Histology

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verschaetse23
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160573
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Histology
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2012-06-30 13:29:48
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Histology
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Histology Midterm
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  1. Location of neurons and glia
    CNS
  2. Location of satellite cells and schwann cells
    PNS
  3. Embryonic CT
    Primarily found in umbliical cord

    Randomly arranged, loose and jelly-like
  4. Adult CT
    Primary connective tissue in the body

    • Two types
    •        Loose and dense CT
  5. Special CT
    • Bone
    • Adipose
    • Bone marrow
    • Cartilage
  6. Cardiac muscle fiber
    • Intercalated disks
    • Uninucleated within cell
  7. Skeletal muscle fiber
    Multinucleated on periphery of cells
  8. Physical Stress Theory
    Changes in the relative level of physical stress cause a predictable adaptive response in all biological tissue
  9. Tissue death due to stress
    Very high or very low stress
  10. Mechanisms of injury due to excessive stress
    • High magnitude in brief duration
    • Low magnitude in long duration
    • moderate magnitude with many repetitions
  11. Psychosocial factors
    • Compliance
    • Motivation
    • Socioeconomics
    • Mental status
  12. Extrinsic factors
    • External support devices
    • Footwear
    • Ergonomic environment
    • Modalities
    • Gravity
  13. Psychological factors
    • Medication
    • Pathology
    • Obesity
    • Age
    •        These all make the body less adaptable to stress
  14. Stress
    Normalized load
  15. Strain
    • Normalized deformation
    • Change in length relative to original length
  16. Stress-Strain curve
    • Elastic region
    • Plastic region
    • Yield strength
    • Ultimate strength
    • Fracture strength
    • Strain energy density
  17. Elastic region
    material deforms under imposition of external forces, and returns to original dimensions when unloaded

    • Stiffness is the slope of the elastic region
    •        Steep slope means more stiff
    •        Also refered to as Young's modulus
  18. Plastic region
    • Material deforms under imposition of external forces and does not return to original dimensions when unloaded
    •        Permanent deformation
  19. Ductility
    amount of plastic strain a material can undergo before failure
  20. Yield strength
    Stress or strain at which plastic deformation begins
  21. Ultimate strength
    Maximum stress or strain, beyond which tissue failure occurs
  22. Fracture strength
    Stress or strain at which tissue failure occurs
  23. Strain-energy density
    Area under stress-strain curve that represents the amount of energy absorbed by tissue before failure
  24. Isotropy
    • Material exhibits identical mechanical properties in all directions during loading
    •        No bodily materials are isotropic
  25. Anisotropic
    All bodily tissues are anisotropic
  26. Viscoelasticity
    • Time-dependent response of a material
    •        Deformation inversely related to velocity of loading
    •        The faster you move, the less the tissue gives way
  27. Viscoelasticity (creep)
    Load stays constant, and the shape changes
  28. Viscoelasticity (stress relaxation)
    Decrease in load experienced by a material over time when deformed to a constant length
  29. Fatigue failure
    Failure of a material at a stress level lower than ultimate stress due to repeated loading cycles
  30. Mast cell
    • Releases vasoactive mediators such as histamine and heparin to
    •        1. Increase vascular supply
    •        2. Facilitate edema to dilute toxic substances
    •        3. Attract in immune response
  31. Macrophage
    • Degrade foreign substances or injured tissues by digesting them, and sending these pieces to the cell surface which are known as antigens
    • Cytokines are released to attract plasma cells
  32. Plasma cell
    Secretes antibodies that bind to free antigen in extracellular space
  33. Fibroblast
    Synthesizes proteoglycans and glycoproteins, and precursor molecules for collagen and elastin
  34. Collagen
    Makes up most of the ECM

    Resists tension, not compression
  35. Procollagen
    Packed into the golgie, which is then secreted into ECM

    Once procollagen is seceted, an enzyme comes along to degrade the non-helical end

    This forms a tropocollagen molecule, which then self aggegates and crosslinks to form a tropocollagen array

    This is now collagen
  36. Collagen (Type I)
    • Synthesized by fibroblasts and osteoblasts
    • Provides tensile strength
    • Present in bone, tendon, ligaments, skin, cornea, internal organs, and dentin
    • Accounts for 90% of the bodies collagen
  37. Collagen (Type II)
    • Synthesized by chondrocytes
    • Thinner fibrils than type I
    •        Found in hyaline and elastic cartilage, and intervertebral disks
  38. Collagen (Type III)
    • Synthesized by fibroblasts
    • First collagen synthesized during wound healing, later replaced by type I
    • Present in skin, loose CT in blood vessels, and internal organs
  39. Elastin (found in ECM)
    • Highly elastic recoild after stress
    • Stress strain slope very flat for elastin
  40. Reticulin fibers (found in ECM)
    • Meshwork for fluid passage
    • Common in bone marrow and lymphoid organs
    •        Like a sponge network
  41. Proteoglycans (found in ECM)
    • Gelatinous
    • Source of viscoelasticity
    • various types of glycosaminoglycans (GAGS) linkked to core protein
    • Hydrophilic (resists compression)
  42. Breakdown of ECM
    • Cytokines indicate injury, bring in immune cells, break it down to be resynthesized
    • If collagen, elastin, and other fibers overgrow, it stimulates the breakdown of the matrix
  43. Dense CT
    Tendon
  44. Tendon
    • High collagen:elastin ratio
    • Parallel collagen fiber alignment
    • Transmit muscle force from bone to fascia
    • Shock absorption
  45. Endotenon
    • Surrounds subfibrils, fibrils, and fascicles
    • Minimizes shear forces during gliding of fiber bundles
    • Provides pathway for blood vessels, nerves
  46. Epitenon
    CT capsule covering tendon
  47. Paratenon
    Loose sheath surrounding the whole tendon + fluid
  48. Steroid use and tendons
    The use of steroids degrades tendons
  49. 4 zones of tendon insertion to decrease stress concentration
    • 1. Connective tissue (least stiff)
    • 2. Uncalcified fibrocartilage (avoids breakage)
    • 3. Calcified fibrocarilage (resists shear)
    • 4. Bone (most stiff)
  50. Inflammatory phase of tendon healing
    3-5 days

    • Release of vasoactive mediators by mast cells in ECM
    • Phagocytosis by macrophages and other immune cells

    • Primary goal is to control edema and pain
    •        Most often done thru passive movement
    •        RICE
  51. Proliferative phase of tendon healing
    day 3 up to 8 weeks

    Increased collagen deposition by myofibroblast, scar tissue

    Influx of fibroblasts which synthesize new fibrocartilage material --> begin as Type III to give initial structure and strength, but later changed to type I

    Primary risk is adhesions, so passive ROM is very important
  52. Remodeling phase of tendon healing
    3 weeks - 4 months

    Here, type III collagen is broken down and replaced with type I

    Fibers oriented parallel to direction of stress

    All activity should now be active
  53. Ligament
    High collagen:elastin ration

    Can increase 7% in length before failure

    Has same 4 zones as cartilage
  54. Ligament healing
    Blood clot forms between ruptured cells

    Clot remodeled by fibroblasts (Type III --> Type I)

    After rupture, go thru inflammatory phase

    Ends of clot define borders, if close together do not need surgical intervention
  55. Adaptations of ligaments
    • Increases of stress of 3-4% lead to hypertrophy, with increase in CSA
    •        Above 4% strain, you get injury
    •        The faster the strain, the faster and higher the adaptation
  56. Hyaline cartilage
    Found in articular cartilage of movable joints, and cartilage of the respiratory tract

    Hyaline cartilage is Type II collagen

    Cartilage is avascular and receives nutrients via diffsion

    Purpose is to increase surface area of joint through which load is dispersed

    Primarily loaded in compression
  57. Articular cartilage structure
    • Superficial tangential zone (20%) - collagen (resists shear)
    • Middle zone (50%) resists compression (proteoglycans)
    • Deep zone (30%) (resists tension)
    • Calcified cartilage (anchors to bone)
    • Solid matrix (20-40%) meshwork to hold proteoglycans
    • Water conent (60-80%)
  58. Elastic cartilage
    • A lot of elastin
    • Found in external ear, epiglottis, and auditory tube
    • Made of type II collagen and elastin
  59. Fibrocartilage
    • Very fibrous, dense, and not highly organized
    • Found in intervertebral disks, articular disks of knee, mandible, SC joint, and pubic symphysis

    Made of type I collagen

    Have lower proteoglycan content

    Found anywhere we have disks that withstand high tensile and compressive forces
  60. What do all cartilgae have in common
    Chondrocytes live within lacuane
  61. Interstitial growth
    Chondroblasts form centers of chondrogenesis and divide by mitosis forming daughter cels within the same lacuane
  62. Appositional growth
    Chondrogenic layer of perichondrium (outermost layer) differentiates into chondroblasts which add new layers of cells and ECM to surface of cartilage
  63. Load-bearing properties of cartilage due to interstitial fluid flow through permeable solid matrix
    • Swelling pressure in solid matrix created by expansion of proteoglycan solution
    •        Protein backbone of proteoglycan is hyalurinon formed by GAGS, with lots of ions that repel each other, giveng them a swelling pressure that creates a cushion
  64. During loading in cartilage
    • Stress within collagen matrix
    • Pressure with fluid phase (first to resist load)
    • Frictional drage due to fluid flow (takes energy out)
  65. Healthy cartilage
    Low permability = increased stiffness = better able to withstand compressive loads

