Cardiovascular Disease Flashcards

(43 cards)

1
Q

What is atherosclerosis

A

buildup of plaque in the artieries

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2
Q

What does the fibrous cap do?

A

protects the plaque build-up

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3
Q

Fatty deposit (aka plaque)

A

Fats, cholesterol, and other substances build up in the artery wall

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4
Q

Vulnerable plaques

A

susceptible to rupture due to high lipid content, increased inflammation, and thin fibrous cap

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5
Q

plaque inflammation and increased arterial pressure can trigger______

A

plaque rupture

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6
Q

When plaque ruptures, exposure to blood flow triggers _____

A

A thrombus

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7
Q

Thrombus

A

blood clot consisting of platelets and insoluble fibrin forms at the site of injury

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8
Q

Myocardial infarction (heart attack)

A

occurs when a clot completely blocks blood flow to an area of the heart

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9
Q

Heart tissues die when ___

A

oxygen (supplied by blood) is denied to the tissues

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10
Q

Steps to plaque formation

A
  1. Arterial wall damage
  2. Chemokines secretion
  3. Foam cell formation
  4. SMC migration
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11
Q

What happens when the arterial wall is damaged?

A

LDL enters the blood stream and then LDL is oxidized and retained

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12
Q

What happens when LDL is oxidized?

A

Endothelial cells are activated secreting chemokines and then monocytes adhere to receptors ICAM and VCAM

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13
Q

Endothelial cell activation leads to :

A
  • Adhesion is molecularly activated
  • Secrete chemokines
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14
Q

How are foam cells formed?

A

monocytes differentiate into macrophages which are then filled with LDL

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15
Q

What is a foam cell?

A

macrophage filled w/ LDL

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16
Q

What causes SMC’s to proliferate?

A

Foam cells secrete growth factors that tells the SMCs to multiply

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17
Q

What causes the SMC’s to migrate?

A

OxLDL binds to the proliferated cells and this causes the release

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18
Q

What do the SMC’s do when they are released?

A

they begin extracellular matrix formation which is comprised of proteins such as collagen and elastin.

19
Q

How should the fibrous cap form?

20
Q

What happens if the fibrous cap forms quickly?

A

the cap doesn’t form well and its likely to rupture

21
Q

Intima

A

the area between SMC’s and EC’s

22
Q

When subendothelial proteins are exposed, this leads to _____

23
Q

What is bad cholesterol

A

LDL- low density lipid protein

24
Q

What is good cholesterol

A

HDL- High density lipid protein

25
HDL function
moves cholesterol from the body to the liver for clearance (removes cholesterol)
26
LDL function
moves cholesterol to arteries
27
Why is HDL more dense than LDL?
More protein per lipid
28
WHat do statins do?
they inhibit HMG=CoA reductase, which is the rate-limiting step of CHolesterol synthesis
29
Statins ____ and they increase the ____ in the liver which decreases _____
reduce cholesterol synthesis LDL receptors LDL by 25%-50%
30
Vascular grafts are usually made of _____ and are only useful for ______
polymers large arteries
31
Vascular grafts are coated with ____ which _____
heparin prevents clotting
32
How are stents implanted
1. stent is inserted into the artery 2. The stent is expanded via a balloon 3. The balloon is removed and the stent remains expanded in the artery
33
Stents are typically made of
metal coated with a polymer
34
Biggest problem with stents and grafts is that ____
they tend to form a thrombus
35
Types of anticoagulant coatings
Hirudin Heparin
36
TFPI and Thrombodulin both _____
Inhibit binding process of thrombin
37
Albumin is ____
protein that prevents things from binding
38
GAGs are
(glycose amino glycans) found on the surface of EC's and prevents platelet binding
39
PC is
a phospholipid found in cell membrane that inhibits platelet binding
40
PEG can
prevent platelet binding
41
EC's release nitric oxide which ____
inhibits platelet binding and SMC proliferaiton
42
Tissue engineered vascular grafts process
1. Cells extracted from patient 2. Cells expanded in culture 3a. Cells mixed with polymer scaffold material and shaped in mold 3b. Vells seeded into porous polymer scaffold 4. COnstruct matured in a bioreactor
43
Nonthrombogenic engineering methods
1. Anticoagulant coatings 2. Inhibit platelet adhesion/ activation 3. In vitro endothelialization 4. In situ endothelialization