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Pharmacology III > Block I: CAD > Flashcards

Block I: CAD Flashcards

1
Q

epicardial vessel atherosclerosis can lead to []

A

coronary heart disease/ Coronary artery disease

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2
Q

what are some presentations of CAD?

A
  1. acute coronary syndrome
  2. chronic stable exertional angina pectoris
  3. ischemia w/o clinical symptoms
  4. heart failure
  5. arrythmias
  6. cerebrovascular disease
  7. periperal vascular disease
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3
Q

squeezing, pressure, heaviness, tightness, pain in chest are signs of []

A

angina

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4
Q

[] is a type of angina with a fixed stenosis

A

chronic stable

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5
Q

[] is a type of angina that involves vasospasm of coronary arteries

A

variant (printzmetal’s sign assoc.)

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6
Q

what are some precipitating factors for variant angina?

A
  1. pregnancy
  2. drugs (cocaine)
  3. cold weather
  4. emotional stress
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7
Q

[] is a type of angina involving a fixed stenosis rupture

A

untable angina

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8
Q

what is L main/ L main equivalent CAD

A

blocking entire L coronary artery

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9
Q

what is the 12 yr. survival rate for 0 occluded vessels

A

88%

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10
Q

what is the 12 yr. survival rate for 2 occluded vessels

A

59%

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11
Q

what is the 12 yr survival rate for one occluded vessel

A

74%

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12
Q

what is the 12 yr survival rate for three occluded vessels

A

40%

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13
Q
  1. pressure/bruning near sternum
  2. chest tightness, SOA
  3. visceral pain lasting 0.5-30 minutes
    - precipitated by exercise, cold, anger, coitus, freight

this describes symptoms of []

A

stable angina

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14
Q

deep, poorly localized chest/arm discomfort
-rarely described as pain
that is producable (brought about by exercise, freight, emotional distress)

usually relieved in 5-10 minutes with rest or NTG

describes []

A

stable angina

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15
Q

angina or ischemic discomfort while

  • at rest
  • lasts > 10 minutes
  • severe pain
  • occurring in a crescendo pattern

this describes []

A

unstable angina

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16
Q

dull discomfort brought about by exrtion that lass under 10 minutes is likely []

A

stable angina

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17
Q

sharp pain lasting more than 10 minutes in a crescendo pattern is []

A

unstable angina

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18
Q

what are some ekg changes you may expect to see in an acute coronary patient

A
  1. St depression
  2. ST elevation
  3. T wave inversion
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19
Q

exertional hypotension and reduced exercise tolerance indicate [] ischemia

A

significant

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20
Q

what are 2 signs significant ischemia

A
  1. hypotenion on exertion

2. reduced exercise tolerance

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21
Q

what is the gold standard to evaluating coronary anatomy to quantify the presence and severity of atherosclerotic disease

A

coronary angiography (AKA cardiac catherterization)

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22
Q

when are good times to order coronary angiography

A
  1. markedly positive stress test
  2. suspected non-arthersclerotic cause ischemia (congenital abrnom.)
  3. recurrent chest pain despite aggressive medical therapy for angina
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23
Q

what is a treatment goal for stable ischemic heart disease

A

reduce/prevent angina symptoms that limit exercise capability & impair QOL

prevent CHD event (mi, arrythmia, heart failure)

exten pt. life

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24
Q

what is a class 1 rec. immediate relief pain asoc. with stable ischemic heart disease?

A

NTG

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25
Q

what is the initial therapy that should be rx’ed for relief of symptoms for stable ischemic heart disease (class 1 guideline)

A

BB

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26
Q

what is a second line for symptom relief of stable ischemic heart disease if BB is contrainindicated or not tolerated (class 1 guideline)

A

CCB/ long acting nitrate

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27
Q

what can be added to treatment of stable ischemic heart disease if BB alone are not efficacious (class 1 guideline)

A

CCB/long acting nitrate

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28
Q

what is a class 2a rec. for symptomatic relief of stable ischemic heart disease for symptom relief

A
  1. long acting non-DHP (dipine drugz)

* instead of BB as initial therapy for relief of symptoms

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29
Q

what are substitutes for BB in SIHD?

