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PATH300 > cardiovascular > Flashcards

cardiovascular Flashcards

1
Q

what is the #2 cause of death in Canada?

A

Atherosclerosis

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2
Q

what are the consequences of atherosclerosis?

A

myocardial infarct, stroke, aneurysm, peripheral vascular disease

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3
Q

what event initiates atherosclerosis?

A

endothelial injury and dysfunction

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4
Q

what is called the build-up in the intima in atherosclerosis?

A

buildup of atheroma

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5
Q

do veins have smooth muscle?

A

yes but thinner than arteries because they carry blood at lower pressure

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6
Q

do arteries or veins have valves? why?

A

veins: to maintain unidirectional blood flow against gravity

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7
Q

describe the 3 layers in the artery wall from inner to outer

A

intima: single layer of endothelial cells (all vessels)
media: smooth muscle
externa: connective tissue

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8
Q

describe the 3 layers of veins wall from inner to outer

A

endothelial cells
smooth muscle
external wall

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9
Q

what deposit on walls of the aorta?

A

cholesterol (fatty streak)

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10
Q

what is atherosclerosis?

A

harmful fibrous tissue accumulation in the intima

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11
Q

what are the 2 outcomes of atherosclerosis?

A

plaque rupture or grows until complete occlusion

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12
Q

what is an angina?

A

chest pain caused limited blood flow through coronary artery due to atherosclerosis

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13
Q

what is stenosis of the lumen?

A

narrowing of the lumen

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14
Q

what is a thrombus?

A

blood clot that can form on the plaque and cause vessel to rupture (stays there)

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15
Q

what can be caused by vessel occlusion in the periphery?

A

gangrene in extremities

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16
Q

what is the other term for angina?

A

transient ischemic attack

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17
Q

what causes the pain of angina?

A

inadequate blood flow during physical activity

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18
Q

what are the CNS symptoms of angina?

A

difficulty speaking and moving (happen transiently)

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19
Q

what is a myocardial infarction?

A

ischemic stroke: vessel occludes completely and causes death of cells in the brain or heart

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20
Q

what are the symptoms of peripheral arterial disease?

A

intermittent claudication (on and off blood flow to the legs causing pain during exercise)

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21
Q

what are the key components of atherosclerosis pathogenesis?

A

endothelial dysfunctions and chronic inflammation in the arterial intima

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22
Q

3 things that cause endothelial injury

A

hyperlipidemia, hypertension, smoking

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23
Q

how do vessels respond to injury of endothelial cells? what do these responses do?

A

retract (increase permeability) and release signaling molecules. this initiates atherosclerotic plaque formation

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24
Q

where is hemodynamic stress the most notable?

A

at branch points (area more susceptible to injury)

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25
Q

what are the 3 big sections of atherosclerosis pathogenesis?

A

hemodynamic stress, cell mediators/cytokines, lipoprotein accumulation

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26
Q

where is hemodynamic stress most notable?

A

at branch points

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27
Q

what induces smooth muscle proliferation after an injury?

A

mediators (macrophages, platelets, lymphocytes, fibroblasts, SM cells) and the growth factors they release

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28
Q

what kind of process is atherosclerosis development?

A

inflammatory process

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29
Q

what are foam cells?

A

modified macrophages formed after taking up LDL that release inflammatory cytokines/mediators

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30
Q

describe the function and structure of lipoproteins

A

carry lipids in blood.
inside = triglycerides and cholesterol
surface = phospholipids, free cholesterol, apoprotein

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31
Q

what type of lipoprotein has the most protein content? what does it do?

A

high-density lipoprotein HDL: brings lipids back to the liver

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32
Q

which lipoproteins are considered bad?

A

LDL and VLDL. they can deposit cholesterol to blood vessel walls

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33
Q

what are chylomicrons?

A

triglycerides from which we absorb lipids from intestines

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34
Q

how are LDLs a risk for atherosclerosis? (2 reasons)

A

their Apo B protein gets recognized by LDL receptor on cells -> LDL gets internalized and broken down in lysosome -> free cholesterol.
also, they activate inflammatory processes

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35
Q

what type of LDLs are most present in atherosclerosis plaques?

