Ischemic Heart Disease, MI, Anti-clotting drugs, Vasodilators Flashcards

1
Q
A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is important to remember about Aerobic Energy Production?

A

O2 is needed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the Primary Cardiac Fuel Sources?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the requirement for Mitochondrial Energy Production?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the Effects of Ischemia & Reperfusion on Aerobic Energy Production?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the Consequences of Reperfusion?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the Reactive Oxygen Species?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe a ROS mediated reperfusion injury

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the relationship between Infarct Size and Time

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe Ischemic Conditioning and Reperfusion Injury

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe Energy Transfer via Creatine Kinase

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the components of Creatine Kinase

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the Plasma Levels of CK-MB and Cardiac Troponin Following MI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the Consequences of Hypoxia?

A
  • Aerobic glycolysis and fatty acid oxydation slow down
  • ATP in short supply
  • Anaerobic glycolysis speeds up (if glucose available, normally comes from blood)
  • Cardiac cells have limited glycogen stores (compared to skeletal muscle)
  • Lactate increases and pH drops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Percutaneous Coronary Intervention (PCI)?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Describe the Treatment of Stable Angina

A
  • Treatment of aggravating symptoms
  • Adaption of activity
  • Treatment of risk factors
  • Beta-Blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the ECG progression in STEMI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the common PTs who have Silent Ischemia/Asymptomatic Ischemia

A

More common in women later decades
More common in diabetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Describe the Physical Exam for IHD

A
  • BP and Pulse
  • New Murmurs
  • Aortic Stenosis can be associated with angina and syncope
  • Carotid bruit
  • S4 can be associated with IHD (nonspecific)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the differences in NSTEMI vs STEMI

A
  • EKG ST elevation (STEMI)
  • Enzymes elevated
  • Occasional develop Q wave
  • Tx antiplatelet, heparin, admission (NSTEMI)
  • Tx Reperfusion (STEMI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Describe the Exercise Stress Test

A
  • Reach 85% of max HR
  • 12 ECG and BP monitoring
  • ST depression 2mm
  • Ventricular Tachyarrhythmia
  • Limitations: abnormal ECG baseline, cannot exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe an Inferior STEMI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Relate Unstable Angina and NSTEMI

A

EKG may show ST depression
Angiogram - partial obstruction
ENZYMES ELEVATED - only NSTEMI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is Acute Coronary Syndrome (ACS)?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Describe a Lateral Wall MI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Describe Unstable Angina

A
  • increased intensity or frequency, does not go away with demand reduction, or occurs at rest
  • ST depression or Normal ECG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

How do CCBs relate to Stable Angina?

A

Second line if Beta-Blockers are not tolerated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

How do NSAIDs relate to Stable Angina?

A

Small but finite increased risk of myocardial infarction and mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What are the Ischemic Heart Disease Risk Factors?

A
  • FmHx premature CAD 1st degree relative
  • male < 55 female < 65
  • Tobacco products
  • Diabetics 2-4 times the risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Describe an Anterior STEMI

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Describe the relationship between Nitrates and Stable Angina

A
  • Systemic venodilation
  • Dilation of coronary vessels and collateral
  • Short acting - NTG spray/tablets
  • Long acting - Transdermal paste/patches
  • Tablets - isosorbide dinitrate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Describe what a Coronary Artery Bypass Graft (CABG) is

A
  • Bypass portion of artery with segment of donor artery or vein
  • Left internal mammary artery is preferred over saphenous vein
  • Artery > Vein
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How do you dx an MI?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are the Tests for IHD?

A
  • Exercise Stress Test
  • Stress Echo
  • Stress Radionuclide Myocardial Perfusion Scan
  • CT for Calcium scoring
  • Angiography (CT or Coronary)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What are the Anginal Equivalents and what is Atypical Presentation?