    The faster you load cartilage, the less the fluid flows out
  66. Increased deformation in cartilage leads to
    reduction of pore size, meaning less fluid flows out
  67. Cartilage stress-strain curve
    No plastic deformation, has an abrupt rupture at yield point
  68. Cartilage injury
    • In healthy cartilage, collagen matrix bears only 15% of the load
    •        If cartilage tears, fluid flows out and the matrix must pick up the slack, which cauess injury and healing is limited due to avascularity
  69. Cartilage repair
    • Zone 1 - Fibrin
    •       First tissue laid down from blood clot
    • Zone 2 - granulation tissue
    • Zone 3 - fibrous tissue (initially type III then type I)
    • Zone 4 - fibrocartilage
    • Zone 5 - hyaline-like cartilage
  70. Organic matrix organization of bone
    • 35% of matrix
    • Type I collagen (90%)
    • Proteoglycans enriched in chondroitin sulfate
    • Kartin sulfate
    • Hyaluronic acid (primary GAGS in bones)
  71. Inorganic matrix in bones
    • 65%
    • Calcium phosphage forms hydroxyapatite crystals distrubuted along length of collagen fibers
  72. Osteon
    • Osteocytes reside in lacunae, which are spaces surrounded by mineralized bone
    • Lacunae are conncected by canaliculi which transport nutritients
    • Nutrients supplied by blood vessels in haversion canal
  73. Intramembranous ossification
    primary bone tissue deposited by osteoblasts derived from mesenchymal cells in embryo (flat bones)
  74. Endochondral ossification
    Hyaline cartilage templates replaced by bone
  75. Osteogenesis
    • Appositional growth - bone is added between periosteum and lamellae to increase width
    • Resporption/remodeling occurs at endosteal surface
  76. Wolff's Law of bone remodeling
    • Thickness, number, and orientation of trabeculae correspond to quantitative distribution of mechanical stress
    • Greatest strength is along the primary axis of lading
    • Mechanical stress is a necessary stimulus for bone growth
  77. Inflammatory phase of bone
    • 1-5 days
    • Local dammage to marrow and blood vessels
    • Osteocyte death leads to enzymatic ECM degredation
    • Platelets release cytokines/growth factors that are attracted by the hematoma
    • Removal of dead bone done by osteoclasts and macrophages
    • Influx of edema to clear out the damaged tissues
  78. Proliferative phase of bone
    • 4 days to 1-4 months
    • Fibroblasts and capillaries form granulation tissue to bridge gap between fragments
    • Chondroblasts lay down ECM and type II collagen to form a 'soft callus'
    • Osteoblasts synthesize type I collagen and regulate mineralization of matrix into hard callus of spongy bone
  79. Remodeling phase of bone
    • 1-4 months up to 4 years
    • Osteoclasts remove patches of bone from callus which are replaced by mature bone synthesized by osteoblasts
    • Ossification begins at periphery where compressive forces are lowest and proceeds toward center of callus
  80. Epimysium
    Dense CT sheath covering entire muscle
  81. Perimysium
    Sheath covering muscle fascicles
  82. Endomysium
    Delicate sheath of reticular fibers and ECM covering each muscle
  83. Arrangement of muscle fiber
    • Can be arranged in parallel, or series
    • Both increases force of muscle
  84. Sarcomeres
    functional muscle unit
  85. Z disks
    • connect each end of sarcomere on thin filaments
    • Titin connects myosin to Z disks
  86. Muscle contraction of filaments
    During muscle contraction, the myosin pull the actin toward the center and the z disks shorten
  87. A band
    Overlapping of thick and thin filaments
  88. I band
    Thin filaments only
  89. M line
    Represents the alignment of the lateral assembled tails of myosin
  90. Thin filament
    • Actin
    • Troponin
    • Tropomyosin
  91. Actin
    Double stranded helix of globular monomers
  92. Troponin
    • Tn I: inhibits binding of myosin to actin
    • Tn C: Binds Ca2+ to initiate contraction
    • Tn T: binds tropomyosin
  93. Tropomyosin
    • Lies in actin groove
    • Binds Tn T to cover myosin binding site during rest
  94. Thick filament
    • Myosin
    • Titin
  95. Myosin
    • Reversibly binds actin
    • ATPase activity to break cross bridges
