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Cardiovascular System > Blood Vessels and Atherosclerosis > Flashcards

Blood Vessels and Atherosclerosis Flashcards

1
Q

What are the basic components of the vessel wall?

A
  • Endothelium
  • Intima
  • Internal Elastic Lamina
  • Media
  • External elastic lamina
  • Adventitia
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2
Q

What are the three types of arteries?

A

Large or elastic

Medium sized or muscular

Small arteries (<2mm) and arterioles (20-100microns)

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3
Q

What are examples of the large or elastic arteries?

A

Aorta and major branches; pulmonary artery

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4
Q

What are two examples of medium-size or muscular arteries?

A

Coronary arteries; renal arteries

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5
Q

In large arteries, elastic fibers alternate between _____ ______ _____ in media

A

smooth muscle cells

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6
Q

In muscular arteries media is primarily ______ _____ ____

Where are elastic fibers in muscular arteries?

A

Smooth muscle cells

Elastic fibers are limited to internal and external elastic lamina

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7
Q

For small arteries/arterioles What makes up the media? What is the purpose of the media?

A

Essentially all smoth muscle cells

Smooth muscle cell contraction adjust blood pressure and flow

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8
Q

Which arterioles have no elastica?

A

Terminal arterioles

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9
Q

What is the average diameter of a capillary?

Are there smooth muscles in capillaries?

A

7-8 microns in diameter

Partially surrounded by smooth muscle-like cells = pericytes

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10
Q

Where do leukocytes commonly emigrate in inflammation?

A

Venules

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11
Q

How much blood volume is contained in veins?

A

2/3 blood volume

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12
Q

What vessels drain interstitial fluid into blood and are a pathway for dissemination of disease?

A

lymphatics

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13
Q

How to endothelial cells respond to injury?

A

Stimulation - rapid reversible response independent of new protein synthesis (response to histamine)

Activation - Elaboration of gene products with biologic activity requires hours/days to develop

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14
Q

What happens in endothelial cell activation?

A
  • Increased expression of procoagulants, adhesion molecules, and proinflammatory factors
  • Altered expression of chemokines, cytokines and growth factors
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15
Q

How do vascular smooth muscles contribute to vascular repair?

A

Migrate to intima and proliferate (also occurs in pathologic processes like athersclerosis)

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16
Q

What is synthesyzed by Vascular smooth muscle cells?

A
  • Collagen
  • Elastin
  • Proteoglycans
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17
Q

What are the two basic pathologies of vascular disease?

A
  1. Narrowing or obstruction (thrombosis)
  2. Weakening of vessel wall (aneurysm and rupture)
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18
Q

What are three steps in intimal thickening?

A
  1. Recruitment of smooth muscle cells or smooth muscle precursor cells to the intima
  2. Smooth muscle cell mitosis
  3. Elaboration of extracellular matrix
19
Q

Why does smooth muscle move to the intima and why is this potentially harmful?

A

This is a stereotyped response to vascular injury of ANY KIND

Intimal smooth muscle cells cannot contract and healing response may narrow or occlude the vessel

20
Q

What is the difference between arteriosclerosis, atherosclerosis and arteriolosclerosis

A
  • Arteriosclerosis - hardening of the arteries (generic term
    • Atherosclerosis - elastic arteries and large/medium muscular arteries
    • Arteriolosclerosis - small arteries and arterioles
21
Q

What is Monckeberg arteriosclerosis?

A

Calcific deposits in media of medium sized muscular arteries

22
Q

What is atherosclerosis

A

A progressive disease of elastic arteries and large to medium-sized muscular arteries

23
Q

What are the two basic types of damage in atherosclerosis?

A

Aneurysm formation - leading to rupture and hemorrhage

Stenosis - by atheroma leading to ischemia/thrombosis

24
Q

In atherosclerosis what clinical syndromes are associated with the elastic arteries?

