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Cardiovascular > Pathology of Atherosclerosis > Flashcards

Pathology of Atherosclerosis Flashcards

1
Q

Types of Blood Vessels: Arteries

A

Large or elastic: -Aorta and major branches (innominate, subclavian, common carotid, & iliac) and pulmonary artery. Medium-sized or muscular - Coronary arteries, renal arteries Small arteries (< 2mm) and arterioles (20-100 microns) course within connective tissue of organs

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2
Q

Muscular artery

A

Media is primarily smooth muscle cells and elastic fibers are limited to internal and external elastic lamina.

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3
Q

Small arteries & arterioles

A

Media: essentially all smooth muscle cells. Arterioles: thin elastic membrane; terminal arterioles-no elastica - Points of physiologic resistance - Medial Smooth muscle contraction: adjusts blood pressure & blood flow.

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4
Q

Capillaries

A
  • Large cross-sectional area with slow blood flow and thin walls - 7-8 microns in diameter - partially surrounded by smooth muscle-like cells -> pericytes.
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5
Q

Venules

A
  • points where leukocytes emigrate in inflammation
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6
Q

Veins

A
  • Large caliber, thin walled - Contain 2/3 of blood volume
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7
Q

Lymphatics

A
  • Drain interstitial fluid into blood - Pathway for dissemination of disease
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8
Q

Endothelial Cell Properties and Functions:

A
  • Maintenance of permeability barrier - Elaboration of anticoagulant, antithrombotic, fibrinolytic regulators - Elaboration of prothrombotic molecules - Extracellular matrix production - Modulation of blood flow and vasculat reactivity - Regulation of inflammation and immunity - Regulation of cell growth - Oxidation of LDL
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9
Q

What are the mediators for the elaboration of anticoagulant, antithrombotic, fibrinolytic regulators?

A

Prostacyclin Thrombomodulin Heparin-like molecules Plasminogen

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10
Q

What are the mediators for the Elaboration of prothrombotic molecules?

A

Von Willebrand factor Tissue Factor Plasminogen activator inhibitor

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11
Q

What are the mediators for extracellular matrix production?

A

Collagen Proteoglycans

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12
Q

What are the mediators for the modulation of blood flow and vascular reactivity

A

Vasoconstriction: endothelin, ACE Vasodilators: NO, prostacyclin

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13
Q

What are the mediators for the regulation of inflammation and immunity

A

IL-1 IL-6 Chemokines Adhesion molecules: VCAM-1, ICAM, E-selectin, P-selectin Histocompatibility antigens

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14
Q

What are the mediators for the regulation of cell growth

A

Growth stimulators: PDGF, CSF, FGF Growth inhibitors: heparin, TGF-beta

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15
Q

Endothelial Cells: Response to Injury: Stimulation

A

Rapid, reversible responses, independent of new protein synthesis (ex. contraction in response to histamine)

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16
Q

Endothelial Cells: Response to Injury: Activation

A

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

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17
Q

Endothelial cell activation: “Basal State”

A

Non-adhesive, non-thrombogenic surface

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18
Q

Endothelial cell activation: “Activated state”

A

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

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19
Q

Endothelial cells activation: Factors that cause a “Basal State”

A

Normotension Laminar Flow Growth factors (e.g. VEGF)

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20
Q

Endothelial cell activation: Factors that cause an “Activated State”

A
  • Turbulent flow - Hypertension - Cytokines - Complement - Basterial products - Lipid products - Advanced glycation end-products - Hypoxia - Acidosis - Viruses - Cigarette Smoke
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21
Q

Vascular Smooth Muscle Cells

A
  • Vasoconstiction/dialation - Synthesis of collagen, elastin, proteoglycans - Elaboration of growth factors and cytokines - Migration to intima and proligeration in normal vascular repair & pathologic processes (atherosclerosis) - Pro-growth factors: PDGF, endothelin, thrombin, FGF, IFN-gamma, IL-1
22
Q

Vascular Disease - Clinical Significance

A

Responsible for more morbidity and mortality than any other category of disease

23
Q

What are the basic pathologies for vascular disease?

A

Narrowing or obstruction: - Atherosclerosis and associated thrombosis Weakening of the vessel wall - Dilatation (aneurysm) and rupture Specific types of vessels are effected in different ways by these diseases.

