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Pathology > Atherosclerosis & Vascular Pathology > Flashcards

Atherosclerosis & Vascular Pathology Flashcards

1
Q

Under normal conditions, what are the features and functions of blood vessels?

A

The normal function of blood vessels is (mainly) to:

  • Contain blood (which can sometimes be under pressure; without letting it clot (or forcing it to clot) and without letting it leak)
  • Interact with blood components when necessary (ie. inflammation, coagulation)
  • Normal blood vessels have: intima, media & adventitia
    (except capillaries which are mostly just endothelium with pericytes - but they have their own specialisations)
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2
Q

What are some features of the tunica intima?

A

The T.I is lined by endothelium which is more than just a ‘teflon coating’:

  • interacts with blood cells and platelets
  • influences vascular tone and blood flow
  • actively prevents coagulation
  • can promote coagulation if ‘activated’ or damaged (by high blood pressure, toxins, turbulence etc.)

The T.I also contains a thin layer of connective tissue (collagen, elastin, fibroblasts) and can heal after damage but will thicken/ fibrose as a result.
- smooth muscle cells migrate in, and produce more ECM - like healing in any other structure.

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3
Q

What are some features of tunica media?

A

The T.M is made up of smooth muscle cells and elastin:
- ‘elastic arteries’ have many layers of elastin
- ‘muscular arteries’ have internal and external elastic lamina
The media is thicker in arteries than in veins:
- with extra elastin, allowing pulsatile blood flow and maintenance of blood pressure.

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4
Q

What are some features of the tunica adventitia?

A

Connective tissue: collagen, fibroblasts, blood vessels

The T.A is thicker in veins than in arteries allowing venous capacity to be very large.

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5
Q

What are some diseases and conditions that can occur in the vessels when things go wrong?

A
  • Diseases of wear & tear: arteriosclerosis, arteriolosclerosis
  • atherosclerosis
  • aneurysms & dissection
  • thrombosis
  • embolism
    All of these affect blood supply and lead to:
  • Ischaemia & infarction
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6
Q

Explain some general features of the conditions: Arteriosclerosis & Arteriolosclerosis

A

Wear & tear happens to blood vessels; more with age and worse with hypertension or diabetes.
Quite often, there is intimal damage due to this wear and tear which causes thickening in the arteries. This is the intimal response to injury: healing but with additional thickening/fibrosis - this process (as well as any other type of arterial hardening) is known as arteriosclerosis.

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7
Q

With which group of individuals is arteriosclerosis most common?

A

Arteriosclerosis is common with aging, or with hypertension as arteries lose their elasticity, and may become narrowed.

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8
Q

What are the sequelae of arterisclerosis?

A

Sequelae:

  • impairs artery’s role in controlling BP
  • can impair blood supply to downstream tissues due to impaired luminal diameter.
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9
Q

What is the mechanism by which arterioles become thickened?

A

Wear and tear can also cause intimal damage and thickening of the arterioles.
Mechanism:
- smooth muscle cells produce too much matrix
- proteins from blood (ie. Ig, albumin etc) can leak across damaged endothelium
- known as ‘hyaline arteriolosclerosis’

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10
Q

What are the sequelae of arteriolosclerosis?

A

Sequelae:

  • poor blood supply to tissues (ischaeia)
  • possibility of microaneurysms and hemorrhage
  • -> possible cerebral hemorrhage (bleeding due to weakened arterioles)
  • -> ‘benign nephrosclerosis’ (ischaemia of kidneys from narrowed arterioles)
    • hypertensive retinopathy
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11
Q

What are some features of atherosclerosis?

A

Atherosclerosis occurs when there is a build up of inflammatory, fibrotic, necrotic and fatty material in arteries - best describes as a fibroinflammatory lipid plague or atheroma.

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12
Q

What is an atheroma?

A

The atheroma is a fibrous cap with a necrotic lipid core.

This atheroma can slowly narrow arteries or can rupture catastrophically. Atherosclerosis is usually only ever seen in arteries and not veins.

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13
Q

How does atherosclerosis form?

A

The formation seems to happen in stages however it is still not completely understood:

  1. Fatty Streaks
  2. Damage, inflammation, cholesterol and fibrosis
  3. Stable atherosclerotic plaque
  4. Unstable atherosclerotic plaque
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14
Q

What are fatty streaks?

A
  • Collections of foam cells in the intima (macrophages & smooth muscle cells that have ingested lipid)
  • Clinically insignificant
  • Common from birth
  • Develop at ostia and branch points where atherosclerotic plaques are common
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15
Q

What are some features of atherosclerotic plaques?

A
  • fibrous cap, chronic inflammatory cells, necrotic lipid core
  • likely asymptomatic but can encroach on the lumen over time (stable angina etc)

Microscopic Features:

  1. foam cells
  2. inflammatory cells (mononuclear)
  3. cholesterol clefts
  4. calcification
  5. thickened intima
  6. narrowed lumen
  7. fibrous cap
  8. necrotic core
  9. thinned media
  10. neovascularisation
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16
Q

What is calcification?

A

Pathologic calcification arises in two ways:

  1. Dystrophic Calcification - appears in areas of cell degeneration (TB, breast legions, atherosclerosis)
  2. Metastatic Calcification - serum Ca and Phosphate levels are too high, they reach their precipitation threshold and fall out of solution: calcification in blood vessels, kidneys etc.
17
Q

What is the difference between stable and unstable plaques?