A

class 1a:

  • CCB
  • long acting nitrate

class 2a:

  • non-DHP CCB
  • ronolazine
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30
Q

what 2 drugs can be used as sdjuvant therapy when BB alone are innefective in SIHD?

A

class 1a:

  • CCB
  • long acting nitrate

Class 2a:
-ronolazine

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31
Q

if a patient with SIHD has high lipids (try > 150, LDL > 100)
what should be added to their therapy?

A

moderate-high dose statin

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32
Q

whats the BP goal for SIHD pts.

A

= 140/90

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33
Q

whats the A1C goal in SIHD pts.

A

< 7%

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34
Q

whats a good physical activity goal for SIHD pts.

A

30-60 minutes of mod intensity aerobic activity at least 5-7 days per weak

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35
Q

how should pts. sith SIHD cut saturated fat?

A

< 7% calories sat fat

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36
Q

whats a systolic BP goal for SIHD

A

< 130 mmHG

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37
Q

whats a LDL goal for SIHD pts.

A

< 70 (< 100 good)

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38
Q

whats a BMI goal for SIHD pts.

A

< 25

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39
Q

what are mainstays of ischemic heart disease optimal therapy?

A
  1. aspirin daily

2. statin: max tolerated dose

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40
Q

what statins are most rec?

A

Rosuvastatin 20-40mg

atorvastatin 40-80mg

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41
Q

a IHD pt. with hypertension or requires waht regimen?

A
  1. ASA
  2. Statin (max)
  3. ACEI/ARB
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42
Q

a IHD pt. with DM requires what regimen

A
  1. ASA
  2. Statin (max)
  3. ACEI/ARB
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43
Q

a IHD pt. with LVEF < 40 % requires what regimen

A
  1. ASA
  2. Statin (max)
  3. ACEI/ARB
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44
Q

a IHD pt with eGFR < 60 requires what regimen

A
  1. ASA
  2. Statin (max)
  3. ACEI/ARB
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45
Q

what is optimal therapy for a IHD pt. with MI or LVEF < 40%

A
  1. ASA
  2. Statin
  3. BB
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46
Q

what can be added to a pt. where ASA in contraindicated or who need an adjuvant to ASA?

A
  1. P2Y12 receptor agonists
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47
Q

if a patient is unable to reach LDL goal with max statin, what can be added?

A

ezetimibe

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48
Q

what can be added to a statin and exetimibe if pt. still is not at LDL goal?

A

evolcumab, alicromab

monoclonal ab for LDL receptors (to keep high numbers of them active to less LDL is stuck in blood)

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49
Q

what should be recomended anually for SIHD pts

A

flu vax

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50
Q

what is the MOA for nitrates

A

potent vasodilatory (primarly venous) and diminish platelet aggregation

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51
Q

nitrate primarily vasodilate [] vessels

A

venous

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52
Q

[] is essential exogenous NO

A

nitrates

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53
Q

what is the role of NO

A

released from endothelial cells to increase cyclic guanosine monophosphate (cGMP) levels through activation of guanylate cyclase

platelet agreggation diminished, vasodilation

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54
Q

what are some indications nitrates

A
  1. terminate acute anginal attacks
  2. prevent effort/stress-induced attacks (prophylactically before exercise)
  3. can be used for long-term prophylaxis
    - usually in combo with BB< CCB
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55
Q

what are some AE nitrates

A
  1. postural hypotension
  2. HA
  3. nausea
  4. reflex tachycardia
  5. rash
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56
Q

what happens when beta receptors are activated by NE

A
  1. AV node conduction accelerated
  2. increase HR and contractility
  3. increased myocardial oxygen demand
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57
Q

during MI [] receptors become activated which exacerbate the MI how?

