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162 Cards in this Set

  • Front
  • Back
single most preventable cause of death in the US and globally
smoking
- 100 million deaths in the 20th century
smoking worldwide death toll
same as one jumbo jet crashing and everyone dying every hour
smoking is responsible for what percent of CV deaths
40%
effects of smoking depend on
# of years u smoked
how much you smoked
depth of inhalation
within seconds of inhaling
u get the release of dopamine in the brain
what kind of drug is a cig
psychoactive
addictive part and the cancerous part
addictive- nicotine
cancerous- tar (60ish carcinogens)
reproductive system and smoking
ye
impedance and erectile dysfunction is 85% higher in male smokers than nonsmokers
yea
in females, smoking fux with ability to produce estrogen
60% more likely to be infertile
other female smoking facts
- decreases uterine blood flow
- embryo transport problems
- endometrium problems
- increased chance of ADD
start then stop smoking
effects can linger
smoking is a predictor of
divorce
1st hand
2nd hand
mainstream
sidestream
both kinds increase mental stress
yea
smoking causes brain atrophy
yea
smoking doubles risk for
parkinsons and alzheimers
smoking contributes to dementia and cognitive issues
yea
smoking and metabolism
speeds it up by 10%
substitute for speeding up metabolism
- exercise. its been used to help ppl quit since metabolism slows down after u quit
more addictive than
cocaine, heroin
cigarette smoking causes decrease in weight by
the overexpression of a gene that is used in fact
15 cigs a day
puts u at risk for Crohn's disease
every organ and tissue in ur body is negatively affected by smoking
yea
radon
risk for lung cancer
more than 20 known carcinogens in a cig
yea; found in the tar
polycyclic aromatic hydrocarbon (PAH)
- carcinogen found in the tar
- doesnt dissolve in water, hard to get rid of
benzopyrene
- type of PAH
- permanently attacks DNA. if it doesnt kill the cell, it causes a genetic mutation to it so that it becomes carcinogenic
Acrolein
irreversibly binds with DNA; binds with guanine and causes a mutation, and ultimately, cancer
- it is the stench you smell
- irritates eyes
- 1000 times more abundant than PAH carcinogens
sidestream smoke
- smoke from tip of cigarette- worse than having someone blow smoke in ur face
- 85% of bad stuff are from tip
- makes platelets stickier
- damages lining of blood vessels
- causes problems with endothelium
- decreases coronary blood flow
- increases arterial stiffness
- leads to inflammation of endothelium
- causes oxidative stress
- larger infarct size if u have a MI
- these things can kick in 30 min--1 hour after
smoking process
injury-->recovery-->injury-->recovery
- stiffens arteries, then they recover, but they get hard over time
Exhaled smoke
more likely to be reactive chemically bc its a cooler temperature; and the particles are smaller
nicotine
- addictive; physical and psychological dependance
- 5-10 sec to reach ur brain
- affects dopamine release
how much nicotine u get depends on
- how much u inhale
- type of tobacco
- filter or not
5 months after u start smoking, ur addicted
yea
states with lowest smoking frequency
- utah
- minnesota
- california
- hawaii
states with highest smoking frequency
- ohio
- michigan
- west virginia
- tennessee
James Duke
bought rights to cig rolling machines and promoted selling them to women
- bought duke U
acute effects of smoking
- increases myocardial oxygen demand (check for the by checking RPP, RPP=hr x sbp/100)
- increases hr and bp
acute effects con't
- reduces oxygen transport
- carbon monoxide takes place of hemoglobin
- arteries contain 20/21ml oxygen per 100 ml of blood
- veins have 5 ml per 100 ml
systemic circulation= 15 ml per 100ml
- increaes susceptability to malignant ventricular arrhythmias
- can cause coronary artery spasm
- makes platelets stickier
chronic effects of smoking
- deicreases hdl
- promotes oxidation of ldl
- increases fibrinogen concentration
- increases blood viscosity
- damages endothelial lining (the tar does)
kicking the habit
- over 70% of people quit smoking bc their physician told them to
- 1/3 of smokers who quit relapse
- only 5% successfuly quit
