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Unit Test 2 Flashcards

1
Q

what are the 3 major causes of death in the Canada?

A
  1. cancer
  2. CAD
  3. stroke
    stroke and CAD together amount to more than cancer
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2
Q

stress test

A

ECG measured on a treadmill at different intensities and used as a diagnostic tool for CVD

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3
Q

CHD

A

Coronary Heart Disease

  • coronary heart damage, the largest portion of deaths attributed to this part of CVD (42%)
  • artery damage, not being able to deliver enough O2 to heart muscle
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4
Q

mortality from heart disease in the US patterns

A

it has decreased to 59% since the 1960s

  • primarily due to smoking awareness/prevention, better technology and medicine for treatment and diagnosis
  • awareness of risk factors and people are surviving heart attacks more
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5
Q

CHD is the #_ cause of death in the US? in Canada?

A

1 in both

accounts for about 20% of deaths annually
also costs a lot of money

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6
Q

AMI

A

acute myocardial infarction

heart attack

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7
Q

what proportion of heart attacks are sudden?

A

half; no signs or symptoms; people die

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8
Q

male vs female risk for CVD

A

males have greater risk up to age 74
females have greater risk than men after age 50 (post menopause, atherosclerosis takes time to develop but is speed up by lack of estrogen present)

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9
Q

ischemic heart disease

A

anything that causes a decrease in blood flow

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10
Q

how is all cause mortality described?

A

as death rates in the population

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11
Q

male vs female life expectancy

A
  • females live longer than males on avg
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12
Q

life expectancy

A

the number of years you’re expected to live from the year you’re born

  • on average, half lives to be above this and half dies before then
  • can also be measured from different points in life
  • max is 122 years
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13
Q

Health Adjusted Life Expectancy (HALE)

A

the number of healthy years you’re living

  • PA can improve this
  • canada’s is 10th in the world: we drive everywhere and it;s killing us
  • in Canada it’s about 72
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14
Q

physical inactivity as a risk factor for all cause mortality

A

wasn’t a problem before because people had to be active as a part of their daily lives at work, they had non processed food
- they also died of infectious disease around age 40 before chronic disease was an issue

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15
Q

disturbing trends in PA and the impact it has on overall health/all cause mortality

A

with these large amounts of screen time, the resulting physical inactivity leads to increased levels of obesity, which is linked to CVD

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16
Q

trends for countries with longer life expectancies

A

mostly European countries with more active transportation

- they also have lower obesity rates due to their being more physically active

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17
Q

what is the relationship between obesity prevalence and active transportation?

A

an inversely proportional relationship

- when people are more physically active, they are less obese

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18
Q

what proportion of deaths do chronic diseases contribute?

A

63%
(only developed nations really deal with chronic disease because undeveloped nations are dying from infectious disease as they have inadequate healthcare)
- almost half of these are due to CVD

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19
Q

PA and harvard alumni study

A
  • death rates were 25-30% lower in alumni expending 2000kcal or more per week
  • active men gained 1-2 years of life for every hour of PA they did per week
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20
Q

person years

A

the number of people in your study times the number of years they were in your study

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21
Q

where is the greatest reduction in overall death risk seen?

A
  • from people going from sedentary to lightly active lifestyles
  • generally a drop and plateau
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22
Q

moderately fit men and women have __ reduction in risk of all cause mortality compared to unfit

A

moderately fit people have a 50% reduction in risk

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23
Q

what is a common relative risk in studies on PA and mortalitu

A

a RR of 0.5 is common; it means that you half the risk or reduce it by 50%

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24
Q

risk is reduced another __% in highly fit compared to moderately fit individuals

A

10-15% lower in highly fit

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25
Q

with regards to when you’re physically active during your life, how does risk look in terms of all cause mortality?

A
  • the risk b/w people who were active their whole lives and those who became active later in life was about the same
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26
Q

dose-response relationship b/w PA and mortality?

A

yes, reduction in risk seen largest by people who meet PA guidelines and are most active

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27
Q

what percentage of Canadians are meeting the PA guidelines?

A

15%

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28
Q

how does age influence our PA rates? why?