A
  1. beta receptors
  2. increase contractility and HR thereby increasing myocardial oxygen demand

the whole reason they are having an MI is because they dont have o2!

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58
Q

what are the effects of blocking beta receptors?

A
  1. decrease HR/contractility
  2. decrease AV node conduction
  3. decrease O2 demand
    - decreased angina both at rest and exercise
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59
Q

what is the first line in chronic angina that requires daily maintenance therapy

A

BB

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60
Q

what is the benefit of BB in angina

A
  1. reduce MI, CAD. mortality
  2. can be used prophylactically in pts. with multiple anginas a day
  3. reduce need for revascularization surgery
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61
Q

[] can decrease anti-anginal effects of BB

A

smoking

62
Q

what are some AE or BB

A
  1. hypotension
  2. bradycardia
  3. bronchospasm
  4. altered glucose metabolism
  5. fatigue
  6. malaise
  7. depression
63
Q

what should you counsel your patient on about abruptly stoping BB?

A
  1. assoc. with increased severity and number of pain episodes if stopped abruptly
64
Q

MOA CCB

A

improve coronary blood flow through coronary atery vasodilatoin to decrease myocardial oxygen demand

blocks long Ca2+ channels in myocytes

65
Q

who are good candidates for CCB?

A
  1. cont/intolerance BB
  2. printzmetal angina
  3. peripheral vascular disease
  4. concurrent uncontrolled HTN
66
Q

printzmetal angina is best treated with []

A

CCB

67
Q

peripheral vascular disease is best treated with []

A

CCB

68
Q

what CCBS can be used to treat arrythmias

A

non DHP

69
Q

what CCBs can be used to vasodilate and cause reduction in BP?

A

all of them, DHP and non DHP

70
Q

what is the moa of ronalozine

A

reduce CA2+ overload in ischemic myocye through selective inhibition of late NA_ current (lna)

71
Q

what drug has an MOA that

reduced Ca2+ overload in ischemic myocyte through selective inhibition of late Na current

A

ronalozine

72
Q

what drug has an MOA that improves coronary blood flow through coronary artery vasodilation by decreasing oxygen demant, wby blocking Ca2+ long channels in myocytes

A

CCB

73
Q

what drug has an MOA that

is a potent vasodilator and diminished platelet aggregation

A

nitrate

74
Q

what drug does NO affect HR, inotropic state, hemodynamic state or increase coronary blood flow?

A

ronolazine

75
Q

what are some indications for ronolazine

A
  1. chronic angina treatment

- reserved for pts. who have no achieved adequate response with other antianginal agents (BB,CCB)

76
Q

what drugs can cause bradycardia

A
  1. non DHP

2. BB

77
Q

what drug causes prolonged QT interval

A

ronolazine

78
Q

what drug can cause HA

A

nitrates

79
Q

what drug can cause depression

A

BB

80
Q

what is an adverse effect of ronalazine?

A

prolonged QT interval

81
Q

what are some contraindications for ronalazine?

A
  1. pre-existing QT interval prolongation

2. hepatic impairment

82
Q

what re drug interactions for ronalazine?

A
  1. other QT prolongating drugs

2. cytochrome P450 3A decrease ranalazine clearance and will cause torsades des points

83
Q

prior to undergoing revascularization surgery for stable exertional angina pectoris what should you do?

A
  1. max 2-3 anti-anginal therapies
84
Q

[] is generally recommended to improve survival in patients with DM and CAD for which revascularization can improve survival

A

CABG (pref. over PCI)

85
Q

patients shold [] taking ASA before their CABG

A

continue

86
Q

a patient on clopidogrel or ticagrelor should [] treatment before CABG

A

d/c for 24 hrs

87
Q

ticagrelor should be help for [] days in elective CBG

A

3

88
Q

clopidogrel should be held for [] days in elective CBG

A

5

89
Q

prasurgrel should be held for [] days in elective CBG

A

7

90
Q

what pharm should be dispensed post op CABG

A
  1. ASA within 6 hours post-op

- continued indefinitley

91
Q

all PCI pts. receive [] to take indef. post procedure

A

ASA

92
Q

how long should clopidogrel be given after drug eluting PCI placed?