- according to center for disease control- 80% of smokers quit when they began running
- exercise= reduce craving
one of the reasons people dont quit
dont wanna gain weight
- about 10% increase in calories occurs if u quit (5-10 lbs)
CAD
yea
not the same as CVD
- responsible for 25% of all deaths
major risk factors
- family history- if one of ur family had a MI, revascularization, or sudden death in a father before 55 or mother before 65
- male gender
- increasing age (after 45 in men, 55 in women)
- cigarette smoking- if u smoke 10 cigs a day, or u quit within the last 6 months
- high blood cholesterol
- hypertension
- physical inactvity
high blood cholesterol
- if total >200 or HDL <40 or LDL >160, you have a risk factor; LDL is more important; we get total cholesterol measured most of the time bc its easier to measure but its not the most important

- as total cholesterol increases, LDL increases. as cholesterol decreases, LDL decreases
- you're also at risk if you're taking lipid lowering medications
- a good LDL level is <130; ideally <100
hypertension
modifiable; borderline is >140/90, confirmed on 2 separate occasions, or taking antihypertension meds
physical inactivity
- every other risk factor is quantitative
- if u are less active than 25% of the population, you are a risk factor for CAD
what does it take to get angina?
a clinically significant lesion- 70% occluded artery
- you have a clinically significant lesion before u feel the effects of it
- you can detect a 50% lesion by exercise test
- chest pain is less likely in women, they get short of breath instead
silent ischemia
- ECG changes without symptoms; changes in ST segment
#1 cause of heart attack
bc a plaque plugs coronary artery
- the more well developed a plaque, the more stable it is, and the less likely you are to have a piece break off and plug the artery
clinical outcomes of coronary artery disease
MI
- ST segment changes- depression; horizontal or downsloping depression. 2 mm drop for .08s; the more depressed, the bigger the problem
- if the depression comes early in exercise, you have a bigger problem than if it comes later in exercise
- transient perfusion problems
- angina
angina
- stable- predictable; usually lasts 20-30s, relived by nitroglycerin
- unstable- unpredictable; usually last longer than 20min; precursor to MI; usually means some sort of plaque erosion or rupture thats going on
- Variant angina (prinzmetal angina)- coronary artery spasm- you'd see no obstruction if u did an angiogram
- silent ischemia- changes in ST segment, changes in T wave, but no common symptoms. common in diabetics; common in older people; old ppl tend to have shortness of breath
- angina- discomfort, feels retrosternal (under the breast bone) often radiates, squeezing or restricting feeling
other things w similar pain
acid reflux
highaytal hernia
spasm of esophagus
another characteristic of angina
diaphoresis- sweating
by age 35, CVD is among the 10 leading causes of death
yea
CAD=
CHD=IHD
- responsible for 1/2 of all cv deaths; 25% of all deaths
aerobic exercise
- increase HDL
causal risk factors for CAD
- cigarette smoking (most impt)
- hypertension
- total cholesterol (in particular, LDL)
- diabetes
predisposing risk factors for CAD
obesity
family history
physical inactivity
male gender
aging
poor socioeconomic status
CAD is responsible for deaths
1/2 of all cv deaths
1/4 of all deaths
CAD=
CAD=CHD=IHD
CAD def
- narrowing (stenosis) of the lumen of the artery
- result of plaque formation
- the fatty streaks become plaques
by age 15, u can have fatty streaks in arteries
yea
how soon u have plaques depends on lifestyle
ye
ultimately, there can be an obstruction of the coronary artery. the plaque can lead to a
focal spasm- in some part of the artery, it contracts and flow is obstructed, leads to angina
referred pain
not pain in the immediate area of blockage, but in other areas
- ischemia can result in this
ischemia can end up in
injury, then MI
most MI's occur in
vessels less than 50% occluded; what you have are young plaques that are likely to have a piece broken off i.e. by hypertension
we always have some injury to the endothelium
but the insults are withstood bc its pretty strong
- nitrous oxide- vasodilator; helps repair endothelium; it si produced as a result of the insults
