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Flashcards in Pathology Deck (158):
1

Definition of atherosclerosis? (Pg 83)

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2

What are plaques made of? (Pg 83)

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3

Where do the plaques occur in atherosclerosis? (Pg 83)

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4

Structure of Tunica Intima (Pg 84)

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5

Tunica Media structure and function (Pg 84)

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6

Structure and contents of Tunica Externa (Adventitia

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7

What are the four (five) major positive risk factors for Atherosclerosis? (Pg 85)

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8

Three negative risk factors for atherosclerosis? (Pg 85)

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9

Have general understanding for Metabolic syndrome (Lecture slides or maybe Pg 85)

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10

What is the structure of lipoproteins and how do they modify the risk of atherosclerosis? (Pg 85)

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11

What does atherosclerosis appear like? (Pg 85)

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12

What is the first part of pathogenesis for atherosclerosis? (Pg 86)

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13

What is endothelial damage caused by? (Pg 86)

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14

What may endothelial damage lead to? Pg 86

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15

What is the second part of pathogenesis for atherosclerosis? (Pg 86)

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16

What occurs in the process of leukocyte migration in atherosclerosis? Pg 86

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17

Third pathogenesis step for atherosclerosis? Pg 86

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18

What activates smooth muscle cells and what do they turn from and what do they turn to? Pg 86

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19

What do smooth muscle cells do once activated in atherosclerosis? Pg 86

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20

What accelerates migration of smooth muscle cells from the Tunica media to the Tunica intima?

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21

3 Consequences of atherosclerosis? Pg 87

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22

Difference of fatty streak and vulnerable plaques? Pg 87

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23

Features of a pre clinical silent plaque in early age?

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24

How do vulnerable plaques suddenly cause symptoms? Pg 87

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25

What is haemostasis? Pg 155

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26

Haemostasis is accomplished by the co-operation of what 3 things? Pg 155

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27

What are the three ways endothelial cells inhibit haemostasis in healthy vessels? Pg 155

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28

What is an example of a chemical and an enzyme that is secreted by endothelial cells to inhibit platelet activation? Pg 155

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29

What does antithrombin do? Pg 155

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30

Two ways endothelial cells promote haemostasis after injury to a vessel? Pg 155

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31

What does von willebrand factor do and what is it secreted by? Pg 155

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32

What is thromboplastin, what secretes it and what does it do? Pg 155

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33

What is platelets made of? Pg 155

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34

What are platelets activated by? Pg 155

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35

What chemicals do platelets secrete and what do they do? Pg 155

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36

What is coagulation? Pg 155

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37

What is thrombin, what is it involved in, and what does it do? Pg 156

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38

What is the fibrinolytic system, and when is it activated? Pg 156

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39

What is a thrombi composed of? Pg 158

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40

What is thrombosis? Pg 158

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41

Where are two places thrombosis can occur? Pg 158

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What is the difference between a blood clot and a thrombus? Pg 158

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43

What are the three main predisposing factors known as? What are they? Pg 158

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44

What causes changes in vessel wall? Pg 158

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45

What are examples of changes in vessel walls? Pg 158

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46

Why is anti-coagulation medication given to post-op vascular implant patients? Pg 158

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47

What changes in blood flow in arteries or cardiac chambers cause thrombosis? Pg 159

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48

What changes in blood flow in veins cause thrombosis? Pg 159

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49

What are the most common veins that are affected by thrombosis? Pg 159

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50

What causes stasis in veins? Pg 159

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51

What causes a change in blood constituents/hyper-coagulability? Pg 159

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Five fates of thrombi Pg 159

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53

What is an embolus? Pg 159

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54

Types of emboli? Pg 159

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What causes the effects of an emboli? Pg 159

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56

What are examples of emboli on the right side of the heart and what do they cause? Pg 159

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57

What are examples of emboli on the left side of the heart and what do they cause? Pg 159

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58

What is the function of heart valves? Pg 195

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59

What are the two main types of heart valve diseases? Pg 195

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60

Six common pathogenic mechanisms in valvular heart disease? Pg 196

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61

What is myxomatous mitral valve degeneration? Pg 196

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62

Why can mitral valve prolapse cause endocarditis? Pg 196

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63

How does dystrophic calcification occur? Examples of it in heart valves? Pg 196

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64

What is infective endocarditis? Pg 197

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65

What is a physical property of heart valves shown in infective endocarditis? Pg 197

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66

What is the properties of acute endocarditis and what is it caused by mainly? Pg 197

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67

What is the properties of sub-acute endocarditis and what is it caused by mainly? Pg 197

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68

What is shown under histological slides for bacterial endocarditis? Pg 198

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69

What is the current believed pathogenesis for rheumatic fever? Pg 198

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70

What is rheumatic fever and what is it caused by? Pg 198

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71

What does rheumatic fever lead to? Pg 198

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72

What is the main problem with rheumatic fever? Pg 198

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73

What are aschoff bodies? Pg 198

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74

What cardiac conditions recommend an endocarditis prophylaxis? Pg 198

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75

What are the difference of Non-bacterial thrombotic endocarditis and infective carditis? Pg 199

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76

What may be the causes of NBTE? Pg 199

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77

What is a carcinoid tumour? Pg 199

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78

What causes a carcinoid tumour, what do they cause, and why does it occur on the RHS valves mainly? Pg 199

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79

What is the definition of syncope and what are some of its features? Pg 161

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What do we sort presentations of LOC in to? Pg 161

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What are some disorders that can mimic syncope? Pg 161

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What is the most important and high yielding diagnostic tool for syncope? Pg 161