A

6 months (3 if bleeding risk)

93
Q

how long should clopidogrel be given post bare metal stint placing?

A

1 month

94
Q

[] plays a key role in arhterosclerosis

A

inflammation

95
Q

what factors can lead to endothelial dysfunction? (which can lead to atherosclerotic plaques)

A
  1. HTN
  2. smoking
  3. dyslipidemia
  4. male
  5. age
  6. tobacco
  7. obesity
96
Q

[] results from myocardial ischemia due to imbalance between myocardial O2 demans and supply

A

ACS (acute coronary syndrome)

97
Q

exposure of collagen & tissue factor from plaque leads to platelet activatoin and adhesion and the release of what vasoactive substances?

A
  1. adenosine diphosphate

2. thromboxane 2

98
Q

[] is defined as changes in shize, shape, and function of L ventricle

A

ventricular remodleing

99
Q

ventricular remodeling can lead to []

A

heart failure

100
Q

what 4 drugs can slow down or reverse ventricular remodeling to improve change of survival

A
  1. ACEI
  2. ARB
  3. BB
  4. aldosterine agonists
101
Q

what are three examples of acute coronary asyndromes

A
  1. STEMI
  2. NSTEMI
  3. unstable angina
102
Q

what complication of ACS do you want to avoid at all costs?

A

cardiogenic shock, high mortality rate

103
Q

[] is a rare complication of MI and occurs when the heart is not able to pump enough blood to meet body’s demand

A

cardiogenic shock

104
Q

[]% STEMI pts. will exerpience cardiogenic shock

A

5-6

105
Q

[]% non stemi pts with experience cardiogenic shock

A

2

106
Q

what is the morality rate of cardiogenic shock

A

60

107
Q
  1. middle anterior anginal chest pain
  2. severe new onset angina
  3. increasing angina duration > 20 min
  4. radiating pain
  5. N/V
  6. diaphoresis
  7. SIA

these are signs of []

A

ACS

  1. unstable angina
  2. MI
    - STEMI
    - NSTEMI
108
Q

what populations may present with abnormal/minimal ACS symptoms

A
  1. women
  2. elderly
  3. diabetics
109
Q

if you suspect ACS, an ECG needs done [] amount of time

A

10 minutes of arrival,

every 15-30 minute intervals during first houe

110
Q

what are key findings on ECG of ACs

A
  1. ST segment elevatoin
  2. ST segment depression
  3. T wave inversion
111
Q

what biomarker can you order if you suspect ACS

A

troponin

released when myocardial cells die

order

  1. at presentation
  2. 3-6 hrs after symptom reset
  3. after 6 hrs in patient with initial normal troponins with ECG change and/or intermediate high risk clinical features
112
Q

[] is the best predictor of mortality after an MI

A

left ventricular function

113
Q

LVEF of [] has a high risk of death

A

< 40%

114
Q

infarction in [] has worse outcomes

A

hyperglycemia

115
Q

what is the best treatment for STEMI

A
  1. coronary reperfusion via primary PCI, fibrinolysis or emergent CABG to restore coronary blood flor
116
Q

what non=pharm revascularization is preferred in STEMIpts

A

PCI

117
Q

high risk NSTEMI may be candidates for []

A

PCI, CABG

early invasive therapy

118
Q

what is pharmacotherapy

ptotocol for ACS

A
  1. Morphine
  2. oxygen (when sat < 90%)
  3. NTG
  4. aspirin
  5. BB
    - within first 24 hours in absence of acute HF exacerbation, low output state, risk coardiogenic shock or con. BB