- vasa vasorum- the arteries have their own blood supply and the endothelium releases it
diabetics have more issues with
cardiomypathy
ischemia can result in
angina
angina
- symptomatic or asymptomatic
- squeezing or constricting of the chest
- in older people; more shortness of breath
- unstable lasts longer than stable
stable
- predictable
- mayb 20 sec
- might sweat
- relieved by nitroglycerin given sublingually
- typically occurs when someone has advanced lesions
- recommend exercise to them and have them grade the angina to +1-->+4 (stop at +3)
unstable
- scab or cap is not stable
- underlying factor for plaque rupture
- dont recommend exercise to them
- usually lasts 20min+
- doesnt go away easily
variant (prinzmetal) angina
- causes spasm
- the spasm may be due to nitrous oxide as a result of endothelium dysfunction
- males are more likely to have calcium deposits in arteries
ischemic cascade
diastolic dysfunction
- heart doesnt fill the way it should
- from diastolic dysfunction, it advances to systolic dysfunction; the heart doesnt empty the way it should
hypokinesis
the heart cant move the way it should in terms of emptying
if u wanna measure how hard the heart is working
measure RPP
left ventricle work is very important
measure thru lvef
- percentage of blood in the heart at the end of filling that gets ejected
- during exercise, ef goes up bc of sympathetic
nervous system
- i.e. if only 20% of blood is ejected, the blood leftover tends to clot; bc of this, blood thinners are usually given;
all of this leads to ecg abnormalities
- heart has problems polarizing and repolarizing
- t wave inversion
- electrical instability

- in cardiac patients during exercise, ef stays the same or goes down
ischemic heart disease
- brought about by a narrowing of the lumen (opening of the artery
- progressive degenerative disease
- results in a narrowing of the lumen by formation of a plaque
arteries consists of tunics
- 1st- tunica intima (innermost layer)
- 2nd- tunica media (middle layer)
- 3rd- tunica adventitia (outer layer)
CAD affects what layer
1 and 2
endothelium
single layer of cells that lines all the arteries
- adjacent to lumen; deeper than tunica intima
- functioning entity
- when it gets damaged you have a problem
ischemia
demand for oxygen
- u can test for this by doing an exercise test to see if the supply for oxygen meets demand
atherosclerosis
- general; more of a pathological process
arteriosclerosis
specific to the arteries; more of an aging process of the arteries
by age 20, 75% of males have some coronary artery disease
ye, streaks are evident as early as age 15
sclerosis
hardening
atheroma
tumor (plaque)
myocardial ischemia results in chest pain and
injury. injury leads to MI
ischemia-->injury-->MI
necrotic tissue
once u have a MI, you have necrotic tissue. necrotic tissue becomes fibrotic tissue that stiffens the heart
angiogram
shows occlusion. you get a revascularization to prevent an MI
- injury and ischemia are reversible, MI is not; streaks are reversible, plaque is not
regression
- if u have coronary artery disease, you cant undo the plaques, but you can regress the streaks
- this is all a result of injury or dysfunction of the endothelium
- clinically significant lesions are 70% or more occluded
pathogenesis of CAD
typically starts out as injury or dysfunction
types of injury
- mechanical stress associated w hypertension
- carbon monoxide from smoking
- toxic chemicals
- hyperglycemia
- high blood glucose associated w diabetes
- infectious agents- herpes, Chalmydia
- nutrition
monocytes and platelets go to injury sites
- bind to inner lining of the artery and hold onto endothelial lining
- then they are converted to macrophages
- macrophages have enzymes that cause cell death
- macrophages become foam cells
- foam cells become part of fatty streaks that become plaques
- once they are plaques, it is irreversible
o monocytes->macrophages->foam cells->fatty streaks->plaques
c-reactive protein
you can measure if the endothelium is injured thru inflammation; c reactive protein is an indicator of inflammation
cholesterol
yeaa
lipids are causative factor for cv
ye
what is the typical cholesterol associated w cvd?
