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Pathophysiology of atheroma Flashcards

(45 cards)

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1
Q

What is atheroma’s alternative clinical name?

A

Atherosclerosis

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2
Q

What is atheroma?

A

Formation of focal elevated lesions (plaques) in intima of large and medium-sized arteries

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3
Q

Why is atheroma damaging to health?

A

Atheromatous plaques narrow the lumen of the blood vessels

Narrow lumen can cause angina

Potential complications ie thromboembolism

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4
Q

What is arteriosclerosis?

A

Non atheromatous narrowing of lumen

Caused by Smooth muscle hypertrophy, apparent reduplication of internal elastic laminae, intimal fibrosis

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5
Q

What is the commonest cause of arteriosclerosis?

A

Old age

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6
Q

Arteriosclerosis contributes to ischaemia in the elderly in what areas?

A

cardiac, cerebral, colonic and renal ischaemia

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7
Q

What conditions can exacerbate the effects caused by arteriosclerosis?

A

Clinical effects most apparent when CVS further stressed by haemorrhage, major surgery, infection, shock

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8
Q

What are the layers of the wall of an artery?

A

Tunica Intima - inner

Tunica Media - Smooth muscle layer

Tunica Adventitia

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9
Q

What is the earliest significant stage/lesion of an atheroma?

What age group is this most likely to present in?

A

Fatty streak in the T. Intima

Young children - neonates

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10
Q

Describe the appearance & histology of a fatty streak

A

Yellow linear elevation of intimal lining

Comprises masses of lipid-laden macrophages

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11
Q

What is the clinical significance of a fatty streak?

A

It poses no immediate risk, and may just disappear

However, there is a risk that it will develop into an atheromatous plaque

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12
Q

What is the appearance & histology of an early atheromatous plaque?

A

Smooth yellow patches in intima

Lipid-laden macrophages

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13
Q

Who is at risk of developing an early atheromatous plaque?

A

Young adults onwards

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14
Q

Describe the basic components/structure of a Fully developed atheromatous plaque

A

Central lipid core

‘Fibrous cap’ between CLC & the lumen

Surrounded by arterial endothelium

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15
Q

What is contained/histologically visible in the central lipid core of a FD atheromatous plaque?

A

Rich in cellular lipids, LDL’s & debris derived from macrophages

May have:

“Foamy macrophages” - often present due to uptake of oxidised lipoproteins via specialised membrane bound scavenger receptor

Haemorrhage

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16
Q

Describe the structure of the fibrous cap, in a FDAP

A

Fibrous tissue:

Collagen - produced by smooth muscle cells
( + elastin )

Inflammatory cells - macrophages, T cells, mast cells - recruited from arterial endothelium

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17
Q

What process occurs in atheromatous plaques, late in their development, once they are very large?

A

Dystrophic calcification:

  • This occurs in necrotic tissue (which a large plaque contains in the lipid core)
  • Dystrophy = tissue wasting away (necrosis causes this)
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18
Q

Late stage plaques are often described as ‘confluent’

What does this mean?

A

Multiple plaques merging together

This means they cover extensive areas

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19
Q

Why might a plaque cause turbulent flow?

Study These Flashcards
A

If they form at arterial branching points/bifurcations

Or probably if theyre just massive

20
Q

What feature of a plaque can be identified in imaging?

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A

Dystrophic calcification

Shows up in angiograms/CT

Marker for atherosclerosis

21
Q

What is a risk associated with calcification of a plaque?

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A

Haemorrhage into lipid core of plaque

22
Q

What are the local risks associated with a very large plaque, that could cause a ‘complicated atheroma’?

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A

Haemorrhage into LC

Plaque rupture / fissuring

Thrombosis

23
Q

What are the main risk factors for Atheroma?

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A

Hypercholesterolaemia & Hyperlipidaemia

Smoking
Hypertension
Diabetes Mellitus

Male
Elderly

24
Q

What are the less important risk factors for atheroma?

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A

Obesity
Sedentary lifestyle
Low socio-economic class
Low birthweight

^Many of the above basically just contribute to main risk factors - ie Low SE class tends to smoking & a diet high in fat leading to hyperlipidaemia etc

