Histology of Blood Vessels_Fishbein

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  1. Basic structure of blood vessels

    - components
    - layers
    • components
    • - endothelial cells
    • - smooth muscles cells
    • - elastica interna
    • - fibroblasts

    • from inner to outer:
    • intima -> media -> adventitia
  2. Tunica intima

    - what is it?
    - consists of
    - Innermost layer of blood vessels

    • consists of:
    • endothelial layer:
    • —- Direct contact w/ blood—

    - Basement membrane separates endothelium from subendothelium

    • subendothelial layer
    • - Delicate connective tissue and scattered stromal cells

    • elastic/fenestrated layer:
    • - Membrane consisting of elastic fiber network

    - —Forms bulk of tunica intima

    —- Thickness depends on type and size of vessel
  3. Tunica Media

    what is it?
    consists of?
    middle layer in blood vessels

    • —Consists of concentric layer of
    • smooth muscle cells
    • extracellular matrix

    • —Smooth muscle cells
    • - —Thickness depends on type and size of blood vessel

    —- Produce extracellular matrix

    • —Extracellular matrix:
    • - —Elastic fibers, reticulin fibers, proteoglycans

    - —Main functions:

    —Conduction of blood along vascular system

    —Control of peripheral vascular resistance

    —Maintenance of blood hydrostatic pressure
  4. Tunica adventitia

    - what is it?

    - consists of?
    - outermost layer of blood vessels

    - —Connective tissue layer surrounding blood vessel

    - —May be important in vascular healing and pathology

    • —Consists of
    • collagen

    elastic fibers

    • —Vasa vasorum: supplies nutrients to
    • media of larger blood vessels (e.g. aorta)

    Nerves: regulate vascular muscle tone
  5. arterial vs. venous vs. capillaries

    - velocity, pressure, and cross sectional area
    • arterial system:
    • high velocity
    • high pressure 
    • least cross sectional area

    • venous system:
    • low velocity
    • low pressure system

    • capillaries
    • greatest cross sectional area
    • slowest velocity

    - vessels that have elastic arteries
    - what forms most of the wall?
    - function
    - —Aorta & main branches, pulmonary trunk

    • - —Media forms bulk of wall
    • —1/3 smooth muscle cells
    • —2/3 concentric layers of elastic tissue

    —Due to elasticity of its wall, elastic arteries are suited for conducting blood, i.e., they are conducting arteries

    —Maintains blood pressure during diastole

    types of muscle arteries and its functions
    —Possess a prominent media with well-formed internal and external elastic lamina

    • —Larger muscular arteries
    • - Functions as distributing arteries

    - —Media comprises 3/4 of wall thickness

    • —Smaller muscular arteries
    • - Functions as resistance arteries

    - contains —layers of smooth muscle cells
  8. what is blood pressure determined by?

    what determines peripheral vascular resistance?
    —Blood pressure is determined by peripheral vascular resistance

    • —This is determined by degree of muscle tone (i.e., muscle contraction) in small muscular arteries and arterioles via:

    • —- Autonomic nervous system
    • - Circulating hormones
    • - Local, endothelial-derived vasoactive mediators

    These mech. also act on arteriolar smooth muscle

    - function
    • —Main site of BP regulation
    • - Finely regulated process

    —- Small changes in muscle tone induce large changes in resistance

    • —Other functions:
    • —- Redistribution
    • —- Shunting of blood
  10. —Metarterioles
    - —Connects arterioles & capillaries

    • —- Individual smooth muscle cells form precapillary sphincter which constricts to reduce or shut off blood flow to their
    • respective capillaries, shunting blood elsewhere
  11. capillaries

    - consists of what cell layer
    - function
    • Consist of a single layer of:
    • - endothelial cells
    • - basement membrane
    • - pericytes: contractile cells that reside outside of the basement membrane

    —- Specialized for nutrient and gas exchange
  12. —3 main types of capillaries
    - Continuous

    - —Fenestrated

    —- Sinusoids (or discontinuous)
    - Most common type of capillary found in skeletal muscle, cardiac muscle, brain, skin, lung, exocrine glands

    • —- Endothelial cells have no fenestrae and are anchored together by tight junctions, which
    • prevent diffusion between cells

