Path Blood Vessels I (9)

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Path Blood Vessels I (9)
2014-02-15 18:28:18
MBS Pathology
Exam 2
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  1. Normal Blood Vessel Layers (Inside to Out)
    • Tunica Intima: endothelium → basement membrane → lamina propria (SM muscle + CT, aka ECM)
    • Tunica Media: internal elastic membrane → SM muscle → external elastic membrane
    • Tunica Adventitia: CT & vasa vasorum
  2. Elastic/Large Arteries
    • have a tunica media with alternating layers of elastic membranes & smooth muscle cells
    • includes Aorta, its branches, & the pulmonary arteries
  3. Muscular/Medium-size Arteries
    • have a tunica media made mostly of smooth muscle that regulates regional blood flow via contraction (vasoconstriction) or relaxation (vasodilation)
    • includes smaller branches of the Aorta (eg. coronary arteries, renal arteries)
  4. Small Arteries & Arterioles
    • are found w/in the CT of organs
    • have a tunica media made up of smooth muscle
    • arterioles are responsible for regulating blood flow resistance (regulate = reduce both pressure & velocity)
    • small changes in arteriolar lumen diameter can have profound flow-limiting effects (50% decrease in diameter = 16-fold increase in resistance)
    • small arteries are those w/ a diameter less than or equal to 2 mm; the diameter of arterioles range from 20-100 μm
  5. Capillaries (7-8 μm)
    • wall is made up of endothelium partially surrounded by pericytes
    • capillary beds have the largest total cross-sectional area & lowest rate of blood flow in the human circulatory system
  6. Veins
    • have larger diameter lumins, thinner walls w/ less distinct layers in comparison w/ arteries at the same level of branching
    • are more prone to dilation, external compression, & penetration by tumors or inflammatory processes
  7. Lymphatics
    thin walled, endothelium-lined channels that in times of infection can disseminate disease by transporting microbes or tumor cells to distant sites
  8. What types of vessels does Atherosclerosis (ATH) mainly affect? Hypertension (HTN)?
    • ATH affects mainly elastic & muscular arteries (large & medium)
    • Hypertension mainly affects small muscular arteries & arterioles
  9. Endothelial Basal v. Activated State & What Causes Either
  10. Vessel Smooth Muscle Cells
    • participate in normal vascular repair & pathologic processes (eg. ATH)
    • can proliferate whens stimulated
    • synthesize ECM collagen, elastin, & proteoglycans
    • elaborate growth factors and cytokines
    • are responsible for vasoconstriction & dilation
  11. What is the stereotypical response of a vessel wall to any insult?
    • Intimal Thickening
    • any vascular injury - with EC loss or just dysfunction - stimulates SM muscle growth & associated synthesis
    • a thickened intima ITSELF does NOT contain lipid droplets - it thickens due to SM muscle cell proliferation
  12. Arteriosclerosis
    • a general term describing any hardening, loss of elasticity, & thickening of medium or large arteries
    • 3 types:
    • 1. Atherosclerosis (ATH)
    • 2. Mönckeberg's Arteriosclerosis
    • 3. Arteriolosclerosis
  13. Atherosclerosis (ATH)
    • a specific form of arteriosclerosis in which hardening of the arteries is characterized by irregularly distributed lipid deposits in the tunica intima of large & medium-sized arteries
    • this causes a narrowing of arterial lumens which results in less blood being able to travel through increasing BP
    • proceeds eventually to fibrosis & calcification
    • causes more morbidity and mortality (~half of all deaths) in the Western world than any other disorder
    • otherwise known as Arteriosclerotic Vascular Disease (ASVD)
  14. Mönckeberg's Arteriosclerosis (Medial Calcific Sclerosis)
    • arterial sclerosis involving the peripheral (muscular) arteries, especially of the legs of older people, w/ deposit of calcium in the tunica media (pipe-stem arteries) but with little or no encroachment on the lumen
    • is an example of dystrophic calcification
  15. Arteriolosclerosis
    • arterioLOsclerosis affects mainly the small arteries and arterioles especially in chronic hypertension & diabetes mellitus
    • it may cause downstream ischemic injury
  16. C-Reactive Protein (CRP)
    • protein made by the liver found in high levels in the blood in response to inflammation (is an acute-phase protein), specifically in response to factors released by macrophages & adipocytes
    • purpose is to bind to phosphocholine expressed on the surface of dead or dying cells there to activate the complement system
    • high levels of CRP can be more diagnostic for ATH than cholesterol levels
  17. What is the response-to-Injury hypothesis of atherosclerosis pathogenesis?
    • the idea that atherosclerosis can be viewed as a chronic inflammatory response of the arterial wall to endothelial injury - it's possible that such a condition won't occur unless endothelial injury occurs first
    • a lesion will worsen through contact w/ modified lipoproteins, monocyte-derived macrophages, T lymphocytes, & the normal cellular constituents of the arterial wall
  18. What are 3 important causes of endothelial dysfunction?
    1. hemodynamic disturbance: plaques have a tendency to form at ostia (opening) of exiting vessels, branch points, & along the posterior wall of the abdominal aorta where they disturbed flow patterns