A

as we get older, our PA rates decrease

  • because physiological changes make this more difficult
  • possibly bc of biological reasons as this trend is also seen in monkeys
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29
Q

coronary risk factors def’n

A

characteristics that tend to increase the chances of developing coronary artery disease
- usually general narrowing/ blocking of arteries

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30
Q

major modifiable risk factors for CHD

A
  1. tobacco use
  2. hypertension
  3. high blood cholesterol (LDL)/ lipids
  4. physical inactivity
  5. overweight/obesity
  6. diabetes
  7. unhealthy diet (incl alc abuse)
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31
Q

major non-modifiable risk factors for CHD

A
  • age: older more risk
  • sex: male early in life, females later in life
  • race
  • genetic predisposition
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32
Q

host susceptibility

A

can be measured by the number of non-modifiable risk factors that someone has

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33
Q

widow maker artery

A

anterior interventricular branch
aka the left anterior descending
- because ventricles need to pump blood to body and it can’t if it has no blood supply itself

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34
Q

pathology

A

the anatomical changes underlying the condition

  • structure change and result in condition
  • use to come up with diagnosis
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35
Q

etiology

A

the development of the condition and how the disease progresses

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36
Q

symptoms reflect ___ and result from ___

A

pathology; etiology

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37
Q

symptoms of MI

A
  • often unrecognized and are confused w heartburn
  • 21% of heart attacks can be silent and thus left untreated
    diff for men than women:
    men- classic signs usually after physical activity
    women- usually after emotional stress, usually don’t go to doctor in time or have higher pain tolerance
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38
Q

atherosclerosis

A

often etiology for heart disease

  • the build up of calcium and fats inside the inner walls of an artery causing it to become narrowed
  • an intimal disease in intima layer
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39
Q

arteriosclerosis

A
  • stiffening of arteries

- happens in CT layers of artery

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40
Q

stenosis

A

narrowing of a structure

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41
Q

where in vessels is atherosclerosis usually found?

A

often in vessels that bifurcate or bend

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42
Q

intravascular ultrasound (IVUS)

A
  • putting ultrasound probe through blood vessel and it sends a radio signal from the middle of the tube
  • allows us to see plaque and how thick it us
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43
Q

cardiac catheterization

A

could insert catheter into brachial or femoral artery (pref. femoral since it’s larger and can still allow blood flow around the catheter)

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44
Q

coronary angiogram

A
  • cheaper and quicker than catheterization, hits lots of vessels at once
  • radio-opaque dye injected into the coronary arteries and gives picture of obstruction where you don’t see the black and an artery should be there (X-ray)
  • you can only see black areas of reduced blood flow, but can’t see the stenosis itself
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45
Q

methods of screening for atherosclerosis

A

cardiac catheterization
coronary angiogram
intraventricular ultrasound (IVUS)

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46
Q

using a stent to treat atherosclerosis

A

inflating a balloon on the end of a catheter in an area where stenosis is and balloon pushes fat out of the way and inflates the stent which holds lumen open

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47
Q

coronary artery bypass graft (CABG)

A

if there are multiple stenosed regions, they can do bypass surgery which often uses a subclavian branch of an artery and attach it to the area the artery is blocking flow to using a vein from the leg

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48
Q

there are 2 types of stenosis of arteries:

A

fixed obstructions
OR
dynamic blockages

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49
Q

fixed obstructionof a coronary artery

A

ex. atherosclerotic plaque that blocks blood flow through artery, most likely to result in heart attack if clot ruptures and blocks off vessels (the results from an inflammatory response)

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50
Q

dynamic obstruction of a coronary artery

A

caused by coronary arterial spasm that decreases blood flow to heart tissue

  • typically transient, not lasting long enough to cause heart attack
  • smoking, stimulant drugs, and diabetes can cause spasms
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51
Q

thrombus (clot) formation

A

at a bifurcation, vessel diameter gets smaller and endothelial wall deals with more stress at the bifurcation
- when plaque has ruptured, a clot forms, blocking blood flow so it can’t move through the vessel

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52
Q

turbulent flow theory of artery injury

A

at a bifurcation, the fastest moving cells are in the centre of the blood vessel and so they hit the area where the vessel splits, causing more damage due to the sheer stress put on endothelial cells