Aorta:

Carotid:

Iliac:

A

Aorta: aneurysm with rupture

Carotid: Occlusion causing stroke (possibly associated with thrombosis)

Iliac: Occlusion causing gangrene (possibly associated with thrombosis)

25
Clinical syndromes associated with athersclerosis in large/medium sized muscular arteries? Coronary arteries: Popliteal arteries: Renal artery: Mesenteric arteries:
Coronary arteries: occlusion causing MI Popliteal arteries: occlusion causing gangrene Renal artery: narrowing/occlusion causing secondary hypertension Mesenteric arteries: narrowing/occlusion causing bowel infarction
26
What is atherosclerosis progression during the "pre clinical phase"?
Normal artery → Fatty streak → Fibrofatty plaque → Advanced/vulnerable plaque
27
How does an advanced vulnerable plaque advance in the evolution of atherosclerosis (3 outcomes)
1. Aneurysm and rupture 2. Occlusion by thrombis 3. Critical stenosis
28
How does a fatty streak appear morphologically?
Multiple yellow, flat dots to streaks, usually in aorta and later in coronaries
29
Describe _lipid incorporation_:
* _Low-density lipoprotein (LDL) cholesterol is transported into the vessel wall_ * Endothelial cells and monocytes/macrophages: * _generate free radicals_ ⇒ _oxidize LDL_ (oxLDL) ⇒ lipid peroxidation * oxLDL is taken up by macrophages via _‘scavenger’ receptors_ ⇒ _activates macrophages_ ⇒ _releases proinflammatory cytokines_
30
Describe the morphology of a fibro-fatty plaque:
* Raised yellow-white plaque in intima with soft yellow core and white fibrous cap * Often eccentric (involve only part of vessel circumference) & patchy; may coalesce & become diffuse
31
What can a fibro-fatty plaque impinge on?
**lumen**
32
What is the **risk** for advanced/vulnerable plaques?
* **Rupture ulceration, erosion, & hemmorhage** * Lead to thrombosis, embolism * Progressive luminal narrowing (leading to critical stenosis) * **Atheroembolism** * **Aneurysm formation** * Wall weakening leading to aneurysm & rupture
33
**Vunerable plaque vs. Stable plaque**
* **Vunerable:** * thin fibrous cap * large lipid core * inflammation * **Stable:** * thick fibrous cap * small lipid core * minimal inflammation
34
What is the morphology of complicated atheromatous lesions?
Caused by **calcification** within the atheromatous plaque **Surface defects:** * ulceration * erosion * overlying thrombus
35
What is the consequence of hemorrhage into a plaque?
likely to cause further narrowing of vessel lumen
36
What happens if there is thrombosis (partial or complete) of the vessel lumen?
* **thrombus may be incorporated into the lesion, further narrowing it** (if it is not already occluded!) * likely happens repeatedly
37
**Factors contributing to thrombosis:**
1. shear stress 2. high levels of LDL 3. smoking (? through elevation of fibrinogen)
38
What causes aneurysm formation? What can an aneurysm lead to?
* **Atrophy** (due to pressure and or ischemia) **of media**, **destruction of elastic fibers** * **Leads to thinned weakened wall prone to rupture**
39
What is the **hypothesis** of atherosclerosis?
**Hypothesis: chronic inflammatory response of arterial wall to endothelial injury** * Components of process: * Endothelial injury * Hemodynamic disturbances * Lipid accumulation * Inflammation * Infection * Smooth muscle proliferation
40
Chronic endothelial injury/dysfunction ⇒ ... What are some strongly suspected causes?
Chronic endothelial injury/dysfunction ⇒ **↑ permeability, enhanced leukocyte adhesion** * **Strongly suspected causes:** * **Hemodynamic disturbances:** _plaques occur in areas of disturbed flow patterns_ (at ostia and vessel branch points) * **Hypercholesterolemia** * Other possible contributors: 1. Hypertension 2. Cigarette smoke toxins 3. Homocysteine 4. Infectious agents
41
How does **inflammation** play a role in the pathogenesis of atherosclerosis?
* **Adhesion molecules** (from endothelial cells) _attract leukocytes_ * **Monocyte adhesion, migration & transformation to macrophages** * _Initially protective response_, but ultimately _cause lesion progression_ * **T lymphs:** _secretion of cytokines & fibrogenic mediators_
42
How does **infection** play a role in atherosclerosis pathogenesis? How do **smooth muscle cells** play a role?
* **Infection:** Importance is unclear at present * Herpes virus * CMV * Chlamydia pneumoniae * **Smooth muscle cells:** * Proliferation and migration into intima with production of matrix proteins
43
How is **chronic hyperlipidemia** related to atherosclerosis?
**Chronic hyperlipidemia:** * Can _directly impair endothelial cell function_ * _Lipoproteins accumulate in intima_

Cardiovascular System (35 decks)

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