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PHSL 232 > L27 > Flashcards

L27 Flashcards

1
Q

what is atherOsclerosis :

A

hardening of the arteries, narrowing or blocking the vessel lumen

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2
Q

in atherOsclerosis, after initial intima injury, what happens to the media

A

remodelling of media (atrophy, loss of

SMC’s) occurs to accommodate plaque and preserve lumen diameter

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3
Q

hypertrophy of vascular walls can cause growth….

A

inward and outward

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4
Q

what is inward vascular remoderling called

A

atherOsclerosis

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5
Q

which is the most common/most clinically relevant form of vascular remodeling because of hypertension

A

atherOsclerosis

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6
Q

what is aneurysm

A

when vessel wall mass increases but wall thickness decreases

Aneurysms = bulge in a artery – life threating if burst

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7
Q

what is restenosis

A

an atherOsclerosis vessel PTCA

after you have clinically dealt with it

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8
Q

Atherosclerosis in the body is defined to specific areas

what are the different names for Atherosclerosis over the body

theres 4

A

Coronary arteries = coronary artery disease

Cerebral (carotid) arteries = transient ischemic attack (TIA), or stroke

Limb arteries = peripheral artery disease

Renal arteries = hypertension, or kidney failure

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9
Q

where do Aneurysms usually occur

A

usually happen in large arteries

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10
Q

Process of Atherosclerosis is because of…

A

Endothelial Dysfunction

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11
Q

in atherosclerosis, what are the risk factors which could cause the Initial injury of endothelium

A

Hypercholesterolemia (most important)
Hypertension
High triglycerides (FFA)
Inflammation

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12
Q

what are the 2 different types of cholesterole (that we learn about) and which is the good and bad one

A

Low-density lipoprotein (LDL)
- This is the one that sticks to the artery walls and causes the plaques to form

High-density lipoprotein (HDL)
- This is the con that carries LDL away (the good one)

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13
Q

why is Low-density lipoprotein (LDL) bad

A

it sticks to the artery walls and causes the plaques to form

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14
Q

what is the desirable levels of HDL and what is a high risk level for atherosclerosis

A

normal > 1.6 mmol/L

high risk < 1mmol/L

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15
Q

what is the optimal levels of LDL and what is a high risk level for atherosclerosis

A

optimal <2.6mmol/L

high risk > 4.1mmol/L

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16
Q

why do you need to measure for specific types of cholesterol and not just the total

A

total is misleading because as long as the different types of cholesterol are in balance with each other, therefore if they are both elevated then you are ok it it just if they become imbalanced that you have a problem

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17
Q

as you get older cholesterol levels get higher

what ages should you be checking your cholesterol levels to make sure they are still in ballance to try and prevent atherosclerosis

A

35-56

men have slightly higher levels

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18
Q

after the initial injury of the intima what is the first steep in the process of atherosclerosis formation

A

formation of a fatty steak

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19
Q

what is the first steep in fatty streak formation

A

LDL circulating in the body is able to migrate between the endothelial cells into the intima . If the influx of LDL exceeds the elimination pool and are not eliminated by the HDL then there is a buildup of LDL within the intima. You then get an LDL pool within the intima

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20
Q

what happens to LDL in the presents of reactive oxygen species or radicals (inflammatory factors)

A

LDL gets oxidised which is bad

LDL on its own aren’t that bad, but once they become oxidised then they are really bad as they do lots of things

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21
Q

oxidised LDL (oxLDL) causes many things to happen

in terms of formation of fatty streak what d they do

A

Ox LDL attracts monocytes by expression of leucocyte adhesion molecules on the endothelium.

If there is a lot of Oxidation then it could release cytokines which further damage the endothelium making gaps to let more LDL in. It will also leads to monocytes

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22
Q

what happens in fatty streak formation when monocytes enter the intima

A

Once monocytes are in the intima they become macrophages which uptake the oxidised LDL (this is an immune response) they interalise oxLDL, causing them to die and become foam cells.