A

An unstable plaque is prone to rupture, leading to acute plaque events. Plaques which rupture often have:

  • thinner fibrous caps (or even ulceration)
  • larger necrotic cores
  • more inflammatory cells
  • less than 50% stenosis (likely asymptomatic)
18
Q

What is an acute plaque event?

A

Something has gone wrong in the plaque such as a rupture, hemorrhage into the plague or erosion to the endothelium.

19
Q

What is the sequelae of an acute plaque event?

A

Sequelae:

  • thrombosis (clotting)
  • thromboembolism (clotting that happens elsewhere because the clot breaks off)
  • atheroembolism (clotting that happens elsewhere because the plaque breaks off)
  • chronic ischaemia when lumen >70% stenosed (such as in stable angina or peripheral vascular disease)
  • aneurysm (due to weakened media, risk of ripture/hemorrhage)
20
Q

What are some risk factors of atherosclerosis?

A

Non-Modifiable: age, gender, family history, certain genes, (*already having atherosclerosis)
Modifiable: hypertension, smoking, diabetes, cholesterol, sedentary lifestyle

The risk factors relate to the pathogenesis.

21
Q

What are some of the roles of endothelium in atherosclerosis?

A

Endothelial activation/dysfunction is important in the start of atherosclerosis. Many risk factors can be linked to endothelial dysfunction:

  • hypertension has a low-grade ‘shear’ effect
  • smoking has toxic and pro-inflammatory effects
  • high blood sugar and lipids can damage endothelium.

Normal endothelium does not interact with inflammatory cells. Activated endothelium behaves differently in that it:

  • becomes leaky
  • expresses adhesion molecules
  • produces cytokines and GFs
  • changes from anti-coagulant to pro-coagulant

Activated Endothelial also takes up LDLs into the intima which becomes oxidised and pro-inflammatory. It also allows monocytes into the intima:

  • activated endothelium expresses adhesion molecules
  • monocytes enter the intima and become macrophages
  • macrophages phagocytose oxidised LDL and produce inflammatory cytokines.
22
Q

What is the role of cholesterol/LDL in atherosclerosis?

A

High cholesterol is a strong risk factor for atherosclerosis. Genetic abnormalities of cholesterol metabolism can result in premature atherosclerosis (can cause death in young people even without other risk factors)

HDL is though to take up lipid from the periphery and remove lipid from plaques.

LDL accumulates in the intima and oxidises to become toxic to endothelial and other cells. It is also taken up by macrophages and smooth muscle cells (to become foam cells). This simulates inflammatory cytokines and produces free radicals in the intima.

23
Q

What is the role of inflammation in atherosclerosis?

A

Inflammatory milieu - cytokines etc. (from macophages and T cells):

  • perpetuates endothelial dysfunction
  • attracts more inflammatory cells (more RoS, more cytokines, more MMPs (matrix metalloproteinases)
  • perpetuates inflammatory process: ‘vicious cycle’
24
Q

What is the role of smooth muscle cells in atherosclerosis?

A

Migrate into the intima and changes phenotype:
- can proliferate
- can produce ECM - like fibroblasts in the healing process)
They also produce collagen which produces a thicker fibrous cap

25
Q

Give a general summary of atherosclerosis.

A

“Atherosclerosis is an intimal-based lesion composed of a fibrous cap and an atheromatous core; the constituents of the plaque include smooth muscle cells, extracellular matrices, inflammatory cells, lipids, and necrotic debris

Atherogenesis is driven by an interplay of vessel wall injury and inflammation. The multiple risk factors for atherosclerosis all cause endothelial cell dysfunction and influence inflammatory cell and smooth muscle cell recruitment and stimulation

Atherosclerotic plaques develop and grow slowly over decades. Stable plaques can produce symptoms related to chronic ischemia by narrowing vessel lumens, whereas unstable plaques can cause dramatic and potentially fatal ischemic complications related to acute plaque rupture, thrombosis, or embolization

Stable plaques tend to have a dense fibrous cap, minimal lipid accumulation and little inflammation, whereas “vulnerable” unstable plaques have thin caps, large lipid cores, and relatively dense inflammatory infiltrates”

26
Q

What is an aneurysm?

A
  • Abnormal dilation of blood vessel (or heart)
  • Due to a weakness in the media (ie. inflammation, infection (syphilis), congenital)
  • Risk is of rupture and hemorrhage (ie. intracranial, from aorta)
27
Q

What is AAA? What are some features of it?

A

AAA (Abdominal Aortic Aneurysm):

  • Associated with atherosclerosis:
    • inflammatory environment weakens ECM (MMPs again)
    • intimal thickening interferes with wall perfusion
  • Often contain thrombus (which can embolise)
  • Risk of rupture increases above 5cm diameter
28
Q

What is a berry aneurysm?

A

Berry Aneurysm:

  • in the cerebral circulation (“Circle of Willis”)
  • weakening of a congenital defect
  • major cause of subarachnoid hemorrhage
29
Q

What is a dissection?

A
  • Blood in the media under arterial pressure (between the inner 2/3 and our 1/3)
  • Very strong association with hypertension (>90%)
  • Generally affects the aorta, especially ascending:
    • can involve or compress important arteries
    • can rupture into pericardium (cardiac tamponade)
    • can rupture into thorax (exsanguination)

Pathology (23 decks)

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