24
Q

Mechanism of Intimal Thickening

A
  1. Recruitment of smooth muscle cells or smooth muscle precursor cells to the intima 2. Smooth muscl cell mitosis 3. Elaboration of extracellular matrix
25
Q

Intimal smooth muscle cells cannot _____

A

Contract

26
Q

Intimal thickening is a natural healing response which may _____ or ____ the vessel

A

narrow; occlude *Occurs with aging - not clinically significant *Occus in atherosclerosis

27
Q

Arteriosclerosis: Types

A

“Hardening of the arteries” - Atherosclerosis - Arteriolosclerosis - Monckeberg medial calcific sclerosis

28
Q

Atherosclerosis: General discription

A

Hardening of the elastic arteries & large/medium muscular arteries - Most common: contributes to 50% of all death (Western World)

29
Q

Arteriolosclerosis

A

Hardening of small arteries and arterioles

30
Q

Monckeberg Arteriosclerosis

A

Calcific deposits in media (& internl elastic lamina) of medium-sized muscular arteries (typically radial and ulnar arteries) - 50 years of age -No obstruction to the blood flow - Usually not clinically significant - Unrelated to atherosclerosis - Its cause is not completely understood.

31
Q

Atherosclerosis: Types of damage

A

Aneurysm formation - leading to rupture and hemorrhage Stenosis - by atheroma leading to ischemia and/or thrombosis and embolism.

32
Q

Atherosclerosis: clinical syndromes = Aorta

A

Aneurysm with rupture

33
Q

Atherosclerosis: clinical syndromes = Carorid arteries

A

Occulusion causing stroke - possibly associated with thrombosis

34
Q

Atherosclerosis: clinical syndromes = Iliac arteries

A

Occlusion causing gangrene - possibly associated with thrombosis

35
Q

Atherosclerosis: clinical syndromes = coronary arteries

A

Occlusion causing myocardial infarction - possibly associated with thrombosis

36
Q

Atherosclerosis: clinical syndromes = Popliteal arteries

A

Occlusion causing gangrene - possibly associated with thrombosis

37
Q

Atherosclerosis: clinical syndromes = Renal artery

A

Narrowing/occlusion causing bowel infarction -possibly associate with thrombosis

38
Q

Atherosclerosis: Evolution

A
39
Q

Fatty Streak: morphology

A

Multiple yello, flat dots to streaks, usually in arota and later in coronaries. May be precursors of artheromas, but not all fatty streaks develop into more advanced lesions

40
Q

Lipid incorporation

A

Low-density lipoprotein (LDL) cholesterol is transported into the vessel wall Endothelial cells and monocytes/macrophages generate free radicals that oxidize LDL (oxLDL), resulting in lipid peroxidation. The oxLDL is taken up by macrophages via scavenger receptors. Uptake of oxLDL activates macrophages and releases proinflammatory cytokines.

41
Q

Fibro-fatty plaque: morphology

A
  • Raised yellow-white plaque in intima with soft yellow core and white fibrous cap.
  • Often eccentric (involve only part of cessel circumference) & patchy; may coalesce & become diffuse
42
Q

Risk for advanced/vulnerable plaques

A
  • -Rupture ulceration, reosion, & hemmorhage
    • Lead to thrombosis, embolism
    • progressive luminal narrowing (leading to critical stenosis)
  • Atheroemoblism
  • Aneurysm formation
    • Wall weakening leading to aneurysm & rupture
43
Q

Complicated ateromatous lesions: Hemorrhage

A

Hemorrhage into plaque likely to cause further narrowing of vessel lumen

44
Q

Thrombosis (partial or complete) of vessel lumen

A

Thrombus may beincorporated into the lesion, further narrowing it (if it is not already occluded! This is a repetitive process.

Factors contributing to thrombosis:

  • shear stress (turnulent flow)
  • high levels of LDL
  • smoking (increasing endothelial damage and stress)
45
Q

Aneurysm formation

A

Atrophy (due to pressure and or ischemia) of media, destruction of elastic fibers,

Leads to thinned weakened wall prone to rupture.

46
Q

Athrosclerosis: Pathogenesis - Compoenents of process

A

Chronic inflammatory response of arterial wall to endothelial injury

  • Components of process:
    • endothelial injury
    • Hemodynamic disturbances
    • Lipid accumulation
    • inflammation
    • infection
    • smooth muscle proliferation
47
Q

Atherosclerosis: Chronic endothelial injury/dysfunction

A

Increases permeability, enhanced leukocyte adhesion.

Suspected causes:

  • hemodynamic disturbances: plaques occur in areas of disturbed flow patterns (at ostia and vessel branch points)
  • hypercolesterolemia
  • Hypertension, smoking, homocysteine, and infectious agents
48
Q

Atherosclerosis: Inflammation

A

Adhesion molecules (from endothelial cells) attract leukocytes

Monocyte adhesion, migration & transfomation to macrophages

  • initially protective response, but ultimately cause lesion progression.

T-lymphs: secretionof cytokines & fibrogenic mediators

49
Q

Atherosclerosis: Infection

A

Importance is unclear presently

Herpes virus

CMV

Chlamydia pneumoniae

50
Q

Atherosclerosis: Smooth muscle cells

A

proliferation and migration into intima with production of matrix proteins

Cardiovascular (7 decks)

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