These then attack more monocytes which will then form a fatty streak. Fome cell also activate T cells

(T cell = immune response)

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23
Q

describe the formation of a fatty streak

A

Influx of LDL exceeds eliminating capacity – extracellular LDL pool

LDL migrate to subendothelial intima

LDL oxidized by radicals - oxLDL

oxLDL- expression leucocyte adhesion molecules - chemokine secretion to attract monocytes

Monocytes enter the intima

Monocytes turn into Macrophages to take up the excessive oxLDL

Macrophages internalize oxLDL

Dead macrophages - Foam cells

Foam cells attract more monocytes and form a fatty streak

Foam cells also activate T-cell immune response

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24
Q

faty streaks are formed by oxidized LDL deposition ->
inflammation, macrophages -> foam cells

how clinically significant is this

A

In general not directly clinical significant or life threatening risk factor

Many just disappear and only some progress to atherosclerotic plaques

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25
Q

how do fatty streaks disappear

A

If you start exercising, losing weight and start eating healthy these will disappear

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26
Q

when does fatty streak formation occur

A

This occurs during the first decade of the disease

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27
Q

in the process of atherosclerosis

initial injury –> formation of fatty streak –>?

what happens next

A

formation of a plaque

28
Q

what causes the formation of a plaque

A

in the last steep of fatty streak formation foam cells trigger an immune response (T Cell activation)

Smooth muscle cells (SMCs)
migrate from media into the
intima, and are triggered to grow

Macrophages, foam cell and smooth muscle cells within the intama then trigger the formation of extracellular matrix. This is a immune response (t cells) which trigger the formation of collagen, eleaston (ECM) and calcium crystals (inflammatory response because of c-reactive protein)

29
Q

what does the inflammatory response in plaque formation cause

A

This forms a fibrous cap around the lipid core which isolates and stiffens the lipid core to stop the blood from clotting.

30
Q

what causes the inflammatory response in plaque formation

A

immune response causes smooth muscle cells to migrate into the intima

in the intima a combo nation of Macrophages, foam cell and smooth muscle cells trigger the formation of extracellular matrix. This is a immune response (t cells) which trigger the formation of collagen, eleaston (ECM) and calcium crystals (inflammatory response because of c-reactive protein)

31
Q

what is a plaque

A

The plaque is the lipid core and the fibrous cap (cologen, elestin and Ca).

32
Q

fatty streaks are harmless but if they keep growing then the body needs to do a repair response (plaque formation)

why is this

A

to stop blood clotting from happening.

33
Q

what is the concequences of plaque formation

A

However if it keeps growing then it can block the vessel causing changes in blood flow which has concequences

If thing get worse again then the plaque could move and form a thrombus and then an embolus

34
Q

are plaques a clinical problem

A

Plaques are not a major clinical problem as long as they don’t grow into the leman or form a thrombus

35
Q

what causes activation of a plaque

A

for whatever reason they become lesioned or fissured (small tear) in the endothelium and you get a blood cloth formation on the plaque

36
Q

where can plaque activation occur

A

This can occur in the arteries and the veins

37
Q

what are the 2 things that can happen when a plaque becomes activated

A

It can remain attached to the lipid core or it can move away from it but it will still be attached to the vessel wall
thrombosis

when it becomes detached from the wall it is a embolism

38
Q

Typically in peripheral arteries disease where are thrombosis formed

A

in the legs in the veins around the valves

39
Q

what is the difference between a thrombosis and an embolism

A

When the thrombus disattaches from the wall it becomes an embolism

The embolus will eventually get stuck somewhere causing blockage of blood flow. This is life threatening

40
Q

the process of atherosclerosis is what kind of response

A

a vascular repair response to arterial trauma

it is a defense mechanism in the body that develops over years

41
Q

During the formation of a fibrous cap:

a. monocytes turn into macrophages and take up the excessive oxLDL particles.
b. smooth muscle cells migrate into the media.
c. the clinical risk for an arterial thrombus is very high.
d. calcium crystals are formed in the intima

A

a. happens before
b. they are already in the media they migrate into the intima
c. no its not

D is correct

42
Q

atherosclerosis is a local phenomenon

where does it usually happen

A

Aorta, carotid arteries, iliac arteries
Large-medium sized muscular arteries (coronary + femoral)

Seldom in small arteries

43
Q

what are the risk factors for atherosclerosis

A

Atherosclerosis is local but risk factors are systemic

eg hypertension, smoking, diabetes, hyperlipidemia and can be genetic

Systemic factors act in concert with local factors

44
Q

what are some local abnormalities that cause atherosclerosis

A

Abnormalities of blood vessel wall: vascular repair response

Abnormalities of blood constituents: coagulation, platelet activation

these cause abnormalities of blood flow: shear stress! (mechanical and physical characteristics)