A

modified / oxidized LDLs

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36
Q

what are the 2 types of receptors that take up LDLs?

A

LDLR and scavenger receptors

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37
Q

what apoprotein is found on HDL surface?

A

Apo A

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38
Q

smooth muscle cells can form a fibrous cap on antheroplaque that has what function?

A

helps reduce risk of plaque rupture

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39
Q

how else do smooth muscle cells contribute to atherosclerosis?

A

accumulate lipids, synthesize collagen, elastin, glycoprotein, synthesize ECM -> enlarges the plaque / forms fibrous cap

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40
Q

what is an embolus?

A

something that moves through blood vessels and eventually blocks one that is too small to let it pass

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41
Q

name the cells involved in formation of a plaque

A

stem cells from bone marrow, foam cells

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42
Q

risk factors for atherosclerosis

A

hyperlipidemia, hypertension, smoking, toxins, obesity, metabolic syndrone, type 2 diabetes

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43
Q

what is caused by T2DM (type 2 diabetes mellitus)

A

high LDL, high triglycerides, high BP, low HDL

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44
Q

complications of atherosclerosis

A

ischemia (complete occlusion), renal ischemia, intermittent claudication, thrombus, embolus, plaque rupture (causes blood clot)

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45
Q

what is an aneurysm

A

weakening of vessel wall causes the vessel to bulge out because the artery is under pressure

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46
Q

how do cigarettes increase risk of atherosclerosis?

A

activates platelet aggregation, increased CO, impaired oxygen delivery, interferes with HDL production, hypertension,

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47
Q

what is familial hypercholesterolemia?

A

rare genetic defect in LDL receptors causing too much LDL in circulation, dengerous for atherosclerosis

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48
Q

what is PCSK9?

A

loss of function mutation that causes degradation of LDL receptors

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49
Q

what is the difference between saturated and unsaturated fat?

A

saturated = bad! lacks double bonds. decreases LDL receptors
unsaturated = good. protect you

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50
Q

which oil is the best?

A

canola; low saturated fat, high unsaturated

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51
Q

what is type 1 diabetes?

A

islets of langherhans are not making enough insulin

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52
Q

what is type 2 diabetes?

A

insulin resistance due to lifestyle (obesity)

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53
Q

what are metabolic syndrome symptoms?

A

abdominal obesity, hyperinsulinemia, high glucose levels, hypertriglyceridemia, low HDL, high HDL, hypertension

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54
Q

what does the activation of insulin receptors cause?

A

uptake of glucose, free fatty acids, and amino acids

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55
Q

how does diabetes affect LDL levels?

A

increases LDL in circulation

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56
Q

what % of people with T2DM die of coronary heart disease?

A

80%

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57
Q

how can insulin resistance affect endothelium?

A

glucose derivatives damage endothelium and ECM and can generate free radicals.
also increases vessel permeability.
can cause edema, ischemia, neovascularization

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58
Q

how are plasma C reactive proteins (CRP) related to coronary vascular disease?

A

higher CRP levels = more inflammation = diabetes

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59
Q

what is thrombosis?

A

formation of blood cloth in the vasculature

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60
Q

how is thrombosis developped from atherosclerosis?

A

platelets aggregate, adhere, and degranulate -> thrombosis

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61
Q

what is PGI2?

A

prostacyclin, an antithrombotic released by healthy endothelium

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62
Q

what does prostacyclin do?

A

promotes vasodilation and blocks platelet aggregation

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63
Q

3 contributors to thrombosis

A

endothelial injury -> abnormal blood flow and hypercoagulability

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64
Q

what can cause hypercoagulability?

A

changes in blood composition after childbirth or surgery (increased platelets, prothrombin, and fibrinogen)

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65
Q

what causes thrombosis in different vessels?

