Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

HLB > Artherogenesis > Flashcards

Artherogenesis Flashcards

1
Q

Non-modifiable arterial disease risk factors (4):

A
  • genetic abnormalities
  • family history
  • increasing age
  • male
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Modifiable arterial disease risk factors (4):

A
  • smoking
  • hypertension (high blood pressure)
  • high cholesterol levels
  • diabetes mellitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Structure of the arterial wall

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Atherosclerosis structure consists of (2):

A
  • fibrous cap
  • necrotic core
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Atherosclerosis structure: fibrous cap:

A
  • smooth muscle cells
  • foam cells
  • macrophages
  • lymphocytes
  • proteoglycans
  • collagen
  • elastin
  • neurovascularisation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Atherosclerosis structure: necrotic core:

A
  • cell debris
  • cholesterol crystals
  • calcium salts
  • foam cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lipid Hypothesis:

A
  • 1980s
  • virchow specifically linked artherosclerosis
    to high LDL cholesterol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Lipid Oxidation Hypothesis:

A
  • atherosclerosis as the consequence of free-radical driven oxidative modification of LDL cholesterol:
    - OH radical (hydroxyl)
    - O2- radical (superoxide)
    - O2 radical (singlet)
  • modified LDL is taken up more rapidly by macrophages: LDL binds to non-specific scavenger receptors
  • led to the hypothesis that: oxidative stress was a prerequisite for lipid uptake and thus a primary cause of atherosclerosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Reasons why lipid oxidation is a contributing factor but is not the primary cause of atherosclerosis:

A
  • the distribution of atheroma in the arterial tree
  • the role of non-lipid risk factors: hypertension, smoking, genetics
  • the complications of atherosclerosis
  • clinical trials with anti-oxidant drugs had no effect on the course of atherosclerotic disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which experimental models does most atherosclerosis data come from? What are the disadvantages of these experiments?

A
  • LDL receptor deficient mice
  • Apolipoprotein E deficient mice
  • the mice develop atherosclerosis on a
    normal diet
  • may not be extrapolated correctly to
    human disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Response to Injury Hypothesis Steps:

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Atherosclerosis is seen as an acute inflammatory response to endothelial injury.

True or False?

A

False
a chronic response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Endothelial Injury Risk Factors:

A
  • haemodynamic stress (high BP, arterial branch points)
  • toxins (cigarette smoke)
  • hyperlipidaemia
  • aging
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

In health, macrophages normally take up very little native LDL cholesterol.

True or False?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What receptor deficiency results in the accumulation of large amounts of cholesterol in macrophages? Elaborate.

A
  • LDL receptor deficiency causes a large
    amount of cholesterol accumulation in
    their macrophages
  • circulating LDL must undergo modification
    to become atherogenic
  • these modifications allow LDL uptake via
    scavenger receptors
  • modification = oxidation/ oxidative stress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why is atheroscleorsis more likely to occur at arterial branch points?

A

More likely to occur where there is turbulent flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Endothelial Injury Response:

A
  • endothelial cells release cytokines
  • endothelial cells express adhesion
    molecules
  • allow leukocytes (monocytes) to bind and -
    infiltrate (macrophages)
  • injury leads to reduced NO production
  • Nitric Oxide (NO) was originally called EDFR endothelium derived relaxing factor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the four classes of small molecules involved in atherosclerosis and what are their purposes?

A
  • Cytokines: regulate inflammatory response
  • Growth factors: stimulate the growth of
    specific cell lines
  • Chemokines: attract monocytes
  • Adhesion molecules: allow adhesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Two examples of the four classes of small molecules involved in atherosclerosis:

A
  • Cytokines: IL-1, TNF-alpha
  • Growth Factors: PDGF, VSMGF
  • Chemokines: MCP1
  • Adhesion molecules: ICAM-1, VCAM-1
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Response to Injury Hypothesis: Step 2:

  • name
  • common lipoprotein abnormalities lead to
    (3)
  • endothelial injury causes
  • in the intima — forms of lipid accumulates
    (2)
  • which stimulates the release
A
  • Lipoprotein Accumulation
  • common lipoprotein abnormalities lead to:
    - increased LDL cholesterol
    - reduced HDL cholesterol
    - increased Lipoprotein (a)
  • Endothelial Injury causes:
    - increased O2 free radicals and
    - reduced NO levels
  • in the intima two lipid forms accumulates:
    - oxidised LDL
    - cholesterol crystals
  • stimulates the release of inflammatory
    mediators
21
Q

Foam Cell Development

A
  • oxidised lipids are ingested by
    macrophages
  • cells become foam cells
22
Q

What are monocytes that move into tissues called?

