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Physiology 2 > KIN 407 > Flashcards

KIN 407 Flashcards

1
Q

What is heart disease?

A

An umbrella term for a number of different diseases that affect the heart. Examples include CAD, CHD, cardiomyopathy, and heart failure.

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2
Q

What are other names for coronary artery disease?

A

Coronary heart disease and ischemic heart disease

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3
Q

What is the number one killer for heart disease?

A

Coronary Artery Disease

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4
Q

What is coronary artery disease?

A

Fatty deposits build up in blood vessel walls and narrow the passageway for the movement of blood. The resulting condition, called atheroscelerosis, often leads to eventual blockage of the coronary arteries, angina pectoris (chest pain), and myocardial infarction (heart attack)

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5
Q

Athersosceloris?

A

Some blood flow is still allowed`

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6
Q

Atherosceloris with a clot?

A

No blood flow

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7
Q

Spasm?

A

Occludes blood flow or completely blocks it

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8
Q

Ischemia?

A

Reduced blood flow

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9
Q

3 symptoms of coronary artery syndrome?

A

Reduced blood flow, chest pain (angina), and myocardial infarction (MI)

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10
Q

What is a hypoxic heart?

A

Low oxygen

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11
Q

What are the signs of a hypoxic heart?

A

Angina pectoris, arrhythmia, and heart failure

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12
Q

What is an anoxic heart?

A

No oxygen

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13
Q

What does an anoxic heart cause?

A

Infarction (death) of the tissue supplied by that artery

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14
Q

Primary prevention of heart disease is?

A

Health promotion and education

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15
Q

Secondary prevention of heart disease is?

A

Cardiac rehab

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16
Q

What is cardiac rehab?

A

The sum total of all interventions, physiological and behavioural, designed to favourably modify an individual’s lifestyle and enhance adherence and compliance with long-term behaviours compatible with minimizing disease progression

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17
Q

4 main parts of cardiac rehab?

A
  1. Medical evaluation 2. Physical activity and exercise 3. Lifestyle education (risk factor ducation) 4. Support
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18
Q

Ultimate purpose of the cardiovascular system?

A

Exchange gases, fluids, elextrolytes, large molecules, and heat

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19
Q

Where is the heart located?

A

Beneath the sternum, on the left of the body

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20
Q

Purpose of valves?

A

TO ensure one way flow

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21
Q

Where is the tricuspid valve located?

A

Between the right artium and right ventricle

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22
Q

Where is the mitral/bicuspid valve located?

A

Between the left atrium and left ventricle

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23
Q

Where are the semilunar valves located?

A

Between the ventricles and arteries (aorta and pulmonary)

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24
Q

Layers of the heart from superficial to deep?

A

Pericardium (fibrous and serous), pericardial cavity, epicardium, myocardium, endocardium

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25
Q

What is the purpose of the pericardium?

A

Prevents over-distension

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26
Q

What is the purpose of the pericardial cavity?

A

Contains a small amount of fluid to prevent friction when the heart beats

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27
Q

2 cell types to consider in the heart?

A
  1. myocyte…mature myocardial cell; contraction 2. autorhythmic cell…electrical activity
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28
Q

Differences in cardiac muscle versus skeletal muscle?

A
  1. Smaller, single nucleus 2. High density of mitochondria 3. Presence of intercalated discs to allow for quick transmission of action potential through the heart
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29
Q

What troponin isoforms are different in cardiac muscle?

A

TN-I and TN-T…TN-C is the same

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30
Q

Cells capable of electrical excitation in the heart?

A

Ventricular and atrial cells (normally not spontaneous), Purkinje fibres (specialized, rapidly conducting tissue), pacemakers (SA node, preferred. AV node, backup)

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31
Q

Resting membrane potential of ventricle?

A

-90 mV

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32
Q

RMO of Purkinje fibres?

A

-95 mV

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33
Q

RMP of SA node?

A

an unstable -60 mV

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34
Q

Ions move by…

A
  1. Diffusion, down their concentration gradients through specialized gates dependent on voltage 2. Active transport against their concentration gradient
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35
Q

Resting potential?

A

Electrical charge difference between inside and outside the cell

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36
Q

MP determined by?

A
  1. Concentration of ions on the inside and outside of the cell 2. The permeability of the cell membrane to those ions through specific ion channels 3. The activity of the pumps (Na+/K+ pump) that maintain hte ion concentrations across teh membrane
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37
Q

Steps in an action potential in a NON-PACEMAKER cell?