A
  • Indigestion
  • Nausea
  • SOB
  • Diaphoresis
  • Dizziness
  • Syncope
  • Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Describe an Angiography

A

Visualizing vessel lumen

Contrast agent with XR, CT or MRI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Describe the relationship between Women and Heart Disease

A
  • More likely atypical presentation
  • 5-10 years older at time of presentation
  • Higher incidence of vasospastic heart disease
  • Less likely to undergo procedures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Describe what a Coronary Angiography is

A
  • Catheter placed in arterial circulation and advanced to coronary arteries both right and left
  • Injection of contrast
  • Measure EF (ventriculogram)
  • 70% obstruction considered significant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is Revascularization?

A

CABG and PCI (percutaneous coronary intervention)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is a Stress Radionuclide Myocardial Perfusion Scan?

A

Compares Rest and Exercise images

Inability to dilate shows less uptake of radioactive tracer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is a Stress Echocardiogram?

A
  • Ischemia presents as wall motion abnormality (US)
  • Dobutamine and Adenosine for pt who cannot exercise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Describe the relationship between Antiplatelets and Stable Angina

A
  • Aspirin
  • P2Y12 Inhibitors (ADP receptor antagonists)
  • Clopidogrel
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Describe what Reperfusion Treatment Therapy is

A
  • Tx within 3 hours = 50% reduction in mortality
  • Can treat up to 12 hours after onset
  • Limit infarct size and preserve LV function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Relate Fibrinolysis and MI Treatment

A
  • Administer in less than 30 minutes
  • tPA, TNK, rPA
  • Administer along with ASA and/or P2Y12 Inhibitor and Heparin
  • Only effective in case of a STEMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the Indications for thrombolytic therapy?

A
  • STEMI onset within 12 hours
  • Most effective in 90 minutes
  • ST elevation of at least 1 mm in 2 contiguous leads
  • 2 mm in leads V2 and V3 for men, 1.5 for women
  • New LBBB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the Fibrinolysis Contraindications and major risk?

A
  • Intracranial hemorrhage in approximately 1% of patients treated with fibrinolytics for MI
  • Higher risk in patient’s over 75 yo
  • Use PCI instead
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Describe PCI: post op care

A

Dual antiplatelet therapy for 12 months, ASA and P2Y12 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

When do you use PCI or Fibrinolytics?

A

When PCI cannot be done in 120 minutes use FIBRINOLYTICS

Any contraindications for fibrinolytics or cardiogenic shock use PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

When do you use PCI or Fibrinolytics?

A

When PCI cannot be done in 120 minutes use FIBRINOLYTICS

Any contraindications for fibrinolytics or cardiogenic shock use PCI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Describe PCI: post op care

A

Dual antiplatelet therapy for 12 months, ASA and P2Y12 inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Describe the uses of Cardiac US and Echocardiography

A

View for regional or global wall abnormalities

Ischemic muscle - wall motion abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Describe the how Pericarditis relates to MI

A
  • Pain decreases with sitting up
  • Dressler Syndrome - post MI syndrome
  • Pericardial and pleural effusions
  • May be inflammatory or immune related with fever and malaise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Describe a Right Ventricular Infarct

A
  • RCA 85%, LCX 15%
  • Fluid back up in systemic circulation
  • Distended neck veins
  • Hypotensive
  • Right sided EKG, elevation RV4
  • IV fluid bolus without NITRATES (AVOID)
69
Q

Describe a Right Ventricular Infarct

A
  • RCA 85%, LCX 15%
  • Fluid back up in systemic circulation
  • Distended neck veins
  • Hypotensive
  • Right sided EKG, elevation RV4
  • IV fluid bolus without NITRATES (AVOID)
70
Q

What are the Q Wave ECG Findings?

A
  • consistent with previous MI
  • Transmural ischemia
  • 1mm wide
  • 1/3 amplitude of R wave
71
Q

What is the treatment for Post-MI Infarction?

A
  • Lifelong aspirin and/or P2Y12 inhibitor
  • Stent placed - aspirin and P2Y12 inhibitor for a year
  • Beta-blocker within first 24 hours unless contraindicated
  • Lifelong high intensity statin
  • Cardiac rehab program
72
Q

What is the treatment for Post-MI Infarction?

