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Osteoarthritis

Osteoarthritis. Randa Mahmoud Al-HarizyInternal Medicine departmentFaculty of Medicine, Cairo University. 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

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Osteoarthritis

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    2. Osteoarthritis Randa Mahmoud Al-Harizy Internal Medicine department Faculty of Medicine, Cairo University

    3. 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. 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.

    6. 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.

    7. 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.

    9. 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

    11. Obesity Heredity Gender Hypermobility Osteoporosis Trauma Congenital joint dysplasia Occupation Sport

    12. Primary OA: No known cause Secondary OA Pre-existing joint damage:   RA, Gout, Seronegative 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.

    14. 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.

    16. 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.

    19. 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.

    20. CONSERVATIVE CARE Weight control Appropriate rest and Exercise Physical therapies Occupational therapies

    21. 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

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

    26. 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

    27. 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

    28. 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

    32. 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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