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Pharm II Exam 3 > Chronic CHD and Chronic Stable Angina > Flashcards

Chronic CHD and Chronic Stable Angina Flashcards

1
Q

What is coronary heart disease (CHD)?

A

General term that describes various phases a patient may cycle in-between for several decades:
-Asymptomatic disease
-Stable angina
-Unstable angina
-NSTEMI and STEMI

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2
Q

Which phases are considered “ACS”?

A

Unstable angina, NSTEMI and STEMI

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3
Q

What is chronic stable angina?

A

A patient w/ predictable angina symptoms during exertion

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4
Q

Is atherosclerosis an inflammatory disease?

A

Yes

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5
Q

What is atherosclerosis?

A

Over time, plaque builds up on the endothelial lining of a BV, triggering an inflammatory response leading to enlargement and increased endothelial injury over time

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6
Q

???? Atherosclerosis pics

A
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7
Q

What are chronic stable angina (CSA) symptoms associated with?

A

Myocardial ischemia, supply and demand mismatch for oxygen

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8
Q

Are chronic stable angina (CSA) symptoms present at rest?

A

No, predictable EXERTIONAL angina

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9
Q

What is the O2 mismatch in CSA?

A

O2 delivery does not meet aerobic O2 demands

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10
Q

Presence of occlusion in CSA may be due to?

A

Lipid-rich plaques, thrombus, vasospasm

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11
Q

Myocardial ischemia in CSA will lead to…?

A

Buildup of metabolites (lactate, AMP), metabolic changes, remodeling

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12
Q

What can meds for CSA prevent?

A

Hypertrophy, remodeling and progression from CSA to ACS by increasing O2 delivery

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13
Q

Oxygen consumption is mainly driven by what factors?

A

Heart rate, ventricular contractility (force of contraction), afterload (systolic wall tension, vascular resistance)

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14
Q

What does the body release to compensate for O2 demand/delivery mismatch?

A

Releases NE (increases ventricular contraction, HR, & afterload)

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15
Q

What medication can be used to counteract the increased contraction, HR, and afterload in response to body releasing NE?

A

Beta Blockers

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16
Q

When does blood fill the coronary arteries?

A

During diastole

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17
Q

What can be used to increase coronary blood flow?

A

Nitroglycerin (vasodilation), and BB or CCB (dec. HR)

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18
Q

What causes myocardial ischemia?

A

Inadequate oxygen supply plus increased oxygen demand that results in predictive anginal pain

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19
Q

Common manifestations of CSA?

A

Anginal pain or discomfort on presentation, ST-segment changes on ECG, reduced LV function on echo

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20
Q

Medical management of CSA?

A

Medical therapy and lifestyle modification

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21
Q

Diet/lifestyle changes for CSA?

A

-DASH Mediterranean diet
-Fasting: can help w/ fluctuating blood sugar in DM
*Physical activity, goal setting

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22
Q

Meds for control of HTN in CSA?

A

ACEi/ARBs, BBs, BP control

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23
Q

Meds for dyslipidemia in CSA?

A

Diet, activity, statins

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24
Q

Other medications for CSA?

A

Antiplatelet therapy, diabetes management, tx to target doses/parameters

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25
Q

What is important to check in CSA follow up?

A

A1C & LDL in 3 months

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26
Q

The “A” of CSA management?

A

Aspirin, ACEi’s, anti-anginals

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27
Q

The “B” of CSA management?

A

Beta blockers, BP control (140/90 mmHg or lower)

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28
Q

The “C” of CSA management?

A

Cholesterol and cigarettes
*High intensity statins (atorvastatin and rosuvastatin)

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29
Q

The “D” of CSA management?

A

Diet, diabetes management, depression

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30
Q

The “E” of CSA management?

A

Exercise: calorie targets, physical activity
(800 kcal/wk vs. 2400 kcal/wk vs. 3000 kcal/wk)

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31
Q

Relative risk reduction of Aspirin in post-MI?

A

25%

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32
Q

Relative risk reduction of B-Blockers in post-MI?

A

25%

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33
Q

Relative risk reduction of ACEi’s in post-MI?

A

25%

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34
Q

Relative risk reduction of lipid lowering agents in post-MI?

A

30%

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35
Q

5 year CV-event recurrence risk percentage if no medical therapy post-MI?

A

20%

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36
Q

5 year CV-event recurrence risk percentage if on only aspirin post-MI?