    —- Basal lamina is continuous
  14. Fenestrated Capillaries
    —Have fenestrae (holes) with or without diaphragms that allow relatively free passage of substances

    —Basal lamina is continuous
    —AKA discontinuous capillaries

    - —Large diameter, discontinuous endothelial layer, and discontinuous basal lamina

    —- Macrophages are usually within the vicinity
    - Function mostly as reservoir vessels

    —- As venules become larger, they have fewer pericytes and more smooth muscle to form muscular veins (not as thick as arteries)—

    - Discontinuous elastic lamina with relatively thick adventitia

    - —Large veins have valves to maintain unidirectional flow

    • —Post-capillary venules
    • - receive blood from capillaries

    —-Appear similar to capillaries except wider lumens and more pericytes

    - —Preferential site for WBC migration
    - Drainage system that removes excess interstitial fluid and immune cells to lymph nodes

    - have blind ends and valves

    - —Larger vessels have thin muscle layer and adventitia

    - —Similar histologically to veins except have no red blood cells
  18. aneurysm
    —Localized dilatation of vessel or heart

    blood-filled balloon-like bulge in the wall of a blood vessel
  19. True aneurysm

    what is it?
    - involves all 3 layers of arterial wall or heart

    —- Atherosclerotic, syphilitic, congenital, left ventricular aneurysm post-MI
  20. —False aneurysm (pseudoaneurysm)
    - a contained rupture

    —- Injury of vessel wall leading to extravascular hematoma that communicates w/ intravascular space

    - —Post-MI (heart attack) rupture contained by pericardial adhesion, leakage at anastomotic site of vascular graft

    - primary causes
    - other causes
    • —Most important causes of aortic aneurysms:
    • - Atherosclerosis

    - Cystic medial degeneration

    —Other causes of aortic aneurysms:

    —- Infections (AKA mycotic aneurysms)

    —- Traumatic

    —- Inflammatory (e.g. vasculitides)

    —- Congenital defects (e.g. berry aneurysms)

    —- Syphilitic aneurysms
  22. abdominal aortic aneurysms
    - —Most common atherosclerotic aneurysm

    - —Rare <50 years old and more frequently seen in men

    —- Majority occur below renal arteries and above aortic bifurcation

    —- Complicated atherosclerotic plaques result in destruction and thinning of aortic media

    - —Often partially or completely filled by thrombus
  23. Aneurysms: Complications
    - Rupture w/ massive, potentially fatal, hemorrhage

    - —Risk of rupture directly related to size of aneurysm

    - —Vascular obstruction with distal organ ischemia

    —- Atheroembolism

    - —Compression of adjacent structure (e.g. ureter)

    - what is it?
    - association w/ other disease?
    - 2 groups it affects?
    - other predisposing factors?
    - tear in inner walls of aorta that allow passage of blood within the layers

    - often ruptures outward causing massive hemorrhage

    - may or may not be associated w/ aortic aneurism

    —>90% occur in men btwn 40-60
    ears w/ antecedent history of hypertension

    —Usually younger patients with systemic or localized connective tissue disorder that affects aorta (e.g. Marfan syndrome)

    • predisposing factors 
    • - iatrogenic (e.g. arterial catheterization),
    • - pregnancy
    • - bicuspid aortic valve

  25. Aortic Dissection: Histology

    key feature?
    characterized by?
    seen in what Syndrome?
    Cystic medial degeneration

    —Characterized by elastic tissue fragmentation, “cyst”-like areas of amorphous ECM  and absence of inflammation

    —Frequently seen in Marfan syndrome
  26. Aortic Dissection Classifications (2)
    1. —DeBakey classification: based on site of intimal tear

    2. Stanford classification: based on site of dissection

    —Type A = ascending aorta involvement (higher risk of rupture)

    —Type B = descending aorta only
  27. Aortic Dissection: Complications
    • 1. rupture
    • 2. occlusion in aortic branch vessels
    • 3. distortion of aortic annulus
  28. vasculitides
    • Inflammatory conditions of blood vessel walls
  29. vasculitis: Infective disease

    • —Syphilis
    • TB
    • bacterial
    • fungal
    • rickettsial
    • viral
  30. vasculitis: Non-infective Disease

