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Pharmacology > Antianginals > Flashcards

Antianginals Flashcards

1
Q

What are three examples of drugs that are metabolized into nitric oxide?

A

Amyl nitrite
Nitroglycerin
Isosorbide dinitrate

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2
Q

What is sildenafil?

A

A type 5 phosphodiesterase inhibitor

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3
Q

What are nifedipine, amlodipine and felodipine?

A

Dihydropyridine calcium channel blockers

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4
Q

What are verapamil and diltiazem?

A

Non-dihydropyridine calcium channel blockers

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5
Q

What is propranolol?

A

Beta adrenergic receptor antagonist

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6
Q

What is metoproplol?

A

Beta1 adrenergic receptor antagonist

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7
Q

What causes angina (when does angina occur)?

A

When oxygen demand exceeds oxygen supply

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8
Q

What are the three types of angina?

A

Stable (angina of effort)
Unstable
Vasospastic (Variant; Prinzmetal’s)

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9
Q

Describe stable angina

A

It is the most common (atherosclerosis with cap)
A fixed narrowing of the coronary artery (partial occlusion to flow)
Onset is associated with a given level of activity (it’s predictable)

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10
Q

Describe unstable angina

A

Onset is at rest or increased physical activity (not predictable)
Related to coronary arteriosclerotic plaque rupture (emboli) - dislodged clots lodge in the coronary blood vessels
Could also be due to platelet accumulation and breaking off of a thrombus

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11
Q

Describe vasospastic angina

A

Occurs at anytime

Spasms of the coronary artery

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12
Q

How is angina treated?

A 
Increase the oxygen supply
and/or
Decrease the oxygen demand
Modify/treat risk factors
Pharmacological treatment
Surgical intervention
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13
Q

What can increase oxygen supply?

A 
pO2 and hemoglobin concentration (can't really change)
Oxygen extraction (can't really change)
Coronary blood flow (site for pharmacological intervention)
Micro-circulation (site for pharmacological intervention)
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14
Q

What can decrease oxygen demand?

A 
Heart rate (site for pharmacological intervention)
Ventricular wall stress (intraventricular pressure, ventricular wall radius, wall thickness; site for pharmacological intervention)
Contractile state (site for pharmacological intervention)
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15
Q

What risk factors should we modify/treat to treat angina?

A

Smoking, dyslipidemias, diabetes, hypertension, sedentary, obesity, stress
Family history is important (but unable to modify)

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16
Q

What are pharmacological treatment options for angina?

A

Nitrates/nitrites
Beta adrenergic receptor blockers
Calcium channel blockers
Aspirin

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17
Q

What are surgical intervention options for angina?

A

Angioplasty

Revascularization

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18
Q

How is nitroglycerin used in angina?

A

Acutely (when there is pain) - sublingual, lingual spray (rapid onset 2-5 minutes, duration 15-30 minutes)
Prophylactically (to prevent pain with exercise). There is a patch (onset 30 min, duration 8-14 hours) or oral (long acting, duration 6-8 hours)

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19
Q

How is isosorbide dinitrate used in angina?

A

Prophylactically (prevent pain with exercise)
Sublingual - onset 2-5 minutes, duration 1.5-2 hours
Oral - onset 15-30 minutes, duration 3-6 hours

20
Q

Describe the mechanism of nitrates

A

They are metabolized into nitric oxide (mainly in the veins)
Nitric oxide increases cGMP which mediates dilation (important to avoid giving drugs that block cGMP breakdown, such as sildenafil aka Viagra)
Nitrates can relax veins (at low doses) and larger arteries (at higher doses). They decrease preload (venous return) which decrease heart rate (which decreases wall stress) and may redistribute blood to ischemic areas. They decrease pulmonary artery resistance which is useful in pulmonary hypertension seen in COPD

21
Q

How do nitrates affect the endocardium?

A

When the heart constricts, the pressure inside is going to squeeze on the endocardium and that tissue is not getting much blood flow. If the heart isn’t constricting as hard, it helps blood flow not drop for as long of time

22
Q

How do nitrates prevent coronary steal?

A

Smaller arterioles and pre capillary sphincters are less affected by nitrates (good thing). This prevents blood flow to ‘healthy’ regions. The arterial vessels that are effected then to be larger and this increases blood flow to healthy and ischemic regions

23
Q

How does hydralazine affect angina?

A

Some vasodilators may worsen angina (including hydralazine)

24
Q

Why do nitrates need to be taken in 12 hour treatment intervals?

A

Because tolerance develops

25
Q

What are the adverse effects of nitrates?

A 
Orthostasis
Throbbing headache
Reflex activation of SNS
Salt and water retention
High doses may decrease BP and increase sympathetic nerve activity (results in increased oxygen demand and decrease perfusion pressure may be problematic)
26
Q

How should nitrates be used?