A

15%

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37
Q

5 year CV-event recurrence risk percentage if on aspirin + BB post-MI?

A

11.3%

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38
Q

5 year CV-event recurrence risk percentage if on Aspirin + BB + ACEi post-MI?

A

8.4%

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39
Q

5 year of CV-event recurrence risk percentage if on Aspirin + BB + ACEi + lipid lowering agent post-MI?

A

5.9%

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40
Q

Cumulative risk reduction if ASA + BB + ACEi + Lipid lowering are used?

A

~70%

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41
Q

Number needed to treat (NNT) to prevent 1 major CV event in 5 years?

A

7 (7 people treated will result in reduction of 1 bad outcome, measures effectiveness of therapy post-MI)

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42
Q

What is the role of platelets in atherothrombosis?

A
  1. Activation by collagen/thrombin after vascular injury
  2. Adhesion (to wall)
  3. Aggregation (platelets stick together, build)
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43
Q

What is the preferred anti-anginal agent (when tolerated)?

A

Beta blockers (Metoprolol, Bisoprolol, Carvedilol, Atenolol)
*best data for reducing CV events

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44
Q

Which beta-blocker acts on both B1 and a1 receptors?

A

Carvedilol

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45
Q

What can be used as an alternative for Beta blockers?

A

Calcium channel blockers (CCBs)

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46
Q

Some CCBs can be used with BBs for what purpose?

A

Vasodilation

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47
Q

Which CCBs can be used with BBs?

A

Dihydropyridines: Amlodipine, Felodipine, Nifedipine

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48
Q

Which CCBs are not commonly used with BB due to the risk of bradycardia?

A

Non-dihydropyridines: Verapamil, Diltiazem

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49
Q

Which nitrate is used as an anti-anginal?

A

Nitroglycerin (in short and longer acting forms)

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50
Q

Does nitroglycerin have any outcome effect, or just symptom relief?

A

Only for symptoms, no outcome data

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51
Q

What form of nitroglycerin is short-acting?

A

Sublingual

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52
Q

What form of nitroglycerin is long-acting?

A

Oral (can be controlled or immediate release)

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53
Q

Outcome benefits of beta blocker treatment are derived from what?

A

Lowering myocardial oxygen demand

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54
Q

Effects of BBs in CSA?

A

Reduced ischemic time, decreased HR, decreased BP/workload, decreased contractility

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55
Q

How does slower HR (from BBs) improve outcome of CSA?

A

Improves venous perfusion and ventricular filling

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56
Q

What reflects BBs use (before vs. after differences)?

A

EKGs

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57
Q

Caution using BBs in patients with what condition?

A

Pulmonary disease

58
Q

What can sudden d/c of BBs lead to?

A

Rebound tachycardia (must taper BBs if d/c)

59
Q

What can BBs mask in patients with DM?

A

Can mask signs of hypoglycemia (ex. tachycardia)

60
Q

What effect can BBs have on EKG?

A

Slowed PR-interval, ventricular rate

61
Q

What effect do BBs have on the renal system?

A

Reduction in renin output, reduces RAAS activity

62
Q

What other condition can BBs be useful for?

A

Open-angle glaucoma (enhanced outflow and drainage)

63
Q

What kind of selectivity is important to consider when choosing BBs for therapy?

A

Beta-1 vs. Beta-2 selectivity
*All BB’s have dose-related B-1/B-2 activity

64
Q

What can selective Beta-1 drugs do at higher doses?

A

They can also block B-2 receptors at higher doses

65
Q

Bronchioles and peripheral vascular tissue uses what activity for some vasodilation?

A

Beta-2 activity

66
Q

Blocking Beta-2 receptors may result in what?

A

Unopposed alpha constriction

67
Q

Ideally, what treatment w/ BBs will avoid excessive alpha constriction/increased afterload?

A

Minimize use of nonselective BBs with some Beta-2 blockade

68
Q

Non-selective BBs?

A

Labetalol, Carvedilol, Nadolol, Sotalol, Timolol

69
Q

Selective BBs?

A

Metoprolol, Atenolol, Bisoprolol

70
Q

Many patients with pulmonary disease can tolerate BBs at what doses?

A

Lower doses

71
Q

Typically, CCBs are given in what setting for CSA & at what dose?

A

The ER, and typically dosed once daily

72
Q

Blocking of calcium channels inhibits what?

