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CVS-charis > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

3 major factors contributing of CVD

A

Hypertension
Smoking
Cholesterol

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2
Q

Where do LDLs depsit and bind?

A

Deposit: subintimal space
Bind: Matrix proteoglycans

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3
Q

Main inflammatory cells in atherosclerosis?

A

Macrophages

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4
Q

2 main classes of macrophages and functions?

A

Resident (normally homeostatic)

Inflammtory (kill microorganisms)

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5
Q

How are macrophage subtypes regulated?

A

By combinations of transcription factors binding to regulatory sequences on DNA

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6
Q

What is reverse cholesterol transport

A

When HDL carries cholesterol from “peripheral tissues” incl arteries back to the liver

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7
Q

What are oxidised/modified LDLs and how are they produced?

A

Family of highly inflammatory and toxic forms of LDL found in vessel walls

Produced due to the action of free radicals on LDL
note one single substance

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8
Q

Type of membrane in LDL

A

Lipid monolayer

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9
Q

LDL membrane what does it include

A

Phospholipids, cholesterol, apoproteins, cargo (fat for fuel)

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10
Q

How do LDLs become trapped

A

Leak through the endothelial barrier by uncertain mechanisms

LDL trapped by binding to sticky matrix carbohydrates (proteoglycans) in the sub-endothelial layer

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11
Q

What happens to LDLs after they become trapped in the subendothelial layer

A

Modification

Oxidation by free radicals

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12
Q

Significance of modified LDL

A

Oxdised LDL is phagocytosed by macrophages and stimulates chronic inflammation

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13
Q 
Familial hyperlipidemia
Inheritance 
Characteristics (2)
Physical signs (2)
Consequences if left untreated
A 
Autosomal genetic disease
Massively elevated cholesterol(20mm/L)
Failure to clear LDL from blood
Xanthomas
Early athersclerosis
Fatal myocardial infarction before the age of 20
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14
Q

What is the cause of familial hyperlipidemia

A

No LDL receptor

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15
Q

Mechanism of familial hyperlipidemia

A

No LDL receptor, macrophages accumulate cholesterol
Second LDL receptor deduced in atherosclerotic lesions, not under feedback control
removes oxLDL

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16
Q

What are scavanger receptors?

A

Family of pathogen receptors that accidentally bind to oxLDL and remove it by reverse cholesterol transport

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17
Q

Macrophage scavenger receptor A

A 
CD204
Binds to
oxLDL
gram +
dead cells
18
Q

Macrophage scavenger receptor B

A 
CD36
Binds to:
oxLDL
malaria parasites
dead cells
19
Q

What is the function of macrophages within plaques (4)

A

Generate free radicals (further ox of LDL)
Phagocytose oxLDL –> foam cells
Become activated by oxLDL/free intracellular chol to secrete substances
Die by apoptosis - contributing to the lipid - rich core of the plaque

20
Q

What kind of substances do macrophages secrete when they become activated by oxLDL/free intracellular cholesterol (4)

A

Cytokine mediators that recruit more monocytes
Chemoattractants an growth factors for vascular smooth muscle cells
Proteinases that degrade tissue
Tissue factor that stimulates coagulation upon contact with blood

21
Q

Give 2 examples of oxidative enzymes that macrphages have

A

NADPH oxdase

Myeloperoxidase (HOCL, HONOO)

22
Q

Definition of chemokines released by macrophages

and 1 example

A

small proteins chemoattractant to monocytes

MCP-1

23
Q

Definition of cytokines released by macrophages

and 1 example

A

Protein immune hormones that activate endothelial cell adhesion molecules IL-1

24
Q

Give two examples of growth factors released by macrophages

A

Platelet derived growth factor

Transforming growth factor beta

25
Q

Function of Platelet derived growth factor

A

VSMC chemotaxis
VSMC survival
VSMC mitosis

26
Q

What does VSMC mean

A

Vascular smooth muscle cell

27
Q

Function of Transforming growth factor beta

A

Increased collagen synthesis
Matrix deposition
This strengthens the plaque
works on VSMC

28
Q

Difference between normal and atherosclerotic VSMC

A

Normal: Increased contractile filaments, decreased matrix deposition
Atherosclerotic: Decreased contractile filaments, increased matrix deposition

29
Q

Give a general example of proteinases that degrade tissue and function

A

Metalloproteinases (MMPs)
Family of 28 homologous enzymes
activate each other by proteolysis
degrade collagen

30
Q

What is the catalytic mechanism of metalloproteinases based on?

A

Zinc

31
Q

Give 5 characteristics of vulnerable and stable palques

A

Large soft eccentric lipid-rich necrotic core (non-cellular material)
Thin fibrous cap
Reduced VSMC and collagen content
Increased VSMC apoptosis
Infiltrate of activated macrophages expressing MMPs

32
Q

How do macrophages die by apoptosis?

A

oxLDL derived metabolites are toxic
Macrophage form cells have protective systems that maintain survival in face of toxic lipid loathing
Macrophages can be overwhelmed and die by apoptosis

33
Q

What does macrophage apoptosis result to

A

Release of macrophage tissue factor and toxic lipids into the central death zone called lipid necrotic core

Thrombogenic and toxic material accumulates, walled off, until plaque rupture causes it to meet blood

34
Q

What is NFkB

A

Transcription factor

35
Q

What is the function of NFkB

A

Maser regulator of inflammation, switches on numerous inflammatory genes e.g. matrix metalloproteinases
inducible NO synthase

36
Q

What is NFkB activated by

A

Numerous inflammatory stimuli such as
Scavenger receptors
Toll-like receptors
Cytokine receptors

37
Q

5 factors that predispose to atherosclerosis

A 
Smoking
Hyperlipidaemia
Location - disturbed flow
Diabetes
Hypertension
38
Q

other name for Scavenger receptor

A

pathogen recognition receptor

39
Q

What happens when collagen gets destroyed

A

Collagen keeps things together, if it is digested this creates a hole/weakening that then allows the fat in the vessel (which is intensely pro-coagulant and intensely toxic) to touch the lumen of the artery  immediate clot formation, thrombosis

40
Q

What are endothelial erosion lesions

A

You have an area where the endothelial cells -possibly because of the macrophages- are lost/dying, this stimulates a thrombus directly on the collagen in the fibrous cap

41
Q

General function of growth factors

A

Generates more smooth muscle cells that are going to be able to switch on to generate more collagen, makes the arteriole stronger and rupture resistant

CVS-charis (7 decks)

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