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D1 Spring > Pharmacology - Anti-Anginal Drugs (Exam 4) > Flashcards

Pharmacology - Anti-Anginal Drugs (Exam 4) Flashcards

1
Q

Heart-attack like symptoms due to emotional and physical stress; more prone to post-menopausal women

A

Takotsubo cardiomyopathy (broken heart syndrome)

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2
Q

Which part of the heart is affected in Takotsubo cardiomyopathy (broken heart syndrome)?

A

Left ventricle is enlarged

(looks like an octopus pot)

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3
Q

What are the symptoms of Takotsubo cardiomyopathy (broken heart syndrome)? (8)

A

Angina pectoris (sudden severe chest pain)
Shortness of breath
Arrhythmia
Cardiogenic shock
Fainting
Low BP
Heart failure
Nausea

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4
Q

Chest pain

A

Angina pectoris

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5
Q

Usually manifested as severe, transient, retrosternal pain that can radiate to arms, back, or jaw

A

Angina pectoris

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6
Q

What is the cause of angina pectoris?

A

Cardiac ishemia/hypoxia

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7
Q

What is the main culprit of angina pectoris?

A

Atherosclerosis (coronary artery disease)

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8
Q

What are the 4 risk factors of atherosclerosis?

A
  1. High cholesterol
  2. High BP
  3. Diabetes
  4. Genetics
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9
Q

What are the steps leading to angina pectoris? (10)

A
  1. Stress/exertion
  2. Sympathetic discharge
  3. Catecholamine release (epi + norepi)
  4. Vasoconstriction
  5. Increased venous return, preload, HR, & O2 demand
  6. Autoregulation
  7. Coronary artery dilation
  8. Atherosclerosis of coronary artery causes narrowing & fixed blood flow
  9. Cardiac ischemia
  10. Angina pectoris
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10
Q

What are the 4 types of angina pectoris?

A
  1. Stable
  2. Unstable
  3. Variant
  4. Cardiac syndrome X
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11
Q

Which types of angina pectoris are caused by atherosclerosis (coronary artery disease)

A

Stable
Unstable

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12
Q

Which type of angina is described as vasospastic or prinzmetal (abnormal coronary artery spasm)?

A

Variant

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13
Q

Which type of angina is described as microvascular and has signs associated with decreased blood flow to heart tissue, but with normal coronary arteries?

A

Cardiac syndrome X

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14
Q

What type of angina?

Pain during stress and exertion
Predictable and manageable
Stable plaque

A

Stable

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15
Q

What type of angina?

Sudden, irregular, unpredictable (even at rest)
Sudden platelet aggregation or plaque breaking away from an artery wall
Unstable plaque

A

Unstable

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16
Q

Which angina is a “walking time bomb” for myocardial infarction?

A

Unstable

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17
Q

What is an example of non-pharmaceutical management for atheroscleorsis?

A

Stent with balloon angioplasty

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18
Q

What is the balloon coated with for an angioplasty?

A

Drugs to prevent clotting

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19
Q

T/F stent with balloon angioplasty is a transient solution for atherosclerosis

A

True

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20
Q

What type of angina?

Pain at rest, often when sleeping
Caused by vasospasm of coronary artery

A

Variant (aka vasospastic or prinzmetal)

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21
Q

What is the mechanism for drugs for angina pectoris?

A

Increase O2 supply
Increase coronary blood flow
Decrease cardiac workload
Decrease O2 demand

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22
Q

What are the 3 types of drugs used for angina pectoris?

A
  1. Nitrates/nitrites
  2. Ca2+ channel blockers
  3. B blockers
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23
Q

Which drug is a nitrate/nitrite?

A

Nitroglycerin

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24
Q

Nitrates/nitrites are a component of what?

A

Nitric oxide

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25
Q

What does nitric oxide cause at low doses vs high doses?

A

Low doses = vasodilation in veins
High doses = vasodilation in arteries

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26
Q

T/F nitric oxide is a free radical gas

A

True

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27
Q

What was previously known as endothelium-derived relaxation factor?

A

Nitric oxide

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28
Q

What happens when nitric oxide dilates arteries at high doses?

A

Increase coronary blood flow
Increase O2 supply

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29
Q

What happens when nitric oxide dilates veins at low doses?

A

Decrease venous tone, preload, CO, O2 demand

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30
Q

T/F nitric oxide (NO) is the same as nitrous oxide (N2O)

A

FALSE, they are NOT the same

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31
Q

Explain how nitrates cause relaxation (5 steps)

A
  1. Nitrate enters SM cell and becomes NO
  2. NO causes guanylyl cyclase + GTP to become cGMP
  3. MLC phosphatase is activated
  4. Increase in myosin LC
  5. Relaxation
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32
Q

What breaks down cGMP to GMP in the SM cell to cause contraction?

A

PDE (phosphodiesterase)

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33
Q

What can inhibit PDE to prevent the break down of cGMP to GMP in the SM cell (prevents contraction)?

A

Sildenafil (PDE-5 inhibitor)

(aka Viagra)

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34
Q

Which drug is used for acute episodes of angina pectoris?

A

Nitroglycerin

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35
Q

Which drug is administered via sublingual tablets, has a rapid onset of 1-3 mins, and a duration of 30-60 mins?

A

Nitroglycerin

36
Q

What is another form of Nitroglycerin administration?

A

Skin patch (for slow, continuous release)

37
Q

T/F Nitroglycerin is unsuitable for long-term prophylaxis

38
Q

T/F Nitroglycerin is metabolized via first-pass

39
Q

Which drug must be kept in emergency kits in dental offices?

A

Nitroglycerin

40
Q

Which drug is a NO donor?