A
  • Lifelong aspirin and/or P2Y12 inhibitor
  • Stent placed - aspirin and P2Y12 inhibitor for a year
  • Beta-blocker within first 24 hours unless contraindicated
  • Lifelong high intensity statin
  • Cardiac rehab program
73
Q

What are the Q Wave ECG Findings?

A
  • consistent with previous MI
  • Transmural ischemia
  • 1mm wide
  • 1/3 amplitude of R wave
74
Q

Describe the how Pericarditis relates to MI

A
  • Pain decreases with sitting up
  • Dressler Syndrome - post MI syndrome
  • Pericardial and pleural effusions
  • May be inflammatory or immune related with fever and malaise
75
Q

Describe the uses of Cardiac US and Echocardiography

A

View for regional or global wall abnormalities

Ischemic muscle - wall motion abnormalities

76
Q

What are the Fibrinolysis Contraindications and major risk?

A
  • Intracranial hemorrhage in approximately 1% of patients treated with fibrinolytics for MI
  • Higher risk in patient’s over 75 yo
  • Use PCI instead
77
Q

What are the Indications for thrombolytic therapy?

A
  • STEMI onset within 12 hours
  • Most effective in 90 minutes
  • ST elevation of at least 1 mm in 2 contiguous leads
  • 2 mm in leads V2 and V3 for men, 1.5 for women
  • New LBBB
78
Q

Relate Fibrinolysis and MI Treatment

A
  • Administer in less than 30 minutes
  • tPA, TNK, rPA
  • Administer along with ASA and/or P2Y12 Inhibitor and Heparin
  • Only effective in case of a STEMI
79
Q

Describe what Reperfusion Treatment Therapy is

A
  • Tx within 3 hours = 50% reduction in mortality
  • Can treat up to 12 hours after onset
  • Limit infarct size and preserve LV function
86
Q

Describe an MI Complication AV Block

A
  • RCA supplies blood flow to the SA and AV nodes
  • Block may be transient and related to vagal tone
  • May respond to atropine since it is at the AV level
87
Q

Describe MI Complications of LBBB

A
  • Damage to conducting system
  • Presents with new LBBB
  • Clinical symptoms of MI and new LBBB treat as MI
88
Q

Describe MI Complications of LBBB

A
  • Damage to conducting system
  • Presents with new LBBB
  • Clinical symptoms of MI and new LBBB treat as MI
89
Q

Describe an MI Complication AV Block

A
  • RCA supplies blood flow to the SA and AV nodes
  • Block may be transient and related to vagal tone
  • May respond to atropine since it is at the AV level
91
Q

What are the pitfalls of ECG?

A

Diagnostic in 50% of AMI cases

Entirely normal in 20% of AMI cases

92
Q

What are the pitfalls of ECG?

A

Diagnostic in 50% of AMI cases

Entirely normal in 20% of AMI cases

93
Q

What are the steps of Hemostasis?

A
95
Q

What are the “substances”?

A
96
Q

What receptor do platelets use to attach to one another?

A
97
Q

What are the 2 substances responsible for stimulating platelet aggregation?

A
98
Q

What molecules do Antiplatelet agents inhibit?

A
99
Q

What inhibitor platelet aggregation drug does this describe?

Blocks ADP receptors on platelets

A
100
Q

What inhibitor platelet aggregation drug does this describe?

Blocks the receptor used for platelet aggregation

A
101
Q

What is the MOA for Aspirin?

A
102
Q

What is aspirin used for?

What are its PKs?

A
103
Q

What are the DDIs and ADRs for aspirin?

A
104
Q

How does aspirin affect Cox-1 vs Cox-2?

A
105
Q

What are the ADP Receptor Antagonists?

A

Clones Prepared to be ADePt

Tony the Tiger reversed

Ticagrelor is reversible

106
Q

What is the MOA for ADP Receptor Antagonists?

A

Irreversibly inhibit ADP receptor on surface of platelets (necessary for platelet aggregation)

108
Q

What are ADP Receptor Antagonists used for?