A

arteries: endothelial injury and plaque rupture
veins: slow blood flow, hypercoagulability & injury

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66
Q

what is deep vein thrombosis

A

DVT: stasis of blood flow in legs after sitting for long. possibility of thrombus forming

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67
Q

what can cause a thrombus in the heart?

A

infarct (damage to heart surface promotes platelets)

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68
Q

3 common sites of thrombus formation

A

heart, brain, periphery

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69
Q

what is the classical case of embolism

A

embolus form around the valves in deep vein in the legs, goes to heart then lungs -> pulmonary embolus

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70
Q

what can help in a small pulmonary embolus?

A

collateral circulation from bronchial artery

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71
Q

where will an embolus cause instant death?

A

if it’s stuck at the bifurcation to the heart

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72
Q

what happens if there is no collateral circulation?

A

infarct

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73
Q

what is blood flow proportional to?

A

the 4th power of the diameter of a vessel

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74
Q

what are the 2 main forces acting on artery?

A

BP and resistance to distension

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75
Q

where can micro-aneurysms be seen?

A

brain and retina

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76
Q

describe the 2 types of aneurysms

A

fusiform: bulges all around
saccular: localized on one side

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77
Q

where is berry aneurism?

A

in circle of Willis

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78
Q

what is cardiac tamponade?

A

tear in aortic wall and blood accumulates in pericardial sac; heart can’t pump properly

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79
Q

what causes varicose veins?

A

increased pressure in feet when standing up causes valves to not close properly

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80
Q

what proportion of blood is always in our venous system?

A

2/3

81
Q

pathogenesis of varicose veins (4 things)

A

prolonged standing, pregnancy, obesity, cellulitis

82
Q

what is the biggest risk factor for heart diseases?

A

hypertension

83
Q

what is the best value for blood pressure?

A

120/80 mmHg

84
Q

what is the cut-off BP value for risks of coronary heart disease?

A

140/90

85
Q

what happens with each 20/10 mmHg increase in BP?

A

cardiovascular mortality risk doubles

86
Q

how do high temperatures affect BP? why?

A

blood vessels vasodilate so BP decreases

87
Q

should BP increase with age? why does it do so in Canada and US?

A

no.
because we eat too salty

88
Q

what are the factors involved in essential/idiopathic hypertension?

A

salt, lack of exercise, obesity, drinking, smoking, stress, inadequate electrolytes, family history

89
Q

examples of how BP is controlled by body

A

arteries contract/relax,
autonomic nervous system,
endocrine system,
kidneys (renin-angiotensin system),
diet

90
Q

what is the “formula” of BP?

A

cardiac output x peripheral resistance

91
Q

how does salt affect BP?

A

more salt -> more water retention -> higher blood volume -> higher CO -> higher BP

92
Q

hypertension complication related to the heart?

A

cardiac hypertrophy

93
Q

which ventricle gets enlarged? why?

A

left. it enlarged to accommodate the increased blood volume and pressure

94
Q

hypertension complication related to arteries?

A

hypertrophy and hyperplasia of smooth muscle cells,
fibroblast proliferation into myofibroblasts, leukocytes recruitment,
arteriolosclerosis in small eye, kidney, adrenal vessels,
vascular damage

95
Q

3 random complications of hypertension on arteries?

A

renal failure, impaired vision, necrosis with fibrosis

96
Q

how can hypertension cause atherosclerosis?

A

causes vessels to narrow and have a thickened wall which increases pressure on branch points.
vicious cycle of one leads to the other

97
Q

what neurological disease can be caused by hypertension?

A

Alzheimer’s disease

98
Q

how does hypertension affect blood brain barrier?

A

increases permeability (bad because more things can enter and injure the brain)

99
Q

what is Charcot-Bouchard aneurysm?

A

weakening of the wall of vessel in the brain can lead to vessel repture

100
Q

what is fibroid necrosis?

A

formation of fibroid due to sever hypertension

101
Q

what is a transient ischemic attack?

A

TIA is a stroke that lasts a few minutes

102
Q

symptoms of hypertension syndrome

A

obesity, abnormal lipid and carbohydrate metabolism, diabetes, renal failure, blood clotting

103
Q

how does high salt intake affect vascular smooth muscle? how does it affect BP?

