Blood Vessels and Atherosclerosis Flashcards Preview

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Flashcards in Blood Vessels and Atherosclerosis Deck (43):

What are the basic components of the vessel wall?

  • Endothelium
  • Intima
  • Internal Elastic Lamina
  • Media
  • External elastic lamina
  • Adventitia


What are the three types of arteries?

Large or elastic

Medium sized or muscular

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


What are examples of the large or elastic arteries?

Aorta and major branches; pulmonary artery


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

Coronary arteries; renal arteries


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

smooth muscle cells


In muscular arteries media is primarily ______ _____ ____

Where are elastic fibers in muscular arteries?

Smooth muscle cells

Elastic fibers are limited to internal and external elastic lamina


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

Essentially all smoth muscle cells

Smooth muscle cell contraction adjust blood pressure and flow


Which arterioles have no elastica?

Terminal arterioles


What is the average diameter of a capillary?

Are there smooth muscles in capillaries?

7-8 microns in diameter

Partially surrounded by smooth muscle-like cells = pericytes


Where do leukocytes commonly emigrate in inflammation?



How much blood volume is contained in veins?

2/3 blood volume


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



How to endothelial cells respond to injury?

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


What happens in endothelial cell activation?

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


How do vascular smooth muscles contribute to vascular repair?

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


What is synthesyzed by Vascular smooth muscle cells?

  • Collagen
  • Elastin
  • Proteoglycans


What are the two basic pathologies of vascular disease?

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


What are three steps in intimal thickening?

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


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

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


What is the difference between arteriosclerosis, atherosclerosis and arteriolosclerosis

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


What is Monckeberg arteriosclerosis?

Calcific deposits in media of medium sized muscular arteries


What is atherosclerosis

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


What are the two basic types of damage in atherosclerosis?

Aneurysm formation - leading to rupture and hemorrhage

Stenosis - by atheroma leading to ischemia/thrombosis


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




Aorta: aneurysm with rupture

Carotid: Occlusion causing stroke (possibly associated with thrombosis)

Iliac: Occlusion causing gangrene (possibly associated with thrombosis)


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


What is atherosclerosis progression during the "pre clinical phase"?

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


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


How does a fatty streak appear morphologically?

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


Describe lipid incorporation:

  • Low-density lipoprotein (LDL) cholesterol is transported into the vessel wall
  • Endothelial cells and monocytes/macrophages: 
    • generate free radicalsoxidize LDL (oxLDL) ⇒ lipid peroxidation
  • oxLDL is taken up by macrophages via ‘scavenger’ receptors ⇒ activates macrophages ⇒ releases proinflammatory cytokines


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


What can a fibro-fatty plaque impinge on?



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


Vunerable plaque vs. Stable plaque

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


What is the morphology of complicated atheromatous lesions?

Caused by calcification within the atheromatous plaque

Surface defects:

  • ulceration
  • erosion
  • overlying thrombus


What is the consequence of hemorrhage into a plaque?

likely to cause further narrowing of vessel lumen


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


Factors contributing to thrombosis:

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


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


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


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


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


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


How is chronic hyperlipidemia related to atherosclerosis?

Chronic hyperlipidemia:

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