PATH 20 MUSCULOSKEL DS

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njards
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174382
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PATH 20 MUSCULOSKEL DS
Updated:
2012-09-30 06:48:46
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PATHOLOGY MUSCULOSKELETAL
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Description:
Overview of musculoskel pathology
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  1. Skel fntns:
    • Mechanical: protection for brain / spinal cord / chest organs, rigid internal support for limbs. Mechanical properties relate to specific construction and internal architecture. Although extremely light, bone has high tensile strength. The combination of strength and light wt is a result of hollow tubular shape, layering of bone tissue, and
    • internal buttressing of matrix.

    • Metabolic/ Mineral Storage: principal
    • resovoir for Ca, other ions (P, Na, Mg)

    Haematopoietic: bone is a host for haematopoietic BM   
  2. Osteoclasts
    • Multinucleate giant cells responsible for removal of bone matrix, and are found in surface depressions at bone surfaces referred to as Howship’s lacunae.
  3. Osteoblasts
    • (osteoBlast = osteoBuilder)
    • - produce bone matrix and control its mineralisation

    • The non-mineralised matrix synthesised by osteoblasts is osteoid.
    • When osteoblasts incorpd into bone = osteocytes, and occupy lacunar spaces.
  4. Osteoid
     = non-mineralised matrix synthd by osteoblasts
  5. Woven bone 
    • immature and disorgd precursor of lamellar bone
    • (collagen fibres in the matrix are irregularly arranged)
  6. Lamellar bone 
    has an organised and layered structure (collagen fibres aligned to form lamellae), and represents mature bone
  7. Bones comprise an external ................... and an internal ..........
    comprising ............. and ...............
    an external shell or cortex and an internal medullary cavity comprising cancellous bone and marrow
  8. Cancellous bone is formed by avascular plates - ‘..........
    Cortex is composed of ...................................................
    'trabeculae'

    dense compact cylindrical units (osteons or haversian systems)
  9. OSTEOMYELITIS = ?
    • Infection of bone and marrow
    • Virtually any pathogen
    • Pyogenic bacteria, mycobacteria

    • Classification
    • Aetiological
    • Acute / chronic
    • Routes of infection
  10. Routes of infection
    1) Blood borne (haematogenous)

    2) Secondary to a contiguous focus of extra-osseus infection (Diabetic foot infections, dental)

    3) Direct implantation(trauma, surgery, e.g. joint prosthesis)
  11. Osteomyleitis can occur in .................
    Virtually any bone

    • Site / location dependent on:
    • Route of infection
    • Nature of vascular supply

    and there are Age related differences
  12. Haematogenous Osteomyelitis
    • Paediatric
    • Staph. aureus most common > 3 yrs
    • Metaphyseal regions (high vascular flow)
    • Femur, proximal tibia and humerus, distal radius

    • Neonatal
    • Often also involves adjacent joint
    • Staph. aureus, group B strep., E.coli.

    • Adults
    • Spread probably via periosteal vessels cortex long bones / flat bones, eg vertebra

    • IV drug users
    • spine or pelvis, unusual sites
  13. Direct Introduction Pathogens
    Most commonly affects bones prone to injury (least covering): phalanges, tibia and forearm bones

    Often polymicrobial

    Compound / comminuted fractures, puncture wounds iatrogenic infection (after internal fixation, joint replacement)
  14. Haematogenous Osteomyelitis
    • Bacteria lodge in marrow
    • Trauma - ?
    • predisposing factor(with stasis / thrombosis)
    • Acute inflammatory response
    • Increased intracompartmental pressure


    bact in bone...divide & prolif.....inflam response.....swell....no where to go....pressre increases......vasc flow decreases......death of bone and marrow
  15. Clinical Aspects of haematogenous osteomyelitis
    • Paediatric : local pain and fever
    • Plain X-rays : often initially normal
    • Intense uptake isotope scans
    • MRI detects abnormality quicker
    • Conclusive diagnosis : identification of organism
    • Blood cultures +/- from lesion itself
  16. Haematagenous osteomyelits outcome:
    Determined by:

    • anatomic location
    • host response / “resistance”
    • the number / virulence of pathogens
    • effectiveness of therapy
  17. Osteomyelitis Ideal Outcome:
    • Resolution and repair
    • Sequestrum resolved
    • Organisms dealt with
    • Defect fills with granulation tissue
    • Ossification + healing
  18. Chronic osteomyelitis (what can go wrong)
    • Inadequate host response
    • Inadequate antibiotic therapy
    • Inadequate removal of sequestrum
  19. Chronic Osteomyelitis
    • Sequestrum, bacteria persist within non-healing cavity. 
    • Infection may gradually spread beyond involucrum into soft tissues: sinuses