    • 2 heavy chains form globular head with 3 binding regions
    • 2 pairs of light chains
  96. Titin
    • Anchors myosin to Z disk
    • Major contributor to passive elasticity of myofibril
  97. Motor unit
    Single motor neuron + all fibers it inervates
  98. Neuromuscular junction (aka motor end plate)
    • Axon terminate in primary synaptic clefts containing receptors which bind ACh released from vesicles in active zones of axon terminal when depolarized
    •        ACH release from cleft then binds to sarcolemma causing T-tubules to release calcium, which is the trigger for contraction
  99. Sliding filament theory
    • Myosin heads bind to actin when Ca2+ is released from SR
    • ATP hydrolysis causes conformational change in myosin head, pulling thin filaments past thick flaments to decrease sarcomere length
    • Cross-bridge cycling continues until membrane depolarization ends and Ca2+ is pumped back into SR
  100. Type I (slow twitch oxidative)
    • Slow ATPase activity (slow twitch)
    • High SD activity (oxidative)
    •        means resistant to fatigue
    • Low alpha-GP activity (non-glycolytic)
    • Low twitch-force and slower rise to peak
  101. Type IIx/b (fast twitch glycolytic, white)
    • Fast ATPase activity (fast twitch)
    •        Allows for fast contraction - also more often found in thicker diameter muscle fibers
    • Low SD activity (non-oxidative)
    • High alpha GP activity (glycolytic)
    • Highly fatigueable, and high twitch-force and faster rise to peak
  102. Type IIa (fast-twitch oxidative, glycolytic)
    • Fast ATPase activity (fast twitch)
    • Intermediate SD activity (oxidative)
    • Intermediate alpha-GP activity (glycolytic)
    • Fatigue resistant
    • Intermediate twitch-force and rise to peak
  103. Mechanical properties
    Muscle that contracts while elongating is less prone to injury because it dissipates energy while elongating
  104. Chronic shortening
    Loss of sarcomeres
  105. Chronic stretch
    Gain of sarcomeres
  106. Disuse of Type I
    Coverts to type II in postural muscles
  107. Type IIx/b --> type IIa
    Conversion with endurance training
  108. Inflammatory phase of muscle
    • Day 1-3
    • Serum enzymes elevated due to fiber necrosis and sarcolemma rupture
    • Phagocytosis of necrotic tissue
  109. Proliferative phase of muscle
    • Begins by day 3
    • Satellite cells = source of myoblasts for muscle fiber regeneration
    • Mitosis stimulated by growth factors released by macrophage
    • CT regeneration by fibroblsats
    • Angiogenesis
  110. NSAIDs
    • Inflammation and pain; arthritis (use)
    • Potent anticoagulant: risk bruising, bleeding, and hemorrhage
    • Supressed cartilage repair and synthesis
  111. Immunosuppresants
    • Organ transplants, autoimmune diseases, neoplasms
    • Risk of infection, decreased bone density, myopathy, bruising, bleeding
    • Peripheral neuropathies may cause weakness in intrisic muscle of hand and feat
    • Delayed healing
  112. Corticosteroids
    • Glucocorticoids (cortison)
    • Mineralcorticoids (aldosterone)
    • Androgens (testosterone)
  113. Glucocorticoids (cortisone)
    Increased protein and CHO metabolism; reduced immune function
  114. Mineralcorticoids (aldosterone)
    Electrolyte and water metabolism
  115. Androgens (testosterone)
    Anabolic function
  116. Adverse effects of prolonged corticosteroid use
    • Reduced collagen synthesis, delayed wound healing, impaired epithelialization
    • Anticoagulation: brusing, bleeding, hematoma
    • Inhibited protein synthesis, weight loss, muscle atrophy (espeically type II), increased intramuscular CT, myopathy, focal myositis, proximal muscle weakness
    • Osteoporosis/osteonecrosis due to inhibited osteoblast collagen synthesis, increased osteoclastic bone resorption
    • Increased tendon strain (biceps, patellar)
  117. Diabetes mellitus
    Cross linking of collagen leads to stiffness
  118. COPD, CHF, CAD, PVD
    Impaired O2 delivery leads to impaired tissue healing
  119. Neurologic impairment
    Impairs rate of neuron firing
  120. Infection
    Delays time to get through inflammatory phase
  121. Poor nutrition
    To build tissues, you need the substrates

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