A

Phase 4: flat slope, Na+/K+ channels closed. Phase 0: Increase in Na+ conductance, the more + cell becomes, more Na+ channels open, at -70 mV (threshold potential) self-sustaining inward flux of Na+ leads to an action potential and stimulates the cells to contract. Phase 1: Na+ channels close, K+ and Cl- open, which starts repolarizing the cell. Phase 2: Ca2+ influx to stabilize cell (offset by K+ out), lengthens the depolarixed stage allowing Ca2+ to trigger Ca2+ in myocyte and to prevent another AP and contraction (want blood to completely empty). Phase 3: Rapid repolarization, K+ diffuses out, return to -90mV

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38
Q

Action potential in pacemaker cells?

A

Phase 4: the resting potential of a pacemaker cell (-60mV to -70mV) is caused by a continuous outflow or “leak” of potassium ions through ion channel proteins in the membrane that surrounds the cells. The difference is that this potassium permeability decreases as time goes on, partly causing the slow depolarization. As well as this, there is a slow inward flow of sodium, called the funny current, as well as an inward flow of calcium. This all serves to make the cell more positive.
This relatively slow depolarization continues until the threshold potential is reached. Threshold is between -40mV and -50mV. When threshold is reached, the cells enter phase 0. Phase 0: Though much faster than the depolarization caused by the funny current and decrease in potassium permeability above, the upstroke in a pacemaker cell is slow compared to that in an axon.
The SA and AV node do not have fast sodium channels like neurons, and the depolarization is mainly caused by a slow influx of calcium ions. (The funny current also increases). The calcium is let into the cell by voltage-sensitive calcium channels that open when the threshold is reached. Phase 3: The calcium channels are rapidly inactivated, soon after they open. Sodium permeability is also decreased. Potassium permeability is increased, and the efflux of potassium (loss of positive ions) slowly repolarises the cell.

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39
Q

Spread of depolarization in heart?

A

SA node–>across both atrium–>AV node–>AV node delay–>AV bundle/bundle of Hiss–>Left and Right bundle branches–>Purkinje fibres

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40
Q

P wave?

A

Atrial contraction

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41
Q

QRS complex?

A

ventricular contraction and atrial repolarization

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42
Q

T wave?

A

Ventricular relaxation

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43
Q

Excitation-contraction coupling?

A

o Action potential enters from adjacent cell via gap junctions in the intercalated disk
o Voltage-gated Ca2+ channels open, and Ca2+ enters the cell
o Ca2+ induces Ca2+ release through ryanodine receptor-channels (RyR)
o Local release causes a Ca2+ spark
o Summed Ca2+ sparks create a Ca2+ signal
o Ca2+ ions bind toTN-C, which allows TN-I t move out of the way, thus exposing the active site on actin for myosin to bind, this initiates contraction
o Relaxation occurs when Ca2+ unbinds from TN-C
o Ca2+ is pumped back into the SR for storage
o Ca2+ is exchanged with N1+ by the NCX antiporter
o Na+ gradient is maintained by the Na+/K+ ATPase

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44
Q

Path of blood flow through the heart?

A

SVC and IVC to right atrium through tricuspid valve to right ventricle through the pulmonary semilunar valve to the pulmonary trunk to the lungs through the pulmonary veins to the left atrium through the mitral/bicuspid valve to the left ventricle through the aorta valve to the aorta to the rest of the body

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45
Q

3 main coronary arteries?

A

Right coronary artery, left anterior descending artery, and left circumflex artery

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46
Q

When do the coronary arteries and heart muscles receive blood?

A

During diastole (when the aortic valve is closed)

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47
Q

If the right coronary artery is blocked, where will an MI occur?

A

Inferior and posterior right heart heart

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48
Q

If the left anterior descending coronary artery is blocked, where will an MI most likely occur?

A

Left ventricular anterior wall, anterior septal wall, anterior right ventricular wall

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49
Q

Is the left circumflex artery is blocked, where will an MI most likely occur?

A

Lateral and posterior left ventricle

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50
Q

Systole?

A

Contraction of heart

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51
Q

Diastole?

A

Relaxation of heart

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52
Q

ESV?

A

blood remaining in left ventricle following contraction

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53
Q

EDV?

A

blood remaining during ventricular relaxation

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54
Q

Stroke VOlume?

A

EDV-SV

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55
Q

Preload?

A

pressure (force) on the left ventricle prior to contraction

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56
Q

Afterload?

A

pressure (force) against which the left ventricle is working during contraction (measured as the pressure in the aorta during contraction)

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57
Q

Cardiac output?

A

total amount of blood ejected from ventricle in 1 min… = HR x SV

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58
Q

Normal resting CO (Q) value?

A

5 L

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59
Q

Normal CO (Q) value during exercise?

A

25 L

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60
Q

Spontaneous rate of SA node?

A

100-115 bpm

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61
Q

Why is RHR lower than the spontaneous rate in the SA node?

A

PNS stimulation of Ach on muscarinic receptors via the vagua nerve lowers it to 60-8- bpm

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62
Q

How is HR increased during exercise?

A

Remove PNS stimulation, then SNS stimulation and increased catecholamines increases it above 100-115 bpm

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63
Q

How does the SNS increase HR?

A

Releases NE from sympthathetic neurons that act on Beta-2 receptors, which increases Na+ and Ca2+ influx, causing earlier depolarization, and thus an increased HR. E from the adrenal medulla works the same way.

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64
Q

How does the PNS slow HR?

A

Releases Ach onto muscarinic receptors, which increases K+ efflux and Ca2+ influx, so hyperpolarizes cell, slowing the rate of depolarization, which decreases HR

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65
Q

Mechanisms that increase EDV by increasing venous return?

A

Venoconstriciton, respiratory pump, muscle pump, and increased blood volume

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66
Q

What is the Frank-Starling mechanism?

A

states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant. The increased volume of blood stretches the ventricular wall, causing cardiac muscle to contract more forcefully (the so-called Frank-Starling mechanisms

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67
Q

How do neuronal and hormonal mechanisms increase SV?

A

NE and E decrease ESV by increasing the force of contraction by letting in more Ca2+ for the myocardial muscle cell to use

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68
Q

How does afterload affect SV?

A

It decreases it!

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69
Q

Ejection fraction?

A

Amount of blood ejected from the left ventricle as a % of total volume of blood in left ventricle prior to contraction… SV / EDV x 100%

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70
Q

Normal ejection fractioN?

A

50-70%

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71
Q

Ejection fraction that may confirm diagnosis of systolic heart failure?

A

35-40%

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72
Q

Ejection fraction that may cause a person to be at risk for life-threatening irregular heart beats?

A

<35%

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73
Q

Systolic BP?

A

Pressure in arteries during contraction…110-120 mmHg

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74
Q

Diastolic BP?

A

Pressure during relaxation…80 mmHG

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75
Q

Pulse pressure?

A

Systolic - Diastolic pressure. pressure that is felt when feeling the pulse

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76
Q

Mean arterial pressure?

A

average blood pressure in an individual. t is defined as the average arterial pressure during a single cardiac cycle. [2 DBP + SBP] / 3

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77
Q

The 3 things that regulate BP?

A
  1. Autonomic nervous system 2. Hormonal responses 3. Local control
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78
Q

How does the autonomic nervous system regulate blood pressure?

A

By its action on HR and SV and through the constriction of blood vessels by NE working on alpha1-adrenergic receptors

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79
Q

How do hormones regulate BP?

A

E works on beta receptors in the heart to cause vasodilation?

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80
Q

What does angiotensin II do?

A

Has both direct and indirect effects. Causes adrenal cortex to secrete aldosterone, the brain to release vasopressin, and stimulates thirst all of which increase Na+ and water retention. Also vasoconstricts the veins. All of these things increase/restore BP

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81
Q

What is vasopressin?

A

It is an anti-diuretic hormone that senses low blood volume and then causes smooth muscle constriction and reabsoprtion of water

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82
Q

Atrial natriuretic factor?

A

Released in atria when stretch via an increase in blood volume. Acts to reduce blood volume via inhibiting renin (no ANG II produced) and causing direct vasodilation

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83
Q

How does the local control system regulate BP?

A

Vasodilation in arterioles through changing [CO2], [H+], [K+], adenosine, and nitric oxide. Endothelin causes vasoconstriction, and so do oxygen.

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84
Q

KNOW SUMMARY OF BP CONTROL! (draw it out)

A

fdasoifh oa

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85
Q

What is oxygen uptake (VO2)?

A

Energy expended by the body in meeting the demands to perform work

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86
Q

Maximal oxygen uptake (mVO2)?

A

the maximal energy expenditure of the body…how much oxygen the body can take in and use

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87
Q

Myocardial oxygen uptake (mVO2)?

A

the demands placed on the heart to perform work

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88
Q

Fick equation?

A

VO2 = Q x (a-v)O2

89
Q

What is so different about the VO2 of the heart?

A

CO can increase as the demands of the heart increase, but O2 extraction is already near max at rest

90
Q

How is the myocardial oxygen consumption estimated?

A

The Rate Pressure Product

91
Q

What is RPP?

A

Rate Pressure Product and is equal to HR x SBP

92
Q

What is the RPP commonly used for?

A

To design rehabilitation programs for cardiac rehab patients so that they can achieve lower HR and SBP, so they can do more work before reaching the RPP that induces angina

93
Q

What are the 3 layers of the coronary arteries?

A

The intima, the media, and the adventia from innermost to outermost

94
Q

What does nitric oxide do in coronary arteries?

A

It’s a primary mediator of endothelial function (vascular relaxation) and dysfunction (contraction). Also, inhibits platelet, leukocyte activation and adhesion, inhibits smooth muscle cell proliferation

95
Q

Endothelial derived vasodilators?

A

NO, Prostacylclin, and Endothelium-derived hyperpolarizing factor

96
Q

Endothelial derived vasocontrictor?

A

Endothelin-1

97
Q

What causes tje endothlial-dependent vasodilators to be released?

A

Ach, serotonin, thrombin, and shear stress

98
Q

What causes endothelin-1 to be releaseed from the endothelium?

A

Thrombin, ANG II, and Epinephrine

99
Q

What is the intima?

A

Vascular endothelium, made up a single-cell and semi-permeable barrier

100
Q

4 ways intima is a mediator of vascular and hemodynamic homeostasis?

A
  1. Maintain vascular tone 2. Anti-thrombotic 3. Modualte immune response 4. Anti-proliferative
101
Q

How does the intima maintain vascualr tone?

A

Endothelin-1 (constrict) and NO, EDHF-1, and PGI2 (dilation)

102
Q

How is the intima anti-thrombotic?

A

Heparan sulfate, thrombomodulin, and plasminogen activators on the endothelial surface. And releases PGI2 and NO into the circulation.

103
Q

How does the intima modulate an immune response?

A

Resists leukocyte adhesion, opposing local adhesion an scavenges supoeroxide anions to prevent ROS formation

104
Q

How is the intima anti-proliferative?

A

NO inhibts smooth muscle proliferation, forcing them to stay in the media. Also, acts as a barrier to prevent blood cells from leaving and larger molecules from circulation entering

105
Q

What does the media consist of?

A

Vascular smooth muscle and ECM

106
Q

What are the contractile capabilities of the vascular smooth muscle in the media?

A

Vasoconstriction from ANG II and Endothelin-1. Vasodilation from Ach and NO.

107
Q

What can the media synthesize?

A

Collagen (strength), proteoglyvans (filler substance), and elastin (flexibility)…these make up ECM. Also, synthesizes vasoactive and inflammatory mediators including IL-6 and TNF-alpha that promote leukocyte proliferation and induce endothelial expression of leukocyte adhesion molecules

108
Q

What does the adventia contain?

A

Nerve, blood vessels, and lymphatic system that nourish the cell walls of the artery.

109
Q

What is endothelial dysfunctioN?

A

Refers to the pathophyiological disease state in which endothelial cells are perturbed promoting vasospasms, thrombus, intimal growth, inflammation, and plaque rupture leading to tissue ischemia, thrombosis, and MI

110
Q

How is endothelial dysfunction measured?

A

Via ultrasound

111
Q

Vascular damage to endothelial cells causes?

A
  1. Inc. permeability 2. Inc. inflammatory cytokines 3. Inc. leukocyte adhesion molecules 4. Dec. vasodilatory molecules 5. Dec. antithrombotic molecules
112
Q

Vascular damage leads to what in smooth muscle cells?

A
  1. Inc. inflammatory cytokines 2. Inc. ECM synthesis 3. Migration and proliferation into subintima
113
Q

6 key components of atherosclerosis?

A
  1. Endothelial dysfunction 2. Accumulation of lipids within the intima 3. Recruitment of leukocytes 4. Formation of foam cells 5. Smooth muscle cell migration 6. Deposition of ECM/hardening
114
Q

What 2 things can lead to endothelial dysfunction/vascualr damage?

A
  1. Physical force 2. Chemical irritants
115
Q

What areas of the vessels are most prone to injury?

A

Branch points…distrubed flow impairs normal endothelial protection

116
Q

What are chemical irritants that cause vascular damage?

A

Tobacco smoking, abnormal curculating lipid levels, diabetes, and increased production of ROS

117
Q

What happens during the accumulation of lipids within the intima?

A
  1. LDL enters into the intima 2. Once inside, LDL is trapped to proteoglycans and undergoes chemical modification by oxidation or glycation to become modified-LDL
118
Q

Steps in the recruitment of leukocytes?

A
  1. Leukocytes (monocytes) induced by mLDL and pro-inflammatory cytokines adhere and penetrate the intima 2. Monocyte differentiation into phagocytic macrophages that express receptors for mLDL
119
Q

Steps in the formation of foam cells?

A
  1. Scavenger mLDL forms foam cell 2. Pathological hallmark of the fatty streak (not reversible and only seen in autopsy) 3. Impaired efflux of these cells, leads to their accumulation in intima, which leads to apoptosis and release of proinflammatory cytokines that promote artheroscelrotic plaque progression
120
Q

Steps in smooth muscle migration?