A
109
Q

What are PKs for ADP Receptor Antagonists?

A
110
Q

What are the DDIs and ADRs for ADP Receptor Antagonists?

A
111
Q

What are the GP IIb/IIIa Receptor Antagonists?

A

ATE GP

112
Q

What is the MOA for GP IIb/IIIa Receptor Antagonists?

A
114
Q

Describe the PKs and ADRs for GP IIb/IIIa Receptor Antagonists

A
115
Q

What are the types of Anticoagulants and what are they used for?

A
116
Q

Where is heparin found?

What are the types of Heparin?

A
117
Q

What is the MOA of Heparin?

A
118
Q

What is the MOA of Unfractionated heparin (HMW)?

What effect does it have on factor Xa?

What are its drawbacks?

A
119
Q
  • What is the MOA of Low molecular weight heparin (LMW)?
  • What drug is an example of it
  • What effect does it have on factor Xa? Thrombin?
  • What are its drawbacks? advantages?
A
120
Q

What are the DDIs and ADRs for Low molecular weight heparin (LMW)?

A
121
Q

What are the Factor Xa Inhibitors?

What DDI do they all share?

A

Fondaparinux

Rivaroxaban

Fond of Rivers

122
Q

Describe the MOA and PK for Fondaparinux

A
123
Q

Describe the MOA, PK, and ADRs for Rivaroxaban

A
124
Q

What are the Direct thrombin inhibitors and their PKs?

A

Dab Again

125
Q

What are the uses of Direct thrombin inhibitors?

What use is specific for Dabigatran?

A
126
Q

What are the ADRs of Direct thrombin inhibitors?

A
127
Q

What are these examples of?

A

Warfarin

128
Q

What is the MOA for Warfarin?

A
129
Q

What are the PKs for Warfarin?

What do you need to monitor?

What is it used for?

A
130
Q

What are the DDIs for Warfarin?

A
131
Q

What are the Pharmacogenomic Considerations: for Warfarin

A
132
Q

What are the ADRS for Warfarin?

Describe Warfarin reversal

A
133
Q

What are the Fibrinolytics/Thrombolytics?

A

ART PLASE

134
Q

What is the MOA for Fibrinolytics/Thrombolytics?

A
135
Q

What are the uses and PKs for Fibrinolytics/Thrombolytics?

A
136
Q

What is Streptokinase?

Describe its PKs and ADRs

A
137
Q

What are the Hemostatics?

What are they used for and what their MOAs?

A
139
Q

What inhibitor platelet aggregation drug does this describe?

Blocks formation of TxA2

A

Aspirin

148
Q

What is Ticagrelor?

A

A reversible ADP receptor antagonist

154
Q

What do you use GP IIb/IIIa Receptor Antagonists for?

A

Patients with recent MI or stroke or PCI

155
Q

Describe the Mechanisms of Ischemia

A
156
Q

Describe the Clinical Utility of Vasodilators

A
157
Q

What is the The “Steal Phenomenon”

A
159
Q

Describe the Blockade of endogenous vasoconstrictors

A
160
Q

Describe the Direct relaxation of vascular smooth muscle

A
161
Q

Describe the Non-endothelium-dependent vasodilators

A
162
Q

Describe what Sodium Nitroprusside is used for

A
163
Q

Describe what Nitroglycerin is what its MOA

A
164
Q

Describe the PKs and ADRs of Nitroglycerin

A
165
Q

Describe Isosorbide dinitrate

A
166
Q

Describe Nifedipine

A
167
Q

Describe Dipyridamole

A
168
Q

What are the “Other Vasodilators”

A
169
Q

Describe EDRF and Endothelin

A

● Endothelin has structural similarities to venom of the Israeli burrowing asp
○ Victims die of heart attack (likely due to severe vasoconstriction)

172
Q

What are the Vasodilator Mechanisms?

A
  • Blockade of endogenous vasoconstrictors
  • Direct relaxation of vascular smooth muscle
  • Non-endothelium-dependent vasodilators
184
Q
A