3.What ways does cholesterol surrounded by food contribute to arterial sclerosis?
please help me with this request for information.. thank you very much!!
Answers:
that particular fat is what help block the arteries. makes it so blood platelets stick in the narrowed nouns causing a blood clot that causes heart attacks or strokes.
Please see the webpages for more details on Cholesterol. Source(s): http://en.wikipedia.org/wiki/Cholesterol
http://www.nlm.nih.gov/medlineplus/ency/…
I did a presentation on the topic last week so:
excess LDL (the doomed to failure cholesterol) is oxidized by free radicles & taken up by macrophges (white blood cells) & become "foam cells", these foam cells start secreting substances that promote endothelial cell prolifration (cells bin liner the vesseles from the inside). foam cells will accumulate on injured endothelium & form "fatty streaks" which will progress into "atherosclerotic plaques"..this will produce the symptomes of angina (heart ischemia). consequently the disease progress, & platelets are activated, these activated platelets will cloak thromboxan A2 which will promote vasoconstriction (constriction of the artery) & further platelet aggregation. activated plateletes have the gycoprotein 2b/3a receptor which will interact beside fibrinogen to form the more stable fibrin... Source(s): medical student...
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Answers:
that particular fat is what help block the arteries. makes it so blood platelets stick in the narrowed nouns causing a blood clot that causes heart attacks or strokes.
Please see the webpages for more details on Cholesterol. Source(s): http://en.wikipedia.org/wiki/Cholesterol
http://www.nlm.nih.gov/medlineplus/ency/…
I did a presentation on the topic last week so:
excess LDL (the doomed to failure cholesterol) is oxidized by free radicles & taken up by macrophges (white blood cells) & become "foam cells", these foam cells start secreting substances that promote endothelial cell prolifration (cells bin liner the vesseles from the inside). foam cells will accumulate on injured endothelium & form "fatty streaks" which will progress into "atherosclerotic plaques"..this will produce the symptomes of angina (heart ischemia). consequently the disease progress, & platelets are activated, these activated platelets will cloak thromboxan A2 which will promote vasoconstriction (constriction of the artery) & further platelet aggregation. activated plateletes have the gycoprotein 2b/3a receptor which will interact beside fibrinogen to form the more stable fibrin... Source(s): medical student...
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