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52 Cards in this Set

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what will a diest high in omega 3 reduce the risk of? will it affect platelet aggregation or coagulation
v fib

Decrease platelet aggregation
intima
media
adventitia
layers of vessels

intima: endothelium, lines lumen: elastic, proteoglycans, collagen
Media: Smooth MM
Adventitia: CT,
what are 4 fx of healthy endothelium
1. dilation
2. inhibit coagulation: inhibit clot formation, inhibit platelet activation, stimulat fibrinolysis
3. inhibit imflammation
4. Inhibit migration/differentiation of: monocytes, T cells, VSM (vascular SM)
name 3 ways healthy endo prevents coagulation
1. inhibit clot formation
2. inhibit platelt activation
3. stimulate fibrinolysis
what does healthy endothelium inhibit the migration/differentiation of?
1. monocytes from blood
2. t cells from blood
3. VSM
What are 4 Fx of NO?
1. dilation
2. inhibits platelet adhesion (antithrombosis)
3. inhibits leukocytes from attacheing to endo, anti inflammatory
4. inhibits growth/migration of VCM
how does NO prevent thrombosis?
not letting plateles adhere
what is the precursor to NO?
WHat enzyme?
where does NO bind?
Arginine
NOS
guanyl cyclase on VCM,
what is artherogensis?
plaque formation

*response of endo to injury
what are the 4 general phases of plaque formation (artherogenesis)
1. Endo damage, this alerts monocytes to become macrophages and LDL oxidation in sub endo

2. Foam Cells: macrophages use scavernger receptor to eat up LDL

3. Fibrous plaque: Fibrous cap from secretions of VCM, Necrotic core, foam cell necrosis

4. Advanced Lesion: plaque rupture, thrombis or Growing plaque leading to stenosis
we know that plaque formation begins with endo damage. how is endo damage and what happens when its damaged?
smoking
turblance due to branching or HTN
infection

**when injured the endo is permiable and lets LDL in and macrophages. Cytokines are released that recruit more macrophages/monocytes Less NO is made so vessels constrict
why dont we want macrophages in the vessels?
**remember they ge there when vessels are injured bc of increased permiability and recruitment by cytokines

**they make ROS, and try to eat up the LDL via scavenger receptors. they also make things that turn off NO synthesis
so the sedonc step of artherogenesis, fatty streak. how does it happen?
1. endo damage
2. FOAM CELL: fatty streak

**macrophages make ROS that oxidize LDL, the oxidLDL is then taken up by macrophages via scavenger receptors (cant stop it). The macrophages cant degrade cholesterol and become foam cells
where is foam cell formation common? why?
branch points

**high turbulence, this leads to endo damage, this leads to increased LDL and macrophages entering BV walls

**also HTN will increase turbulence and increase foam cell formation
how do levels of LDL and HDL affect foam cell formation
LDL, increased foam cell
HDL, decreased foam cell
what layer does foam cell formation occur?
intima
what is the necrotic core of a plaque
dying foam cells,

covered by fibrous cap in step 3 of artherogensis
how is the fibrous cap (step 3) formed?
who secretes what where and what happens
1. endo damage
2. foam cell
3. Fibrous Cap: macrophages/endo make cytokines that tell SM to enter the intima where the action is occuring

**VCM in the intima secrete EMC which is the cap, the cap is hardened with Ca
what happens when the firbours cap of a plaque is unstable
it can rupture, thrombosis
what are demographic features that increase ones risk of CVD that CANT be changed
man
over 40
family Hx
what are lipid risk factors for increased risk of CVD
1 high total cholesterol
2. low HDL
what are 5 things that a 45 yo man whos mom died of CVD do to prevent his risk? what cant he change?
1. HTN- turbulence increased
2. DM (glycation, endo damage)
3. Smoking- increased damage
4. Obesity- IR and fat metabolism
5. Inactive

**he cant change that hes a man, hes old, and his momma died
what does cholesterol need to be under to decrease risk of CVD
200 or less
why is hi HDL good to lower risk of CVD
reverse cholesterol transport

**removes cholesterol from endo/peripheral tissue and brings it to the liver
is having high HDL AND LDL as good as HIGH HDL and low LDL
better to have high HDL nad low LDL than high both
how are SFA related to CVD? what is the mech
SFA increase CVD

