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Cardiovascular System > Pathology of Atheroma > Flashcards

Pathology of Atheroma Flashcards

1
Q

Define Atheroma/Atherosclerosis

A

The formation of focal elevated lesions (plaques) in the intima of large and medium sized arteries

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2
Q

What happens as a result of atheromatous plaque in coronary arteries?

A

Myocardial Ischaemia -> Angina

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3
Q

What is a common complication of atheroma?

A

Thromboembolism

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4
Q

Remember Arteriosclerosis is not the same as atherosclerosis!!! wat is it dogh?

A

Arteriosclerosis is an age-related change in muscular arteries.
Smooth muscle hypertrophys, apparent reduplication of IEL with intimal fibrosis. All leads to a decreased vessel diameter.

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5
Q

What CV conditions does arteriosclerosis contribute to?

A

Cardiac, Cerebral, colonic and renal ischaemia.
Obviously in the elderly given its an age related condition.

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6
Q

When is arteriosclerosis likely to become apparent to a clinician?

A

When the CVS is further stressed by haemorrhage, surgery, infection or shock.

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7
Q

What are the phases of atheroma?

A

-> Fatty Streak
-> Early Atheromatous Plaque
-> Fully developed atheromatous plaque

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8
Q

A fatty streak is the earliest phase of an atheroma, what does it look like and what comprises it?

A

A yellow linear elevation within the intimal lining of the artery.
Its made of masses of lipid laden macrophages.

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9
Q

What is the significance of a fatty streak?

A

It has no clinical significance as it causes no effects and it may well disappear on its own,
However these patients are considered ‘at risk’ of developing atheromatous plaques.

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10
Q

In what age is it common to see fatty streaks in arteries?

A

Young children

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11
Q

An early atheromatous plaque is the first non-reversible stage of atheroma development, what does it look like and what is it made of?

A

Early atheromatous plaque looks like smooth yellow patches in the T. Intima.
Its made of lipid laden macrophages much like a fatty streak

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12
Q

In what age do we commonly see an early atheromatous plaque?

A

Young adults and up.

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13
Q

What makes up a fully established atheromatous plaque?

A

A central lipid core covered by a fibrous tissue cap all within the intimal lining.

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14
Q

What fibrous tissue provides structural strength to the atheromatous plaque, and what produces it?

A

Collagen in the fibrous cap provides structural strength to a plaque.
The collagen is made in smooth muscle cells

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15
Q

What cell types are found within the fibrous tissue cap?

A

Inflammatory cells such as macrophages, T lymphocytes and mast cells.

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16
Q

Other than the obvious lipids, what is found in the central lipid core of a fully developed atheromatous plaque?

A

Cellular debris derived from macrophages that died in the plaque.

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17
Q

What gives many atheromatous plaques a ‘foamy’ rim?

A

Macrophages that have partially broken down lipoproteins to give the foamy appearance.

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18
Q

What feature of a fully developed atheromatous plaque is a useful marker in angiograms/CT?

A

The extensive dystrophic calcification

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19
Q

Where do atheromas most often form?

A

At points of turbulent flow.
Such as the branchin points of arteries.

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20
Q

What do we call a late stage plaque that covers a large area?

A

Confluent

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21
Q

What are the features of a complicated atheroma?

A

The same as a fully developed atheromatous plaque (lipid core + fibrous capsule)
Plus:
- Haemorrhage into the plaque
- Plaque rupture or fissuring
- Thrombosis

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22
Q

Atheroma can be caused by one major risk factor alone, what is this?

A

Hypercholesterolaemia (hyperlipidaemia)

23
Q

How do genetics cause hypercholesterolaemia?

A

The présence/function of LDL receptors is determined genetically.
1/500 are heterozygous for mutations resulting in reduced function and therefore increased blood LDL.
1/1million are homozygous and usually die of coronary atheroma before adulthood.

24
Q

What are the signs of major hyperlipidaemia?

A

LDL, HDL, total cholesterol and triglyceride levels.

Corneal arcus (cholesterol deposit around iris)
Xanthelesmata (cholesterol deposit in periorbital region)
Tendon Xanthomata (On the tendons of knuckles or achilles usually)

A family history of MI or atheroma

25
Q

What are the types of hyperlipidaemia?

A

Primary or Familial
Acquired or Secondary
Idiopathic

26
Q

What other strong risk factors accelerate the process of plaque formation?

A

Smoking
Hypertension
Diabetes Mellitus
Being Male
Being Elderly

27
Q

What other risk factors contribute in some way to atheroma but not hugely?

A
  • Obesity
  • Sedentary lifestyle
  • Low birthweight
  • Low socio-economic status
28
Q

What are the 2 major steps in formation of atheromatous plaques?

A
  • Injury to the endothelial lining
  • Chronic inflammatory and healing response of vascular wall
29
Q

What is the more detailed process of development of the lipid core of an atheroma?

A

Essentially. circulating lipid along with smooth msucle and inflammatory cells form a large mass within the endothelium that drives continued inflammation adding to itself.

  • Endothelial injury & dysfunction
  • LDL accumulates in the exposed vessel wall
  • Monocytes adhere to the endothelium, migrate into the intima and convert macrophages
  • Platelets adhere to the injury.
  • Activated platelets & macrophages release growth factors that drives smooth muscle cell recruitment
  • Smooth muscle proliferates, ECM is produced and T cells are recruited
  • Lipids accumulate, both extracellular and within foamy macrophages.
30
Q

What are the 2 most important ways the endothelium becomes injured?

A

By haemodynamic disturbances (turbulent flow)
By hypercholesterolaemia (lipoproteins are partially degraded when stuck to the wall by inflammatory cells releasing toxic growth factors and cytokine that directly damage the wall.)

31
Q

How is the function of injured endothelial cells different?

A

+ The injured cells have a high permeability for LDL hence why it accumulates so much.
+ Increased Thrombogeneicity
+ Incread expression of cell adhesion molecules which help form the messy sticky atheroma.

32
Q

How does the fibrous cap form on an atheroma?

A

Chronic inflammation leads to tissue repair.
Growth factors like PDGF are released leading to synthesis of collagen, elastin and mucopolysaccharide much like a scar along with smooth muscle proliferation.
The growth factors are released by platelets, the endothelium, macrophages and smooth muscle cells.

33
Q

How does an established plaque spread?

A

Patches of endothelium covering are destroyed by organisation (smooth muscle invades and collagen is deposited). This also forms microthrombi (blood clots) on the surface/

34
Q

How serious is atheromatous disease?

A

Can be benign all the way to life threatening.
Complications of atheroma can also be life threatening

35
Q

What are the common consequences of atheroma?

A
  • Progressive narrowing of lumen (stenosis)
  • Acute atherotrhombotic occulusion
  • Embolisation to a distal arterial bed
  • Ruptured atheromatous aortic aneurysm
36
Q

What happens if stenosis of the vessel lumen gets to 50-75%?

A

Thers a critical reduction of blood flow in the distal arterial bed and reversible tissue ischaemia occurs.

37
Q

Give an example of reversible tissue ischaemia due to atheromatous stenosis?

A

A stenosed atheromatous coronary artery can lead to stable angina

38
Q

What do we mean when we say reversible tissue ischaemia?

A

It is triggered by something and can be relieved.
E.g. myocardial ischemia occurs on exertion and is relieved by rest.

39
Q

What happens if the stenosis is very severe (i.e. >75% of the lumen)?

A

Ischaemic pain occurs at rest.
e.g. unstable angina in a stenosed atheromatous coronary artery

40
Q

What do we call stenosis of the peripheral arteries (ilieal/femoral/popliteal etc)

A

Peripheral Arterial Disease

Most often due to atheroma.

41
Q

What is the major symptom of peripheral arterial disease?

A

Intermittent Claudication (on exertion usually so its clearly reversible tissue ischemia)

42
Q

What happens to the tissue if theres longstanding tissue ischemia?

A

The affected organ atrophys.

E.g. longstanding severe atherosclerotic renal artery stenosis leads to renal atrophy

43
Q

How does an acute atherothrombotic occlusion occur?

A
  • The plaque ruptures
  • Exposes highly thrombogenic plaque contents
  • Activates coagulation cascade
  • Very quick thrombotic occlusion
44
Q

What happens if a thrombotic occlusion is total?

A

-> Total occlusion
-> Irreversible ISchaemia
-> Necrosis (infarction) of tissue

45
Q

How does an embolisation to a distal arterial bed occur?

A

Small thrombus fragments detach from the atheroma.
They travel to distal vessels and get stuck, occluding the vessels of the capillary bed.
This gives you small local infarcts

46
Q

What happens if small emboli occlude heart vessels?

A

Dangerous small foci of necrosis within the myocardium leading to life threatening arrhythmias

47
Q

What happens if emboli detach from an atheroma in the carotid artery?

A

Either a cerebral infarct causing full blown stroke
Or Transient Ischaemic Attack (mini-stroke, TIA)

48
Q

How does a ruptured atheromatous abdominal aortic aneurysm occur?

A

Inflammatory activity due to the lipid plaque causes the T. Media underneath to erode.
The vessel gradually dilatates until it suddenly ruptures.
Result: massive retroperitoneal haemorrhage and often death.

49
Q

What else can occur due to an aneurysm in the abdominal aorta?

A

Prior to rupturing the atheromatous plaque can form a mural thrombus which gives off emboli to the legs.

50
Q

What is mural thrombus?

A

A thrombus in the wall of a heart chamber of large artery (provided it doesnt totally occlude it)

51
Q

What is a vulnerable atheroma?

A

One at high risk of becoming complicated. i.e. rupturing and forming a thrombosis.

52
Q

How do we recognise vulnerable atheroma?

A

Thin fibrous tissue cap
Large lipid core
Prominent Inflammation

53
Q

What preventative measures can be taken to lower risk of atheromatous disease?

A
  • Smoking cessation
  • BP control
  • Weight loss
  • Regular exercise
  • Improve Diet
54
Q

What preventative measures can we take to control the impact of existing atheromatous plaques?

A

Cholesterol lowering drugs.
Aspirin (inhibits platelets thus decresing risk of thrombosis
Surgery

Cardiovascular System (49 decks)

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