A

Plaque progression (fatty streak –> fibrous plaque)…SMS migrate into intima and proliferate ecause of signals from foam cells, activated platelets, and endothelial cells release of growth factor

121
Q

Steps in deposits of ECM?

A

Secretion of collagen and elastin to form the fibrous cap…forming atheroma, gorwing lipid core (outward/positive remodeling) that can evolve into thrombogenic lipid core that underlies a protective fibrous cap. Determines overall integrity of plaque.

122
Q

Stable plaque?

A

Lesion with a thick fibrous cap and small lipid core, pronounced arterial narrowing…complicated lesion walled of by Ca2+, lumen narrowing >70%, grows until full blockage or rupture

123
Q

Vulnerable plaque?

A

Plaque with thinner caps, rich lipid core are less obstructive but are more likely to rupture and incite thrombosis,… <40% narrowing, but more susceptible to rupture…forms thrombus (can break off) or can be absorbed into plaque or cause a complete block

124
Q

Outward remodeling?

A

Positive…Away from the lumen and maintains lumen size (initial changes)

125
Q

Inward remodeling?

A

Negative…pushes into lumen and narrows it

126
Q

Complications of atheroscelrosis?

A
  1. Narrowing or occlusion 2. Calcification 3. Rupture 4. Hemorrhage into plaque 5. Embolism 6. Aneurysm
127
Q

Non-modifiable risk factors?

A

Advanced age, male gender, heredity

128
Q

Modifiable risk factors?

A

Tobacco smoking, hypertension, dyslipidemia, diabetes, metabolic syndrome, lack of physical activity

129
Q

What is a risk factor?

A

Characteristcs that appear to be assoicated with the development of heart disease…difficult to identify a cause-effect relationship

130
Q

Criterion for risk factors?

A
  1. Strength of association 2. Consistency of the relationship (under diverse circumstances) 3. Specificty 4. Temporality 5. Biological gradient 6. Plausibility 7. Coherence 8. Confirming animal or human research 9. Analogy
131
Q

Absolute risk?

A

probability of developing the disease over a certain period

132
Q

Relative risk?

A

Individual risk is compated to the average risk for age and gender, or compare to person with no risk

133
Q

Low absolute risk?

A

<10%

134
Q

Intermediate absolute risk?

A

10-20%

135
Q

High absolute risK?

A

> 20%

136
Q

Very high absolute risk?

A

?20% + history of CHD events and additional high risk features (diabetes, metabolic disease)

137
Q

Defining criteria for age as a risk factor?

A

Men greater than or equal to 45, women greater than or equal to 55

138
Q

Gender as a risk factor?

A

45-49 yrs CAD 4x more in male versus female. 65-69 yrs CAD 2x more in male vs female. 85 yrs is the same

139
Q

Why is the onset of symptoms 10 yrs earlier in males for CVD?

A

Protective effects of estrogen in premenopausal women…diabetes removes this protectection

140
Q

Genetics as a risk factor?

A

Strong independent risk factor for MI, coronary revascularization or sudden death in males <65 yrs. Positive family history relative risk = 1.5. Multiple family members increase the risk substantially.

141
Q

How much of CVD is controlled by genetics? By environmental factors?

A

40% genetics, and 60% environment

142
Q

Single most modifiable risk factor?

A

Smoking…accounts for 14.5% deaths per year. RR = 3 in people who lived with current smokers, progression 20% higher

143
Q

How does nicotine increase the risk of CVD?

A
  1. Induction of a hypercoaguable state due to nicotine (inc. thrombaxane A2 –> activates new platelets and increases platelet aggregation, inc. fibrinogen –> clotting, inc. factor Vii –> initiates clotting 2. Vasoconstriction of the coronary arteries due to nicotine (binds to nicotinic receptors in the adrenal medulla, releasing E and NE, which bind to alpha-adrenergic vasoconstriction, increasing TPR, which decreases flow), Causes direct damage to the epithelium 3. Direct effect on the heart (Binds to nicotinic receptors in adrenal medulla, release E and NE, increases the work of the heart, bind to beta receptors, inc. HR and in SV so inc Q, and therefore the RPP, which can trigger arrhythmias from ischemia. Nicotine causes inc O2 demand (work on heart) and arterial constriction and an increase to clot, causes the O2 cupply to NOT equal the O2 demand
144
Q

How does CO increase the risk of CVD?

A

Reduces oxygen delivery. Hb has 20x the affinity for CO, it inhibits the release of oxygen, and also causes osidative stress due to CO being highly reactive (injure the epithelium, oxidize LDL, and heart compensates by pumping harder to get more blood = more work put on heart)

145
Q

What does acrolein in smoke do?

A

Increase LDL (allows oxidation of LDL) and Decrease HDL (decrease HDL via reducing exercise capacity and inhibiting enzyme in HDL synthesis)

146
Q

What does smoking do to blood viscosity?

