Cardiovascular Disease (3) Flashcards
what pop is living w heart disease in canada and what % can be avoided
1/12 Canadians over 20 are living w dx heart disease
-80% can be prevented by adopting healthy behaviours
risk factors for CVD seen in framingham study
- smoking
- physical inactivity
- overweight/obese
- hypercholesterolemia
- elevated cholesterol (high LDL, low HDL)
- hypertension
- diabetes
why does smoking lead to CVD
- due to oxidative stress
- may be related to inability for nitric oxide generation and bioavailability which influences the vascular walls
- oxidation of material that can collect on inside of arteries and cause atherosclerotic diseases that can relate to platelet aggregation
new categories of hypertension (normal, pre, hypertension, stage 1, stage 2)
normal- <120/80 pre- 120-139/80-89 hyper- >140/90 stage 1- 140-159/90-99 stage 2- >160-180/100+
what stage of hypertension needs to be addressed pharmacologically and why
stage 3
- high risk of dissemination/stroke from too much vascular pressure
why tx hypertensionn- how much does it reduce risk by
if we can decrease systolic by 2mmHg, we can reduce mortality due to CVD by 3%
-diet and exercise interventions can make sig changes in mortality
what is sustained hypertension, masked and white coat
sustained- occurs no matter what
masked- transient elevation of BP, but no changes over time, 8% of pop
white coat- in office, 12-18% of pop
framingham 10 year risk assessment 3 steps
- assess risk factors
- 10 year cardiovascular risk % (anybody over 10% needs intervention)
- Heart age based on points from step 1
exogenous pathway of lipid biogemestry
chylomicrons assembled in intestinal mucosa as a means to transport dietary cholesterol and trigylerides
remnants are absorbed by liver and FFA are put into adipose tissue for storage or into mm tissue for energy
what do capillaries of adiose tissue and mm do to chylomicrons
FA are removed from chylomicrons and triglycerides by lipoprolipase
-FFA are absorbed into tissues and glycerol backbone returned to liver and kidneys
mediated by LDL receptors and LDL receptor related pros
what does excess dietary fat and cars convert to
trigylerides
endogenenous pathway of lipid metabolism
triglycerides in the liver are packaged into VLDL and released back into circulation
-VLDLs aere molecules formed to transport endogenous fat via hepatic tissue
What does APO E and APO B do
- Presence of APO E enables lipoprotein particles to have high affinity for LDL receptors on the hepatocytes and adrenal cortex cells
- LDL particles also possess APO B, which is required for LDL receptor binding
primary pharm intervention of CVD and how to determine if needed
Those with CVD potential are tested for non fasting lipid level
- max 20% variance in lipids fated vs non
- -if <10 no intervention
- -if 10+ statin initiated, ASA for clotting risk
what do statins do and why
- inhibit HMG CoA reductase
- -the intracellular synthesis of cholesterol is inhibited and cells are therefor dependent on extracellular sources of cholesterol
- -net result is an increased cellular uptake of LDLs