    2. lipoprotein abnormalities: can result from gene mutations, dyslipoproteinemia, ↑ LDL, ↓ HDL

    3. inflammation: inflam. cells & mediators are directly responsible for the initiation, progression, & complications of ATH lesions (eg. foam cells, + T-cells in the intima generate a chronic immune inflammatory state)
  19. Foam Cells
    • fat-laden macrophages formed when the body sends macrophages to the location of a fatty deposit on the blood vessel walls
    • the macrophage surrounds the fatty material in an attempt to destroy it but the cell becomes filled with lipids (fats)
    • become a problem when they accumulate at particular foci thus creating a necrotic centre of atherosclerosis
  20. Based on inflammation's role in endothelial dysfunction, what might the correlation be between anti-inflammatory drugs & cardiovascular risk?
    anti-inflammatory drugs can lower a person's cardiovascular risk
  21. Most Extensively Involved Vessels Affected by Atherosclerosis
    • 1. Lower abdominal aorta
    • 2. Coronary arteries (MI)
    • 3. Popliteal arteries (back of knee)
    • 4. Internal carotid (neck → stroke)
    • 5. Vessels of the circle of Willis (brain)
  22. Intimal Cell Mass
    • white, thickened areas at branch points in the arterial tree that contain SM muscle cells & ECM but NO lipid
    • these ‘cushions’ are located at arterial branch sites & they correlate well w/ the locations of later atherosclerosis
  23. Fatty Streak
    • the first grossly visible lesion in the development of atherosclerosis
    • it appears as an irregular yellow-white discoloration on the luminal surface of an artery & consists of aggregates of foam cells beneath the inner, endothelial layer of an artery
    • it doesn't protrude significantly & does not cause any disturbance in blood flow
    • may also contain T cells, aggregated platelets, & SM muscle cells
    • it is a precursor lesion of atheromas that may become atheromatous plaques
    • blue: endothelial cell
    • red: internal elastic membrane
    • black: lipid droplets in intima
  24. Atheroma
    • an accumulation & swelling in artery wall intima that is the characteristic lesion of atherosclerosis
    • has a core made up of macrophages, muscle cells, leukocytes (WBC), ECM, calcium, & intra + extracellular lipid deposits with a covering fibrous cap
    • may cause stenosis of the vascular lumen, weakens vessel's wall, & can cause rupture of the vessel
    • intimal thickening + high lipid diet → atheroma
  25. What are the 3 main components of atherosclerotic plaques?
    • 1. Cells: SM muscle cells, macrophages, T cells
    • 2. Extracellular matrix: collagen, elastic fibers, proteoglycans
    • 3. Lipid: both intra & extracellular
  26. Atherosclerotic Plaques
    • also contain a superficial fibrous cap composed of SM muscle cells & dense collagen
    • beneath and to the side (shoulder) of the cap is a more cellular area w/ macrophages, T cells, & SM muscle cellsa necrotic core contains lipid, debris from dead cells, foam cells (macrophages & SM muscle cells), fibrin, & plasma proteins
    • the plaque is neovascularized & dystrophic calcification of cells can be seen
  27. Plaque Neovascularization
    growth of atherosclerotic plaques is accompanied by neovascularization from vasa vasorum microvessels extending through the tunica media into the base of the plaque and by lumen-derived microvessels through the fibrous cap
  28. Cholesterol Clefts
    • the microscopic manifestation of extracellular accumulations of cholesterol in an atherosclerotic plaque
    • if released can travels w/ the bloodstream to other places in the body where it may obstructs blood vessels (embolism)
  29. Clinical Complications of Atherosclerotic Plaques
    1. Rupture, ulceration, or erosion of the luminal surface (exposes bloodstream to highly thrombogenic substances, induces thrombus formation which can partially or completely occlude the lumen → ischemia)