A

Sublingual nitrates should be use for acute episodes of angina
Contact a physician if the pain persists or worsens 5 minutes after one tablet

27
Q

How do Asians responsd to nitrates?

A

30 -50% of Asians may be poor responders due to decreased mitochondrial aldehyde dehydrogenase (ALDH2) which is needed to convert nitrate to nitric oxide
ALDH2 is also needed to breakdown aldehyde associated with alcohol metabolism (a flush response to alcohol suggests a lack of ALDH2)

28
Q

What are propranolol and metoprolol? What are they used for?

A

Beta adrenergic receptor blockers
First line treatment in chronic stable angina (not for acute angina attacks)
They are recommended as initial treatment in relief of angina symptoms in stable ischemic heart disease

29
Q

Describe the mechanism of beta blockers

A

They decrease oxygen demand (decreased heart rate, blood pressure and contractility)
May produce reverse steal (increase flow to ischemic regions)

30
Q

What are the benefits of beta blockers?

A

Improved survival (important)
Following an MI, it’s the only antianginal proven to decrease incidence of reinfarction and improve patient survival (if there is no previous MI, they are as good as CCBs and nitrates but prophylactic use to prevent the first MI appears to be ineffective)
They are also a benefit in systolic heart failure

31
Q

What are the adverse effects of beta blockers?

A

Slowing of the heart, increased EDV, increased oxygen demand (may use with nitrates to decrease preload and EDV)
Not for vasospastic angina because you want to relax the vessels (may worsen if beta2 is blocked)

32
Q

What do dihydropyridines do?

A

They decrease afterload (peripheral resistance) and may also decrease coronary vascular tone (arterial vessels are more sensitive than veins)
They may cause reflex SNS in cardiac beta receptor activity
They decrease coronary artery spasm (good for Primzmetal angina)
They do not change “double product” value where angina is felt
They work by decreasing oxygen demand
The arterial vessels are more sensitive than vein; little cardiac suppression

33
Q

What are verapamil and diltiazem?

A

Non-dihydropyridines

34
Q

What does verapamil do?

A

Decreases oxygen demand (negative inotrope, chronotrope and lowers blood pressure)
Poor vascular dilator

35
Q

What does diltiazem do?

A

Decreases oxygen demand (negative inotrope, negative chronotrope and lowers blood pressure)
Effective coronary arterial dilator (less peripheral)

36
Q

What are the benefits of calcium channel blockers?

A

They decrease symptoms, increase exercise tolerance/time
If beta blocker is ineffective or contraindicated, we can substitute a CCB or combine with a CCB
They are effective for vasospastic angina (dihydropyridines are preferred)

37
Q

What are the adverse effects of CCBs?

A

Serious cardiac suppression (verapamil and beta blocker can cause possible heart block)
Constipation, ankle oedema
Sympathetic reflexes (nifedipine vs verapamil)
Dizziness, hypotension, headache, flushing

38
Q

What is angina of effort? What should be done about it?

A

Stable angina
Patients should be on aspirin or clopidogrel
Nitrates and beta-adrenergic receptor blockers are initial treatment (or CCB is there is problems with these two)

39
Q

How should unstable angina be treated?

A

With anti platelet therapy (aspirin, clopidogrel, IV heparin)
Oxygen
Nitroglycerin sublingual, or give IV if pain persists after three tablets
Morphine, IV for pain and anxiety
Oral beta-adrenergic receptor blockers IV
Statins
Beta-adrenergic receptor blockers decrease ischemic episodes but not mortality

40
Q

What should be taken for vasospastic angina?

A

CCBs (vascular) and/or nitrates

41
Q

What should be avoided with vasospastic angina?

A

Beta-adrenergic receptors blockers may worsen the condition (beta1 selective blockers may be okay)
Aspirin decreases prostacyclin which is a vasodilator
Sumatriptan is used in migraines and may constrict coronary arteries

42
Q

If someone has concomitant asthma, what is the preferred drug and what is the least preferred?

A

Preferred: CCBs, nitrates

Least preferred: beta blockers

43
Q

If someone has concomitant diabetes mellitus, what is the preferred drug and what is the least preferred?

A

Preferred: CCBs, nitrates

Least preferred: beta blockers

44
Q

If someone has concomitant heart failure, what is the preferred drug and what is the least preferred?

A

Preferred: nitrates, beta blocker

Least preferred: Non-dihydropyridines

45
Q

If someone has concomitant hypertension, what is the preferred drug and what is the least preferred?

A

Preferred: beta blockers, CCBs

Least preferred: nitrates

46
Q

If someone has concomitant peptic ulcer, what is the preferred drug and what is the least preferred?

A

Preferred: beta blockers, nitrates

Least preferred: CCBs

Pharmacology (15 decks)

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