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83

What kind of things in the history should be taken? Pg 161

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84

Why is more caution with diagnoses taken with elderly? Pg 161

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85

What is examined with initial examination when presented with syncope? Pg 161

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What are some investigations to do when appropriate for syncope? Pg 161

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What is the diagnosing method for syncope? Pg 161

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What is the most common syncope? Pg 161

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89

What are the causes of neurally-mediated syncope? Pg 161

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What are the physiologic reflex mechanisms that neurally mediate neurally-mediated syncope? Pg 162

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What is a treatment strategy for neurally mediated syncope? Pg 162

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92

What are some causes of orthostatic hypotension syncope? Pg 162

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What are treatment strategies for orthostatic hypotension syncope? Pg 162

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Why is it important to distinguish cardiac syncope from the other types of syncope? Pg 163

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What CV diseases may cardiac syncope be warning of? Pg 163

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What is the definition of a palpitation? Pg 164

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Are they benign or malignant mostly? Pg 164

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Main way to asses palpitations? Pg 164

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99

How do the ventricles work in utero? Pg 177

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100

What is hydrops and what does it indicate? Pg 177

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101

What problems can effect pump function and cause hydrops in a foetus? Pg 177

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102

What is the major problems that occur in a sick newborn? Pg 177

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103

What happens to circulation when transitioning from foetal to neonatal life? Pg 177

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104

What presentations in the first 24 hours after birth might be the sign of a congenital heart disease? Pg 177

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105

What will heart murmurs in a neonate NOT be? Pg 177

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106

What do patients with PDA dependant lesion for pulmonary blood flow present with and why? What happens when it gets worse (ductus arteriosus closes)? Pg 177

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107

How do you treat patients with PDA dependant lesions for pulmonary blood flow? Pg 177

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108

What do patients with PDA dependant lesion for systemic flow present with and why? What happens when it gets worse (ductus arteriosus closes)? Pg 177

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109

How do you treat patients with PDA dependant lesions for systemic blood flow? Pg 177

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110

What do patients with PDA dependant lesion for mixing present with and why? What happens when it gets worse (ductus arteriosus closes)? Pg 177

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111

What congenital abnormalities present at age 2-6 weeks, and why then? Pg 176

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112

What happens to the heart and lungs in VSD's at 4-6 weeks if still undetected? Why? Pg 176

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113

What are the symptoms and signs of heart failure in infants? Pg 177 (LECTURER MENTIONED THIS IS ALL YOU REALLY NEED TO KNOW FOR THIS LECTURE)

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114

What murmurs are heard in large VSD's and small VSD's and why? Pg 178

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115

When do ASD's present? Pg 178

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116

What does a decrease in ventricular compliance cause in ASD'S? pG 178

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117

What do ASD's usually present with? Pg 178

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118

What's the difference between closing an ASD in childhood and later in life? Pg 178

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119

How are ASD's detected? Pg 178

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120

What is the cardinal diagnostic sign of a ASD? Pg 178

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121

What is the definition of ischaemia? Pg 167

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122

What is hypoxia, and what is it in relation to ischaemia? Pg 167

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123

What is a complete lack of oxygen called? Pg 167

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What else does ischaemia cause in addition to hypoxia? Pg 167

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125

What are possible causes of ischaemia and examples of them? Pg 167

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126

How does septic shock cause ischaemia? Pg 167

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127

What are examples of increased O2 demand? Pg 167

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128

In order from most sensitive to least, name cell types that are sensitive to ischaemia. Pg 168

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129

What happens to neutrophils in normoxia and hypoxia? Pg 168

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130

What transcription factor is activated in neutrophils in hypoxia? Pg 168

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131

What does the outcome of vessel occlusion additionally depend on? Pg 168

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132

What is opposite to collateral circulation/organs and what is more resistant to ischaemia? Pg 168

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133

Is vessel diameter directly or inversely proportional to volume of ischaemic tissue? Pg 168

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134

How does speed of onset of ischaemia determine the outcome of vessel occlusion? Pg 168

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135

The outcomes of ischaemia on the cellular level? Pg 169

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136

Range of possible outcomes of ischaemia on tissue level? From least to worst. Pg 169

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137

What are some tissue adaptations that occur in ischaemia? Pg 169

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138

What is the definition of infarction? Pg 169

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139

What are most infarctions caused by? Pg 169

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140

What are the different types of infarctions? Pg 169

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141

What type of infarction does re-perfusion injury cause? Pg 169

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142

What are the main characteristics of a white infarction? Pg 169

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143

What is the dominant appearance after infarction in most solid organs? Pg 169

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144

Describe the process of acute inflammation caused, where does this process occur? Pg 169

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145

What cell types are responsible for the process of organisation in acute inflammation? Pg 169

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146

What is granulation tissue remodelled into? When does this occur? Pg 169

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147

What is ischaemic heart disease (IHD)? Pg 169

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What is IHD usually caused by? Pg 169

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149

List clinical syndromes that occur as a result of IHD listing from least sever to most severe. Pg 169-170

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150

What is angina pectoris? Pg 169

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151

Why does angina pectoris NOT cause cellular necrosis? Pg 169

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152

When does a myocardial infraction commonly occur? Pg 170

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153

What is the difference of a transmural infarction and a subendocardial infarct? Pg 170

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154

How does an MI cause a mural thrombosis? Pg 170

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155

What other complications can occur from and MI? Pg 170

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156

Name some treatment options that aim at rapid restoration of blood flow? Why is rapid restoration needed? Pg 170

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157

What is a major concern of restoring blood flow in an MI? Pg 170

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158

What is the result of re-perfusion after long periods of ischaemia? Is the result the same after short periods? Pg 172

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