A

Isosorbide dinitrate

41
Q

Isosorbide dinitrate comes in _____________ formulations

A

long-acting

42
Q

What is a problematic side effect of isosorbide dinitrate?

43
Q

What is the mechanism of isosorbide dinitrate?

A

NO decreases platelet aggregation/adhesion in acute myocardial infarction

44
Q

What are adverse effects of nitrates and nitrites?

A

Headache
Tolerance
Hypotension (reflex tachycardia)
Cerebral ischemia
Syncope (when standing still or w/ alcohol)

45
Q

Which nitrate/nitrite drug is contraindicated for use in pregnant women?

A

Amyl nitrite

(“my pregnant friend Amy can’t take Amyl nitrite”)

46
Q

What does amyl nitrite cause in pregnant women?

A

Dramatic decrease in placental blood flow

47
Q

What is a drug cannot be taken with nitrates and nitrites?

A

PDE-5 inhibitors (ex: Slidenafil/Viagra)

48
Q

What can happen if you combine nitrates/nitrites and PDE-5 inhibitors?

A

Excessive hypotension

49
Q

What do CCBs block?

A

L-type channels

50
Q

What do CCBs cause in vascular SM?

A

Relaxation and vasodilation

51
Q

What is a treatment for stable angina?

52
Q

Which drug is effective in preventing coronary vasospasm?

53
Q

What are the 2 types of CCBs? What are they used for?

A

Non-dihydropyridine (arrhythmias, cardiac effects)
Dihydropyridine (vasodilate arteries)

54
Q

What drugs are non-dihydropyridine CCBs?

A

Verapamil
Diltiazem

55
Q

What drugs are dihydropyridine CCBs?

A

“-dipines”

56
Q

What CCB is used to treat angina pectoris?

A

Dihydropyridines

57
Q

What CCB is used to treat arrhythmias?

A

Non-dihydropyridines

58
Q

What happens when Ca2+ goes through a Ca2+ channel? (5 steps)

A
  1. Ca2+ enters cell
  2. Binds to calmodulin
  3. Ca2+-calmodulin complex activates MLC kinase
  4. Increase in myosin LC PO4
  5. Contraction
59
Q

What kind of muscle gets Ca2+ externally?

A

Smooth muscle (internal organs)

60
Q

What kind of muscle gets Ca2+ internally (from sarcoplasmic reticulum)?

A

Cardiac muscle
Skeletal muscle

61
Q

What kind of muscle do CCBs block?

A

Smooth muscle

62
Q

CCBs _________ coronary blood flow, myocardial perfusion, and O2 supply; CCBs ___________ myocardial O2 demand

A

increase; decrease

63
Q

What is the mechanism of non-dihydropyridine CCBs?

A

Decrease contractility, HR, CO, & O2 demand
Increase diastolic relaxation of LV

64
Q

What is an adverse effect of the CCB phenytoin? (ON EXAM)

A

Gingival hypertrophy

65
Q

What do B blockers inhibit?

A

Sympathetic discharge and catecholamine release

66
Q

What is the effect of B blockers?

A

Decrease contractility, HR, CO, & O2 demand

67
Q

What do B blockers provide protection from?

A

Reflex tachycardia

68
Q

What are the clinical uses of B blockers?

A

Angina pectoris
Prevent future myocardial infarctions

69
Q

Which anti-anginal drugs are usually used together?

A

Nitrates + B blockers

(nitrates cause reflex tachycardia, B blockers inhibit reflex tachycardia)

70
Q

What are the adverse effects of B blockers?

A
  1. Bronchoconstriction at high doses
  2. Decreases glucose in liver (risk of hypoglycemia)
  3. Myocardial depression/heart failure
  4. Chronic B blockade (B receptor super-sensitivity; slow withdrawal required
  5. CNS effects (depression, weakness, sleep disturbances, dizziness)
  6. Fatigue (from both cardiovascular and CNS effects)
71
Q

What are the contraindications of B blockers?

A

Asthma
COPD
Variant angina

72
Q

Why can’t B blockers be used in variant angina?

A

Can cause vasoconstriction

73
Q

What is the opposing effect of high and low doses of epinephrine on vascular SM?

A

High dose: acts on a1 - vasoconstriction
Low dose: acts on B2 - vasodilation

74
Q

What happens when epinephrine is given at a low dose and the pt is on a B blocker?

A

Vasodilation is inhibited

75
Q

B blockers do NOT mix with what other anti-anginal drug?

A

Non-dihydropyridine CCBs

76
Q

Why can’t you mix B blockers and non-dihydropyridine CCBs?

A

They both decrease HR and contractility

77
Q

What can happen if you mix B blockers and non-dihydropyridine CCBs?

A

Intolerable dizziness
Increased risk of cardiovascular outcomes

78
Q

Which drug is shown to increase the risk of stroke in elderly patients?

A

B blockers

79
Q

T/F B blockers were removed from list of drugs of choice to treat hypertension in 2014

80
Q

What are 2 second-line drugs to treat angina?

A
  1. Statins
  2. Anticoagulants
81
Q

Which drug is an HMG-CoA reductase inhibitor used to prevent further progression of atherosclerosis?

82
Q

Which drug is used to prevent blood clot formation in the coronary artery?

A

Anticoagulants

83
Q

How often does nitroglycerin have to be replaced?

A

Every 3 months

84
Q

Which patients cannot have nitroglycerin?

A

Those who have had PDE-5 inhibitors in the last 24 hours

85
Q

What must you watch out for in the dental office when treating patients with cardiovascular disease?

A

Local anesthetics w/ epi
Retraction cords w/ epi

D1 Spring (47 decks)

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