A

increase calcium uptake through Na+/K+ and Ca2+ exchange, which increases constriction and increases BP

104
Q

how does high salt diet affect the brain?

A

increases sodium in CSF which increases sympathetic activity & vasoconstriction

105
Q

lowering BP by as low as _____ mmHG can have lots of benefits

A

15 mmHg

106
Q

what compound can you increase in diet to help bring BP down? which one should you decrease?

A

increase potassium
decrease sodium and saturated fat

107
Q

what is ischemic heart disease?

A

impaired blood flow to the heart

108
Q

3 major vessels supplying the heart?

A

left anterior descending (most commonly blocked), right coronary artery, left circumflex

109
Q

coronary heart disease

A

Atherosclerotic plaque in arteries of the heart proximal to the main coronary arteries

110
Q

what is stenosis

A

narrowing of the lumen of a vessels

111
Q

at what % of blocked arteries do you start to see symptoms?

A

70% blocked

112
Q

what is angina pectoris and when does it happen

A

chest pain due to impaired blood flow to the heart

113
Q

what determines the preload to the heart?

A

venous return

114
Q

what is the afterload?

A

blood pressure; greater pressure = greater afterload = greater pumping

115
Q

characteristics of cardiac myocytes related to energy

A

high energy requirement (fuel Na/K pumps & need lots ATP)
low energy reserve (no big glucose store)

116
Q

where can angina pain be felt? why?

A

chest, neck, shoulder, left arm, jaw.
due to convergence in afferent pathway on spinal column

117
Q

what other than atherosclerosis can cause angina?

A

coronary artery spasm

118
Q

how are coronary artery diseases detected?

A

ECG treadmill stress test

119
Q

how can angina be treated? in what cases does this treatment not work?

A

vasodilator nitroglycerin. can’t relax smooth muscle if there is a circumferential atherosclerotic plaque

120
Q

what surgery for angina?

A

coronary artery bypass surgery with left internal mammary artery (if LAD is blocked)

121
Q

describe the other procedure (not a major surgery) to solve angina

A

coronary angioplasty: balloon inflated in the vessel to break the atherosclerotic plaque. now, we can also place a stent that can release vasodilators

122
Q

what is myocardial infarct

A

total occlusion of the blood flow to a portion of the heart

123
Q

4 causes of occlusion in myocardial infarct

A

thrombus, embolus, hemorrhage, spasm

124
Q

what is a variant angina?

A

angina caused by coronary artery spasm. can’t cause an infarct

125
Q

what % of myocardial infarct lead to svdden death

A

20%

126
Q

where will you feel pain during myocardial infarct

A

left side of the chest, arm, and face

127
Q

whats the most important variable in an infarct?

A

collateral circulation

128
Q

2 different types of heart failure (consequences of infarct)

A

mechanical failure (section can’t beat)
electrical failure (arrhythmias)

129
Q

what do you see on ECG for coronary artery ischemia, injury, and infarct?

A

ischemia: t wave inversion
injury: S-T segment elevation
infarction: Q wave inversion

130
Q

how does the blood change after myocardial infarct?

A

myocytes enzymes and higher neutrophil count. (can be used to measure severity of injury)

131
Q

3 markers of acute myocardial infarct

A

myoglobin
troponin
CK-MB

132
Q

what is ventricular fibrillation? how to treat it?

A

uncoordinated electrical activity of the ventricles.
treatment = defibrillatory shock

133
Q

what drugs can help in the 4 hours after arrhythmia attack?

A

thrombolytic drugs

134
Q

how will they treat you in coronary care unit?

A

electroshock, antiarrhythmic drugs, thrombolytic drugs, oxygen, morphine, nitroglycerine, B-blockers

135
Q

complications of MI

A
  • thin ventricle wall
  • thrombus
  • cardiac rupture (Death)
  • papillary muscle rupture
  • ventricular septal defect
  • ventricular aneurysm
136
Q

what are C-reactive proteins

A

proteins whose levels are elevated in inflammatory diseases. increase risk of cardiovascular death

137
Q

can heart disease be reversed?