Micro-organisms:
- May have a role

25
Hypercholesterolaemia is the most important risk factor for atheroma Describe what makes it such an important factor...
It can cause formation & growth of plaque in the absence of other risk factors Also: - Rare genetic mutation causing lack of cell membrane receptors for LDL cholesterol is present in 1/1500 caucasians (heteroz) & 1/1million (homoz) - Homozygous sufferers have insanely high LDL cholesterol levels & usually die from coronary artery atheroma in their teens
26
If you suspect hypercholesterolaemia/hyperlipidaemia What biochemical investigations should be undertaken?
Bloods - LDL - HDL - Total cholesterol - Triglycerides
27
What signs on examination are indicative of hyperlipidaemia/hypercholesterolaemia?
1) Inspection of the face: Corneal arcus - Banana shaped cloudy opacity on cornea of eye Xanthalasmata (xanthalasma) - Sharp bump on skin - Deposit of cholesterol - Yellowish 2) Inspection of rest of body: Tendon xanthomata - knuckles, achilles etc - deposits of cholesterol stuff
28
What must happen in order for an atheroma to begin to form?
1) Injury to endothelial lining of artery 2) Chronic inflammatory & healing response of vascular wall to agent causing injury Exposure of arterial wall allows LDL to accumulate & plaque to start forming
29
Describe the formation of an atheromatous plaque on an exposed arterial wall
1) Wall exposed ∴ accumulation of Lipoproteins (LDL) 2) Monocytes see injury: - Adhese to endothelium (& release factors) - Migrate into intima & become foamy macrophages 3) Platelets: - Adhesion & activation - Release factors 4) Factors released by Platelets & macrophages recruit smooth muscle cells 5) Smooth muscle cells proliferate, begin manufacturing ECM & recruit T cells 6) Lipids continue to accumulate in this mess, and form the lipid core
30
In order for a plaque to begin forming, there must be endothelial injury, which allows monocytes & lipoproteins to migrate and all that stuff What are the main causes of endothelial damage?
Turbulent flow (haemodynamic disturbance) Hypercholesterolaemia
31
How does hypercholestrolaemia damage the endothelium of arteries?
Chronic hypercholesterolaemia can increase production of reactive oxygen species It can also cause accumulation of Lipoproteins in the T. intima: - Lipiproteins are modified by free radicals - Modified lipoPs accumulated by macrophages but not destroyed - This makes foamy macrophages - Foamy Macrophages are toxic to endothelium & also release growth factors, cytokines
32
Why is it easier for plaques to form on damaged endothelial cells?
Increased expression of adhesion molecules (ICAM-1 & E-selectin) High permeability to LDL Increased thrombogenicity
33
To put it simply What two things move into the intimal layer to form plaques
Inflammatory cells & lipids
34
How do lipids get into the lipid core?
During plaque formation - large number of macrophages & T-cells: - Macrophages accumulate lipids, and die through apoptosis - The debris & lipids accumulate ∴ form the lipid core The chronic injury response recruits more & more lymphocytes ∴ more lipids are 'fed' to the core
35
What causes smooth muscle cells to proliferate? What is the effect of this?
Platelets, injured endothelium, macrophages & smooth muscle cells release growth factors (PDGF)... Causes: - growth of intimal SM - Synthesis of collagen, elastin & mucopolysaccharides
36
What gives rise to the fibrous cap?
Platelets, injured endothelial cells, macrophages and Smooth muscle cells secrete Growth factors (PDGF) One of the effects of growth factors is to stimulate collagen synthesis Fuck ton of collagen - goes into fibrous cap
37
There are several clinical manifestations of atheromas, related to several different aspects of the disease Summarise what can cause the clinical manifestations of atheromas
Stenosis Acute atherothrombotic occlusion Embolisation of atherothrombus Ruptured atheromatous abdominal aortic aneurysm
38
What clinical manifestations of atheromas are 'Stenosis' related?
High grade stenosis of over 70% causes ischaemia of supplied tissue: ``` Reversible tissue ischaemia Stable angina Unstable angina Peripheral arterial disease Atrophy due to longstanding ischaemia ```
39
What clinical manifestations of atheromas are related to 'atherothrombotic occlusion'
Thrombus from ruptured plaque = total occlusion = infarction of tissue: Myocardial Infarction Stroke Lower limb gangrene
40
What clinical manifestations of atheromas are caused by embolisation of fragments of thrombosed atheromatous arteries?
Embolic occlusions of small vessels = small infarcts of organs: Arrhythmia Cholesterol emboli in kidney, liver, skin Stroke
41
What clinical manifestations of atheromas are caused by aneurysms due to the ruptured plaque?
The media layer beneath the atheromatous plaque is weakened by inflammatory processes from the plaque: Retroperitoneal haemorrhage Mural thrombus - emboli to legs
42
Atheromatous plaques that are likely to rupture have distinct morphological features What are these features?
Thin fibrous cap Large lipid core Prominent inflammation (just think of a big red spot thats about to burst)
43
Inflammatory processes weaken atheromatous plaques and are a main reason for them becoming fragile and likely to burst How do inflammatory cells weaken the plaque?
Secretion of proteolytic enzymes, cytokines and reactive oxygen species
44
Some plaques are highly stable, and cause problems through stenosis of the vessel in which they exist How is the structure/activity of these cells different from that of an unstable plaque?
Highly stenotic, more stable plaques have a much larger fibrocalcific component & less inflammatory activity
45
What are the preventative & therapeutic measures for atheromas?
``` Smoking cessation BP control Weight loss Exercise Diet ``` Statins - if high cholesterol Aspirin - stabilise plaque & reduce thrombosis risk Surgery - if needed

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