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brs2 > atherosclerosis and peripheral vascular disease > Flashcards

atherosclerosis and peripheral vascular disease Flashcards

1
Q

what are some modifiable risk factors for cardiovascular disease

A 
smoking
lipids uptake
blood pressure
diabetes
obesity
sedentary lifestyle
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2
Q

what are some non modifiable factors

A

age
sex
genetic background

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3
Q

what is the total risk if an individual smokes ,has high cholesterol and high blood pressure

A

x16 times more likely to die from heart attack

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4
Q

what are some changes in chd epidemiology over last decade

A

statins to reduce hyperlipidaemia
antihypertensive treatments
increased obesity leading to increased diabetes
new improvements in diabetes treatment have doubtful effect on cvd

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5
Q

why do atherosclerosis occur at bifurcations

A

turbulent blood flow

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6
Q

where does atherosclerosis usually take place

A

internal elastic lamina

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7
Q

where does ldl deposit in?

A

subintimal space and binds to matrix proteoglycans

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8
Q

briefly describe progression of atherosclerosis

A

adaptive thickening of smooth muscle at lesion prone site
type 2 lesion causes macrophage foam cells
in preatheroma - small pools of extracellular lipids
atheroma - core of extracellular lipids
fibroatheroma - fissure and haematoma, thrombosis

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9
Q

what are the main types of cells involved in atherosclerosis

A 
vascular endothelial cells
monocyte-macrophages
vascular smooth muscle cells
platelets
t lymphocytes
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10
Q

what is the role of vascular endothelial cells

A

barrier function e.g to lipoproteins

leukocyte recruitment

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11
Q

what is the role of monocyte macrophages

A

foam cell formation
cytokine and growth faction release
major source of free radicals
metalloproteinases

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12
Q

what is role of platelets

A

thrombus generation

cytokine and growth factor release

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13
Q

what is the role of vascular smooth muscle cells

A

migration and proliferation
collagen synthesis
remodelling and fibrous cap formation

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14
Q

role of lymphocytes

A

macrophage activation and also activated by macrophages themselves

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15
Q

what are the main inflammatory cells in atheroclerosis

A

macrophages derived from blood monocytes

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16
Q

what are the main 2 classes of macrophages

A

inflammatory macrophages - adapted to kill microorganisms
resident - normally homeostatic - suppress inflammatory activity
alveolar resident macrophages - surfactant lipid homeostasis
osteoclasts - calcium and phosphate homeostasis
spleen - iron homeostasis

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17
Q

what is ldl

A

‘bad’ cholesterol - synthesised in liver

carries cholesterol from liver to rest of body incl arteries

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18
Q

what is hdl

A

‘good cholesterol’ - carries cholesterol from ‘peripheral tissues’ icl arteries back to liver

19
Q

what are oxidised ldls/ modified ldls

A

families of highly inflammatory and toxic forms of ldl found in vessel walls

20
Q

what happens when ldls leak through endothelial barrier by uncertain mechanisms

A

ldl is trapped by binding to proteoglycans in sub endothelial layer and becomes susceptible to modification e.g oxidation by free radicals - represents partial burning
phagocytosed by macrophages and stimulates chronic inflammation

21
Q

what is familial hyperlipidaemia

A

autosomal genetic disease
massively elevated cholesterol >20mmol/l
failure to clear ldl from blood
causes xanthomas and early mi

22
Q

treatment for fh

A

hmgcoa reductase inhibitor = statins

to lower plasma cholesterol

23
Q

what are macrophage scavenger receptor a

A

known as cd204
binds to oxidised ldl
binds to gram positive bacteria like staph and strept
binds to dead cells

24
Q

what are macrophage scavenger receptor b

A

aka cd36
binds to oxidised ldl
binds to malaria parasites
binds to dead cells

25
Q

what are some oxidative enzymes that macrophages have that can modify native ldl

A

NADPH oxidase e.g superoxide 02

myeloperoxidase e.g HOCl (bleach) from ros+ and Cl, HONOO

26
Q

what are macrophages 2 roles when it comes to arterial ox ldl deposits

A
  1. detects oxldls as bug causing activation of ‘bug detector’ pathways causing inflammation
  2. re process cholesterol and send back to hdl - reverse cholesterol transport
27
Q

What is the effect of bleach HOCl on ldls

A

ldl gets into artery
activates macrophages
bleach damages inside of artery - plaques start falling apart

28
Q

what are cytokines

A

protein immune hormones that activate endothelial cell adhesion molecules

29
Q

what are chemokines

A

small proteins chemoattractant to monocytes

30
Q

what are the cytokines involved in monocyte recruitment

A

IL1 upregulates vascular cell adhesion molecule 1 VCAM1

VCAM1 mediates tight monocyte binding

31
Q

what are the chemokines involved in monocyte recruitment

A

monocyte chemotactic protein 1 - (mcp1) binds to monocyte g coupled receptor ccr2

32
Q

what is the ‘wound healing’ role of macrophages in atherosclerosis

A

release complementary protein growth factors that recruit VSMC and stimulate them to proliferate and deposit ECM

33
Q

what are the 2 main growth factors involved in wound healing

A

platelet derived growth factor

transforming growth factor beta

34
Q

what is role of platelet derived growth factor

A

VSMC chemotaxis
VSMC survival
VSMC division - mitosis

35
Q

role of transforming growth factor beta

A

increased collagen synthesis
matrix depostition
= thicker fibrous cap

36
Q

overall what does pdgf and tgf beta cause

A

decrease in contractile filaments

increase in matrix deposition genes

37
Q

what is the effect of plaque erosion/rupture

A

blood coagulation at site of rupture may lead to occulsive thrombus and cessation of blood flow

38
Q

what are metalloproteinases

A

family of 28 homologous enzymes
activate each other by proteolysis
degrade collagen
catalytic mechanism is based on Zn

39
Q

what are the characteristics of vulnerable and stable plaques

A

large soft eccentric liquid rich necrotic core
increased VSMC apoptosis
reduced VSMC and collagen content
thin fibrous cap
infiltrate of activated macrophages expressing MMPs

40
Q

how does macrophage activation take place

A

oxldl metabolites are toxic
macrophage foam cells have protective systems that maintain survival in face of toxic lipid loading
once overwhelmed - macrophages die via apoptosis
release macrophage tf and toxic lipids into central death zone - lipid necrotic core
thrombogenic and toxic material accumulates - until plaque ruptures

41
Q

what is nuclear factor kappa b

nfkb

A

transcription factor - major regulator of inflammation

-

42
Q

what is nfkb activated by

A

scavenger receptors
toll like receptors
cytokine receptors e.g il1

43
Q

what does nfkb switch on

A

matrix metalloproteinases
inducible nitric oxide synthase
il1

brs2 (65 decks)

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