200mg%
over 60% of the population has around 200
word
25% have
>240
higher the cholesterol
greater the death rate (CHECK HANDOUT)
good cholesterol
lower than 180
average cholesterol for children and adolescents
160mg%
when ur born, you're
80mg
for every 50mg% increase above 200
you're chance of having a heart attack doubles
not all cholesterol is bad
cholesterol is ubiquitous
- important in growth, structure, transport- in every cell and tissue in the body
- differs in species
- differs in organs
cholesterol is a major building block of
plasma membranes
- makes up 30% of plasma membranes
2 sources of cholesterol
- exogenous- dietary- 300mg/day; beef, dairy, organ meats, processed luncheon meats
- endogenous- ur body makes cholesterol in the liver and small intestines; 85% of ur cholesterol is mad in the liver, make about 1g per day
if u wanna change ur cholesterol
aim for endogenous part
- lower cholesterol= lower death rate= lower risk for cvd
cholesterol is influenced by
obesity and physical actiity
cholesterol is not water soluble
it only becomes soluble when combined w a protein; as a result, lipoproteins exist
classes of lipoproteins
- vary in , weight , size, and density
- the whole purpose is to transport cholesterol
HDL
- about 20-30% of cholesterol. HDL is primarily protein, about 50%; very dense; HDL is inversely related with CHD; as HDL goes up, ur risk goes down. it gathers up the cholesterol in the body, and brings it to your liver, and it gets metabolized there. lowers risk for CVD
LDL
60-70% is cholesterol. collects cholesterol, but drops it off in the walls of the arteries instead of the liver.
- its an atherogenic protein. (initiates formation of plaques)
- most tissues have ldl receptors. the ess ldl receptors u have, the more susceptible u are to atherosclerosis
ldl is most impt
ye
as total cholesterol goes up and down
up- ldl goes up
down- ldl goes down
VLDL
mostly triglyceride
testing cholesterol
u can measure cholesterol easier than LDL; also less expensive and doesnt require fasting
ldl requires
12 hour fast
cholesterol measurement requirements
cant be sick, pregnant, or in a weightloss program
some cholesterol is affected by posture
mhm
the lab can also vary the value
ye
the measure should agree within
30mg%, and should also be done within 8 weeks; average the 2, and thats ur cholesterol
typically cholesterol is measured using
serum, but it can also be done using plasma
serum
portion of blood without clotting factor
- usually taken and put in a red silicon tube
plasma
with clotting factor
- plasma is usually taken then put in a testtube with EDTA (an anticoagulant), purple top tube
cholesterol level measured in serum is different from the cholesterol measured in plasma
when taken from plasma, times it by 1.03 to get the serum equivalent
ldl is usually calculated
based on hdl and triglycerides. but bad bc u might get hdl, vldl, or triglycerdes wrong, which would make ldl wrong
start at age 17-30
ur cholesterol increases 2.2mg% every year. peaks in middle age and declines in old age
there are differences in cholesterol levels in terms of
- race
- season- for men its higher in winter and lower in summer; opposite for women
- pregnancy- increased if pregnant; cholesterol levels decreased during ovulation
men typically have higher
ldl; women typically have higher hdl
risk for cholesterol is highest in
middle age; thats when u should reduce it the most
only about 30% of the cholesterol u ingest is absorbed
yea
enzyme impt for cholesterol absorption
HMG CoA reductase- main enzyme in cholesterol synthesis
- most drugs target this
- most active when ur consuming saturated fat
desirable cholesterol value
<200
high cholesterol
>240
epidemiologically desirable
<180
if u have good cholesterol, measure it every
5 years
if ur cholesterol is >240
get a lipid protein profile
- any other decisions after that is based on ur ldl
