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02. Cardiovascular > L20. Pathology of Arterial Diseases > Flashcards

L20. Pathology of Arterial Diseases Flashcards

1
Q

What is arteriosclerosis?

A

The hardening of the arteries as a result of ageing and the ‘wear and tear’ associated with it.
Arteries lose their elasticity and as a result become narrowed

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2
Q

What conditions accelerate or predispose to arteriosclerosis?

A

Diabetes

Hypertension

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3
Q

What is the pathogenesis of arteriosclerosis?

A

Damage to the intima of the endothelium (normal in ageing) leads to the healing response:

  • recruitment of smooth muscle cells which synthesis collage
  • more collagen = less elastin content (Arteries cannot relax)
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4
Q

What is hyaline arteriosclerosis?

A

thickening of the walls of arterioles by the deposition of homogeneous pink glassy appearance (amorphous) hyaline material
- proteins from the blood leaking into the subendothelium

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5
Q

What are the consequences of arteriosclerosis?

A

Impairment of the arteries control of blood pressure
May result in poor blood supply (due to narrowing) - ischaemia
Possibility of stretching out the vessel = microaneurysm and haemorrhage.
(cerebral haemorrhage, benign nephrosclerosis, hypertensive retinopathy)

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6
Q

What is atherosclerosis?

A

A build up of inflammatory, fibrotic, necrotic and fatty material in the arteries leading to a slow narrowing with potential rupture

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7
Q

What are the 2 main components of the atheroma (plaque)?

A

Fibrous cap + Necrotic Core

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8
Q

What are the stages of pathogenesis of atherosclerosis?

A
  1. Fatty streak formation: collection of foam cells in the intima
  2. Damage: inflammation and accumulation of cholesterol, inflammatory infiltrate and fibrosis
  3. Stable atherosclerotic plaque
  4. Unstable atherosclerotic plaque (rupture)
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9
Q

What are the features of the atherosclerotic plaque? [10]

A
  1. Thickened Intima
  2. Thinned media
  3. Narrowed Lumen
  4. Necrotic Core
  5. Fibrous Cap
  6. Inflammatory Cells
  7. Calcification
  8. Cholesterol Clefts
  9. Foam Cells
  10. Neovascularisation
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10
Q

What are the two types of pathologic calcification?

A
  1. DYSTROPHIC: formation of calcium deposits in cell degeneration (Eg. atherosclerosis, TB, cancer)
  2. METASTATIC: serum calcium and phosphate levels are too high reaching precipitation thresholds in vessels, kidneys and other tissue
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11
Q

Compare and contrast a stable vs. vulnerable plaque

A 
Stable: 
Complete and thick fibrous cap
Small core 
Less inflammatory cells 
Likely asymptomatic
Unstable:
Prone to rupture (Acute plaque events)
Thin fibrosis cap or ulcerations
Large lipid filled and NECROTIC core
More inflammatory cells
<50% stenosis is likely asymptomatic
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12
Q

What is an acute plaque event?

A

Plaque rupture
Haemorrhage into the plaque: thickening = narrowing
from the neovascularisation or shoulder weakness
Erosion of the endothelium

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13
Q

What are the consequences of an acute plaque event?

A
  1. Thombosis
  2. Thromboembolism
  3. Atheroembolism
    (Less common)
  4. Chronic ischeamia = stable angina
  5. Aneurysm due to weakened media- high likelihood of rupture/haemorrhage
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14
Q

What defines chronic ischaemia (in terms of stenosis?) - what are the results?

A

> 70% stenosis of the lumen

= Stable angina and claudication

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15
Q

What are the non-modifiable risk factors of atherosclerosis?

A

Age (old), Male gender, family history, certain genes, history of atherosclerosis

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16
Q

What are the modifiable risk factors of atherosclerosis?

A

Hypertension, smoking, diabetes, cholesterol, sedentary lifestyle

17
Q

What is the role of the endothelium in atherosclerosis?

A

Damaged endothelium becomes activated
= increased permeability
= expression of adhesion molecules, cytokines and growth factors
= inflammatory infiltrate and LDL infiltrate
= Accumulation of oxLDLs + foam cells
= change from anti- to pro-coagulant

18
Q

What is the role of cholesterol (LDL levels) in atherosclerosis?

A

Accumulation of low density lipoproteins (LDLs) in Intima

  • become oxidised and then taken up by macrophages (foam cells)
  • oxLDL is toxic to endothelial and other cells
  • able to stimulate inflammatory cytokines
  • production of free radicals increases inflammation (cycle)
19
Q

What is the role of inflammation in atherosclerosis?

A

They perpetuate the endothelial dysfunction
Attract more inflammatory cells
Macrophages: foam cells, ROS production, cytokines, MMP production

20
Q

What is the role of smooth muscle cells in atherosclerosis?

A

Migrate from the media into the intima and change phenotype
= Proliferative
= synthetic (collagen)
In attempt to make a thick and stable fibrous cap

21
Q

What is an aneurysm and what is it caused by?

A

An abnormal dilation of the blood vessels (or heart)

- due to a weakness in the media (Eg. inflammation due to atherosclerosis, infection or due to a congenital abnormality)

22
Q

What are some consequences of aneurysms?

A

Risk of rupture and haemorrhage

Eg. Intracranial haemorrhage or aortic haemorrage

23
Q

What is the difference between a saccular and fusiform true aneurysm? And the differences between a false aneurysm and a dissection?

A

Saccular: bulging out of the vessel on one side
Fusiform: bulging out of the vessels on both sides
False: Extravasation of blood into the wall leading to aneurysm/bulging out of one part of the wall
Dissection: extravasation of blood into the wall that spreads (doesn’t bulge as much)

24
Q

What is an abdominal aortic aneurysm (AAA)?

A

A fusiform aneurysm
Often the aneurysm contains a thrombus which can embolise

LINES OF ZAHN

25
Q

Why is AAA associated with atherosclerosis?

A

Because the inflammatory environment weakens the ECM and the intimal thickening interferes with the wall perfusion

26
Q

How is the risk of rupture of an AAA defined?

A

> 5cm diameter

27
Q

What is a berry aneurysm?

A

Mainly occurs in the cerebral circulation
Due to weakening of the vessel
And is a major cause of subarachnoid haemorrhage

28
Q

What is a dissection?

A

When blood is present in the media

29
Q

What is dissection strongly associated with and why?

A

Hypertension

Because the high arterial pressure forces blood into the media

30
Q

What are the types of dissection?

A

Type A: (1) dissection and extravasation of blood through the media the whole length of the artery on both sides
(2) extravasation of blood in a localised area of the artery on both sides

Type B: Extravasation of blood through the media of the length of the artery on only one side

31
Q

What artery does dissection commonly occur in and what are the consequences?

A

The aorta (especially the ascending)

  • compresses or block important arteries
  • rupture into the pericardium (cardiac tamponade)
  • rupture into the thorax (esanguination)

02. Cardiovascular (43 decks)

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