Brainscape's Knowledge GenomeTM

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


See full index

cardiovascular system > vescular endotheium 2 > Flashcards

vescular endotheium 2 Flashcards

1
Q

describe the pathogenesis of atherosclerosis

A

occurs when the endothelium of a large vessel receive chronic stimulation eg from smoke - chronic activation of the endothelial cells
leukocytes attach and accumulate uder the endothelium
permeability increases and lipids also accumulate under the endothelium - causing foam cells
the macrophages die
complex atherosclerotic plaque is formed

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

describe the endothelium

A

single layer of cells
grow next to each other
cells talk to each other and send signals

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

describe the basement membrane

A

made of ECM proteins - active

send signals

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

what is in the tunica intima

A

[endothelium] made of endothelium, basement membrane, lamina propia - sm and connective tissue, internal elastic membrane

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

what is in the tunica media

A

[sm cells]

sm and external elastic membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is in the tunica adventitia

A

vasa vasorum, nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

are bv consistant

A

no, they’re different in different places

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are bv mainly composed of

A

mainly endothelium and caste around

in heart there is more bv than myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what do endothelial cells do

A 
matrix proteins and growth factors involved in angiogenesis 
thrombosis and haemostasis 
angiogenesis 
vascular tone permeability 
inflammation

control many processes, there is a balance between pro and anti effects, essential but it is regulated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

describe the regulation of endothelial homeostasis

A

at rest there is a tilt towards antiinf, antithrombotic and anti-proliferative
there are time when the balance needs to tilt eg in chronic disease, the endothelium is chronically activated this is permananet
use transcriptional and proteomic screening to assess this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

stimuli for endothelial cell dysfunction

A

hypercholesterolaemia (oxidatively modified lipoproteins)
DM - produce radicals
hypertension (ANG2 and ROS)
sex hormone imbalance (oestrogen deficiency and menopause)
aging
oxidative stress
proinflammatory cytokines (IL-1 and TNF)
infectious agents (bacterial endotoxins and viruses)
mechanical stress
high glucose

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

describe the normal recruitment of leukocytes

A

leukocytes adhere to the walls of post capillary venuoles

transmigrate into the tissues

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

describe the recruitment of leukocytes in atherosclerosis

A

leukocytes adhere to the endothelium of larger arteries
find the thick wall
and get stuck in the subendothelial spac
monocytes migrate into the subendothelial space and mature into macrophages
newly formed post capillary venules at the base of the developing lesions provide a further portal for leukocyte entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

how do the leukocytes go through the endothelium

A

there are addition molecules on the surface of endothelium

when there is an inflammatory trigger the endothelium present the molecules and the leukocytes bind and go through

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

which part of leukocyte migration is reversibole

A

the rolling of leukocytes along the endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what happens if you lack the mechanism for leukocyte migration

A

disease
mutation in pathway
cant protect from inflammatory stimulation

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

how can it be used clinically that this pathway is used in disease

A

drugs can be produced that target it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

problem with teh fact that the migration of leukocytes is different in different locations

A

the drug may have adverse effects in different tissues to what the drug is intended for

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do we know that leukocyte migration occurs

A

use intra-vital microscopy
on the stage there is an animal with exteriorised tissue
you can see the movement of leukocytes through capillaries and entering the endothelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

how do endothelial junctions form

A

endothelial cells are a singl aer of clls
when they contact each other during divison, they stop dividing - contact inhibition
interact with molecular pathways
endothelial cells dont divide very much - but they have a long life
you can see the lines at the cell junction by using an Ab to a molecule at that junction

21
Q

structure of capillary

A

endothelial cells surrounded by basement membrane and pericapillary cells (pericytes)