NCEP
national cholesterol education program
with definite risk factors
2 or more; if u have a cholesterol >240, then u have a lipid protein profile
LDL desirable level
<130
LDL high risk
> 160
if LDL is <130,
repeat in 5 years
if LDL is >160
diet and lifestyle therapy first, then drug therapy
- diet- reduce total fat to <30% of ur total calories and reduce ur cholesterol intake to less than 300mg% per day; do this for 6 weeks and if nothing happens, reduce ur saturated fat intake to <7% and reduce ur cholesterol intake to less than 200mg% per day
- sat fat is bad
drug therapy
- problems: once u go on them, u dont come off them (particularly with statins)= liver problems down the line
- if u have LDL >225, def need drugs
- >190, ur a candidate, but not definite
- the minimum goal is to reduce LDL to 130mg%
statins
use HMGCoA reductase
- aims at HMGCoA to reduce cholesterol
- HMGCoA reductase converts HMGCoA to cholesterol
- statins act on the reductase, so the conversion of HMGCoA to cholesterol cant happen, therefore, lowers cholesterol and ldl
A CoA- comes from saturated fat, increases HMG CoA levels, and therefore cholesterol synthesis
more statins
mimic HMG-CoA
- taken at night bc cholesterol is synthesized at night
- Lipitor (atorvastatin)- best selling pharmeceutical in history
- can lower ldl by 70mg% aka very effective
- 60% reduction in the number of cardiac events after statins have been prescribed
- better given as secondary prevention rather than primary prevention
- not as good at reducing tryglycerides, but better at lowering LDL
- problem is, theres an increased risk for rhabdomyolysis; rapid breakdown of skeletal muscle (usually happens when u mix statins and nicotinic acid (i.e. niacin))
- symptoms- live enzyme problems and muscle problems like myalgia
nicotinic acid
water soluble b vitamin
- wont reduce as much as a statin though
- lowers ldl, total cholesterol, raises HDL, lowers triglycerides
- side effects- flushing of the skin, but u build tolerance after a few weeks
- to reduce flushing- take the acids in time released preparations, avoid taking on empty stomach, and start w a low dosage, or take aspirin with it
- initial dose- 100-250 mg a day
- usually after dinner, bc u produce cholesterol at night. some ppl take up to 6g, over 2g u should ask ur dr first.
- contraindications- can affect blood glucose, liver function, u can develop uric acid crystals (gouty arthritis- crystals in joint), and ulcers
bile acid sequestrants
- lower LDL
- increase synthesis of bile acids in liver; bile acids are made from cholesterol
- problems- GI side effects- bloating, fullness, constipation, nausea, flatulence, can interfere w absorption of other drugs
top drug
use nicotinic acids first, then statins, then bile acid sequestrants
top ways to lower cholesterol
- weight reduction, lower body fat; 15 miles of aerobic activity a week, or 90 min of exercise
- most impt thing exercise does is lower triglycerdies and raise HDL
- smoking cessation
factors that affect cholesterol
- genetics; family disorders
- gender
- pregnancy
- birth control pills
- saturated fat in diet
- high calorie diets
- gorging
- uncontrolled diabetes
- inactivity (indolence)- exercise raises hdl
- anxiety (raises it)
- cigarette smoking
- excess coffee consumption- coffee causes the release of fatty acids into the blood stream; excess is more than 5 cups a day
HMG stands for
3 hdroxy, 3 methyl glutaryl CoA
taking in less saturated fat can
lower cholesterol
if u reduce ur dietary intake
sometimes what happens is u increase ur cholesterol synthesis; to reduce synthesis, reduce saturated fat
statins general
- improve endothelial function
- modulate (reduce) inflammatory response
- make plaque more stable
- prevent clotting
mevastatin
- produced by a fungus; same fungus that penicillin is produced from
- first statin identified