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53
Q

vasomotor tone

A
  • signals changes that cause blood vessels to change diameter
  • cytosolic calcium stimulated release of NO caused by sheer stress on endothelium, triggers smooth muscle in media layer to dilate
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54
Q

nitric oxide (NO)

A
  • a potent vasodilator, inhibits platelet adhesion and activation therefore also inhibits clotting
  • antiflammatory agent: inhibits adhesion of leukocytes to endothelial surface when there’s damage to endothelium
  • has short half life so doesn’t stay in circulation long
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55
Q

atherogenesis

A
  • the building up of plaque
  • begins w endothelial disruption caused by intimal injury
  • platelets adhere to collagen at site activating fibrinogen
  • fibrinogen increases platelet aggregation and releases platelet derived growth factor (PDGF)
  • macrophages eat damaged cells, debris and oxidized LDL to make fatty streaks
  • smooth muscle cells and fibroblasts migrate to intima to make fibrosis (cap)
  • lipid deposits accumulate to increase stenosis
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56
Q

factors that cause endothelium injury

A
  • LDL
  • tobacco
  • homocysteine
  • oxidized LDL stimulates monocyte secretion
  • high blood glucose
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57
Q

homocysteine

A

an intermediate AA

  • present in people who eat a lot of protein, males, older people, sedentary, environmental toxins
  • high levels increase risk, starting to breakdown an AA
  • decreased by folic acid, exercise, vitamins B6 and B12
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58
Q

why is high blood glucose a problem

A

cells keep trying to take up the glucose, then it gets added to proteins which make them sharp and dysfunctional and causes endothelial damage

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59
Q

when do symptoms of atherosclerosis appear?

A

when the blockage reduces blood flow by about 80%

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60
Q

myocardial ischemia

A

inadequate oxygen supply to part of the heart caused by impaired blood flow
- results in angina

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61
Q

ischemia

A

a reduction in blood flow to anywhere in your body leading to insufficient O2 delivery to tissues

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62
Q

angina

A

symptoms of heart attacks without actually causing tissue damage

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63
Q

symptoms of ischemia

A

chest, arm neck and jaw pain, indigestion type pain

- people take nitroglycerin which stimulates release of NO and increases blood flow again

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64
Q

secondary prevention vs primary prevention

A

primary: trying to keep from getting the disease
secondary: trying to keep the symptoms from getting worse

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65
Q

does primary prevention of atherosclerosis exist?

risk factors of atherosclerosis?

A

not really, 1 in 6 teenagers has coronary plaques; we can’t really stop it but we can slow it down
risk factors: smoking high BL, diet high in saturated fat and cholesterol

66
Q

what types of stenoses cause most infarctions?

A

low grade ones, most people who have heart attacks have less than 50% stenosis and are therefore asymptomatic ; when more stenosed, the plaque has a strong fibrous cap and risk of rupture is lessened

67
Q

what percentage of first heart attacks are fatal?

A

30-50%
- a lot of people don’t know anything is wrong until they die from a heart attack; people don’t usually get cardiac checkups

68
Q

characteristics of plaque prone to rupture

A
  • thin fibrous cap
  • lipid, macrophage rich
  • smooth muscle poor
69
Q

how do we know about the relationship between PA and CHD?

A

evidence from:

  • occupational studies
  • leisure time PA studies
  • studies of fitness
70
Q

london bus study

A
  • showed effects of occupational PA on CHD
  • bus drivers had high BP, were obese and once there were factored out, there was still reduced risk for conductors compared for drivers
  • when conductors had heart attacks, they were less severe
71
Q

problems with PA studies

A
  • might not measure every variable
  • can’t determine cause and effect w cross sectional or retrospective
  • confounders
  • inaccuracy of medical/autopsy records/ recall of habits by family members
72
Q

physical fitness and its relationship to CVD mortality

A

more strongly related to reduce CHD than other estimates of PA
proof: greatest reduction in risk for those who are more physically fit

73
Q

nurses health study

A

a large scale population study on nurses and PA rates

  • when family history of CDV isn’t a factor, risk goes down, thus deeming physical inactivity a risk factor
  • supports that PA works in both women and men to prevent CVD
74
Q

CVD risk in women and men and PA

A
  • there was originally thought to be no relationship b/w PA and CVD in women
  • however, PA reduces the risk of CVD to a similar extent in women as in men
75
Q

PA and its influence on other CAD risk factors

A

it can reduce independent risk factors for CHD but also other risk factors like high BP, weight, lipids

76
Q

PA and risk of recurrent heart attack

A

although there is a reduction in CAD mortality with exercise rehab, there is no reduction in risk of having another non-fatal MI

77
Q

Mill’s Canons for CVD

temporal sequence, strength of assoc, consistency

A

temporal sequence: yes
strength of association: risk is 2x higher if inactive; also note 2000kcal/week protection against CVD
consistency of results: yes

78
Q

fibrinolytic factors

A

break down clots

79
Q

biological plausibility for PA to have an effect on CVD risk

A

exercise:
increases HDL cholesterol and fibrinolytic factors
reduces BP, TG, body fat, blood coagulability and MVO2 (heart is getting more efficient and so needs less O2 during PA)

80
Q

MVO2

A

myocardiac VO2: the amt of oxygen needed for heart to survive to do work
- decreases with exercise training because heart is getting to be more efficient and requires less O2

81
Q

functional adaptation

A

we get healthier endothelium and the release of things like NO contribute to better vasodilation

82
Q

structural adaptation

A

over time, remodelling by significantly increasing the size of your arteries (diameter, thickening)

83
Q

the relationship between functional adaptation and structural adaptation

A

starting by relying more on functional adaptation. then, as structural adaptation increases, then we rely less and less on functional adaptation

84
Q

cerebrovascular disease and stroke definition

A

a stroke is the loss or impairment of bodily function resulting from injury or death of brain cells after insufficient blood supply
- results from hypoxia (inadequate oxygen delivery) caused by ischemia

85
Q

hypoxia

A

inadequate oxygen supply

86
Q

warning signs of stroke

A
  1. weakness
  2. trouble speaking
  3. vision problems
  4. headache
  5. dizziness
87
Q

what is the mnemonic for the public to recognize the stroke?

A 
FAST
face drooping
arm weakness
speech difficulty
time to call 911
88
Q

types of stroke

A 
ischemic
- thrombotic or embolic
- also TIAs
hemorrhagic
- subarachnoid or intracerebral
89
Q

ischemic stroke

A
  • interruption of blood flow to the brain due to a blood clot or possibly swelling of the brain
  • 80% of strokes are ischemic
  • atherosclerosis usually involved
  • either thrombotic or embolic
90
Q

thrombotic stroke

A

category of ischemic stroke

  • a blood clot that forms in an artery directly leading to the brain
  • more typical
91
Q

embolic stroke

A

category of ischemic stroke

  • clot develops somewhere else in the body and travels through the blood stream to the brain
  • usually in older people if someone falls and gets injured, the clot forming might move to the brain and cause a stoke
  • also can be caused by irregular heart rhythm (AFib) where blood spends too much time in ventricles and clots
92
Q

TIA

A

transient ischemic attack
- similar to angina in the heart, called a mini stroke where O2 delivery to brain is interrupted temporarily but no cells die so it’s not really a stroke
- symptoms similar to ischemic stroke except they go away w/in a few hours
1/3 of people who have a TIA have a stroke within 5 years therefore it puts you significantly at risk

93
Q

hemorrhagic stroke

A

caused by uncontrolled bleeding in the brain when a blood vessel bursts
- bleeding interrupts normal blood flow and by flooding the brain (also lots of pressure), kills brain cell because they damage the brain cell env’t
- 20% of strokes
2 types: subarachnoid or intracerebral hemorrhage

94
Q

subarachnoid hemorrhage

A

a category of hemorrhagic stroke

- uncontrolled bleeding on the surface of the brain in the area between the brain and skull

95
Q

intracerebral hemorrhage

A

a category of hemorrhagic stroke

- occurs when an artery deep within the brain ruptures

96
Q

types of hemorrhage

A

both types of hemorrhage can cause hemorrhagic stroke

  • therefore if you take aspirin, it thins your blood and you’ll bleed out
  • aneurysm
  • AVM (atriovenous malformation)
97
Q

aneurysm

A

a weakened area in the blood vessel wall of he blood vessel that fills with blood and bulges
- turbulent flow is here now and puts blood at a greater risk of clotting

98
Q

AVM

A

atriovenous malformation
- a malformation of the brain’s blood vessels usually present at birth, causing the artery walls to be weak and could break over time

99
Q

how much of a problem is cerebrovascular disease and stroke?

A

3rd leading COD is US

5th leading in Canada (5%)

100
Q

incidence of stroke

A

10-15% higher in women than in men

- maybe bc of hormones released during pregnancy or bc of loss of protective estrogen bc of menopause

101
Q

why does someone usually do PA after having a stroke?

A

rehab probably, rather than prevention

102
Q

non modifiable risk factors for stroke

A
  • age: greater than 65 and increases exponentially after this
  • gender: before menopause women have decreased risk but after, their risk is greater than that of men
  • family history: if someone has a stroke before a certain age, it’s likely a result of genetics
  • ethnicity: First Nations and South Africans have higher incidence
  • PRIOR STROKE or TIA puts you at greatest risk of having another
103
Q

modifiable risk factors for stroke

A
  • high BP, blood cholesterol (LDL)
  • heart disease, atrial fibrillation (causes 50% of strokes)
  • diabetes, being overweight
  • excessive alc consuption
  • physical inactivity
  • smoking, stress
104
Q

what is the #1 modifiable risk factor for stroke

A

hypertension

- an estimated 45% of people have high BP

105
Q

how does age influence someone’s risk of having a stroke?

A

after age 55, risk doubles with each decade

106
Q

classifications of blood pressure

A

normal
prehypertension
stage 1 hypertension
stage 2 hypertension

107
Q

normal blood pressure

A

<120/

<80

108
Q

prehypertension

A

systolic: 120-139
disatolic: 80-89

109
Q

stage 1 hypertension

A

systolic: 140-159
diastolic: 90-99

110
Q

stage 2 hypertension

A

systolic: >160
diastolic: >100
- pretty dangerous

111
Q

systolic pressure

A

the peak pressure in arteries during ventricular ejection

112
Q

diastolic pressure

A

the pressure in the arteries during ventricular relaxation

113
Q

what happens when someone’s systolic blood pressure is less than 100mmHg

A

they have almost no risk of CVD

- they also faint a lot if they don’t have sufficient oxygen delivery to body tissues

114
Q

how does high blood pressure work?

A
  • when arterioles constrict, the heart has to work harder to force the blood through and often becomes enlarged which is not good
  • when we have lots of resistance in the system, it’s harder to move blood through, arteries stiffen and increases resistance more
115
Q

framingham results re: BP and stroke risk

A

systolic BP over 150 doubles stroke risk

which is 4x that of risk of heart disease

116
Q

physiological effects of cigarette smoking

A
  • heart rate increases: NE release causes increasing resting heart rate but heart isn’t getting any more O2 supplied bc body is at rest
  • blood O2 carriage decreases: Hgb has a higher affinity for carbon monoxide than O2
  • blood clots form: nicotine causes coagulation of blood which can cause coronary thrombosis or stroke
117
Q

effects of nicotine

A
  • increases BP
  • causes heart to work doubly hard (increases contraction force and stroke volume)
  • dysrhythmias by stimulation of ectopic pacemakers
  • increase in both plasma FFAs and platelet adhesiveness, predisposing someone to atherosclerosis
118
Q

smoking and how it increases stroke

A
  • in general, smoking more than a pack a day has twice the risk of a heart attack and increases risk of stroke 5x over someone who doesn’t smoke
  • when combined with high blood cholesterol and hypertension, smoking increases risk of stroke by 7x (double that of MI)
119
Q

physical activity and risk of stroke trends

A

no trends,

there is no clear associations that show PA as a preventative for stroke, but there probably is some protective effect

120
Q

what do case control studies show in terms of the association between stroke and PA?