A

yeah

138
Q

what are medication against heart diseases?

A

timolol: beta-blocker that keeps BP down
aspirin: reduces clumping of platelets

139
Q

describe the trajectory of an electrical wave in the heart

A

SA node -> through the atria -> AV node -> bundle of His -> right/left bundle branch -> purkinje fibers -> cardiomyocytes

140
Q

what is the main pacemaker of the heart?

A

SA node.
AV node is the back up pacemaker

141
Q

what are the rates of the SA node, AV node, and ventricular system?

A

SA node = 60-100 bpm
AV node and HIs-purkinje system = 40-60 bpm
Ventricular system = 20-45 bpm

142
Q

what are called the specialized connections between myocytes? what is their role?

A

intercalated disks: allows rapid spreading of the action potential and provide better coordination

143
Q

what causes the initial rise in membrane potential that triggers the AP?

A

Na+ inflow through fast V-gated channels opening

144
Q

what happens after the initial Na+ influx?

A

depolarization plateau maintained by Ca++ influx, then K+ outflow allows repolarization

145
Q

what are the effect of the sympathetic stimulation on the heart

A

increases contractility, frequency, conduction velocity, irritability

146
Q

what neurotransmitter transfers sympathetic stimulation?

A

noradrenaline and adrenaline

147
Q

what neurons work to slow the pacemaker down?

A

vagal motor neurons

148
Q

explain the ECG waves

A

P wave = atrial depolarization
QRS complex = ventricular depolarization
T wave = ventricular repolarization

149
Q

what is the type of arrhythmia that slows vs increases heart rate?

A

bradycardia = slow heart rate
tachycardia = rapid heart rate

150
Q

what is sinus bradycardia?

A

impulses originating from SA node at a slow rate

151
Q

what is respiratory sinus arrhythmia?

A

faster heartbeat when breathing in, slow when breathing out (harmless)

152
Q

atrial arrhythmia pathogenesis: what is heart block

A

AV node block. only P wave is seen on ECG

153
Q

atrial arrhythmia pathogenesis: what is ectopic focus?

A

atrial fibrillation: no coordinated contractions due to random electrical activity in the heart. dangerous but doesn’t necessarily kill

154
Q

atrial arrhythmia pathogenesis: what is circus re-entry?

A

damaged purkinje branch causes signal to travel in opposit direction

155
Q

what are the consequences of atrial arrhythmia?

A
  • sinus (SA node) arrest
  • flutter (rate 200-400 bpm
  • fibrillation: unsynchronized contractions
156
Q

what do pacemakers do?

A

kick in when SA node stops functioning

157
Q

why is ventricular function critical in atrial arrhythmias?

A

If the ventricles are functioning normally, the person will most likely stay alive

158
Q

what does it do that the inside of the heart is a thrombogenic surface?

A

increasing risk of thrombus that can lead to stroke if blocking vessel to brain

159
Q

what are the 2 biggest risk factors for a stroke?

A

atrial fibrillation and hypertension

160
Q

what are consequences of ventricular fibrillation?

A

death within minutes

161
Q

when can a defibrillator be used?

A

during ventricular defibrillation

162
Q

what is systole vs diastole?

A

systole = ventricles contract
diastole = ventricles relax, atria contract

163
Q

what is stenosis? what can it cause?

A

narrowing of the opening of a valve. can cause regurgitation (blood flows backward)

164
Q

what is incompetence?

A

valve can’t close properly

165
Q

what causes rheumatic heart disease?

A

ear or throat infection with B-hemolytic streptococcus (similar antigen on heart valves)

166
Q

what is the major cause of heart valve damage?

A

rheumatic heart disease. can become chronis

167
Q

what are causes of valve diseases?

A

rheumatic heart disease, IV drug use, immunocompromission, sepsis, streptococcy, staphylococcy, fungi

168
Q

what is aortic stenosis? what are the symptoms?

