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22 Cards in this Set

  • Front
  • Back
primary prevention
prevention of first occurrence of cardiovascular disease

more expensive because many treated people will never get the disease regardless

risk factor evaluation at age 18
2ndary prevention
prevention of 2nd occurance of CVD

vigorous risk modification

better money spent
nonmodifiable risk factors
age - older

sex - men before 70, women after 70

family history - smoking/dietary habits learned, genetics,
modifiable risk factors
smoking - #1
hypertension
lipid abnormalities (cholesterol)
diabetes

others:
obesity
phys infactivity
left ventricular hypertrophy
magnitude of risk is determined by
amount of a given risk factor

number of risk factors over the lifetime
number of risk factors
2 risk factors doubles a person risk

3 risk factors = 4x the risk

removing one risk factor is a huge change
risk markers
associated with development of artheroscleosis but NOT CAUSITIVE

altering a risk marker does not affect progression or regression of disease

e.g. homocystine, uric acid
global risk score
assess primary risk only - not secondary risk

e.g. framingham risk scores

high risk = 20% or greater risk of event in 10 years

intermediate = 10-19%

low risk < 10%
current guidelines on risk factor identification
every five years after 18 determine risk factors

global risk score every 5 years after 35 for males and 45 for female
primary prevention of atherosclerosis
lifestyle behavior change even more valuable than any drug

smoking cessation, eat less

drugs: weigh cost, toxicity, treat more people to prevent events
2ndary prevention of atherosclerosis
individuals with CVD

single greatest benefit = smoking cessation

lifestyle

more aggressive lipid targeting

diabetes over 40 should be considered for 2ndary prevention
T/F atherosclerosis is a systemic illness
true

likely if you have atherosclerotic disease in one area (like in periphery), likely to have coronary artery disease
patient adherence
intervention is long term and sustained
smoking effects on atherosclerosis
effects endothelial function and vasomotion

plaque formation
hypertension effect on atherosclerosis
elevation of either systolic or diastolic pressure

lifestyle and medication

DASH diet
hyperlipidemia
lipid metabolic abnormalities are often genetically biased

diet and inactivity -> overexpression of abnormalities
LDL
LDL is major component of plaque - most associated with atherosclerotic plaque formation

most useful drug target

control of LDL will cause already formed plaques to regress

caused by increased calories and saturated fats
HDL
inversely associated with atherosclerosis

reverse cholesterol transport from tissue to liver disposal

too high levels not good
triglycerides
2ndary drug target

TGs make LDL more atherogenic

made worse with high carbs

linked with metabolic syndrome and diabetes
metabolic syndrome
cluster of risk factors

defined by:
abdominal obesity

hypertension

glucose intolerance (prediabets or diabetes)

lipid abnormalities - high TGs and depressed HDL

insulin resistance link
diabetes
want to control glucose, BUT most important is controlling macrovascular effects

macrovascular effects contributes the most to deaths and includes eyes, peripheral nevers, and kidney

control LDL, BP, smoking is important
need to focus on what 3 things to reduce atherosclerosis
exercise

diet

smoking