22
Q

structure of post capillary venules

A

similar to capillary

with more pericytes

23
Q

what happens when leukocytes migrate through post capillary venules

A

they chew on the basement membrane and go through to the tissue

24
Q

what happens when leukocytes migrate through arteris

A

they get stuck in the basal membrane

never chew through the arteral wall

25
Q

structure of the artery

A

3 thick layrs

rich in cells and ECM

26
Q

endothelium’s role in permeability

A

regulates t flux of fluids and moleculs from blood to tissues and vice versa

27
Q

what is caused by increased permeability of the endothelium

A

oedema

leakage of plasma proteins through the junctions into the subendothelial space

28
Q

describe the process of lipoprotein trapping

A

lipoproteins move through th endothelium adn bind to proteoglycans
they are oxidesed
macraphages eat the lipds
this forms foam cells ad fatty streaks

29
Q

which points in the cardiac system are prone to atherosclerosis

A

branch points

30
Q

describe lamina flow

A

streamlined
outermost layer slow
innermost fast
porotective flow

31
Q

describe turbulent flow

A

irregular flow
speed continuously changing in magnitude and direction
promotes coagulation and inflammation
prevent NO

32
Q

how can endothelial cells sense changes in flow

A

lamina flow promotes antithromboytic, antiinf factors and NO production, inhibits SMC proliferation
turbulent flow promotes coagulation, leukocyte adhesion, SNC proliferation, endothelial apoptosis and reduced NO production
profile of genes and proteins are regulated by blood flow

33
Q

describe the effect of NO

A

key regulator in cardiovascular health
reduce oxidation of LDL cholesterol - component of plaque
reduces the release of superoxide radicals
reduce proliferation of SMC in the vessel wall
inhibit monocyte adhesion
reduces platelet activation
dilates BV

34
Q

what TF are selectively activated for by lamina flow

A

KFL2 and KLF4

35
Q

what TF is selectively activated by turbulent flow

A

NFkB - involved in inflammation

36
Q

what is epigenetics

A

functionally relevant
inheritable changes to the genome
that don’t involve a change to the nucleotide sequence which affect gene expression

37
Q

what are the 3 main epigenetic mechanisms

A

DNA methylation
histone modification
miRNA

38
Q

why is epigenetics relevant

A

new drugs target the epigenetic pathway - especially in cancer

39
Q

what happens in epigenetics

A

the genome adapts to developmental/environmental cues through modification of the DNA - by methylation, or modifying histones
essential for development and differntiations
twins have different responses to heritable diseases

40
Q

blood flow and epigenetics

A

blood flow regulates chromatin
mechanoreceptor recognises the flow
changes the chromatin
TF is activated
eg stable flow downregulates the expression of DNA methyltransferases - allows promotor of antitherogenic genes to remain demethylated - enabling expression
in disturbed flow - upregulate DNA methyltransferases - hypermethylation of antiatherogenic genes - Klf4 and Hox A5 - repressing their expression

41
Q

what is angiogenesis

A

a way new bv are formed in the body

42
Q

what triggers angiogenesis

A

hypoxia, growth factor bind to end of bv and cause growth

involved in disease eg cancer

43
Q

bad quality of angiogenesis

A

promotes plaque growth

44
Q

good quality of angiogenesis

A

prevent damage post ischemia

angiogenesis reinstate blood vessels and flow to a blocked area - preventing ischemia

45
Q

describe senescence

A

growth arrest that halts the proliferation of aging anmd or damaged cells
it is a response to stress or damage
they have distinctive morphology and markers eg b-gal

46
Q

good affect of senescence

A

prevent transmission of damage to daughter cells

repilactive senescence - the limited proliferative capacity of cells in human nature

47
Q

bad affect of senescent cells

A

pro-inflammatory and contribute to disease
found in atherosclerotic lesions
can be induced by CVD risk factors
proinf and prothrombotic phenotype
may contribute to plaque progression and complications

48
Q

how can we prevent atherosclerosis

A

Ab used against atherosclerosis caused a drop in CVD
stop the ‘bad’ pathways easier but look into ways to maintain the ‘good’ pathways
good health in general eg diet, exercise, statins, novel therapies

49
Q

effect of resveratrol

A 
protective effect on CVD 
promotes eNOS 
reduce senescence 
prevent proinflammatory changes 
improve function in T2DM 
beneficial at lower doses and cytotoxic at higher doses 
clinical benefits not been demonstrated

cardiovascular system (22 decks)

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