Patho

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jessiekate22
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156603
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Patho
Updated:
2012-06-03 04:37:57
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Osteoporosis MM jt disorders
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two lectures
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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
  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
  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
  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
  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
  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
  25. What are teh chemical agents that have effects on the transmission of messages for mm contraction?
  26. What sensory receptros are present in the mm tendons?
    • - golgi tendon organ- detects tension
    • - mm spindle- detects changes in mm length
  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
  30. What tract controls mm contractions etc?
    • corticospinal tract
  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
  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?
  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
  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
  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?
    • - 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)
  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

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