Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
57 Cards in this Set
- Front
- Back
|
What are the 6 different stages of plaque formation?
|
fatty dot --> fatty streak --> intermediate lesions --> fatty atheroma --> fibroatheroma --> complicated atheroma
|
|
|
What is a Type I lesion also known as? (2)
|
Initial lesion or a fatty dot
|
|
|
What is in a fatty dot?
|
A few macrophages with lipids inside
|
|
|
Where are fatty dots located?
|
in the aorta
|
|
|
How early do fatty dots appear and what do they look lie?
|
As early as 1 year and they are yellow dots that are less than 1mm
|
|
|
What is a Type II lesion also known as? (2)
|
fatty streaks or linear lesions
|
|
|
How do the type II lesions change in shape?
|
they are more elongated (up to 1 cm) from fusion of dots.
|
|
|
How do the type II lesions change in composition from type I
|
You have more macrophages/lipids and also some T cells. They can be foam cells.
|
|
|
Where are fatty streaks starting to show up besides the aorta?
|
in the coronary arteries
|
|
|
Are all fatty streaks going to become atherosclerotic plaque?
|
No! Many show up in places that don't get atherosclerosis
|
|
|
Does ever atherosclerotic plaque come from fatty treaks?
|
yes
|
|
|
What determines if a fatty streak is going to turn into a plaque?
|
the presence of risk factors like HTN, DM, and hyperlipidemia
|
|
|
What is a Type III lesion also known as? (1)
|
intermediate lesions
|
|
|
What distinguishes type II from type III?
|
There is fat present outside of macrophages (because they exploded)
|
|
|
When do atheromas actually start? (which type)
|
In type IV
|
|
|
What is a Type IV lesion also known as? (1)
|
fatty atheroma or atheroma
|
|
|
What distinguishes a type IV lesion?
|
a lipid core surrounded by foam cells and other inflammatory cells
|
|
|
What is a Type V lesion also known as? (1)
|
A fibrofatty atheroma or fibroatheroma
|
|
|
What distinguishes a type V lesion?
|
A fibrous cap and neovasclarizations at the corners
|
|
|
What is a Type VI lesion also known as? (1)
|
complicated atheromas
|
|
|
What distinguishes a type VI lesion?
|
There is disturbance of the endothelial layer and platelets are forming a plug or even a thrombus
|
|
|
What are the types of disturbances that can happen to start a complicated atheroma?
|
erosions or fissures or intraplauqe hemorrhage
|
|
|
What happens when there is an intraplauqe hemorrhage?
|
The blood will gather in the center of the plaque and start occluding the lumen
|
|
|
What is another way an intraplaque hemorrhage can be formed?
|
blood from the vessel breaks in and accumulates in the plaque.
|
|
|
What is the driving force behind the formation of types I-IV?
|
the accumulation of lipids
|
|
|
What is the driving force behind the formation of fibroatheromas from type IV?
|
accelerated accumulation of SM and collagen deposition
|
|
|
What is the driving force behind the formation of complicated lesions?
|
inflammation or mechanical stress leading to thrombus formation and hemorrhages
|
|
|
What is an eccentric lesion?
|
the opposite of a concentric lesion, it just occupies one spot of the vessel wall
|
|
|
How do eccentric lesions grow into larger lesions that can take up all or half the circumference?
|
They accumulate more fat and also merge with one another.
|
|
|
What is the mnmonic for memorizing the order of most common vessels to develop atherosclerosis?
|
Aortic CROCOdiles POPping from CAR of WILLIS (Ab Aorta, coronary, popliteal, carotid, circle of willis)
|
|
|
At what stage do lesions stop being silent and MAY start causing problems?
|
Starting at type IV (fatty atheroma)
|
|
|
What is the main complication of atheromas in the large arteries vs muscular arteries?
|
aneurysm for large. obstruction for muscular.
|
|
|
Why may fibrosis form in plaques?
|
due to growth factors (secreted by all cells, but especially endothelial and platelet)
|
|
|
Why may calcifications form in plaques?
|
When the cells get hurt in all the commotion or die, they release negatively charged FA's which attract Ca2+.
|
|
|
What form of calification is this?
|
dystrophic calcifications
|
|
|
Is fibrosis and calcification dangerous?
|
Not really except for if they get so bad and concentric that they make stenosis.
|
|
|
What is the real dangerous progression involving surfact defects?
|
thrombogenesis or atheroembolism
|
|
|
How does an atheroemoblus form?
|
A plaque ruptures so much that the plaque inside comes out and lidges somewhere else
|
|
|
What is the real dangerous progression involving the neovascularizations?
|
intraplaque hemorrhage leading to ballooning out and obstruction
|
|
|
What is the real dangerous progression involving wall weakening?
|
aneurysm and rupture
|
|
|
What are the main fates of atherosclerosis? (4)
|
Stenosis
Occlude Embolize Aneurysm and rupture |
|
|
Generally, when do atherosclerotic complications occur?
|
over the age of 30
|
|
|
What are the two main complication of abdominal aortic anuerysms (from atherosclerosis)?
|
a thrombus can form from all the turbulence and lead to lower limb ischemia OR a rupture
|
|
|
What is the main complication of atherosclerosis in the coronary arteries?
|
Ischemic heart disease
|
|
|
What are the 4 ways in which ischemic heart disease may manifest?
|
1. angina pectoralis
2. MI 3. Sudden cardiac death 4. Chronic IHD which may lead to chronic cardiac failure from loss of myocytes |
|
|
How does sudden cardiac death come about?
|
There is some injury that leads to tachycardia/arrhythmmia the kills you suddenly.
|
|
|
What is the main complication of atherosclerosis in the popliteal arteries?
|
they either occlude, stenose, or embolize, all to lead to distal limb ischemia
|
|
|
What is the main complication of atherosclerosis in the carotid arteries or the circle of willis?
|
1. TIA
2. Stroke |
|
|
Define a TIA.
|
A cardiovascular event that leads to neurological dysfunction that recovers completely in 24 hours.
|
|
|
Define a stroke.
|
Same as a TIA except that you don't recover completely in 24 hours.
|
|
|
What type of atherosclerosis do you get to the gut?
|
Osteal stenosis of the mesenteric arteries due to turbulence at the openings.
|
|
|
What part of the gut usually gets occluded from this type of atherosclerosis?
|
small intestines
|
|
|
What is the main symptom of someone with osteal artherosclerosis of the mesenteric arteries?
|
post prandial abdominal pain from not gettting enough blood to digest.
|
|
|
Where do the renal arteries usually get atherosclerosis? Why?
|
at the ostia because they are relatively perpendicular branch points.
|
|
|
What is leriche syndrome?
|
When you get extensive atherosclerosis to the abdominal aorta and iliac arteries
|
|
|
What kinds of symptoms do you get with leriche syndrome? (1)
|
males- impotence
claudication atrophy of calf muscles |
|
|
What is the difference between primary and secondary prevention?
|
primary is to prevent sx in someone who has never had complications (TIA, MI) and secondary is with someone who has had it already.
|