A

Increases it through RBC production

147
Q

In summary, how does smoking increase risk of CVD?

A

Impaired flow mediated dilation, promotes atherosclerosis, increased work of the heart with reduced bloodflow

148
Q

What is hypertension?

A

Chronically elevated BP, diastolic or systolic

149
Q

Why is hypertension called the silent killer?

A

No symptoms until disease is advanced…70% know they have it/30% don’t know.

150
Q

What is considered normal BP?

A

Systolic <80

151
Q

Prehypertensive BP?

A

Systolic 120-139 and Diastolic 80-90

152
Q

Stage 1 hypertension BP?

A

Systolic 140-159 and diastolic 90-99

153
Q

Stage 2 hypertension BP?

A

Systolic >160 and diastolic >100

154
Q

What is primary hypertension?

A

90% of people. No identifiable cause. Multiple defects of BP regulation that interact with environmental stress

155
Q

What is secondary hypertension?

A

10% of people. Is due to kidney abnormalities, narrowing of certain arteries, rare tumours, adrenal gland abnormalities, and pregnancy

156
Q

What are the causes of essential hypertension?

A
  1. Genetics 2. Heart (high CO due to overactive SNS) 3. BLood vessel vasoconstriction due to inc. SNS activity, ion channels defective, and abnormal regulation by local factors (NO and endothelin) 4. Kidney (volume based hypertenion due to excessive Na and H2O) 5. Elevated insulin 6. Obesity
157
Q

How do the contributions of CO and TPR change with age?

A

High BP in younger people is due to cardiac output, but as age increases it is due to TPR

158
Q

What are the consequences of hypertension?

A
  1. Increased work of the heart 2. Arterial damage resulting from elevated pressure that weaken the vessel walls and accelerated atherosclerosis
159
Q

Effects of hypertension on the heart?

A
  1. Inc BP = Inc afterload. This inc wall tension of the heart, causing left ventricular hypertrophy, so the heart can’t relac as well, leading to diastolic dysfunction, dec the fill, and therefore, O2 delivery. 2. Inc O2 demand because the heart is working harder 3. Systolic disfunction
160
Q

Effects of hypertension on the arteries?

A
  1. Arterial damage, increaed BP weakens the vessel wall, leading to SMS hypertophy in the intima, which inc stiffness. Also, fatigue of the elastic fibres. 2. Atherosclerosis…damage endothleium (vasoconstriction because drop in NO), induce thrombus and induce emboli
161
Q

How does chronic exercise decrease BP?

A

Chronic exercise = anti-inflammatory, improve endothelial function, neural.humeral changes (altered vascular responsiveness to SNS stimulation, and increased production of local vasodilators due to increased muscle BF and muscle contraction)

162
Q

Pharmacological treatment for hypertension?

A

Diuretics, beta-blockers, calcium channel blockers, ACE inhibitors, alpha-blockers, vasodilators, alpha-beta blockers

163
Q

How does exercise acutely effect hypertension?

A

Vasodilation

164
Q

What are chylomicrons?

A

Digested form of lipoprotein which is converted to VLDLs in the liver

165
Q

What are very low density lipoproteins?

A

Major transporter of TG in blood

166
Q

What are indtermediate density lipoproteins?

A

Transitional lipoprotein in the metabolism of LDL, highly related to atherosclerosis

167
Q

What are low density lipoproteins?

A

Major transporter of free cholesterol, most atherogenic

168
Q

What are high density lipoproteins?

A

Transport cholesterol to liver from periphery sites, used to make bile acids…reverse cholesterol transport, anti-inflammatory molecule, “good cholesterol”

169
Q

What is total cholesterol important for?

A

Cell structure, structure of sex hormones, vitamin D, and components of bile acid BUT also the main constituent of atherosclerosis. No threshold or absolute low level below which serum cholesterol ceases to be associated with the development of atherosclerosis

170
Q

Steps in the exogenous cholesterol transport pathway?

A
  1. Dietary fats are absorbed by the small intestines and repackagaed as chlyomicrons, accompanied by apo B-48 2. Apo E and subtypes of apo C are transferred to chylomicrons from HDL particles in the blood stream 3. Apo C enhances interactions of chylomicrons with lipoprotein lipase on the endothelial surface of adipose and muscle tissue 4. Chylomicron remnants are removed from the circulation by the liver, mediated by apo E 5. One fate of cholesterol in the liver is incorporated into bile acid, which is exported to the intestine, completing the exogenous pathway
171
Q

Steps in the endogenous cholesterol pathway?