A

calcification of the aortic valves.
symptoms = angina, syncope

169
Q

what is syncope?

A

fainting due to inadequate blood flow to coronary arteries

170
Q

how does the heart adapt to aortic stenosis?

A

left ventricle hypertrophy

171
Q

what is aortic regurgitation and the symptoms?

A

aortic valve can’t close properly, blood flows back into left ventricle.
symptoms = fatigue, dyspnea

172
Q

how does the heart adapt to aortic regurgitation?

A

left ventricle dilation leading to heart failure eventually

173
Q

what are the symptoms of mitral stenosis? how does the heart adapt?

A

fatigue and dyspnea.
left atrium hypertrophies and dilates. right ventricle hypertrophies

174
Q

what is mitral regurgitation symptoms and adaptations?

A

dyspnea.
left and right ventricles dilate and hypertrophy

175
Q

how can heart valve disease be treated?

A

surgery to repair to valve

176
Q

What is the final outcome of arrhythmias and valvular heart disease?

A

congestive heart failure

177
Q

describe congestive heart failure

A

Inadequate cardiac output leads to tissue that become congested because of edema and fluid flowing out of the vasculature

178
Q

what are the symptoms of congestive heart failure?

A

swollen ankles, kidneys retaining fluid, enlarged heart, congested lungs

179
Q

what are the causes of congestive heart failure?

A

CHD congenital heart disease, hypertension, valvular disease, arrhythmia

180
Q

what is the link between left ventricular hypertrophy, coronary heart disease, renal failure, peripheral vascular disease, retinopathy, brain hemorrhage, stroke?

A

can all be caused by hypertension!

181
Q

sequence of 4 events leading to heart failure

A
  1. loss of myocardia efficiency
  2. initiation of compensatory mechanisms (hypertrophy, dilation, tachycardia)
  3. failure of compensatory mechanisms
  4. heart failure
182
Q

what causes left vs right ventricular hypertrophy?

A

LVH = hypertension
RVH + dilation = COPD
both can be caused by mitral valve disease

183
Q

what is backward failure?

A

blood backs up into venous circulation

184
Q

what is forward failure?

A

insufficient blood flow

185
Q

what do both backward and forward failure lead to?

A

edema and congestion of tissue

186
Q

what are the symptoms of backward and forward failure?

A

edema, cyanosis, dyspnea, orthopnea, fatigue, weakness, nocturia, increased venous pressure

187
Q

what is a cardiogenic shock?

A

drop in blood pressure incompatible with life due to heart failure. caused by heart failure, most often LV

188
Q

what % of CO is directed to the brain?

A

20%

189
Q

what causes a stroke?

A

atherosclerosis in vessels leading to brain and ischemia

190
Q

what is FAST (signs and symptoms of a stroke)?

A

Face dropping
Arm weakness
Speech difficulty
Time to call 911

191
Q

what are the causes of intracranial hemorrhage?

A

hypertension, amyloid, ruptured aneurysms

192
Q

where in the brain do aneurysms tend to occur?

A

circle of willis

193
Q

what is treatment to avoid rupture (against intracranial hemorrhage)

A

coils inserted in the aneurysms to stabilize it

194
Q

what is the risk with saccular aneurysm and subarachnoid hemorrhage?

A

if they rupture there is a 50% chance of death

195
Q

which artery of circle of Willis is the most frequent site of damage?

A

middle cerebral artery

196
Q

what are the consequences of an incident at the middle cerebral artery?

A

contralateral hemiplegia, hemianesthesia, speech impairment (half of the body is affected)

197
Q

how can neuronal plasticity help after intracranial hemorrhage?

A

can rescue symptoms; possibility of functional recovery

198
Q

what is multi-infarct dementia?

A

small areas of injury all over the brain (mini-emboli)

199
Q

what are the risk factors for stroke?

A

elevated systolic blood pressure, diabetes, cigarette smoking, prior atrial fibrillation, prior CVD, alcohol, high cholesterol

PATH300 (10 decks)

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