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  1. What is the function of a bone?
    • - support, framework and protection
    • - hematopesis (bone marrow)
    • - involved in Ca metabolism and storage
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  2. What is the bone structure?
    • - Bone matrix- haversian system are made up of collagen fibres and Ca phosphate salts, containing blood vessels
    • - Bone Cells- osteoclasts (destroy old bone tissue), osteoblasts (create new bone matric), osteocytes (former osteoblasts- controlling/signalling function
  3. What is bone remodelling?
    • - bone reabsobed (osteoclasts)
    • - new bone formation (osteoblasts)
    • - bone may or may not change its density and thickness
    • - purpose: repair micro damage; supply calcium to serum
    • in adults- equilibrium; in
    • in children- formation > resorbtion
    • Aging- bone loss accentuated (resorbtion> formation)
  4. How is bone remodelling controlled?
    • - mechanical stress (weight bearing or mm contraction); osteoblastic vs osteoclastic activity
    • - hormones: lengthening via growth plate- growth hormone and sex hormone: parathyroid hormone or cortisol
    • - RANK ligand
    • - Osteoprotegerin
  5. What is local tissue signalling factors?
    • - rank ligand- RANKL- a regulatory cytokine expressed by osteoblasts. It bins to RANK receptor on osteoclast and activates them. RANKL overproduction> degenerative bone disease
    • -osteoprotegerin- OPG- a glycoprotein decoy receptor to which RANKL binds and thereby prevents RANKL binding to RANK
    • - bone remodelling
  6. How does bone grow?
    • - chondrocytes (produce cartilage)
    • - osteoblasts (produce bone matric and facilitate its mineralization
    • - action of GH on bone is indirect, via IGF-1. By binding to its specific recptor, IGF- 1 causes mitogenic effects in chondrocytes (hypertrophy and proliferation), activated osteoblasts and inhibits of osteoclasts.
  7. What happens after bone fracture?
    • 1. mechanical strain
    • 2. breaking the bone and damage to blood vessels
    • 3. bleeding
    • 4. hematoma and inflammation

