Antianginals Flashcards

1
Q

3 triggers for angina

A
  1. Physical exertion
    1. Mechanical stress
    2. Increased contractility, pulse rate and BP
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2
Q

What is angina?

A

Pain when the heart becomes anoxic (oxygen deprived)

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3
Q

When does anginal pain occur most often?

A
  • At nighttime - midnight to 8 am.

Clusters of chest pain for months followed by weeks with no symptoms

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4
Q

What things might be a trigger for angina?

A
  • Stress
  • Cold
  • Hyperventilation
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5
Q

Describe Typical (exertional) angina

A
  • Coronary arteries not able to transport enough oxygen to meet myocardium demand
    • Oxygen imbalance causes ischemia
    • Stress, exertion, eating, etc. (block flow of blood)
  • *If demand exceeds available oxygen, then necrosis occurs = myocardial infarction
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6
Q

Describe the amount of alpha and beta receptors in a normal coronary artery

A

When they are normal, mainly beta 2 receptors are present.

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7
Q

Epinephrine acts on what receptor and has what effect?

A
  • Acts on both beta 2 and beta 1.
    • On beta 2, it causes vasodilation ( improves bloodflow to heart)
      • On beta 1, it increases demand of the heart
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8
Q

Individuals with variant angina have what type of receptors in their coronary arteries?

A

They have more alpha 1 receptors than beta 2 receptors = vasoconstriction

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9
Q

What is the effect of having more alpha 1 receptors in coronary arteries than beta 2 receptors?

A
  • Epinephrine usually increases heart rate and cardiac output but with the amount of alpha 1 receptors, also vasoconstricts the coronary arteries, reducing amount of blood delivered to heart.
    - Results in lack of oxygenation due to vasospasm
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10
Q

EKG diagnosis of variant angina consists of what?

A

Elevated S-T segment which is not present in normal angina

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11
Q

What general categories of drugs may be used in treatment of unstable angina?

A
  1. Nitrates
    1. Beta blockers
    2. Calcium channel blockers
    3. Antiplatelet drugs
      1. Antithrombin therapy
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12
Q

Nitrites and Nitrates cause what?

A
  • Relaxation of all smooth muscle
    • Results in arterial and venous vasodilation
      • Drugs work on endothelial cells that produce nitric oxide
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13
Q

What is the biochemical process behind the action of nitrites and nitrates

A

Nitric Oxide activates guanylyl cyclase which converts GTP to cGMP, which then causes dephosphorylation of light chain myosin (2nd messenger system)

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14
Q

4 general effects caused by nitrites and nitrates

A
  1. Produce vasodilation
    1. Decrease venous return to the heart (decrease preload)
    2. Decreased work
      1. Decrease O2 demand
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15
Q

Side effects of Nitrites and Nitrates

A
  1. Vasodilation = intense and fast = causes headache
    1. Weakness, dizziness
    2. Flush
    3. Postural hypotension and syncope = accentuated by alcohol
    4. Reflex sympathetic activity - tachycardia and increased peripheral resistance
      a. Beta blockers are used to keep tachycardia under control
    5. Rash
    6. Nitrates oxidize hemoglobin to methemoglobin
      1. Large doses of nitrites/nitrates for long-term use decreases oxygen-carrying capabilities
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16
Q

What might be the problem arising from nitrates being able to oxidize hemoglobin to methemolgobin?

A

Blood no longer carries oxygen well! Bad for someone who is experiencing angina

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17
Q

Route of administration for nitrites and nitrates

A
  1. Sublingual
    1. Topical
    2. Oral
      1. Transdermal
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18
Q

Describe the onset, duration, and purpose for amyl nitrate

A
  1. Onset
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19
Q

Purpose of Nitroglycerin:

A

Rescue drug = in office emergency kit

20
Q

How is nitroglycerin administered and what is its onset?

A
  • Administered sublingually and absorbs through mucosa

Onset: 1-3 minutes

21
Q

If needed to give in case of emergency, what is the sequence of administration

A

Pill or metered dose spray sublingually = wait 5 minutes; re-administer up to 3 doses, then 911

22
Q

Why is nitroglycerin stored in a small brown vial?