    - 3 types
    • Large vessels
    • - Takayasu
    • - giant cell
    • - rheumatoid
    • - ankylosing spondylitis

    • —Medium-sized vessels
    • - PAN
    • - Kawasaki
    • - Wegener
    • - Churg-Strauss
    • - rheumatoid
    • - SLE
    • - dermatomyositis

    • —Small vessels
    • - Serum sickness
    • - H-S purpura
    • - cryoglobulinemia
    • - drug-induced
  31. —Pathogenesis of noninfectious vasculitis
    —****Result of body’s own inflammatory cell attacking the vessels****

    Immune complex deposition

    —Antineutrophil cytoplasmic antibodies (c-ANCA, p-ANCA)

    —Anti-endothelial cell antibodies
  32. Hypertension

    population affected?
    - Affects ¼ adults in the US general population

    —- Affects ⅓ African American adults

    - —Increased prevalence & incidence with age

    —“Silent killer”

    —- Many asymptomatic

    - —Irreversible vascular damage may occur prior to diagnosis
  33. Hypertension

    - BP classifications
    Image Upload

    - aka
    - prognosis
    - characterized by
    —AKA accelerated hypertension

    —5% hypertensive persons w/ rapidly rising BP leading to death in 1-2 years if left untreated

    • —Characterized by:
    • - very high BP
    • - renal failure
    • - retinal hemorrhages
    • - exudates ± papilledema

    —May develop in previously normotensive persons, but more commonly superimposed on pre-existing benign hypertension
  35. malginant hypertension:Effects on Organs

    - Small arteries/arterioles
    - Medium & large arteries (including aorta)
    —- Heart
    - —Brain
    - —Retina
    • Small arteries/arterioles
    • - —Arteriolosclerosis (especially kidneys)

    • —Medium & large arteries (including aorta)
    • - Accelerated atherogenesis

    - Dissection & aneurysm due to medial degeneration

    • —Heart
    • - Concentric hypertrophy of left ventricle

    —- Coronary artery atherosclerosis & consequences

    • —Brain
    • - Hemorrhagic & ischemic cerebrovascular accidents

    - —Acute encephalopathy

    • —Retina
    • - Only site where effects of hypertension directly observable

    - characterized by
    - Seen in both hypertension & diabetes mellitus

    —- Homogeneous, pink hyaline thickening of arteriolar wall with narrowing of lumen

    —- Leakage of plasma components across vascular endothelium

    —- Excessive ECM production by smooth muscle cells

    - char. of what disease?
    - —Characteristic of, but not limited to, malignant hypertension

    - —Onion-skin, concentric, laminated thickening of arteriolar walls with progressive narrowing of lumen

    —- Ultrastructurally, laminations consist of SMCs and thickened and reduplicated basement membrane
  38. homostasis
    Well-regulated processes that serve to maintain blood in fluid, clot-free state in normal vessels

    —Induces rapid formation of blood clot at site of vascular injury
    —1. Intact blood vessel wall

    2. —Normal platelet function

    3. Normal coagulation system
  40. NORMAL HEMOSTASIS involve?

    —Primary hemostasis

    —Secondary hemostasis

    —Anti-thrombotic counter-regulation

    —Antithrombotic properties
    • —Antiplatelet effects:
    • - Acts as barrier btwn platelets and highly thrombogenic ECM

    - —Production of PGI2 (prostacyclin) & nitric oxide

    • - —Elaborate adenosine phosphatase
    • —Anticoagulant effects
    • - —Heparin-like molecules (blood thinner)

    • - —Thrombomodulin (binds to thrombin)
    • —Fibrinolytic effects
    • - Synthesize tissue plasminogen activator
    • - dissolves clots in the body

    note: there are also Prothrombotic properties in endothelium but MAJOR fxn of endothelium is ANTI-THROMBOTIC
  42. Platelet activation steps
    1. Accumulate at site of endothelial injury

    —2. Adhere to exposed collagen

    3. —Secrete granules (ADP + TXA2)

    4. Aggregate to transform temporary hemostatic plug into a more definitive thrombus
  43. what two factors stimulate platelet aggregation?
    ADP and TXA2
  44. end product of coagulation cascade
    Thrombin converting fibrinogen to fibrin
  45. methods to CONTROL COAGULATION
    - Maintenance of flow to remove platelets and to dilute local factors that promote thrombosis