    • Stages of bone healing:
    • - hematoma
    • - granulation
    • - procallus
    • - bony callus
    • - remodlling
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  8. Which factors affect healing after bone fracture?
    • Amount of damage
    • Age
    • Infection
    • Systemic disease affecting circulation (eg diabetes)
    • Mm spasm
  9. What are possible complications of bone fractures?
    • Ischemia
    • compartment syndrome (compresion of nerve, blood vessels, and mm tissue> lack of O2> tissue death)
    • Fat emboli
    • Nerve damage
  10. What os osteoporosis?
    • - metabolic disorder, when bone resorbtion exceed bone formation.
    • - causes decrease in bone matric and mineralization
  11. What are the forms of osteoporosis?
    • - primary- postmenapausal, senile, idiopathic
    • - secondary-following other condition (eg crushing syndrome)
  12. What are the risk factors of osteoporosis?
    • Age- decrease osteoblastic activity
    • decrease mobility- decrease mechanical stress stimulus
    • Hormonal- hperparathyroidism, crushing syndrome, catabolic glucocoricoids
    • nutrients- decrease calcium, vit D, protein, malabsorption sndromes
  13. What are some of the clinical features of osteoporosis?
    • - normal boney density 833mg/cm2- osteopenia 833-648, osteoporotic <648
    • - back pain
    • - kyphosis/ scoliosis- fractures- haunch
  14. How do you manage osteoporosis?
    • - increase Ca and Vit D intake
    • - exercise
    • - inhibitors of bone resorbtion
    • - hormonal therapy
  15. What are ricets and osteomalacia?
    - both are metabolic bone disorders that are expressed as reduced bone mineralization
  16. What is the main cause of rickets and osteomalacia?
    • - dietary problems
    • - malabsorption
    • - lack of sun exposure
  17. What is the process of ricket/ osteomalacia?
    • - deficit Ca/ phosphates/ vit D
    • - lack of bone mineralisation
    • - soft bones
    • -deformations and low heigh in children
    • - vit D is needed for absorbtion of Ca in the intestin
    • NOTE- osteomalacia is the same disorder in adults- soft bones- compression fractures
  18. Skeletal mm structure
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  19. What is the composition of myofilaments, and how do they work?
    • - thin filaments contain proteins- actin, tropomyosin, troponin- they are attached to the Z line
    • - thick filaments- contain myosin
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  20. What is the neural control of skeletal mm?
    • - motor unit is the smallest functional unit for movements. It consists from a single alpha motorneuron, its axon plus all mm fibres inervated by this neuron
    • - alpha motoneuron- in the ventral horn of the spinal cord- ventral root
    • - Motorneuron pool is a group of neurons (a column) that innervate one mm
  21. What is the neuromm junction?
    • - is a synapse between the motorneuron axon terminal and the mm fibre
    • - arrival of electrical pulse (AP) along the motor neuron axon to the terminal causes release of neurotransmitters
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  22. What are the synaptic vessels at the nerve end terminal filled with?
    Ach- acetilcholine
  23. What activates ACh?
    • cholinesterase
    • this then allows pores to open and the AP to be transmitted
  24. Phasic and tonic mm contractions
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  25. What are teh chemical agents that have effects on the transmission of messages for mm contraction?
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  26. What sensory receptros are present in the mm tendons?
    • - golgi tendon organ- detects tension
    • - mm spindle- detects changes in mm length
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  27. What is a reflex?
    • - response to sensory stimuli without participation/ contribution of consciousness
    • - knee (patellar) reflex:
    • 1. Reflexes are elementary acts of behaviour
    • 2. Stimulating of given input produces determined and predicted output
    • 3. Performed without conscious control. Reflexes vs voluntary responses: in reflex, afferent input strictly determines output; no contribution of will
  28. Which areas of the brain control skeletal mms?
    • - primary motor cortex (M1/Area 4)- precentral gyrus (aussie walter campbell)
    • - - precentral gyrus is the motor cortex (wilder Penfield demo via small electrical currents being put into the cortex resulting in twitching around the body
  29. High motor control- corticospinal (pyramidal) pathways
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  30. What tract controls mm contractions etc?
    • corticospinal tract
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  31. What is mm dystrophy?
    - a group genetic disorder that manifests as degneration of skeletal mm
  32. What causes mm dystrophy?
    • - mutations in dystrophin gene
    • - dystrophin is a protein located in the membrane of mm fibres. Essential for maintaining cell shape and survival
  33. What is the pathogenesis of mm dystrophy?
    • - lack of dystropin
    • - degeneration and necrosis of mm cells
    • - mm cells replaced by fat and fibrous connective tissue
    • - mm weak or cannot contract
  34. Mm dystrophy
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  35. What are the clinical signs of mm dystrophy?
    • - mm weakness
    • - tendon reflexes reduced
    • - vertebral deformities
    • - respiratory insufficience > lung infection
    • - cardiac abnormality
    • - mental retardation

    Death usually before 20 due lung and heart failure
  36. What is upper/ lower motor neurone dyndrome?
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  37. How are jts classified and what are the three types?
    • - classified by the degree of movement
    • - synarthroses- immovable (eg cranial sutures)
    • - Amphiarthroses- slightly movable (eg ribs to sternum)
    • - siarthroses (synovial)- freely movabble (shoulder)
  38. What is the structure of a synovial jt?
    • - articular cartilage- covering over ends of bones (very smooth, slippery surface)
    • - Synovial membrane- produces synovial fluid (lubricant) which fills the space between ends of bone
    • -articular capsule- consists of synovial membrane and a fibrous capsule
    • - ligament- reinforce capsule, links bones, supports jt
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  39. What are non-traumatic jt injuries?
    • - overuse injuries such a tennis elbow
    • - repetitive strain injuries (carpal tunnel syndrome)
  40. What are traumatic jt injuries?
    • - jt dislocation
    • - injuries of tendons and ligaments
  41. What is the pathogenesis of jt injuries?
    trauma- inflammation- granulation tissue- collagen fibres- fibrous tissue
  42. What are the classifications of tendon and ligament injuries?
    • - strain- tear in a ligament
    • - sprain- tear in a tendon
    • - avulsion- detachment from a bone
  43. What are the causes and signs and symptoms of lig and tendon injuries?
    - traumna or excessie mm force

