treatment with beta blockers, calcium channel blockers, and nitrates Used either in combination with beta blocker or as a substitute in patients who cannot receive beta blockers
50
Angina Preventative Therapies
Regular aerobic exercise Stress reduction Smoking cessation Weight control Blood pressure control Diabetes management Pharmacotherapies to prevent cardiovascular events: Aspirin (or clopidogrel) HMG-CoA reductase inhibitors (the –statins) ACE inhibitors (the –prils) and ARBs (the –sartans)
51
Three primary drug classes that are utilized in angina
beta blockers, calcium channel blockers, & nitrates
52
Nitrates are the mainstay of treatment for ____ symptoms
acute
53
Cardioselective beta blockers are often recommended as?
initial first-line therapy for long-term prophylaxis
54
Anti-anginal Combinations may be
more effective than monotherapy
55
Only CCBs or nitrates can be used to relieve
vasospastic angina by preventing coronary artery spasm

Cardiovascular II Exam 3 (15 decks)

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