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Pharm 2 Exam SHEA > Angina COPY > Flashcards

Angina COPY Flashcards

1
Q

Definition of what:

an imbalance b/w the oxygen requirement of the heart and the oxygen supplied to it via the coronary vessels

A

Angina Pectoris

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2
Q

Definition of what?

–Inadequate blood flow in the presence of CAD (coronary artery disease)

A

Stable angina (effort; classic)

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3
Q

Definition of what?

–Transient spasm of localized portions of these vessels resulting in significant myocardial ischemia and pain

A

Variant angina (vasospastic; Prinzmetal)

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4
Q

Definition of what?

–Present when episodes of angina occur at rest and when there is an increase in the severity, frequency, and duration of chest pain in patients with previously stable angina.

A

Unstable angina (acute coronary syndrome)

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5
Q

The following is presentation of what?

  • Substernal CP on exertion
  • Pain described as: “squeezing, heaviness, tightness”
  • Radiation to L or R arm, back, down into abdomen or into the neck
  • 5+/10 on pain scale
  • Timing: pain last less than 20 min and usually relieved by rest w/ or w/o sublingual nitro in 5-10 min
A

Stable ischemic heart disease

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6
Q

Which grading of Angina Pectoris according to the Canadian Cardiovascular Society Classification System?

  • Ordinary physical activity does not cause angina such as walking and climbing stairs.
  • Angina occurs with strenuous, rapid, or prolonged exertion at work or recreation
A

Class I

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7
Q

Which grading of Angina Pectoris according to the Canadian Cardiovascular Society Classification System?

  • Slight limitation or ordinary activity.
  • Angina occurs:
    • on walking or climbing stairs rapidly, on walking uphill, on walking after meals,
    • in cold, in wind, under emotional stress
    • only during the few hours after wakening.
    • Walking >2 blocks and climbing >1 flight of stairs
A

Class II

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8
Q

Which grading of Angina Pectoris according to the Canadian Cardiovascular Society Classification System?

  • Marked limitations of ordinary physical activity.
  • Angina when walking 1-2 blocks and climbing one flight of stairs
A

Class III

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9
Q

Which grading of Angina Pectoris according to the Canadian Cardiovascular Society Classification System?

  • Inability to carry on any physical activity without discomfort
  • anginal symptoms may be present at rest
A

Class IV

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10
Q

Which 3 main groups of medications are used in Angina Pectoris?

A

Nitrates, BBs and CCBs

  1. Nitrates
    1. Nitroglycerin
    2. Isosorbide dinitrate
    3. Isosorbide mononitrate
  2. B Blockers
    1. Propanolol
    2. Metoprolol
  3. CCBs
    1. Verapamil
    2. diltiazem
    3. Nifedipine
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11
Q

What 2 Beta Blockers are used in Angina Pectoris

A
  1. Metoprolol
  2. Propanolol
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12
Q

What 3 CCBs are used to treat Angina?

A

1. Verapamil

2. diltiazem

  1. Nifedipine
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13
Q

T/F: Ranolazine can be used to treat Agina?

A

True

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14
Q

MOA of which group of meds?

  • **Release nitric oxide in sm. muscle–> activates guanylyl cyclase–> increases cGMP**
  • cGMP promotes formation of Myosin-LC–> results in vascular smooth mm. relaxation
A

Nitrates (Nitroglycerin)

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15
Q

*What are 3 toxicities of Nitroglycerin?*

A
  1. *Orthostatic hypotension
  2. *tachycardia
  3. *HA
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16
Q

What are the 4 effects of Nitrates (Nitroglycerin) in Angina?