    2. Hemorrhage into a plaque (due to rupture of the fibrous cap or thin-walled vessels in areas of neovascularization; hematoma may expand plaque or induce plaque rupture)

    3. Atheroembolism (plaque rupture releases debris/microemboli into bloodstream)

    4. Aneurysm formation (pressure or ischemic atrophy of tunica media causes vessel wall weakness & aneurysm development that may rupture)
  30. Possible Clinical Outcomes of Arterial Plaques
  31. Mural Thrombi
    • thrombi adherent to the vessel wall that are not occlusive & affect large vessels (eg. aorta)
    • appear grey-red w/ alternating light & dark lines (lines of Zahn) which represent bands of fibrin (lighter) w/ entrapped white & red blood cells (darker)
  32. Vulnerable v. Stable Plaque
  33. Major Consequences of Atherosclerosis
    • Myocardial infarctions
    • Cerebral infarction (stroke)
    • Aortic aneurysms
    • Peripheral vascular disease (gangrene of the legs)
  34. Aneurysms
    • congenital or acquired dilations of blood vessels or the heart
    • true aneurysms is a localized, blood-filled balloon-like bulge in the wall of a blood vessel that involves all 3 layers of the artery or the attenuated wall of the heart (eg. atherosclerotic & congenital vascular aneurysms, ventricular aneurysms resulting from transmural MI)
    • complications arise from rupture, thrombosis, or embolization
  35. False Aneurysm (Pseudoaneurysm)
    • a hematoma that forms as the result of a leaking hole in an artery
    • the hematoma forms outside the arterial wall, so it is contained by the surrounding tissues
    • the extravascular hematoma communicates with the intravascular space (“pulsating hematoma”)
    • eg. ventricular ruptures contained by pericardial adhesions or leaks at the junction of a vascular graft w/ a natural artery
  36. Dissection
    • a tear within the wall of a blood vessel that allows blood to separate the wall layers
    • pressurized blood gains entry to the arterial wall through a surface defect & pushes apart the underlying layers
  37. What is the major risk for aortic dissection?
  38. What are the 2 most important causes of aortic aneurysms?
    • 1. atherosclerosis
    • 2. hypertension
    • others include inadequate or abnormal connective tissue synthesis, TGF-β receptor mutation (elastin, collagen), Marfan syndrome (fibrillin), Ehlers-Danlos (collagen), excessive connective tissue degradation, loss of smooth muscle cells, or a change in the smooth muscle cell synthetic phenotype
  39. Hyaline Arteriolosclerosis
    • thickening of the walls of small arteries & arterioles caused by the deposition of homogeneous hyaline material
    • there's also a loss of underlying structural detail & narrowing of the lumen
    • is associated with age, hypertension, & diabetes mellitus
  40. Hyperplastic Arteriolosclerosis
    • a type of arteriolosclerosis involving a narrowed lumen seen in severe hypertension
    • "onion-skin" is sometimes used to describe this form of vessel w/ thickened concentric smooth muscle cell layer & thickened, duplicated basement membrane
    • in malignant hypertension these hyperplastic changes are often accompanied by fibrinoid necrosis of the arterial intima & media
    • such changes are most prominent in the kidney & can lead to ischemia + acute renal failure