    —- Thrombin depletion by absorption onto fibrin

    - —Natural anticoagulants (antithrombin III, proteins C and S, thrombomodulin)

    —- Activation of fibrinolytic system (dissoves clots)

    - —Clot retraction
    1. —Antithrombin III

    —2. Thrombomodulin

    • 3. —Protein C
    • - Activated by thrombomodulin
    • —- Requires protein S (made by endothelial cells) as cofactor
    • - Both proteins C and S are vitamin K-dependent
    • - Protein C and S deficiency = clotting

    —4. Tissue Factor Pathway Inhibitor


    important enzmyes
    fxn: dissolves clots

    —tPA converts plasminogen to plasmin, which breaks down fibrin to fibrin split products

    —Free plasmin binds to circulating α2-antiplasmin and becomes inactivated

    —Endothelial cells secrete PAIs to abrogate tPA effect
    Extravasation of blood from damaged blood vessel

    —May be external or internal
  49. Hematoma
    accumulation of blood within tissue
  50. hemorrhage: causes

    —Vascular disorders (vasculitis)

    —Platelet disorders (thrombocytopenia)

    —Clotting factor deficiencies

  51. hemostasis and hemorrhage
    • Normal hemostasis is most effective in
    • controlling small vessel bleeding

    —Bleeding from large artery cannot be controlled by body—

  52. hemorrhage in arteries vs veins

    Veins bleed slower than arteries due to lower pressure but also difficult to control
  53. —Hemorrhage: Clinical significance depends on what?
    • - volume and rate of blood loss
    • - site of bleeding
    • - other comorbid conditions

    <20% acute blood loss or a greater loss that occurs slowly may have no clinical significance in healthy adults

    —Patients w/ significant comorbid conditions such as coronary artery disease may not be able to tolerate such blood loss

    —Greater loss may result in hypovolemic shock

    —Small hemorrhages in critical sites, such as pericardium or brain, may be lethal
  54. THrombosis

    what is it?
    Formation of solid mass of blood components in blood vessels or the heart
  55. —Beneficial effects of thrombus
    —Stop exsanguination (blood loss) from external injury

    —Control local hemorrhage
  56. Detrimental effects of Thrombosis
    —Partial or complete obstruction of a vessel with reduced flow causing ischemia to tissues and organs—

    Fragmentation to form an embolus
    describes the three broad categories of factors that contribute to thrombosis

    • 1. endothelial injury
    • - chemical
    • - mechanical
    • - inflammatory

    • 2. alteration in blood flow
    • - turbulence
    • - stasis

    • 3. hypercoaguable states
    • - primary
    • - secondary
  58. Fate of thrombuses
    • 1. resolution
    • 2. embolization to the lungs
    • 3. incorporated to the wall
    • 4. organized and re-canalized
    • 5. propagation towards the heart
  59. embolism
    —Detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin

    —Almost all are fragments of dislodged thrombus
  60. emolism: consequences
    Vascular occlusion with concomitant ischemic necrosis of downstream tissues (AKA infarction)
  61. sites of embolism
    Pulmonary thromboembolism (from venous circulation to lungs)

    —Systemic thromboembolism (from heart or large arteries to distant structures)
  62. systemic embolism: origins
    —Most from mural intracardiac thrombi

    —Ulcerated atherosclerotic plaques, aortic aneurysms, or valvular vegetation comprise remainder

    —Paradoxical embolism rare
  63. site of embolism in systemic embolism
    Lower extremities (75%)

    —Brain (10%)

    —Intestines, kidneys, spleen
    • Gas
    • - —Air (surgical procedures, chest wall injury)

    - Nitrogen (decompression sickness)

    • —Amniotic fluid
    • - Labor & immediate postpartum period

    • —Bone marrow
    • - —Cardiopulmonary resuscitation, trauma

    • —Cholesterol
    • - Atherosclerotic plaques

    • —Fat
    • - Fractures of long bones

    —Foreign bodies

    • —Tumors
    • Atrial myxoma
Card Set:
Histology of Blood Vessels_Fishbein
2014-01-17 04:02:59
Blood Vessel histology
systems 1
Systems: Fishbein Lecture 2.3
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