A
  1. **Smooth muscle relaxation, especially in vessels
  2. other smooth muscle is relaxed but not as markedly
  3. **vasodilation decreases venous return and heart size
  4. may increase coronary flow in some areas and in variant angina
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17
Q

What are the 3 clinical applications of Nitroglycerin

A
  1. Prophylaxis (oral and transdermal)
  2. Acute Coronary Syndrome (IV)
  3. Angina (sublingual for acute episodes)
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18
Q

**Which med has a high first-pass effect, so sublingual dose is much smaller than oral**

A

Nitroglycerin

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19
Q

Nitroglycerin has the following interaction:

**Synergistic hypotension with _________

A

**phosphodiesterase type 5 inhibitors (sildenafil, etc)

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20
Q

What subclass of nitrates is considered long-acting and which are considered ultrashort-acting nitrate (hint: this one is a street drug now)

A

Long acting: Transdermal nitroglycerin

Ultrashort-acting nitrate: Amyl nitrite (obsolete for angina, some recreational use)

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21
Q

What is the clinical application of transdermal nitroglycerin, a long-acting nitrate?

A

**Prophylaxis of angina**

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22
Q

Pharmacokinetics of which med?

Slow onset

  • long duration of absorption: 24 h
  • duration of effect: 10 h (tachyphylaxis)
A

Transdermal nitroglycerin

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23
Q

Which med is it common to have a loss of response after 10-12h exposure to the drug?*

A

Transdermal nitroglycerin, a long acting nitrate

24
Q

What are the results of the follwing potential beneficial effects of nitrates in the tx of angina:

  1. Decreased ventricular volume
  2. Decreased arterial pressure
  3. Decreased ejection time
A

**Decreased myocardial oxygen requirement**

25
Q

What are the results of the follwing potential beneficial effects of nitrates in the tx of angina:

Vasodilation of epicardial coronary arteries

A

**Relief of coronary artery spasm**

26
Q

What are the results of the follwing potential beneficial effects of nitrates in the tx of angina:

Increased collateral flow

A

**Improved perfusion to ischemic myocardium**

27
Q

What are the results of the follwing potential beneficial effects of nitrates in the tx of angina:

Decreased LV diastolic pressure

A

**Improved subendocardial perfusion**

28
Q

What are 3 potential deleterious effects of nitrates in the treatment of angina?

A

1. *Reflex tachycardia

2. *Reflex increase in contractility

3. *Decreased diastolic perfusion time due to tachycardia

29
Q

What are the results of the follwing deleterious effects of Nitrates in the tx of angina?

1. Reflex tachycardia

2. Reflex increase in contractility

3. Decreased diastolic perfusion time due to tachycardia

A
  1. Reflex tachycardia= increased myocardial O2 req.
  2. Reflex increase in contractility= increased myocardial O2 req.
  3. Decreased diastolic perfusion time due to tachycardia= decreased coronary perfusion
30
Q

What is the MOA of beta blockers

A

β-blockers produce a moderate reduction in BP through competitive inhibition of β1-receptors found in the kidney, leading to a reduction in renin release

31
Q

How do beta blockers impact all of the major contributing factors of MVO2?

A

•Reducing HR, myocardial contractility, and intramyocardial wall tension (through BP reduction)

32
Q

β1-selective agents are preferred in patients with angina and what 5 things?

A
  1. COPD
  2. Peripheral arterial disease
  3. DM
  4. Dyslipidemias
  5. Sexual dysfunction
33
Q

What is the main MOA of Propanolol and Metoprolol?

A

**Blocks sympathetic effects on heart and blood pressure**

Also reduces renin release

34
Q

What is the effect of Propanolol and Metoprolol? (4 things)

A
  1. decreased HR, CO and BP
  2. **Decreases myocardial oxygen demand**
35
Q

What is the clinical application of beta blockers (propanolol and metoprolol) in the tx of angina?

A

**Prophylaxis of angina**

36
Q

What are the 4 toxicities of Beta blockers (propanolol and metoprolol)

A
  1. Asthma
  2. AV block
  3. acute heart failure
  4. sedation
37
Q

What interaction is important to know about when considering giving a patient Propanolol or metoprolol (beta blockers) in the prophylactic tx of angina

A

Additive w/ all cardiac depressents

38
Q

MOA of which two meds?

Nonselective block of L-type calcium channels in vessels and heart

A

CCBs- Verapamil and diltiazem

39
Q

What are the 3 effects of CCBs (Verapamil and diltiazem) and what do these result in?