A
  • when comparing people who’ve had a stroke to those who haven’t, a lifelong reduction in risk is present for those who have been physically active throughout their lifespan (50% more)
  • also the greatest reduction in risk is seen in those who are active more recently as well
121
Q

study results re: PA exercise frequency, intensity and amount on stroke

A

Harvard alumni study shows that:

  • lowest amount of PA has greatest reduction in risk regardless of other factors
  • in terms of PA frequency and intensity, PA acts as an effect modifier on stroke where it improves certain risk factors that decrease the likelihood of having a stroke
122
Q

Nurses’ health study results on stroke

A
  • all women study looking at if doing a little PA would reduce risk
  • found that the more PA and at greater intensity had the greatest reduction in risk
123
Q

Mill’s canons for stroke and PA

A
  • temporal sequence: yes, PA later in life was still effective
  • **strength of association: risk reduction 30-60%
  • consistency of results: yes most studies show reduction in risk, consistent w diff pop also
  • does response: not as clear; extra benefit of vigorous controversial opinion
  • biological plausibility: yes. PA reduces risk factors, blood clotting, etc
124
Q

how are people categorized into levels of blood pressure if systolic and diastolic BPs are part of different classifications

A

have to put them in whichever is higher because you don’t want to underestimate someone’s hypertensiveness

125
Q

Korotkoff sounds

A
  • first heard when brachial artery is partially open: pressure at this point is systolic
  • when sound stops, brachial artery is mostly open, the pressure at this point is diastolic
126
Q

cause of hypertension

A

cause is unknown in 95% of cases

127
Q

prevalence of hypertension

A

NHANES III study says that prevalence is 20%, most people don’t know they have it though so it’s estimated to be about 50% of Canadians

128
Q

methods for primary prevention of hypertension

A
  • normal body weight
  • reduce dietary sodium intake so that you can expel water
  • regular aerobic PA
  • limit alcohol consumption
  • maintain adequate dietary K+
  • consume diet that would prevent atherosclerosis
129
Q

drugs for treatment of hypertension

A

generally either decrease HR or help eliminate fluids from body

  • diuretics
  • SNS receptor blockers
  • ACE inhibitors
  • calcium channel blockers
  • also a combo of some of the above
130
Q

fundamental regulatory equation of the circulatory system:

A

flow/cardiac output (Q) = change is pressure / resistance (or total peripheral resistance- TPR)
- anything that affects cardiac output or TPR will effect arterial pressure

131
Q

contributing factors to arterial pressure

A
  • total blood volume (more vol=more pressure)
  • rate of blood flow (CO)
  • blood vessel diameter (bc flow= length of tube X viscosity of blood/radius^4)
  • – arteriolar resistance is important because of total cross-sectional area in the body
132
Q

SNS impact on BP

A

sympathetic nervous system (SNS) increases BP

  • SNS nerves release NE, adrenal glands release epinephrine
  • both bind w adrenergic receptors which act to increase HR and force of contraction
  • this causes vasoconstriction to increase TPR and BP increases
133
Q

PNS impact on BP

A

parasympathetic nervous system (PNS) decreases BP

  • Ach released from vagus nerve of PNS binds with cholinergic receptors
  • this causes vasodilation and BP decreases
134
Q

risk factors for hypertension

A

age - stiffening and changes in CNS increase resistance
ethnicity - african americans have greater resistance and less flow
obesity - more flow because of expanded plasma volume and increased SNS activity

135
Q

PA and hypertension risk

A

epidemiological and clinical experiments both provide evidence that moderate intensity PA is assoc with prevention and treatment of MILD hypertension

  • it doesn’t work well for severe hypertension (greater than stage 1)
  • heavy activity doesn’t have huge reductions in risk
136
Q

PA and treatment of hypertension

A
  • works for mild, not for severe hypertension
  • seems to benefit women more than men (greater BP drop)
  • doesn’t work as well for overweight individuals (systolic drops less) BUT drops are independent of weight change++
  • most benefit is from moderate PA, not much more for high
  • diastolic changes seen most in longer durations of PA
137
Q

