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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
Q

Clinical syndromes associated with athersclerosis in large/medium sized muscular arteries?

Coronary arteries:

Popliteal arteries:

Renal artery:

Mesenteric arteries:

A

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
Q

What is atherosclerosis progression during the “pre clinical phase”?

A

Normal artery → Fatty streak → Fibrofatty plaque → Advanced/vulnerable plaque

27
Q

How does an advanced vulnerable plaque advance in the evolution of atherosclerosis (3 outcomes)

A
  1. Aneurysm and rupture
  2. Occlusion by thrombis
  3. Critical stenosis
28
Q

How does a fatty streak appear morphologically?

A

Multiple yellow, flat dots to streaks, usually in aorta and later in coronaries

29
Q

Describe lipid incorporation:

A
  • 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
Q

Describe the morphology of a fibro-fatty plaque:

A
  • 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
Q

What can a fibro-fatty plaque impinge on?

A

lumen

32
Q

What is the risk for advanced/vulnerable plaques?

A
  • 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
Q

Vunerable plaque vs. Stable plaque

A
  • Vunerable:
    • thin fibrous cap
    • large lipid core
    • inflammation
  • Stable:
    • thick fibrous cap
    • small lipid core
    • minimal inflammation
34
Q

What is the morphology of complicated atheromatous lesions?

A

Caused by calcification within the atheromatous plaque

Surface defects:

  • ulceration
  • erosion
  • overlying thrombus
35
Q

What is the consequence of hemorrhage into a plaque?

A

likely to cause further narrowing of vessel lumen

36
Q

What happens if there is thrombosis (partial or complete) of the vessel lumen?

A
  • thrombus may be incorporated into the lesion, further narrowing it (if it is not already occluded!)
  • likely happens repeatedly
37
Q

Factors contributing to thrombosis:

A
  1. shear stress
  2. high levels of LDL
  3. smoking (? through elevation of fibrinogen)
38
Q

What causes aneurysm formation?

What can an aneurysm lead to?

A
  • Atrophy (due to pressure and or ischemia) of media, destruction of elastic fibers
  • Leads to thinned weakened wall prone to rupture
39
Q

What is the hypothesis of atherosclerosis?

A

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
Q

Chronic endothelial injury/dysfunction ⇒ …

What are some strongly suspected causes?

A

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
Q

How does inflammation play a role in the pathogenesis of atherosclerosis?

A
  • 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
Q

How does infection play a role in atherosclerosis pathogenesis?

How do smooth muscle cells play a role?

A
  • 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
Q

How is chronic hyperlipidemia related to atherosclerosis?

A

Chronic hyperlipidemia:

  • Can directly impair endothelial cell function
  • Lipoproteins accumulate in intima

Cardiovascular System (35 decks)

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