45
Q

what is shear stress and what is it detected by

A

Force resulting from friction of flowing blood on luminal surface

Endothelial mechano-sensing element

46
Q

describe normal shear stress

A

NO production, decrease expression of inflammatory
response mediators, adhesion molecules, vasoconstrictors
and oxidants

Less oxidence means that there is less risk of the formation of oxLDLs, decrease in adhesions molecules means that there is less attraction of monocytes

47
Q

describe low or turbulent shear stress

A

Reduced NO production, enhanced monocyte adhesion, platelet activation, SMC proliferation, oxidant activity, vasoconstriction

48
Q

describe low shear stress

A

low shear stress = low blood flow = Prolonged interaction time between blood constitutions and the endothelium making it more lily to get activation of monocytes and adhesions

Low = shear stress is not aligning the endothelial cells

49
Q

what is the relationship between low shear stress and turbulent shear stress

A

Local areas with low shear stress and altered flow directions during cardiac cycles (making it turbulent)

50
Q

why do elestic arteries develop atherosclerosis

A

Local areas with low shear stress and altered flow directions during
cardiac cycles have higher risk of atherosclerosis (more pulsatile = more risk)

eg arteries with turbulent and pulsatile flow
Elastic (Aorta, carotid arteries, iliac arteries)
Large-medium sized muscular arteries (coronary + femoral)

51
Q

what are some reasons for turbulent shear stress

A

Branches, Bifurcations, Stenosis = Turbulence

52
Q

describe the carotid arteries in terms of atherosclerosis

A

Particularly susceptible to plaque formation

has lower blood pressures because the head above the heart

get turbulent blood flow in the “fork” (Bifurcations) and therefore plaque build up

53
Q

describe the coronary arteries in terms of atherosclerosis

A

Highest blood pressures from aorta

Ageing and Hypertension (Reflections)

Turbulent flow because of constant compressive systolic force means they are susceptible to plaque build up

54
Q

describe how the face of atherosclerosis has changed

A

the traditional stereotypical face of atherosclerosis is a Smoking overweight Caucasian midlife male

now it is a Asian, south Asian, Central and South America, younger women
Obesity because of high consumption of sugar/fructose diets in addition to high fat diets
causing people to have low HDL cholesterol, and high triglycerides

55
Q

what are statins

A

HMG-CoA reductase inhibitors, lowers LDL

LDL lowering drugs

56
Q

what are some examples of statins

A

Cholesterol absorption inhibitors: block absorption cholesterol in intestine

Inclisiran: interferring RNA lowers LDL levels, only twice a year required.

Bempedoic acid: upstream target of statins

PPARalpha agonists to target triglycerides; anti-inflammatory therapies

57
Q

what is angiography

A

Angiography = use of contrast dye and X-ray to see blockages in the vasculature

58
Q

what is an angioplasty

A

ballooning

they shove a balloon in the vessel to open it back up to let blood through

Can cause rupture of plaque which can be dangerous

59
Q

what is stenting

A

this is when they place a stent in the vessel to open it back up. they can now be drug-eluting (things like NO) to further increase dilation of the vessel

60
Q

when would precautions like angioplasty and stenting be used

A

If people don’t adjust their lifestyle

causes restenosis (it will just happen again and you will return to the original situation)

61
Q

what is a endarterectomy

A

surgical removal of atheromatous plaque material

mostly used for peripheral artery disease

62
Q

when would a bypass be used

A

Coronary artery disease

63
Q

what does a bypass involve

A

an artificial, artery or vein

This means that the blockage stays and you make a new artery so that the heart can be perfussed again

64
Q

what are aortic aneurysms caused by

A

Aorta dilatation (atherosclerosis – age)

65
Q

where can aortic aneurysms happen

A

Ascending, arch, descending, infrarenal, juxtarenal, suprarenal

66
Q

why are aortic aneurysms so bad

A

Rupture is almost certain death

Symptoms are rare and non-specific

need to be repaired with stents

You can not know that this is occurring and they are usually discovered by accident. They will then either leave it and monitor it or they can do open heart surgery and replace parts of it

67
Q

Coronary arteries have a high risk of developing atherosclerosis

BECAUSE

coronary arteries have a relative high blood pressure and continuously
turbulent flow.

A

both statements are true and causally related

PHSL 232 (30 decks)

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