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Cardio > Pathophysiology of atheroma > Flashcards

Pathophysiology of atheroma Flashcards

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?

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?

A

Dystrophic calcification

Shows up in angiograms/CT

Marker for atherosclerosis

21
Q

What is a risk associated with calcification of a plaque?

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’?

A

Haemorrhage into LC

Plaque rupture / fissuring

Thrombosis

23
Q

What are the main risk factors for Atheroma?

A

Hypercholesterolaemia & Hyperlipidaemia

Smoking
Hypertension
Diabetes Mellitus

Male
Elderly

24
Q

What are the less important risk factors for atheroma?

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
Q

Hypercholesterolaemia is the most important risk factor for atheroma

Describe what makes it such an important factor…

A

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
Q

If you suspect hypercholesterolaemia/hyperlipidaemia

What biochemical investigations should be undertaken?

A

Bloods

  • LDL
  • HDL
  • Total cholesterol
  • Triglycerides
27
Q

What signs on examination are indicative of hyperlipidaemia/hypercholesterolaemia?

A

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
Q

What must happen in order for an atheroma to begin to form?

A

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
Q

Describe the formation of an atheromatous plaque on an exposed arterial wall

A

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
Q

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?

A

Turbulent flow (haemodynamic disturbance)

Hypercholesterolaemia

31
Q

How does hypercholestrolaemia damage the endothelium of arteries?

A

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
Q

Why is it easier for plaques to form on damaged endothelial cells?

A

Increased expression of adhesion molecules (ICAM-1 & E-selectin)

High permeability to LDL

Increased thrombogenicity

33
Q

To put it simply

What two things move into the intimal layer to form plaques

A

Inflammatory cells & lipids

34
Q

How do lipids get into the lipid core?

A

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
Q

What causes smooth muscle cells to proliferate?

What is the effect of this?

A

Platelets, injured endothelium, macrophages & smooth muscle cells release growth factors (PDGF)…

Causes:

  • growth of intimal SM
  • Synthesis of collagen, elastin & mucopolysaccharides
36
Q

What gives rise to the fibrous cap?

A

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
Q

There are several clinical manifestations of atheromas, related to several different aspects of the disease

Summarise what can cause the clinical manifestations of atheromas

A

Stenosis

Acute atherothrombotic occlusion

Embolisation of atherothrombus

Ruptured atheromatous abdominal aortic aneurysm

38
Q

What clinical manifestations of atheromas are ‘Stenosis’ related?

A

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
Q

What clinical manifestations of atheromas are related to ‘atherothrombotic occlusion’

A

Thrombus from ruptured plaque = total occlusion = infarction of tissue:

Myocardial Infarction
Stroke
Lower limb gangrene

40
Q

What clinical manifestations of atheromas are caused by embolisation of fragments of thrombosed atheromatous arteries?

A

Embolic occlusions of small vessels = small infarcts of organs:

Arrhythmia
Cholesterol emboli in kidney, liver, skin
Stroke

41
Q

What clinical manifestations of atheromas are caused by aneurysms due to the ruptured plaque?

A

The media layer beneath the atheromatous plaque is weakened by inflammatory processes from the plaque:

Retroperitoneal haemorrhage
Mural thrombus - emboli to legs

42
Q

Atheromatous plaques that are likely to rupture have distinct morphological features

What are these features?

A

Thin fibrous cap
Large lipid core
Prominent inflammation

(just think of a big red spot thats about to burst)

43
Q

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?

A

Secretion of proteolytic enzymes, cytokines and reactive oxygen species

44
Q

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?

A

Highly stenotic, more stable plaques have a much larger fibrocalcific component & less inflammatory activity

45
Q

What are the preventative & therapeutic measures for atheromas?

A 
Smoking cessation 
BP control 
Weight loss 
Exercise 
Diet

Statins - if high cholesterol
Aspirin - stabilise plaque & reduce thrombosis risk

Surgery - if needed

Cardio (41 decks)

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