Myocardial Ischaemia Epidemiology and Aetiology Flashcards
1
Q
ischaemic heart disease other names (4)
A
coronary artery disease (CAD), coronary heart disease, heart disease, micro-vascular heart disease
2
Q
heart disease that is more prevalent in women
A
micro-vascular heart disease
3
Q
CAD symptoms (2)
A
none or angina pectoris
4
Q
angina pectoris
A
chest strangling
5
Q
no symptoms
A
silent
6
Q
angina pectoris pain due to
A
lactate and adenosine activation of pain nerve endings
7
Q
CAD mortality rates peaked in
A
1966
8
Q
CAD mortality started to decrease after
A
coronary bypass surgery
9
Q
Framingham study started
A
1945-50
10
Q
CAD mortality rate linked to smoking
A
1955
11
Q
Coronary care units set up in Australia
A
1960-65
12
Q
Coronary bypass surgery used after MI
A
1970
13
Q
beta blockers first used for hypertension
A
1975
14
Q
MONICA study starts
A
1980-85
15
Q
Framingham shows 50% increase in MI with hypertension
A
1980-85
16
Q
Statins lower cholesterol
A
1985-90
17
Q
Statins and ACE inhibitors available PBS
A
1985-90
18
Q
statins most prescribed drug on PBS
A
2000-2005
19
Q
Leading causee of disease worldwide
A
CHD
20
Q
CHD deaths : dementia/stroke
A
2:1
21
Q
Number of Australians dying daily from CHD
A
48
22
Q
Cardiovascular disease with the most hospitalisations
A
CHD
23
Q
hospitalisation for CAD
A
men > women
24
Q
More deaths compared to hospitalisation
A
women
25
what is ischaemic heart disease
imbalance between oxygen supply and demand
26
Oxygen supply to the heart factors (3)
diastolic pressure, coronary oxygen resistance, carrying capacity
27
Oxygen demand factors (3)
ventricular wall stress, heart rate, contractility
28
increased muscle mass leads to
increased oxygen demand
29
ventricular wall stress that leads to increased oxygen consumption
intraventricular pressure (stretch) and systolic pressure (afterloading)
30
Ventricular wall stress that leads to decreased oxygen consumption
increased wall thickness
31
How heart rate increases oxygen demand
cardiac cycle energy expenditure
32
cardiac cycle energy expenditure
ATP splitting
33
ATP splitting (2)
Calcium homeostatis and cross bridge activity
34
how contractility leads to increased oxygen demand
increased ionotropic state (increased energy expenditure) andsympathetic modulation
35
when is coronary flow maximised
diastole
36
what determines coronary perfusion
aortic diastolic pressure
37
normal aortic diastolic pressure
60 mmHg
38
what is oxygen carrying capacity dependent on (2)
Haemoglobin levels and oxygen saturation (stability)
39
oxygen extraction in the heart is
maximised
40
what increases coronary resistance
vessel compression (maximised in systole)
41
vascular tone is
autoregulated
42
coronary resistance can lead to
vessel obstruction
43
Metabolic constrictor
oxygen
44
metabolic dilators (4)
adenosine, lactate, Hydrogen ions, carbon dioxide
45
Endothelial constrictors
Endothelin 1
46
What produces Endothelin 1 (2)
shear force and Angiotensin II stimulation
47
Endothelial dilators (2)
nitric oxide and prostacyclin
48
neural/hormonal constrictors
alpha 1 receptors
49
neural/hormonal dilators
beta 2 receptors
50
coronary dysfunction can lead to
autoregulatory failure
51
contributors to coronary dysfunction (3)
endothelial cell dysfunction, unopposed vasoconstriction, imbalance
52
what leads to endothelial cell dysfunction
nitric oxide defficiency
53
autoregulatory failure means (4)
increased cardiac work, irregular coronary flow, oxygen demand/supply mismatch, clots
54
what can cause clots in autoregulatory failure
loss of nitric oxide mediated suppression of platelet aggregation
55
Main features of coronary pathology (2)
atherosclerosis and thrombi formation
56
thrombus
clot
57
Normal arterial wall layers (3)
endothelial cells, elastic connective tissue, smooth muscle cells
58
Fatty streak features (3)
LDL cholesterol, macrophages, muscle cells
59
How is a fatty streak formed (3)
macrophages ingest lipids, streak forms, smooth muscle migration
60
Stable plaque features (4)
lipid core expansion, smooth muscle proliferation and thickening, plaque bulge, fibrous scar tissue cap
61
Vulnerable plaques (6)
plaque cap ruptures, collagen exposed, platelets aggregate, thrombus formation, downstream blood flow occlusion, calcifications
62
Anterior heart surface anatomy (7)
superior vena cava, right atrium, right auricle, left atrium, aorta, pulmonary artery, conus arteriosus, right ventricle, left ventricle
63
RCA
right coronary artery
64
LAD
left anterior descending branch of the left coronary artery
65
RCA runs between
right atrium and right ventricle
66
LAD runs between
Right ventricle and left ventricle
67
what is present in MI histology
calcifications
68
Plaque obstruction
stenosis
69
<70% stenosis
minimal effect on flow and compensatory dilation
70
70-90% stenosis
espisodic ischaemia
71
>90% stenosis
basal ischaemia
72
100% total occlusion
thrombosis
73
partial transient occlusion
hibernation
74
partial maintained occlusion
hibernation
75
total transient occlusion
stunning
76
total maintained occlusion
stunning
77
hibernation
chronic metabolism suppression
78
hibernation recovery
Re flow
79
stunning
prolonged contractile depression
80
stunning recovery
delayed
81
infarct
irreversible myocardium necrosis
82
what causes infarct
prolonged intense ischaemia
83
How is excitation contraction coupling maintained
ion flow (particularly calcium) and pumps
84
In depolarisation of a cardiomyocyte how does calcium enter the cell
sarcolemmal T tubule L type Ca channels
85
what does intracellular calcium do in a cardiomyocyte (2)
stimulates myofilament contraction and activates sarcoplasmic reticular calcium release
86
how is intracellular calcium reuptaken
SERCA pumps and ATP
87
What is required for calcium to be pumped out of a cardiomyocyte
ATP
88
How does sodium come into a cell
in exchange for hydrogen ions (elevates cardiomyocyte pH)
89
how does sodium leave a cell
sodium potassium exchanger or sodium calcium exchanger
90
What is there a reduction of in ischaemia (3)
oxygen, pH, ATP
91
What is there an increase of in ischaemia (3)
hydrogen, calcium and sodium ions
92
what is inhibited in ischaemia (5)
calcium pumps, sodium potassium exchanger, SERCA channels, mitochondrial function, myofilament contraction
93
Myocardial hypoxia leads to decreased (3)
ATPase pump activity, SR Ca uptake, cell pH
94
Myocardial hypoxia leads to increased (2)
sodium calcium exchanger and anaerobic metabolism
95
reduced ATPase and SR Ca uptake coupled with increased sodium calcium exchanger leads to (3)
increased calcium in, potassium out and sodium in
96
increased calcium in, potassium out and sodium in leads to (2)
lipase and protease activation and altered RMP
97
RMP
resting membrane potential
98
increased anaerobic metabolism coupled with decreased cell pH leads to
chromatin clumping and protein denaturation
99
altered RMP can lead to
arrythmias
100
lipase and protease activation coupled with chromatin clumping and protein denaturation can lead to
cell death