A
  1. The liver packages cholesterol and TAGs into VLDL particles, accompanied by apo B-100 and phospholipid. The TAG content of VLDL is much higher than that of cholesterol, but this is the main means by which the liver releases cholesterol into the circulation 7. VLDL is catabolized by LPL, releasing FAs to the muscle and adipose tissue 8. Approx. 50% of the VLDL remnants (IDL) are then cleared in the liver by hepatic receptors that recognize apo E 9. The remaining IDL is catabolized further by LPL and hepatic lipase (HL), which remove additional trigylceride, apo E, and apo C, forming LDL particles 10. Plasma clearance of LDL occurs primarily via LDL receptor-mediated endocytosis in the liver and peripheral cells, directed by LDL’s apo B-100 and apo-E
172
Q

How does LDL-C progress and promote atherosclerosis?

A

LDL enters via injured endotheliu,, is oxidized, and attracts circulating monocytes, which differentiate in to macrophages, which bring in more choesterol and cause proliferation and migration of SMC to the intima, with the help of growth factors and cytokines

173
Q

How is HDL-C anti-atherogenic?

A

HDL prevents entry of cholesterol from establishing atherosclerotic lesions or actually removes it (reverse cholesterol transport)

174
Q

How is HDL-C anti-inflammatory?

A

Enhancement of endothelial function, rapid clearance of TG rich products and protection against oxidative effects of LDL

175
Q

What are triglycerides?

A

Storage form of fat that provides energy when fatty acids are degraded. Atherogenic. Strong relationship between TG and CAD, especially in combo with other RF (LDL, elevated glucose, etc)

176
Q

What are apoproteins?

A

Several major proteins associated with lipoproteins, function in cell membrane recognition and cofactor in metabolic reactions. ApoB-100 binds to LDL-directly , which reflects the number of circulating atherosclerotic particles.

177
Q

How does physical activity improve dyslipidemia?

A
  1. decrease size/increase density of lipoproteins 2. inc. LDL receptors in liver to take up more cholesterol 3. increase HDL synthesis enzymes 4. enhance FFA oxidation and increae LPL 5. Decrease TG, decrease LDL by 10-15%, and increase HDL by 20% for high intensity aerobic exercise 6. Improve body comp and reduces abdominal adiposity and improved weight control
178
Q

What are the lifestyle changes that improve dyslipidemia?

A
  1. physical activity 2. dietary changes 3. weight loss
179
Q

What are some of the pharmacology interventions for dyslipidemia?

A

nicotinic acid, bile-acid sequestrates (resins), fibrinic-acid derivatives (fibreates), HMG-CoA reductase inhibitors (statins)

180
Q

2 types of obesity?

A

Hyerplasia and hypertrophy

181
Q

Hyperplasia obesity?

A

Increaed number of fat cells

182
Q

Hypertrophy obesity?

A

Normal # of fat cells, but fat cells have an increased trigylceride content. Contributes to adult onset obesity.

183
Q

What does fat infiltration into the myocardium cause?

A

Increased plasma volume (inc work on the heart), increase in circulating FFA, and increased sympathetic tone and arrhythmias (inc HR and dec HR variability), adverse cardianc remodelling (hypertrophy b/c increased load on the heart, leading to imparied systolic and diastolic function)

184
Q

What are the two roles of adipocytes?

A

Lipid storage and active endocrine cells

185
Q

What are come of the adipokines?

A

IL-6, TNF-alpha, Leptin, Adiponectin, Resistin

186
Q

How do IL-6 and TNF-alpha contribute to CAD?

A

Pro-inflammatory, which increases insulin resistance (inc. diabetes, MS, and atherosclerosis) and endothelial dysfunction (dec synthesis and activation of NO via ROS)

187
Q

How is leptin related to CAD?

A

Secreted in direct proportion to fat stores. High levels damage the endothelium and increase pro-inflammatory cytokines (TNF and CRP), increases SNS activity, and causes oxidative stress by decreasing paraoxanase activity.

188
Q

What does CRP in relation to CAD?

A

Acts on endothelial cells to promote platelet aggregation and thrombosis formation

189
Q

How do low levels of adiponectin in obese people contribute to CAD?

A

Low adiponectin increases insulin resistance, which decreases NO, leading to endothelial dysfunction and increases inflammation of promotion of atherosclerosis and decreased FFA oxidation

190
Q

How is resistin related to CAD?

A

Released from macrophages…increased resistin = increased insulin resistance, increased pro-inflammatory by inc in IL-6 and TNF, and promotes vascular dysfunction (promotes foam cells and proliferation and migration of VSM)

191
Q

What is Type 1 diabetes?

A

Autoimmune disease that causes pancreas beta cell destruction

192
Q

What is Type 2 diabetes?

A

insulin resistance caused by inflammation (insulin receptors become less sensitive). Stimulated by pro-inflammatory adipokines

193
Q

What is metabolic syndrome?