    - pain, swelling, limited movements

    - low blood to area- > 6w to heal
  44. What is osteoarthritis?
    • - degenerative jt disease
    • - cause unknown- possibly genetic
  45. What is the pathophysiology of osteoarthritis?
    • - articular cartilage is damaged
    • - surface of cartilage becomes rough and worn
    • - tissue damage causes release of enzymes, accelerating damage of cartilage
    • - subchondral bone my be exposed
    • - osteophystes (bone spurs) develop and may break off
    • - jt cleft becomes narrower
    • - secondary inflammation of surrounding tissue
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  46. What are the signs and symptoms of osteoarthritis
    • - aching pain with Wb and movement
    • - jt movement is limited
    • - activites become limited due to pain
  47. What will OA of the spine result in?
    • scoliosis
    • - asymmetric disk space as well as the larger osteophytes which develop in attempt to bear the weight of the body
  48. What is rheumatoid arthritis?
    - chronic systemic inflammatory disease that affects jts
  49. What are the causes of RA?
    - unknown- autoimmune mechanism is well established: formation of rheumatoid factor (RF)- an auto- antibody againt Ig G
  50. What is the patho of RA?
    • ?- activation of synovial macrophages and fibroblasts
    • this results in the release of enzymes, acitvation and proliferation of chondrocyres and synovical cells, activation of osteoclasts
    • activation of B lymphocytes (release of RF= deposition of immune complexes in jt

    • All result in:
    • -synovitis- marked unflam, cell proliferation
    • - pannus formation- granulation tissue spreads
    • - cartilage erosion- created an unstable jt
    • - fibrosis-calcifies and obliterates jt space
    • - anklyosis- jt fixation and deformity
  51. What are the pathologic changes in jt of RA?
    • Image Upload- boney deformities
    • - ankylosis of jt
    • - ulnar drift
  52. What are the signs and symptoms of RA?
    • local:
    • - affected jts extremely painful
    • - stiffness of jt (especially in the morning)
    • - redness and swelling of jts
    • - jt involvement includes small jts and if often bilateral
    • - jt movement impaired
    • - eventually jt becomes fixed and dformed
  53. What are the systemic signs and symptoms of RA?
    • - fatigue
    • - mild fever
    • - anorexia
    • - generalised lymphadenopathy
  54. What is juvenile RA?
    • - different from adult form
    • - more acute onset
    • - large jts frequently afftected
  55. What are teh three types of JRA?
    • - stills disease (systemic form)- fever, rash, lymphadoenopathy, hepatomegaly, in addition to jt involvemnt
    • - second form of JRA causes polyarticular inflammtion
    • - third form of JRA- four or fewer jts but causes uveitis (inflammation of iris, ciliary body and choroid of eye)
  56. What is infectious (septic) arthritis?
    - infection of a jt that in turn causes arthritis
  57. What are the causes of infectious septic arthritis?
    • - diret introduction of bacteria into jt eg trauma, non sterile injection or surgery
    • - secondary infection due to bacteremia
    • - gonococcus, staphylococcus, spirochete (lymes disease (tick bite)
    • - usually dvelops in single jt
    • - jt is red, swollen, painful and decreased movement
  58. What is the pathogenesis of gout? (gouty arthritis?)
    • - genetic factor (eg deficit of enzyme uricase) or poor renal excretion of urea
    • - hyperurycemia
    • - deposists of uric acid crystals in a jt
    • - inflammation
  59. What are some clinical feature of gouty arthritis?
    • - intermittent course of disease
    • - formation of tophus (nodule of precipitated urate crystal- in soft tissue causes local inflammtion, in jt bursae- extensor surface of forearm, pinnae of ear )
    • - oftenaffects singe jt eg big toe
  60. What is ankylosing spondylitis?
    • - stiff, vertebra
    • - cause is unknow (possibly autoimmune/ genetic)
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  61. What is the pathogenesis of ankylosing spondylitis
    • - inflam of vertebral jts
    • - fibrosis of jt, calcification and fusion of vertebra
    • - lack of movement in the spine
  62. What are the signs and symptoms of ankylosing spondylitis?
    • - back pain and stiffness (initally lower back)
    • - with progression- lack of movement of the spine
Card Set:
2012-06-03 08:37:57
Osteoporosis MM jt disorders

two lectures
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