A

It is photosensitive

23
Q

T or F, Nitroglycerin is only offered as a very rapid onset short term situational drug.

A

False, there is also a transdermal patch that has a longer duration (up to 12 hours). Used as part of a long-term therapy

24
Q

Name the long-acting nitrates

A
  1. Isosorbide dinitrate

2. Isosorbide mononitrate

25
Q

Isosorbide dinitrate onset and duration of action

A
  • Onset = 2-10 minutes
    • Sublingual tablet = 1-2 hour duration
      • Oral tablet = 4-6 hours
26
Q

Isosorbide mononitrate onset and duration of tablet

A
  • Onset = 30-60 minutes

- Oral tablet = half life of 4 hours

27
Q

Indications for Beta Blockers:

A

Indicated for all acute coronary syndromes

28
Q

General mode of action for Beta blockers

A
  • Decrease workload of the heart by decreasing cardiac output (afterload) and arterial pressure, which decreases venous return, decreases preload and decreases oxygen demand
  • *Decreased oxygen demand decreases angina
29
Q

T or F, Beta blockers do not cause vasodilation

A

True

30
Q

Patients with what medical history will ALWAYS be taking beta blockers? Why?

A
  • Patients with history of myocardial infarction
    • They have been shown to decrease mortality after MI
      Also, increase chance of surviving second heart attack
31
Q

5 side effects of beta blockers

A
  1. Bradycardia
    1. Contraindicated in some forms of congestive heart failure
    2. Contraindicated for variant angina
      1. Bronchial constriction/Asthma attacks
32
Q

T or F, Beta blockers are contraindicated for variant angina and typical angina

A

False, contraindicated for variant but ok for typical

33
Q

Why are beta blockers contraindicated for variant angina?

A

Patient does not have enough beta receptors in coronary arteries, then if block, vasospasm = more angina

34
Q

Nonselective beta blockers are contraindicated in what patients?

A

Asthmatics

35
Q

Cardioselevtive beta blockers are preferred for what patients?

A
  • Insulin-dependent diabetics

- Asthmatics

36
Q

Beta blockers are often combined with what anti-hypertensive drug?

A

Diuretic to prevent sodium retention

37
Q

Cardioselective effects of beta blockers are achieved at what level of dosage?

A
  • Low doses

Lost at high doses

38
Q

Oral care considerations with beta blockers

A
  1. Non-selective beta blockers enhance the pressor response to epinephrine: hypertension and reflex bradycardia
    1. OK to use epinephrine with cardioselective agents
    2. NSAIDS may reduce effects of beta blockers when used for >3 weeks
      1. No precautions needed with short term NSAID use
39
Q

T or F, Calcium channel blockers have a positive inotropic effect

A

False, Negative inotropic effect

40
Q

Biochemical action of calcium channel blockers

A

Block Ca+ entry into the myocardial cell = less Ca+ inside of the cell maintains troponin’s inhibitory effects by decreasing contraction of the heart

41
Q

Why use a calcium channel blocker in an antianginal scenario?

A
  • Because the heart does not speed up, no pain from angina.
    • Some of these drugs cause smooth muscle relaxation of coronary arteries = vasodilation.
      • Decreases contraction of the heart
42
Q

Which calcium channel blockers decrease force of contraction of myocardium:

A
  1. Verapamil

2. Diltiazem

43
Q

Which calcium channel blockers vasodilate coronary arteries to improve myocardial oxygenation

A

Amlodipine

44
Q

Which calcium channel blockers vasodilate peripheral arteries and veins, decreasing afterload and preload, which reduces the work of the heart?

A
  1. Nifedipine

2. Nicardipine

45
Q

Oral care considerations with antianginals?

A
  1. Limit extend of procedures per visit
    1. Limit epinephrine in local anesthesis to 2 cartidges
    2. Consider local anesthetics without vasoconstrictor
      1. Remember gingival hyperplasia with some calcium channel blockers