A
  1. Reduced vascular resistance
  2. reduced cardiac rate
  3. reduced cardiac force

All of these results in decreased oxygen demand

40
Q

T/F: clinical applications of CCBs (verapamil, diltizaem) include prophylaxis of angina, HTN and others

A

True

41
Q

What are the 4 toxicities of the CCBs- verapamil and diltiazem?

A
  1. Atrioventricular block
  2. acute heart failure
  3. constipation
  4. edema
42
Q

What interaction is important to know about when considering giving a patient verapamil or diltiazem (CCBs)

A

Additive with other cardiac depressants and hypotensive drugs

43
Q

MOA of which 2 CCBs?

**Block of vascular L-type calcium channels > cardiac channels**

A

Nifedipine

Amlodipine

(dihydropyridine)

44
Q

T/F: the effects of Nifedipine and Amlodipine (CCBs) are like verapamil and diltiazem but they have MORE cardiac effect

A

FALSE

Nifedipine and Amlodipine have less cardiac effect

45
Q

What are the two clinical applications of Nifedipine and Amlodipine?

A
  1. **Prophylaxis of angina**
  2. HTN
46
Q

What are 2 toxicities of Nifedipine and Amlodipine (CCBs)?

A
  1. Excessive hypotension
  2. baroreceptor reflex tachycardia
47
Q

What is an important interaction to keep in mind when prescribing Nifedipine or Amlodipine (CCBs)?

A

Additive w/ other vasodilators

48
Q

What are the effects (decrease or increase) of nitrates alone on the follwing:

  1. HR
  2. Arterial presure
  3. end-diastolic pressure
  4. contractility
  5. Ejection time
  6. Net myocardial oxygen req.
A
  1. HR- reflex increase
  2. Arterial presure- Decrease
  3. end-diastolic pressure- Decrease
  4. contractility- reflex increase
  5. Ejection time- reflex decrease
  6. Net myocardial oxygen req.- decrease
49
Q

What are the effects (decrease or increase) of BBs or CCBs alone on the follwing:

  1. HR
  2. Arterial presure
  3. end-diastolic pressure
  4. contractility
  5. Ejection time
  6. Net myocardial oxygen req.
A
  1. HR- Decrease
  2. Arterial presure- decrease
  3. end-diastolic pressure- increase
  4. contractility- decrease
  5. Ejection time- increase
  6. Net myocardial oxygen req.- decrease
50
Q

What are the effects (decrease or increase) of combined nitrates and BBs or CCBs on the follwing:

  1. HR
  2. Arterial presure
  3. end-diastolic pressure
  4. contractility
  5. Ejection time
  6. Net myocardial oxygen req.
A
  1. HR- Decrease
  2. Arterial presure- decrease
  3. end-diastolic pressure- decrease
  4. contractility- no effect or decrease
  5. Ejection time- no effect
  6. Net myocardial oxygen req.- decrease
51
Q

Which med

  1. Little affinity for α1, β1, or β2 adrenoreceptors
  2. Minimal calcium channel blocking activity
    • no clinical significance
  3. Doesn’t provide benefit by impacting hemodynamics of HR, BP, the inotropic state, or increased coronary blood flow
A

Ranolazine (sodium channel blocker)

52
Q

How does Ranolazine reduce ischemic episodes?

A

by selective inhibition of late sodium current (INa)

53
Q

What is the MOA of Ranolazine?

A

**Inhibits the late sodium current in the heart**

also may modify fatty acid oxidation

54
Q

Effects of which med?

  1. **Reduces cardiac oxygen demand**
  2. fatty acid oxidation modification may improve efficiency of cardiac oxygen utilization
A

Ranolazine (sodium channel blocker)

55
Q

What is the 4 side effects of Ranolazine?

A
  1. **QT prolongation**
  2. Nausea
  3. constipation
  4. dizziness
56
Q

Interaction of Ranolazine (sodium channel blocker)

Inhibitors of ______ increase ranolazine concentration and duration of action

A

Inhibitors of CYP3A

Pharm 2 Exam SHEA (15 decks)

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