A

Inhibits Ca2+ mediated depolarization, facilitates muscle relaxation

73
Q

What kind of CCBs are Verapamil and Diltiazem?

A

Non-dihydropyridines

74
Q

Verapamil and Diltiazem can be used in place of what medications?

A

Beta-blockers

75
Q

What benefits do Verapamil and Diltiazem provide?

A

Rate control, Anti-anginal effects, BP lowering

76
Q

How do Verapamil and Diltiazem lower BP?

A

Depression of AV node conduction, coronary & arterial vessel dilation

77
Q

What kind of vasodilation activity do dihydropyridine CCB’s have?

A

Selective vasodilation with minimal AV node activity

78
Q

Calcium channel blockers have what similar effect between classes?

A

Similar BP reduction

79
Q

Calcium channel blockers may have differences in what effects?

A

Hemodynamics and tolerability may be different among classes

80
Q

Which dosage forms of CCB’s are once daily?

A

XR, ER, XL are once daily (be mindful of dosage form!)

81
Q

In HFrEF, which medications should be avoided?

A

Non-dihydropyridine Calcium channel blockers

82
Q

Which meds can be used in HFrEF?

A

Can use BB, ACEi, diuretics

83
Q

What do Diltiazem and Verapamil reduce?

A

Myocardial O2 demand, HR, contractility, peripheral vascular resistance, ischemic time, BP, workload

84
Q

Do EKGs reflect CCB use (before vs. after)?

A

Yes

85
Q

Which has better effect on cardiac conduction/output: Verapamil or Diltiazem?

A

Verapamil

86
Q

Which dosage forms of Verapamil & Diltiazem give the best 24 hour HR and BP control?

A

Long acting dosage forms

87
Q

Which CCBs are dihydropyridines?

A

Nifedipine, Amlodipine, Felodipine

88
Q

Which dihydropyridine gives the best 24 hour HR and BP control?

A

Long acting drugs (i.e. Amplodipine)

89
Q

Which dihydropyridine is short acting and can be associated with rebound sympathetic activity, rebound HTN, & tachycardia?

A

Nifedipine

90
Q

When can Nifedipine use be dangerous?

A

In BP labile (easily changing/altering) patients w/ severe CAD & HTN

91
Q

What do nitrates dilate: arteries or veins?

A

Mixed venous AND arterial dilating

92
Q

Which vasodilates more from nitrates: arteries or veins?

A

Venous vasodilation > arterial vasodilation

93
Q

Nitrate effects?

A

Increase venous capacity, decrease ventricular preload, improves venous/later arterial filling

94
Q

Benefits of nitrates come from what?

A

Symptom relief, reduced hospitalization (HOWEVER, NO CV OUTCOME BENEFITS)

95
Q

What are nitrates useful for?

A

Controlling symptoms and delaying ED/urgent care visits

96
Q

Which meds for CSA have extensive first pass metabolism?

A

Oral Nitrates (must be broken down by liver before they get to the heart)

97
Q

Which nitrate route of administration can avoid the first pass metabolism?

A

Sublingual (SL)

98
Q

How fast do SL nitrates take effect? How long do the effects last?

A

Rapid vasodilation (fast acting), but only 30 minutes of effect

99
Q

If needed for chronic use, which form of nitrates should be avoided?

A

Short acting nitrates

100
Q

Which dose intervals of nitrates should be used for chronic management?

A

12 and 24 hour dose intervals

101
Q

When should short-acting nitrates be used?

A

To treat occasional angina symptoms

102
Q

If using nitrates chronically, what should be done in order to avoid building a tolerance to the meds?

A

Windows of drug vacation

103
Q

Venodilation is more prominent in what doses of nitrates: higher or lower?

A

Lower doses

104
Q

Arterial dilitation is more prominent in what doses of nitrates: higher or lower?

A

Higher doses

105
Q

What can occur due to venous dilation by nitrates?

A

Orthostasis due to venous pooling: dangerous if dehydrated, upright/not moving, or using alcohol

106
Q

What can happen with temporal and meningeal arteries when using nitrates?

A

Vasodilate triggering intense, throbbing, disorienting migraine-like headaches

107
Q

What percentage of patients experience migraines from temporal and meningeal vasodilation when taking nitrates?

A

> 60% of patients

108
Q

What can happen in patients are using nitrates inappropriately (not using PRN) and then stop using them abruptly?

