L4: Arteritis, atherosclerosis & diseases of arteries Flashcards

1
Q

What is the definition of arteritis?

A
  • Inflammation of arteries
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2
Q

What are the types of arteritis?

A

1- Infective

2- Non-infective

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3
Q

What causes infective arteritis?

A
  • due to microorganisms e.g. (staph aureus). It may be:
    Acute as in arteries passing in area of acute inflammation or,Chronic as in arteries passing in area of chronic inflammation (endarteritis obliterans).
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4
Q

What are the types of non-infective arteritis?

A
  • Polyarteritis nodosa.
  • Systemic lupus erythematosus.
  • Thromboangitis obliterans.
  • Giant cell arteritis.
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5
Q

What is non infective arteritis mediated by?

A
  • These inflammatory and often necrotizing vascular lesions are usually mediated by immune mechanism (immune complex deposition).

“Type III hypersensitivity reaction”

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6
Q

What is the definition of polyarteritis nodosa?

A
  • It is a necrotizing inflammation of small and medium sized arteries caused by immune complex hypersensitivity reaction. It is marked by destruction of arterial media and internal elastic lamina resulting in aneurysmal nodules.
  • Mostly affects kidney, heart, GIT, CNS and musculoskeletal vessels. “Biopsy is taken for diagnosis”
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7
Q

What are the complications of polyarteritis nodosa?

A
  • Ischemia: It may be chronic due to fibrosis or acute due to thrombosis.
  • Rupture due to fibrinoid necrosis leading to heamorrhage. “Acute”
  • Aneurysms due to weak fibrosed media. “Chronic”
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8
Q

What is the definition of systemic lupus erythrematous?

A
  • Multi-system disease, type III hypersensitivity (immune complex).

“Mainly affects females in middle age”

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9
Q

What are the affected blood vessels in SLE?

A
  • Small arteries, arterioles or even venules are affected nearly all-over the body.
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10
Q

What is the fate of SLE?

A
  • Death is usually due to:
    1. Hypertension
    2. Renal failure
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11
Q

What is giant cell arteritis? (Temporal arteritis)

A
  • It seen in medium to large sized arteries with granuloma formation.

“Mainly affects males, especially in temporal artery”

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12
Q

What is Thromboangitis obliterans? (Buerger’s disease)

A
  • It is an acute inflammation (followed by chronic) involving small to medium-sized arteries of the extremities extending to adjacent vein and nerve.
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13
Q

What is the cause of Thromboangitis obliterans?

A
  • Hypersensitivity to tobacco products with hereditary predisposition.

“More in Jewish”

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14
Q

What are The complications of Thromboangitis obliterans?

A
  • Ischemia which may lead to intermittent claudication (chronic ischemia) and gangrene (acute ischemia).

“Pain after walking for some time”

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15
Q

What is the definition of atherosclerosis?

A
  • Chronic degenerative disease characterized by formation of intimal fibro- fatty plaques
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16
Q

What is the most common arterial disease?

A
  • Atherosclerosis
17
Q

where is atherosclerosis more common?

A
  • More common in developed countries
18
Q

What is the pathogenesis of atherosclerosis?

A

1- Reaction to injury formulation

Injury (or dysfunction) of endothelium leads to…
• Entry of monocytes and lipids (hyperlipoproteinemia) to subendothelium.
• Platelet adhesion and aggregation.

2- Release of mitogenic factors from platelets and
macrophages…..proliferation and migration of smooth muscle fibers.

3- Monocytes and smooth muscle cells engulf lipid and
cause lipid deposition into the lesion.

4- Necrosis in the deeper part.

19
Q

What is the N/E of atherosclerosis?

A
  • Sites: Small, medium, and large arteries
  • Aorta, especially descending *Coronaries and cerebrals
  • Femoral , renal, superior mesenteric and internal carotids.
  • Uncomplicated atheroma: “unit lesion for atherosclerosis”
    disc-like patches. Color ranges from yellow to white according to relative amount of fat covered by glistening intima. more around the mouths of the branches.
  • Complicated atheroma: calcification, ulceration, thrombosis
20
Q

What is the M/E of atherosclerosis?

A
  • Intimal lesions:
    Subendothelial fibrous cap, formed of proliferated smooth muscle cells, foam cells and extra cellular matrix, Central core of cholesterol and cholesterol esters, lipid laden macrophages (foam cells), necrotic debris and calcification.
  • Medial lesions:
    Internal elastic lamina: disrupted
    Media: atrophy “due to pressure”
    Vascularisation of plaque
  • Adventitia: lymphocytic infiltrate “to fight infection”
21
Q

What are the complications of atherosclerosis?

“ACUTE”

A

1- Narrowing of vascular lumen…chronic ischemia.

2- Superimposed thrombosis…acute ischemia.

3- Ulceration with liberation of fatty core … acute ischemia, athero emboli, DIC.

4- Pressure atrophy of the media with fibrosis….weakening of the wall …. Aneurysm.

5- Dystrophic calcification.