MONA B

119
Q

when should o2 be admin in ACS

A

< 90% sat, respiratory distresss

120
Q

how often should NTG be given in ACS

A

every 5 minutes

121
Q

what should be discharged after ACS

A
  1. NTG SL
  2. ASA
  3. BB
  4. High intensity statin
  5. ACEI/ARB
  6. *HrfEF patients with aldosterone antagonist
122
Q

what is the MOA ASA

A

irreversible inhibition of platelet cyclooxygenase-1

-may have antiinflammatory effects

123
Q

what are contraindications ASA

A
  1. hypersensitivity
  2. active bleeding
  3. severe bleeding irsk
124
Q

what should NOT be administered with ASA

A

NSAID

125
Q

what kind of drug is ticagrelor

A

cyclopentyltriazolopyrimide P2Y12 inhibitor

126
Q

what is the MOA ticagrelo

A

binds REVERSIBLY to P2Y12 ADP receptor

to reduce rate of combined endpoint CV death, MI, stroke

127
Q

what drugs MOA is

binding reversible to P2Y12

A

ticagrelor

128
Q

what is the indication for ticagrelor

A

indicated to reduce CV thrombotic events in patients with ACD

129
Q

ticagrelor vs. clopidogrel

which is more efficacious

A

ticagrelor

130
Q

what are contraindications ticagrelor

A
  1. hepatic impairment
  2. intracranial hemorrhage hx
  3. active bleeding
  4. ASA > 100
131
Q

what are AE of ticagrelor

A
  1. bleeding
  2. dyspnea
  3. bradyarrythmia
  4. elevated uric acid
  5. elevated Scr
132
Q

what kind of drug of clopidogrel

A

thienopyridine

P2Y12 inhib.

133
Q

moa clopidogrel

A

irreversible bind to P2Y12 reveptor, prevent firbinr clots

134
Q

contra. clopidogrel

A
  1. hypersensitivity
  2. active bleeding
  3. severe bleeding risk
135
Q

AE clopidogrel

A
  1. bleeding

2. N/V/D

136
Q

important drug interaction clopidogrel

A

PPIs may lower effectivement

-omeprazole and esomeprazole esp.

137
Q

what kind of drug is prasugrel

A

thienopyridine

P2Y12 inhib.

138
Q

MOA prasugrel

A

irreversibly block P2Y12 in paltelets

139
Q

which of the thienopyridines acts quicker?

A

prasugrel

140
Q

which thienopyridine is more efficacious in patients undergoing PCI

A

prasugrel

141
Q

which thienopyridine is NOT affected by PPI

A

prasugrel

142
Q

which thienopyridine is affected by PPI

A

clopidogrel (esp. omeprazole and esomeprazole)

143
Q

which thienopyridine is assoc with increased CABG bleeding rates in clinical trials

A

prasugrel

144
Q

P2Y12 should be given to patients undergoin PCI

A

prsugrel

145
Q

what P2Y12 should be given to patients undergoind CABG

A

clopidogrel

146
Q

when is really the only time to use prasugrel

A

pt. undergoing PCI

147
Q

what are contraindications prasugrel

A
  1. active bleeding

2. prior stroke

148
Q

what precautions should you take with prasugrel

A

age >/= 75

body weight < 60

149
Q

what are AE prasugrel

A
  1. bleeding

2. TTP

150
Q

stent thrombosis usually present as []

A

MI, STEMI

151
Q

what are components of drug eluting stint

A

platform

  1. stainless steel
  2. cobalt chrome
  3. platinum

polymer coating
1. controlled release drug carriers

antiproliferative agent

  • lipophilic
  • immunsuppressive
152
Q

what medications should a pt be on to prevent secondary MI

A
  1. ASA
  2. BB
  3. CCB
  4. ACEI
  5. high intensity statin
  6. NTG if ischemic chest pain
  7. Antiplatelet for at leas 12 months
    - ticagrelor
    - clopidogrel
    - prasugrel
  8. annual flu vax
  9. glycemic control

Pharmacology III (6 decks)

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