Mill’s Canons for hypertension

A
  • temporal sequence: yes. also can do experimental studies to show this
  • strength of association: risk reduction 30-50% active
  • consistency of results: most studies show reduced risk w PA and this is across diff pop.s also
  • does response: unclear bc less seems to be more
  • biological plausibility: yes, PA can reduce BP by decreasing Q and/or TPR
138
Q

hyperlipidemia

A

having high blood cholesterol/TG levels

139
Q

4 types of lipids

A

cholesterol
triglycerides
phospholipids
fatty acids

140
Q

cholesterol

A

a modified steroid, made in the liver

  • used to make steroid hormones (testosterone, estrogen)
  • involved in keeping cell membrane fluid, skin waterproofing
141
Q

triglycerides

A

how we store energy in the body

  • a glycerol and 3 FAs
  • an efficient storage method
142
Q

phospholipids

A

make up cell membranes

  • hydrophilic head (phosphate/diglyceride)
  • hydrophobic tail (2 FA chains)
143
Q

fatty acids

A

long hydrocarbon chains with carboxyl groups on the ends

- how we store large amounts of energy

144
Q

lipoproteins

A

transport fats through blood since they aren’t dissolvable in fluid

145
Q

classes of lipoproteins

A 
least dense to most dense, also largest to smallest:
chylomicron
VLDL
LDL
HDL
146
Q

chylomicron

A

least dense lipoprotein, largest in size

- carries fats from food in SI to liver to be processed via the blood

147
Q

VLDL

A

second least dense, second largest in size

- carry from liver to cells of body

148
Q

LDL

A

second most dense, second smallest in size

  • carry primarily cholesterol to body tissues
  • most dangerous bc gets oxidized and can lead to atherosclerosis in our blood vessels
149
Q

HDL

A

most dense, smallest in
size
- carry cholesterol from body tissues and drops off at liver

150
Q

endogenous fats

A

made in the body, not found in our food

151
Q

triglyceride

A

a fatty substance found in the body and our food

  • manufactured by body from excess alcohol, sugar and fats
  • FA chains vary dramatically in length, chains can be saturated or unsaturated (good bc keeps from packing too tightly): the fats we consume have an impact on the type of FA in TG
152
Q

main TG sources

A

adipocytes

intramuscular

153
Q

intramuscular TG

A
  • TG interspersed in muscle fibers
  • when mobilized from adipose tissue during exercise are hydrolyzed into FFAs and glycerol which body can use for energy
  • transported in plasma by albumin to where needed
154
Q

total blood cholesterol and heart disease

A
  • greater levels of overall cholesterol increase risk for CHD
  • higher or equal levels of HDL to LDL cholesterol reduces your risk of CHD
  • — its most important to know how much good to how much bad you have; having more LDL increases your risk the most
155
Q

amount of HDL cholesterol needed to reduce risk of CHD

A

in men: 40-50 mg/dl

in women: 50-60 mg/dl

156
Q

Apo B

A

a protein present on the outside of cell membranes in lipoprotein molecules caring cholesterol
- is a better indicator of CHD risk than LDL cholesterol levels are

157
Q

cholesterol levels, CHD risk and treatment of cholesterol

A

only treat high levels of LDL-C when risk for CHD is also high, otherwise, cholesterol isn’t as big of a problem as we thought it might be

158
Q

risk factors for high hyperlipidemia

A
  • sex (postmenopausal women)
  • age (HDL decreases w age)
  • % body fat causes HDL to be lower and LDL greater
  • diet, alcohol overuse, diabetes all bad for HDL, increase LDL and TG
  • smoking and steroids decrease HDL
  • exercise increases HDL :)
159
Q

prevalence of high blood cholesterol in Canada

A

40% of Canadians have it

160
Q

Mediterranean diet and cardiac events

A

people who eat lots of fish, fruits and veg, olive oils, nuts, seeds, minimal red meat: have a LOT less cardiac events than those consuming the traditional Western diet

161
Q

dietary recommendations by canadian cardiovascular society

A
  • keep fat intake to less than 30%
  • less than 200mg cholesterol
  • v. little saturated fat
  • limit alcohol intake to 1-2 drinks/day
162
Q

PA and training on hyperlipidemia

A
  • most improvement with aerobic exercise (decreases TG)
  • resistance exercise equivocal
  • dose response equivocal
  • also range in amount of aerobic exercise

– exercise needs to be coupled with either diet changes or medication if looking to reduce hypercholesterolemia

Epi (3 decks)

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