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Cardiovascular System > Mechanism of Atheroma & Infarction > Flashcards

Mechanism of Atheroma & Infarction Flashcards

1
Q

What is Atheroma?

A

The degeneration of artery walls caused by the accumulation of fatty deposits and scar tissue leading tot he restriction of circulation and a risk of thrombosis

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2
Q

What is infarction?

A

An obstruction of blood supply to an organ/tissue region, typically a thrombus or embolus causing necrosis

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3
Q

What is a thrombus?

A

A blood clot formed in a vessel and remains there

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4
Q

What is an embolus?

A

A blood clot that travels from it’s site of formation to another location in the body

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5
Q

What is the role of lipoproteins?

A

Transfer fats around the body - make fats available to be taken up via receptor mediated endocytosis

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6
Q

Which lipids are carried via LDLs?

A

Cholesterol
phospholipids
Triglycerides

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7
Q

What is atherosclerosis?

A

A disease in which plaque builds up inside your arteries

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8
Q

What causes the inflammation during atherosclerosis?

A

Complex inflammatory response mediated by LDLs and angiotensin II

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9
Q

What can cause atherosclerosis & inflammation to worsen?

A

An ongoing systemic inflammatory disease makes it all worse

e.g. rheumatoid arthritis

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10
Q

What are the common sites of atherosclerosis?

A

Carotid arteries & Circle of Willis
Coronary Arteries
Iliac Arteries
Aorta

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11
Q

Describe how the inflammatory response is initiated in atehrosclerosis

A
  1. Endothelial cells activated by inflammatory triggers
    • LDL particle oxidation mainly stimulated by necrotic
      cell debris + free radicals in endothelium
  2. Endothelial cells activated and express cytokines and
    adhesion molecules
  3. Circulating myocytes bind to activated endothelium.
    -> start expressing adhesion molecules, move through
    tissue residing in intimal layer
  4. Monocytes differentiate -> tissue macrophages
    • release own inflammatory mediators
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12
Q

What is the issue with the inflammatory response initiation during atherosclerosis?

A

It’s the appropriate immunological response to inflammation but, it’s in the incorrect place

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13
Q

Describe how plaques form within vessels

A
  1. Macrophages accumulate LDL from circulation
    • > become foam cells
  2. Activated foam cells release growth factors, causing
    smooth muscle to leave medial layer and cross internal
    elastic lamina entering intima
  3. Activated smooth muscle cells also release growth
    factors
    • may begin collagen + elastin synthesis in intima layer
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14
Q

Outline the process of plaque maturation

A
  1. Smooth muscle cells accumulate LDL forming a 2nd
    type of foam cell
    • continue to produce extracellular matrix of elastin +
      collagen => fibrous plaque
  2. Cells under plaque = oxygen starved => apoptosis and
    release their fat to form globules which accumulate in
    intima => lipid core
  3. Dying cells release matrix metalloproteinases +
    enzymes -> breakdown fibrous matrix towards plaque
    edge
  4. Large lipid core covered in fibrous plaque - may be
    vulnerable to enzymatic digestion
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15
Q

What is calcification?

A

Hardening of tissue due to deposition / conversion into calcium carbonate or other insoluble calcium compounds

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16
Q

What role does calcification play in atheroma?

A

Later on in life calcium deposits may form around the atheroma (seen via CT)
- role of calcium is unknown

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17
Q

Explain why calcium may be hazardous in vessels?

A

Reduces arterial stretch and compliance

18
Q

Why may calcium deposits be beneficial to vessels?

A

A lot of calcium deposits (compared to a few) could prevent lipid core breaking off, exposing intima full of collagen -> potential to form thrombus

19
Q

When does atheroma formation occur during our lifetime?

A

Macrophage foam cells develop between 0 - 10 yrs
Smooth muscle foam cells develop by puberty
Lipids accumulate
<40 yrs maturation of fibrous cap

20
Q

How does thrombosis occur?

A

If central core becomes too large, plaque rupture can occur and subendothelium is exposed.
The endothelium is normally an anticoagulant surface

21
Q

What causes arteries to become pro-coagulant during thrombosis?

A

Collagen forms a very good base for clotting along with other proteins and factors in the intima -> provides pro-coagulant surface in arteries

22
Q

What is the consequence of a thrombus forming?

A

May occlude the artery

23
Q

What are the consequences of occlusive thrombosis?

A
  • MI (heart attack)
  • Occurs when blood flow decreases / stops to a part of
    the heart -> causes damage to myocardium
24
Q

What are the consequences of atheroma due to thromboembolism?

A
  • Ischaemic Stroke
  • Obstruction due to embolus from elsewhere in the
    body (usually carotid artery) blocking blood supply to
    part of the brain
  • Other types of ischaemic stroke occur
25
Q

Describe the pathology of an aneurysm due to wall thickness

A
  • e.g. Aortic aneurysm
  • causes weakness in aortic wall - increasing risk of aortic
    rupture
  • Rupture causes internal bleeding
    -> can cause shock and death if not treated immediately
26
Q

Give examples of how systemic inflammation promotes atheroma

A 
e.g. rheumatoid arthritis 
Parasite infections lead to chronic inflammation 
Genetic &amp; environmental influences 
- everyone has atheroma
- genes cause vulnerability 
- environment causes manifestations
27
Q

Where does arterial occlusion usually occur?

A

Mainly in carotid and cardiac coronary arteries

28
Q

What is the consequence of arterial occlusion?

A

Anything downstream from an arterial occlusion become starved of oxygen
e.g. Ischaemia
- The reduced blood flow leads to symptoms such as
angina on exercise

29
Q

What are the consequences of a detached arterial thrombus?

A

A thrombus becoming detached can:

  • Block cardiac arteries (MI)
  • block cerebral (stroke)

> can cause serious damage or death

30
Q

Where does venous occlusions occur?

A

In lungs or legs

31
Q

What are the effects of venous occlusions?

A

In legs don’t cut off oxygen supply
Causes pain and swelling
Hydraulic pressure causes oedema

32
Q

What is the consequence of a detached venous thrombus?

A

Could return to right side of heart and enter pulmonary circulation causing pulmonary embolism

33
Q

What causes a stable cardiac angina?

A

Due to permanent flow limitation

Not necessarily infarction

34
Q

What can cause unstable cardiac angina?

A

Due to transient thrombosis

Not necessarily infarction

35
Q

What is the cause of myocardial infarction?

A

Due to complete occlusion

36
Q

Describe the changes you’d see in ECG for a patient with MI

A
  • STEMI (elevated ST level due to MI)

damaged heart tissue doesn’t depolarise properly sp ST elevated above baseline

37
Q

What is the survival rates of MI

A

50% survive their first MI

1/2 won’t live past the month

38
Q

Outline the complications presented with MI

A
  • Acute cardiac failure
  • Conduction issues; arrhythmia
  • Papillary damage; valve dysfunction
  • Mural thrombosis; stroke
  • Wall rupture
  • Chronic heart failure; myocardial scarring
39
Q

Describe the features of a thromboembolic stroke

A

Occurs when thrombus at carotid plaque rupture travels to smaller cerebral vessels

85% from carotid atheroma rupture
15% from stasis in LA due to arrhythmia

40
Q

Outline features of a non-thromboembolic stroke

A

Due to hypo-perfusion, loss of BP

e. g.
- heart failure
- haemorrhage
- shock
- aneurysm rupture
- bleeding in brain

Cardiovascular System (16 decks)

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