A

Rebound tachycardia (preferably prescribe BB or non-dhp CCB along w nitrates)

109
Q

What is nitrate tachyphylaxis?

A

Long term exposure to short acting nitrates will desensitize response to nitrates

110
Q

What medications should absolutely be avoided if using nitrate therapy?

A

Phosphodiesterase inhibitors: Viagra (Sildenafil), Cialis (Tadalafil), etc.

111
Q

How long should phosphodiesterase inhibitors be held after any nitrate?

A

24 hours

112
Q

What interaction can nitrates have with posphodiesterase inhibitors?

A

CAN BE DEADLY, causes a massive shift of blood away from the heart

113
Q

What causes nitrate toxicity?

A

Excess nitrate combines w hemoglobin (Hb) causing methemoglobinemia –> oxygen delivery impaired

114
Q

What is nitrate toxicity/methemoglobinema treated with?

A

Methylene blue

115
Q

Quick acting nitrates to treat angina symptoms?

A

Nitroglycerin (Nitrostat, NitroBID)

116
Q

What is nitroglycerin intended for?

A

Rapid relief of angina (insufficient for background dilation)

117
Q

How does nitroglycerin act on vascular smooth muscle?

A

Relaxes vascular smooth muscle via increased cGMP

118
Q

What are the effects of nitroglycerin?

A

Reduces O2 demand, preload, afterload
Improves collateral/backup circulation
Reduces sx, hospitalization
**NO IMPROVEMENT ON CV OUCTOMES

119
Q

Duration of sublingual (SL) nitroglycerin?

A

20-30 minutes

120
Q

Duration of transdermal (TD) nitroglycerin?

A

6-8 hours

121
Q

When should TD nitroglycerin patches be removed?

A

Before MRI and defibrillation

122
Q

Half life of nitroglycerin?

A

1-4 minutes

123
Q

What nitrate-free interval is necessary for avoiding tolerance of oral nitroglycerin?

A

Interval of 10-12 hours

124
Q

What should you instruct patients to avoid when using nitrates?

A

Alcohol

125
Q

First dose of nitrates should be given where?

A

Under supervision to monitor for headache or reflux

126
Q

Which nitrates are long-acting for angina prevention?

A

Isosorbide mononitrate (Imdur, Ismo, Monoket) and Dinitrate (Isordil)

127
Q

How do long-acting nitrates work?

A

Systemic vasodilation by increasing cGMP

128
Q

What do long-acting nitrates reduce?

A

Reduce preload, LV end diastolic volume & pressure

129
Q

Is there any data of improved CV outcome for long-acting nitrates?

A

NO, only symptom relief data

130
Q

Dosage for chronic use of long-acting nitrates?

A

5-10mg at:
7AM and 3PM
OR
9AM and 5PM
*allows nitrate-free interval to reduce tachyphylaxis

131
Q

Mononitrate formulations allow what duration?

A

XR tablet allows 24 hours (once daily)

132
Q

Dinitrate formulations allow what duration?

A

XR tablet allows 12 hours (twice daily)

133
Q

What is important to educate patients on when using XR tablets (long-acting nitrates)?

A

DO NOT confuse with SL nitroglycerin or chew like aspirin

134
Q

How to manage nocturnal angina with long-acting nitrates?

A

Adjust scheduled doses/dose spacing

135
Q

Medication combo for angina/chest pain?

A

BB + long-acting nitrates + PRN SL/spray nitroglycerin

136
Q

Medication combo for angina/chest pain in unable to take BB?

A

Non-DHP CCB + long-acting nitrates + PRN SL/spray nitroglycerin

137
Q

Management for lipid-lowering in CSA?

A

Counsel on lifestyle habits, baseline lipid and liver panel, if LDL > 190 investigate cause (may be genetically predisposed), high intensity statins

138
Q

When to use PCSK9i’s for lipid-lowering?

A

Not routinely used, but if LDL remains >190 even after high intensity statins, initiate PCSK9i therapy

139
Q

ACEi (or ARB if intolerant) therapy for CSA?

A

Evidence supports dec. in CV events w/ CHD
Also consider for: CKD, DM, EF < 40%
*plaque stabilization

140
Q

Which medication should only be used if necessary?

A

Non-DHP CCBs in place of BB’s - lack data for benefits in preventing MI

141
Q

Meds for plaque stabilization?

A

DAPT, ACEi, statins

Pharm II Exam 3 (6 decks)

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