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Osteoarthritis

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Osteoarthritis Randa Mahmoud Al-Harizy Internal Medicine department Faculty of Medicine, Cairo University OA is a group of diseases and mechanical abnormalities ... – PowerPoint PPT presentation

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Title: Osteoarthritis


1
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Osteoarthritis
  • Randa Mahmoud Al-Harizy
  • Internal Medicine department
  • Faculty of Medicine, Cairo University

3
OSTEOARTHRITIS
  • OA is a group of diseases and mechanical
    abnormalities entailing degradation of joints,
    including articular cartilage and the subchondral
    bone next to it
  • OA is derived from the Greek word ostoe,
    meaning of the bone, arthro, meaning joint,
    and itis, meaning inflammation

4
DEFINITION
  • There is no simple definition of OA as it
    requires consideration of three overlapping areas
    - pathological changes, radiological features and
    clinical consequences. Pathologically, there is
    an alteration in cartilage structure,
    radiologically there are osteophytes and joint
    space narrowing, and clinically some patients
    complain of pain and disability.

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EPIDEMIOLOGY
  • Osteoarthritis is the most common type of
    arthritis.
  • The prevalence increases with age
  • 80 of people over 60 years will have some
    radiological evidence of it, although only 60 of
    those will show symptoms.

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  • O.A.
  • Women over 55 years are affected more commonly
    than are men of a similar age.
  • There is a familial pattern of inheritance
  • The resulting disabilities have major
    socio-economic resource implications,
    particularly in the developed world.

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AETIIOLOGY
  • In OA, a variety of potential forces hereditary,
    developmental, metabolic and mechanical may
    initiate processes leading to loss of cartilage.
  • Subchondral bone may be exposed and damaged, with
    regrowth leading to a proliferation of
    ivory-like, dense, reactive bone in central areas
    of cartilage loss, a process called eburnation.
  • The patient experiences pain upon weight bearing
  • Due to decreased movement from pain, regional
    muscles may atrophy and ligaments may become more
    lax

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PREDISPOSING FACTORS
  • Obesity
  • Heredity
  • Gender
  • Hypermobility
  • Osteoporosis
  • Trauma
  • Congenital joint dysplasia
  • Occupation
  • Sport

12
CAUSES
  • Primary OA No known cause
  • Secondary OA
  • Pre-existing joint damage   RA, Gout, Seronegativ
    e spondyloarthropathy, Septic arthritis, Paget's
    disease, Avascular necrosis, e.g. corticosteroid
    therapy 
  • Metabolic disease Chondrocalcinosis, Hereditary
    haemochromatosis, Acromegaly 
  • Systemic diseases Haemophilia- recurrent
    haemarthrosis, Haemoglobinopathies, e.g. sickle
    cell disease, Neuropathies

13
  • CLINICAL PICTURE
  • OA commonly affects the hands, feet, spine and
    the large weight bearing joints such as hips and
    knees
  • Symptoms
  • Joint pain
  • Joint gelling (stiffening and pain after
    immobility)
  • Joint instability
  • Loss of function.

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  • CLINICAL PICTURE
  • Signs
  • Joint tenderness
  • Crepitus on movement
  • Limitation of range of movement
  • Joint instability
  • Joint effusion and variable levels of
    inflammation
  • Bony swelling
  • Wasting of muscles.

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DIAGNOSIS
  • Investigations in OA
  • Blood tests. There is no specific test the ESR
    and CRP are normal. Rheumatoid factor and
    antinuclear antibodies are negative.
  • X-rays are abnormal only when the damage is
    advanced.
  • MRI demonstrates early cartilage and subchondral
    bone changes.
  • Arthroscopy reveals early fissuring and surface
    erosion of the cartilage.

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TREATMENT
  • Generally speaking, the process of clinically
    detectable osteoarthritis is irreversible, and
    typical treatment consists of medication or other
    interventions that can reduce the pain of OA and
    thereby improve the function of the joint.

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CONSERVATIVE CARE
  • Weight control
  • Appropriate rest and Exercise
  • Physical therapies
  • Occupational therapies

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  • DIETARY TREATMENT
  • Glucoseamine, chondroitin sulphate, antioxidants,
    others
  • SPECIFIC MEDICATIONS
  • Paracetamol
  • NSAIDs
  • COX-2 selective inhibitors
  • Corticosteroids

22
OTHERS
  • Implantation of chondrocytes
  • Local injection of hyaluronic acid
  • Topical treatment
  • Surgical treatment
  • Acupuncture

23
Crystal Deposition Disease
  • GOUT
  • Definition
  • Gout is a disease which is characterized by
    tissue deposition of monosodium urate crystals
    (MSU) due to hyperuricaemia that results in
  • Gouty arthritis
  • Tophi
  • Gouty nephropathy
  • Uric acid nephrolithiasis

24
ETIOLOGY
  • 1- Overproduction of urate
  • Endogenous
  • Hyperactivity of phosphoribosylpyrophosphate
    (PRPP) synthetase
  • Partial deficiency of hypoxanthine guanine
    phospho-ribosyltransferase (HGPRT)
  • Myeloproliferative and lymphoproliferative
    disorders
  • Hemolysis
  • Psoriasis
  • Exogenous
  • Excess dietary purine consumption meat, liver,
    kidney, sea food, legumes, mushrooms

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Underexcretion of Urate
  • Renal disease
  • Lead intoxication
  • Hyperparathyroidism
  • Hypothyroidism
  • Drugs
  • Low dose aspirin
  • Diuretics
  • Ethambutol
  • Pyrazinamide
  • Cyclosporine
  • Alcohol

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CLINICAL PICTURE
  • 1- Asymptomatic hyperuricemia
  • 2- Acute gouty arthritis
  • - precipitating factors excess dietary purines,
    alcohol, drugs, surgery, trauma, dehydration
  • - typically affected joints of lower limb more
    commonly than that of upper limb the first
    metatarsophalangeal joint of big toe, the
    tarsals, ankles, heels, knees, wrists and fingers
    in a descending order
  • Presentation early in the course of the disease
    is monoarticular, of acute onset, often during
    night. The affected joint is exquisitely painful,
    warm, red and swollen. Subsequent attacks become
    polyarticular and persist longer

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CLINICAL PICTURE
  • 3- Intercritical gout asymptomatic intervals
    between the acute attacks
  • 4- Chronic tophaceous gout development of
    subcutaneous nodules of deposits of monosodium
    urate crystals

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INVESTIGATIONS
  • Serum level of uric acid may be elevated
  • Synovial fluid analysis for
  • Cells 25.000 100.000 leukocytes/mm3
  • Polarized microscopy of the synovial fluid
    reveals the typical needle shaped negative
    birefringent crystals
  • Radiology soft tissue swelling, punched out bone
    erosions

29
TREATMENT
  • During the acute attack
  • NSAIDs indomethacin , Colchicine, ACTH,
    Intraarticular steroids, systemic corticosteroids
  • Treatment of chronic tophaceous gout
  • Xanthine oxidase inhibitor (allopurinol)
  • Uricosuric drugs probenecid
  • Diet control

30
PSEUDOGOUT
  • Definition
  • Pseudogout is an inflammatory arthropathy
    resulting from deposition of calcium
    pyrophosphate dihydrate crystals (CPPD) in and
    around joints that results in calcification of
    articular cartilage (chondrocalcinosis)

31
Conditions associated with pseudogout
  • Hyperparathyroidism
  • Haemochromatosis
  • Osteoarthritis
  • Hypothyrodism
  • Neuropathic arthropathy
  • Idiopathic
  • Familial

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Clinical picture
  • Acute pseudogout
  • Acute monoarthritis especially affecting knee,
    ankle, wrist or shoulder. Surgical procedures and
    acute medical illness may precipitate the attack
  • Chronic pseudogout
  • Presenting as osteoarthritis but distinguished
    from it by the involvement of atypical joints as
    wrists and metacarpophalangeal joints

33
INVESTIGATIONS
  • SYNOVIAL FLUID ANALYSIS FOR
  • Cells 25.000 100.000 leukocytes/mm3
  • Polarized microscopy of the synovial fluid
    reveals the typical rhomboid shaped positive
    birefringent crystals
  • RADIOLOGY
  • Chondrocalcinosis with evidence of calcification
    of fibrocartilage as menisci, symphisis pubis and
    triangular cartilage of the wrist

34
TREATMENT
  • NSAIDs
  • Joint aspiration
  • Intraarticular injection of steroids

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THANK YOU
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