A

Macrophages

23
Q

Response to Injury Hypothesis in detail:

A
  • chemical/oxidative stress causes
    endothelial dysfunction
  • allows low density lipoproteins to move
    into the intima and become modified
  • the injured endothelium allows monocytes
    to adhere to the endothelium and migrate
    into the intima where they become
    macrophages
  • the macrophages take up the
    modified/oxidised low-density lipoproteins
    to form foam cells
  • the foam cells release more inflammatory
    mediators, cytokines, growth factors and
    chemoattractants
  • which causes the migration of smooth
    muscle cells from the media into the intima
  • these cells mix together forming a fatty
    streak
  • extracellular matrix formation: made by
    smooth muscle cells that secrete collagen,
    elastin and proteoglycans
  • extracellular matrix stabalises the
    atherosclerotic plaque
24
Q

Fatty Streak Formation:

A
  • ***smooth muscle cells migrate from the
    media
  • ***foam cells and smooth muscle cells
    produce fatty
    streaks
  • foam cells eventually undergo apoptosis,
    when they mix with smooth muscle cells
  • visible in almost everyone from early teens
  • does not obstruct flow but may progress
  • visible in almost everyone from early teens
25
Q

Fatty streaks are found in which part of the vessel?

A
  • the intima
  • hence do not obstruct flow
26
Q

What is the first visible manifestation of atherosclerosis?

A

Fatty streak (in intima)

27
Q

Atherogenesis

A
28
Q

Plaque Stabilisation:
- cells?
- consists of?
- what stabilises the atherosclerotic plaque?
- controlled by a mumber cytokines/growth
factors?

A
  • smooth muscle cells migrate from the
    media and proliferate
  • smooth muscle cells and synthesise
    extracellular matrix:
    - mainly collagen
    - also elastin and proteoglycans
  • **extracellular matrix stabilises the
    atherosclerotic plaque
  • controlled by a number of cytokines/growth factors:
    - Platelet-derived growth factors (PDGF)
    - Fibroblast growth factor (FGF)
    - Tissue Growth Factor alpha (TGF-
    alpha)
29
Q

Plaque Development: what forms the fibrous cap of an atherosclerotic plaque

A
  • smooth muscle cells and extracellular
    matrix
30
Q

What forms the necrotic core of an atherosclerotic plaque?

A
  • foam cells degenerate forming a lipid rich
    necrotic core
31
Q

Atherosclerotic Plaque Progression:

A
  • plaque grows: becomes raised from the
    vessel wall
  • calcium salts deposited: calcium phosphate and calcium hydroxyapitite, hardening of arteries
  • new vessels grow into the edges of the
    plaque (Neovascularisation)
  • tunica media is thinned and weakened
32
Q

What is neovascularisation?

A

when new vessels grow into the edges of the atherosclerotic plaque - can bleed into the plaque

33
Q

Occlusive atherosclerotic plaques can cause

A

angina

34
Q

Unstable Occlusive Atherosclerotic Plaques :

A
  • activated inflammatory in plaques can
    cause:
    - smooth muscle cell apoptosis
    - breakdown of extracellular matrix
  • ***thinning of fibrous cap will lead to
    rupture
  • development of unstable of vulnerable
    plaques
35
Q

unstable plaques diagram

A
36
Q

Unstable plaques can lead to clinical events:(3)(3)

A
  • rupture/erosion/ulceration will expose
    collagen and the lipid core which is
    thrombogenic
  • Thrombus may:
    - occlude the artery (MI)
    - partially occlude the artery (unstable
    angina)
    - become organised into the plaque,
    plaque progression (stable angina)
  • Occlusions or progression can also follow bleeding into the plaque (neovasculature)
37
Q

ST elevation myocardial infarc occurs when

A
  • occlusion atherosclerotic plaque in a coronary artery
38
Q

Stroke occurs when

A

occlusion atherosclerotic plaque in the brain

39
Q

Aneurysm formation:

A
  • weakening of the media, thinning of
    adventitia leads to arterial dilation
  • eventually leads to dissection, and vessel
    rupture
40
Q

Where does aneurysm commonly occur and why

A
  • abdominal aorta
  • tension in the wall is greatest
  • progressive dilation
41
Q

Athero-embolism:

A
  • ruptured plaque material discharged into
    the circulation
  • lands in small vessels (eg legs)
  • necrotic toes
42
Q

Clinical consequences of atherosclerosis: aorta:

A
  • aneurysm formation (abdomen>thorax)
  • renal artery stenosis (hypertension)
43
Q

Clinical consequences of atherosclerosis: coronary arteries:

A
  • angina
  • MI
  • heart failure
44
Q

Clinical consequences of atherosclerosis: cerebral arteries:

A
  • stroke
  • vascular dementia
45
Q

Clinical consequences of atherosclerosis: leg arteries:

A
  • claudication
  • foot ulcers
  • gangrene
46
Q

Atherosclerosis is a degenerative process.

True or False?

A

False
Inflammatory

47
Q

How many deaths in the UK are due to atherosclerosis?

A

1 in 5 deaths in the UK is due to atherosclerosis

48
Q

Plaque instability occurs when the

A

lipid rich necrotic core expands and the fibrous cap thins

49
Q

Plaque - related clinical events most commonly occur due to

A

thrombosis following plaque rupture

HLB (49 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions