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Cardiology > Pathology of Atheroma > Flashcards

Pathology of Atheroma Flashcards

1
Q

Define Atheroma/Atherosclerosis [2]

A

The formation of focal elevated lesions (plaques)[1] in the intima of large and medium sized arteries [1]

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2
Q

What happens as a result of atheromatous plaque in coronary arteries? [2]

A

Myocardial Ischaemia -> Angina

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3
Q

What is a common complication of atheroma? [1]

A

Thromboembolism

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4
Q

DDX between arteriolosclerosis and atherosclerosis

A

Arteriolosclerosis is an age-related change in muscular arteries. Smooth muscle hypertrophys, intimal fibrosis > decreased vessel diameter.
Atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. It is a type of arteriolosclerosis

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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? [3]

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? [2]

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? [2]

A

It has no clinical significance [1] as it causes no effects and it may well disappear on its own,
However these patients are considered ‘at risk’ of developing atheromatous plaques. [1]

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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? [2]

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 cell types are found within the fibrous tissue cap? [4]

A

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

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15
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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16
Q

What feature of a fully developed atheromatous plaque is a useful marker in angiograms/CT? [1]

A

The extensive dystrophic calcification

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17
Q

Where do atheromas most often form?

A

At points of turbulent flow.

Such as the bifurcation points of arteries.

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18
Q

What do we call a late stage plaque that covers a large area? [1]

A

Confluent

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19
Q

What are the features of a complicated atheroma? [3]

A 
The same as a fully developed atheromatous plaque (lipid core + fibrous capsule) 
Plus [3]
- Haemorrhage into the plaque
- Plaque rupture or fissuring
- Thrombosis
20
Q

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

A

Hypercholesterolaemia (hyperlipidaemia)

21
Q

What are the signs of major hyperlipidaemia? [3]

What do lab tests show? [2]

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

LDL high, total cholesterol high

22
Q

What are other strong risk factors accelerate the process of plaque formation? [5]

A 
Smoking
Hypertension
Diabetes Mellitus
Being Male
Being Elderly
23
Q

What are the minor risk factors [4]

A
  • Obesity
  • Sedentary lifestyle
  • Low birthweight
  • Low socio-economic status
24
Q

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

A
  • Injury to the endothelial lining

- Chronic inflammatory and healing response of vascular wall

25
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.)
26
Q

How is the function of injured endothelial cells different? [3]

A

+ The injured cells have a high permeability for LDL hence why it accumulates so much.
+ Increased Thrombogeneicity
+ Incread expression of cell adhesion molecules

27
Q

How does an established plaque spread? [2]

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

28
Q

What are the common consequences of atheroma? [4]

A
  • Progressive narrowing of lumen (stenosis)
  • Acute atherotrhombotic occulusion
  • Embolisation to a distal arterial bed
  • Ruptured atheromatous aortic aneurysm
29
Q

What happens if stenosis of the vessel lumen gets to 50-75%? [2]

A

Thers a critical reduction of blood flow in the distal arterial bed [1] and reversible tissue ischaemia occurs [1]

30
Q

Give an example of reversible tissue ischaemia due to atheromatous stenosis? [1]

A

A stenosed atheromatous coronary artery can lead to stable angina

31
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

32
Q

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

A

Peripheral Arterial Disease presenting as intermittent claudication

33
Q

What is the major symptom of peripheral arterial disease?

A

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

34
Q

What happens to the tissue if theres longstanding tissue ischemia? [1] Give one eg [2]

A

Atrophy of affected organ

E.g. longstanding severe atherosclerotic renal artery [1] stenosis leads to renal atrophy [1]

35
Q

How does an acute atherothrombotic occlusion occur? [4]

A
  • The plaque ruptures
  • Exposes highly thrombogenic plaque contents
  • Activates coagulation cascade
  • Very quick thrombotic occlusion
36
Q

What happens if a thrombotic occlusion is total? [2]

A
  • > Total occlusion
  • > Irreversible ISchaemia
  • > Necrosis (infarction) of tissue
37
Q

How does an embolisation to a distal arterial bed occur?

A

Small thrombus fragments detach from the atheroma [1]
They travel to distal vessels and get stuck, occluding the vessels of the capillary bed.
This gives you small local infarcts [1]

38
Q

What happens if small emboli occlude heart vessels?

A

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

39
Q

What happens if emboli detach from an atheroma in the carotid artery? [2]

A

Either a cerebral infarct causing full blown stroke

Or Transient Ischaemic Attack (mini-stroke, TIA)

40
Q

How does a ruptured atheromatous abdominal aortic aneurysm occur? [3]

A

Inflammatory activity due to the lipid plaque causes the T. Media underneath to erode. [1]
The vessel gradually dilatates until it suddenly ruptures. [1]
Result: massive retroperitoneal haemorrhage and often death. [1]

41
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.

42
Q

What is mural thrombus?

A

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

43
Q

How do we recognise vulnerable atheroma (of rupturing)? [3]

A

Thin fibrous tissue cap
Large lipid core
Prominent Inflammation

44
Q

What preventative measures can be taken to lower risk of atheromatous disease? [5]

A
  • Smoking cessation
  • BP control
  • Weight loss
  • Regular exercise
  • Improve Diet
45
Q

What preventative measures can we take to control the impact of existing atheromatous plaques? [3]

A

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

Cardiology (29 decks)

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