    • Rare complications:
    • Malignant Transformation (SCC)
    • Amyloid
  20. Walled off, localised abscess in bone
    Brodies abscess
  21. Chronic Recurrent Multifocal Osteomyelitis
    • = clinical entity distinct from bacterial osteomyelitis.
    • -Autoinflam disorder, bactl culture usu negative
    • -Kids and adolescents
    • - bone pain and fever prolonged, fluctuating course
    • - often multifocal, most often in tubular bones, clavicle
    • - less frequently the spine and pelvis

    • X-ray appearance suggests subacute or chronic osteomyelitis
    • Biopsy and laboratory findings are nonspecific
    • Aetiology is largely unknown
  22. Tuberculous Osteomyelitis
    • Spread from focus of active visceral disease (usu lungs)
    • Sites : spine, hip and knee (immunocompromised: often multifocal)
    • Chronic granulomatous reaction
    • No raised intracompartmental pressure
    • Little reactive new bone
    • Extension through bone + periosteum into soft tissue and joints
  23.  Potts disease
    • = Tuberculous Osteomyelitis in Spine
    • Collapsed vertebrae, angulation, often kyphosis, extension across and destruction of discs, cord compression, meningitis, thoracic, lumbar psoas frequently affected, ‘cold’ abscess

    • Tuberculous Osteomyelitis can also occur in:
    • Hip / knee destruction of subchondral bone, narrowing of joint space, ankylosis
    • Spinal TB
    • Anterior vertebral elements
    • Destruction vertebral end plate
    • Spread across intervertebral discs
    • Involvement of adjoining vertebral bodies
    • Cold abscesses paravertebral tissues / psoas
  24. Joint Infxn mechnsms:

    • - Blood borne infection of synovium
    • - Extension of an adjoining focus of infection e.g. osteomyelitis
    • - Direct inoculation(trauma/operative)

    • Acute septic arthritis is a medcl emergncy
  25. Acute Septic Arthritis
    • Acute non-gonococcal septic arthritis = medical emergency Early diagnosis, rapid and aggressive therapy
    • Dx - Aspiration and appropriate culture
    • Can lead to significant morbidity (stuffed joints) and mortality
    • Even with prompt diagnosis and treatment, high morbidity rates
  26. Septic Arthritis: Neonates and infants
    • Febrile illness
    • Hip, knee and ankle - usually monoarticular
    • Cartilage readily destroyed
    • Staph aureus, strep, H. influenzae, Gram negative rods
  27. Septic Arthritis Adults
    Traumatic chronic inflammatory arthritides(+/-) immunocompromised

    Iatrogenic joint injection / aspiration / prosthetic joint replacements
  28. Septic Arthritis
    • Swollen, red, warm, painful joint
    • Fever, raised WCC
    • Acute inflammatory reaction
    • joint capsule and synovium = swelling + effusion
    • histol, looks same as other inflam/infxn..eg pimple.
  29. Synovial Fluid Examination
    • Normal: 
    • small volume
    • clear
    • 200 WBC/mL
    • <25 PM's
    • culture negative

    • Septic/bacterial
    • small volume
    • turbid/ yellow/green
    • 100,000 WBC/mL
    • >90 PM's
    • culture positive
  30. Tuberculous Arthritis
    • Large joints
    • Haematogenous spread to synovium
    • Chronic granulomatous inflammatory process
    • Destroys articular cartilage and subchondral bone
    • Joint destruction - fibrous ankylosis

    • Chronic swelling and effusion
    • Few acute signs of inflammation
    • Loss of range of motion
    • Formation of draining sinuses
  31. Fracture
    • = a discontinuity. 
    • Types:

    • Complete
    • Incomplete (greenstick)
    • Simple / closed
    • Open / Compound
    • Comminuted
    • Stress
  32. Fracture Healing
    • The principal factors that affect healing are:
    • 1) Wound immobilisation
    • 2) Vascular supply
    • 3) Presence of infection
    • 4) Physical stress
  33. The ideal situation for fracture healing:
    • Good vascular supply
    • Minimal necrosis
    • Precise anatomical reduction
    • Immobilisation
    • Absence of infection
  34. Bad for fracture healing:
    • Infection
    • Vascular compromise
    • Malignancy
    • Systemic disease
    • Persistent/excessive motion
    • Cleft / non-union
    • ‘pseudoarthrosis’ forms
    • Excessive gap / poor reduction - Fibrous union

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