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18 Cards in this Set

  • Front
  • Back
When does atherosclerosis begin?
post adolescence (it occurs where arteries branch)
Explain the LDL phenomenon again.
Arteries form Apo-B receptors b/c of injury and LDL has Apo-B so it sticks to arterial wall
(LDL part of repair process)
Is the LDL being there reversible?
Yes very..when no more injury, HDL can come and pull off LDL
However what happens sometimes with WBCs?
when there's an injured site, WBCs always like to remove bad things so they go to the site so it engulfs the LDL particle. BUT if the LDL particle becomes oxidized, it can't leave the WBC and damaged cells! so while in the WBC, LDL sends out cytokines to the liver telling it to produce CRP (C-reactive protein)
Thus, what's a good predictor of heart attack anad stroke?
`if CRP levels are high (note: CRP usually a response to infections)
What's a foam cell
structure formed when WBC-LDL complex keep attracting more LDLs (slow process)
how does calcium come into play?
CALCIUM IS starts getting attracted to foam cell (called plaque). The foam cell keeps growing and this is what atherosclerosis is---still damaged cells but w/ increased plaque so getting more damaged
Now RBCs come into play! OH NO!
RBCs can turn on/off stickiness--anyway, the accumulation of RBCs --> less and less blood flow --> thrombosis (blood clot at the site of injury)-can't get any blood through artery--> heart attack
What are the warning signs of a heart attack?
1) discomfort in center of chest. Feels like uncomfortable pressure...squeezing, fullness or pain
2) Pain/discomfort may radiate to arms, back, neck, jaw, or stomach
3) shortness of breath
4) cold sweat, nausea, or lightheadedness.
How long do you have to get to the hospital when this shit happens?
What's the way out of this scary atherosclerosis shit?
What does it mean when fatty acids are saturated?
all carbons staurated with Hs (this is the fat we make/eat)
Plant sources of saturated fats
palm, coconut, cottonseed
What does it mean when fatty acids are unsaturated?
not all carbons saturated w/ Hs--> double bonded carbons
monosaturated: only one C=C double bond (olive oil and canola oil).
polyunsaturated (most frequent type of fatty acids)
(corn oil, soybean oil, safflower, sunflower)
So what's wrong with saturated fatty acids?
sensitivity of Apo receptors on the liver is related to degree of saturation...the more unsaturated the fat, the more seneitve these liver receptors get...if sensitized, it can pick up (IDLs and) LDLs so more will go to the liver than go to injured cells in arteries
what's one way to minimize the risk of atherosclerosis (dealing with fat)
substitute unsaturated fats with saturated fats...most of the cholesterol we have is made by the body (60%) so if we increase cholesterol intake, we decrease the amont made by the body (called downregulation)
What are determinants of cholesterol production?
1. Demand: if intake of fat increases, bile production increases (bile is VLDL--a fat)
(gallbladder is fat store)
what are other things to do to minimize risk of atherosclerosis?
1) supply diet (reduce fat intake--less LDL going to arteries)
2)minimize consumption of fat.