Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
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 |