**SFA increase LDL by decreaseing LDL receptors on liver, this means LDL cant enter the liver so they have to float around and then they get into vessels
what do mryistic acid and palmitic acid do to CVD
these are SFA, they block the bililiy of LDL to get in the liver, LDL circulates and stays in the blood ---> increased CVD
where are lots of mryistic and palmitic acid found
SFA
whole milk, cheese
solid animal fat (red meat)

**less than 7% of calories shoudl be from SFA, typically its 11%
what happens when LDL receptor activity is increased? decreased? give an example that increases or decreases activity
Increased: less LDL in circulation and less risk for CVD, increases LDL receptor with increased MUFA, PUFA (lineolic acid, omega 6)

Decreased: less LDL enters liver and so it floats around and increases CVD, SFA do this
what are MUFA? where are they
monounsat FA

**decrease LDL :)


olive oil
almond oil
canola oil
high oleic safflower oil
what are trans FA? are they good or bad, where are they found?
TFA, MUFA that looks liek a SFA

BAD!!! increase LDL, decrease HDL

Found in processed food, not in plants or animals
what are PUFA's? where are they found
polyunsat FA

omega 3,6
lineolic acid

increase LDL receptor activity to decrease LDL in circulation

**seed oils, walnuts
does omega 3 or 6 affect cholesterol levels
6

*increases LDL receptor activity to decrease LDL in circulation
what kind of fat is lineolic acid, what does it do?
PUFA

decrease LDL
where do ya find omega 3? what does it do to CVD, how?
fish (EPA, DHA)

Salmon
Mackerl
Anchovies
Sardines
Herring

**great reduction in CVD risk, but doesnt alter cholesterol levels. THey decrease platelet aggregation

**omega 3 are weak platelet aggregators, no aggregation, no thrombosis!
if you cut off the fat of a steak are you lowering the amt of cholesterol your eating? will you lower any fat consumption?
not really, lots of cholesterol in the lean meat

you cut off the SFA
is ALL cholesterol abs in mixed micelles?
nope, only 50% abd with micelles
whats a more influential role on LDL cholesterol levels
1. dietary cholesterol intake
2. composition/amt of fats eaten
2. the AMT of TYPE of fat is way more important in determining LDL levels
how are HDL/LDL affected by...
1. TFA
2. SFA
3. MUFA
4. PUFA 6
5. PUFA 3
1. TFA- LDL hi, HDL lo
2. SFA: LDL hi, HDL ---
3. MUFA: LDL low, HDL lo
4. PUFA 6: LDL lo, HDL lo
5. PUFA 3: HDL ---, HDL --
Nuts do what to cholesterol, what kind of fats do they have
decrease cholesterol

MUFA, PUFA

**they are exceptionally good, good beyond pure replacement of fats
do all high fat diets result in CVD?

remember the three nations and their food?
NO!

only diets high in SFA

Japenese: low total fat but lots of SFA, high CVD
North European: HIGH fat dies, high SFA, high CVD
Medeterranian: HIGH fat diet but LOW SFA, low CVD

**quality over quantity
what are sterols/stanols, how do they affect cholesterol levels
lower LDL
nothing with HDL

**found in plants, similiar structure to cholest
how do sterols work to lower LDL
they are incorporated into mixed micelles so cholesterol cant be incorporated
what does fiber do to cholesterol? how?
decrease cholesterol

their digestion interferes with bile salt reabsorption (they are pooped out!) so more cholesterol is used to make bile salts and so is taken out of circulation
what does eating oatmeal, fruit, veggies, legumes do to cholesterol
FIBER!!!

it reduced cholesterol by interfering with bile salt abs. bile salts (and the cholesterol in them) are pooped out and cholesterol is taken from circulation and used to make bile salts
what happens to cholesterol when you loose weight
decreases
how is HDL increased
exercise
what does booze do to cholesterol
increases HDL
what are the 7 things that the ntnl cholest education program recommends?
1. eat lean meats and plants
2. dont eat visible fat, milk products
3. eat carbs: complex from grain/veggies/fruit
4. fish 2x/week
5. replace SFA with MUFA/PUFA
6. Loose weight
7. exercise
what are the reccomendations

SFA
PUFA
MUFA
Cholesterol
Total Fat
SFA <7% total cal
PUFA 10% total cal
MUFA 20% total cal
Cholest <200mg/day
Total Fat 20-35% total cal, remember its what KIND of fat, not how much!
do all ppl with MI have high cholest
nope, 50% dont
if you.... you are 95% liekly to have CVD
1. smoke
2. DM
3. HTN
4. Hypercholesterolemia