A

Cluster of pathological conditions related to insulin resistance: abdominal obesity, highTG, low HDL-C, high blood pressure, high fasting glucose

194
Q

What is the fasting blood glucose level for diabetes diagnosis?

A

greater than or equal to 7.0 mmol/L

195
Q

What is the A1C level for diabetes? Normal?

A

Less than 7 for diabets and less than 6 for normal

196
Q

What does diabetes do to the vessels?

A

Causes both macrovascular and microvsacular disease

197
Q

What are the large vessel diseases caused by diabetes?

A

CVD (heart disease, stroke, peripheral vascular disease) and High BP

198
Q

What are the small vessel diseases caused by diabetes?

A

Retinopathy, npehropathy, neuropathy, and autnomic neuropathy

199
Q

What are the 2 main ways T2D cause/contributes to CAD independent of other risk factors?

A
  1. hyperglycemia 2. hyperinsulinemia
200
Q

How does hyperglycemia contribute to CAD?

A

Glycatation of lipoproteins (m-LDL). Pro-thromobtic and anti-fibrinolytic, impaired endothelial dysfunction, increased leukocyte adhesion (all becaue of dec NO)

201
Q

How is hyperinsulinemia contribute to CAD?

A

Stimulates growth of SMS within atherosclerosis, increases lipid metabolism, decreases synthesis and activation of NO, and causes endothelial dysfunction and oxidative stress

202
Q

What is the treatment for T2D?

A

normalize plasma glucose, prevent or delay chronic complications, lifestyle changes of weight reduction, exercise and diet, pharmacological treatment may be necessary with one or a combination of anti-hyperglycemic agents

203
Q

What are the 2 main ways exercise helps with T2D and its complications for CAD?

A
  1. cardiorespiratoty fitness increases HR, SV, and oxygen extraction, increases muscle blood flow and NO, and maintenance of weight loss 2. Gylcemix control/increase insulin sensitivity by increasing the # of receptors, increasing GLUT4, and enzymes in uscle (increased glucose extraction). Increases # of receptors and GLUT 4, and TNF-alpha in adipose tissue (inc FFA and glucose uptake) amd increases insulin sensitivity in the liver.
204
Q

What is physical activity?

A

Any body movement, actively produced by skeletal muscle that increases energy expenditure levels above resting levels; any activity that is not sedentary or quiet sitting

205
Q

What is exercise?

A

Planned, structured, purposeful, and repetitive. Designed to maintain or improve physical fitness

206
Q

What is leisure time physical activity?

A

Exercise, sports, recreation, or hobbies that are not associated with activities as part of one’s regular job duties, household or transportation

207
Q

Are Canadians physically active?

A

53% self reported they got 30 mins of walking per day

208
Q

Are Canadians physically fit?

A

32% have “good” fitness

209
Q

Do Canadians meet the new international and Canadian guidelines recommended to obtain substantial health benefits?

A

15% of Canadian adults attain 150+ mins of moderate to vigorous physical activity per week

210
Q

How is PA and exercise measured?

A

VO2, MET, kcals, steps per day, intensity, duration, and frequency

211
Q

Hoes does physical activity protect/prevent CAD independent of traditional risk factors?

A

inhibits the progress of atherosclerosis

212
Q

How does exercise make the heart more efficient?

A

Improves autonomic tone (SNS/PNS balance), decreases heart rate and contractility via Beta receptors and decreases arrhythmias

213
Q

How does exercise improve vascular function?

A

Enhances endothelial function, collaterals, and blood flow, which increases NO. Also causes vasodilation, anti-inflammatory, anti-coagulation, and mobilizes endothelial progenitor cells that repair endothelium and long term structural adaptations that increase lumen diameter. Increases the # of capillaries through angiogenesis and improved autonomic tone (SNS/PNS balance), which causes vasodilation

214
Q

How does exercise decrease inflammation?

A

Reduced systemic inflammation, working muscles (myokines) increase IL-6 with has anti-inflammatory properties, decreases levels of TNF-alpha, and decreases CRP, which decreases vascular adhesion molecules

215
Q

What hemostatic effects does exercise have?

A

Decreased blood coagulation through decreased platelet aggregation, decreased plasma fibrinogen, increased plasma tissue plasminogen activity

216
Q

What is the optimal amount of exercise?

A

2000 kcal.week. 35-55 minutes most days of the week + high levels of LTPA (8000-12000 steps per day)

217
Q

What are the three hormones/NT that CVD is related to in respect to mental disorders?

A

cortisol, epinephrine, and serotonin-NT

218
Q

KNOW THE PATHWAYS FOR HOW MENTAL PROBLEMS LEAD TO CVD

A

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Physiology 2 (16 decks)

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