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Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
Osteoarthritis
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Osteoarthritis

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  • 1. OSTEOARTHRITIS Presenter: Robin Gulati
  • 2. CONTENTSAbout OsteoarthritisOccurrencesCausesSymptomsEtiopathogenesisDiagnosisTreatment & Management
  • 3. What is Osteoarthritis? Type of arthritis Caused by the breakdown and eventual loss of the cartilage of one or more joints. Cartilage is a protein substance that serves as a "cushion" between the bones of the joints. Also known as degenerative arthritis.
  • 4.  Osteoarthritis commonly affects:- Hands Feet Spine Large weight- bearing joints, such as the hips and knees.
  • 5.  As defined by the American College of Rheumatology (ACR), OA is a heterogeneous group of condition that leads to joint signs and symptoms which are associated with defective integrity of articular cartilage, in addition to related changes in the underlying bone at the joint margins.
  • 6. OCCURENCES Before the of age 45, osteoarthritis occurs more frequently in males. After 55 years of age, it occurs more frequently in females. Higher incidence in the Japanese population South-African blacks, East Indians, and Southern Chinese have lower rates.
  • 7. Primary osteoarthritis: Have no known cause.Secondary osteoarthritis: When the cause of the osteoarthritis is known.
  • 8. CAUSES: PRIMARY OA AgingWater content of the cartilage increases Protein makeup of cartilage degenerates. Cartilage begins to degenerate by flaking or forming tiny crevasses.
  • 9.  Advanced cases: Total loss of cartilage cushion between the bones of the joints. Repetitive use of the worn joints over the years can irritate and inflame the cartilage, causing joint pain and swelling. Loss of the cartilage cushion causes friction between the bones, leading to pain and limitation of joint mobility.
  • 10.  Inflammation of the cartilage can also stimulate new bone outgrowths (spurs, also referred to as osteophytes) to form around the joints. Can develop in multiple members of the same family, implying a hereditary (genetic) basis for this condition.
  • 11. SECONDARY OACaused by another disease orcondition.Conditions that can lead to secondaryOA include:• Obesity• Repeated trauma or surgery to the joint structures,• Abnormal joints at birth (congenital abnormalities),• Gout• Diabetes• Hormone disorders
  • 12. Obesity: Increases the mechanical stresson the cartilage.The most powerful risk factor, next toaging, for osteoarthritis of the knees.Crystal deposits in the cartilage can causecartilage degeneration and OA.Uric acid crystals cause arthritis ingout, while calcium pyrophosphate crystalscause arthritis in pseudogout.
  • 13. Congenital abnormalities: Vulnerable tomechanical wear, causing earlydegeneration and loss of joint cartilage.Structural abnormalities (Hips): Presentsince birth.Hormone disturbances: Such as diabetesand growth hormone disorders, are alsoassociated with early cartilage wear andsecondary osteoarthritis.
  • 14. SYMPTOMS1. Pain in the affected joint(s) after repetitive use.2. Swelling, warmth, and creaking of the affected joints.3. Pain and stiffness of the joints after long periods of inactivity.
  • 15. 4. In severe OA, complete loss of the cartilage cushion causes friction between bones, causing pain at rest or pain with limited motion.5. Progressive cartilage degeneration of the knee joints can lead to deformity and outward curvature of the knees, which is referred to as being "bowlegged."6. People with OA of the weight- bearing joints (like the knees) can develop a limp. The limping can worsen as more cartilage degenerates.
  • 16. 5. Osteoarthritis of the cervical spine or lumbar spine causes pain in the neck or low back. Bony spurs, called osteophytes, that form along the arthritic spine can irritate spinal nerves, causing severe pain, numbness, and tingling of the affected parts of the body.
  • 17. 6. Formation of hard, bony enlargements of the small joints of the fingers.  The bony deformity is a result of the bone spurs from the osteoarthritis in that joint.7. Appearance of finger nodes  Classic bony enlargement of the small joint at the end of the fingers is called a Heberdens node  Common bony knob (node) occurs at the middle joint of the fingers in many patients with osteoarthritis and is called a Bouchards node.
  • 18. ETIOPATHOGENESIS Cartilage matrix: made up of:- a. Proteoglycans (chondrotin sulfate) b. Glycosaminoglycans (carbohydrates that contain amino sugars found in proteoglycans) c. Chondrocytes d. Collagen
  • 19. 1. Proteoglycans Huge molecules made up of protein and sugars that are woven around and through collagen fibres forming a dense netting inside the cartilage. These molecules make cartilage so resilient that it can stretch and then bounce back when moved. They also trap water molecules much like a sponge.
  • 20. 2. Chondrocytes Special cells sprinkled throughout the matrix. They are the only cells found within the matrix and are continually producing new collagen and proteoglycan molecules. Also responsible for releasing enzymes that dispose off ageing collagen and proteoglycan molecules that have surpassed their usefulness.
  • 21. 3. Collagen Provides elasticity and the ability to absorb shock at the joints. Creates a framework to hold the proteoglycans in place and can be referred to as the "glue" that holds the cartilage matrix together.
  • 22. Abnormal integrin expression Modified chondrocyte synthesisImbalance of destructive cytokines over regulatory factors Degradation of cartilage matrix due to activity of cytokines by increased production of MMP No adequate synthesis of inhibitors Metalloproteinases activated Loss of articular cartilage
  • 23.  A key role is played by cell/extra-cellular matrix (ECM) interactions, which are mediated by cell surface integrins. Integrins modulate cell/ECM signalling, essential for regulating growth and differentiation and maintaining cartilage homeostasis. During OA, abnormal integrin expression alters cell/ECM signalling and modifies chondrocyte synthesis, with the following imbalance of destructive cytokines over regulatory factors.
  • 24.  IL-1, TNF-alpha and other pro-catabolic cytokines activate the enzymatic degradation of cartilage matrix and are not counterbalanced by adequate synthesis of inhibitors. Enzymes involved in ECM breakdown: Metalloproteinases (MMPs), activated by an amplifying cascade. MMP activity is partially inhibited by the tissue inhibitors of MMPs (TIMPs), whose synthesis is low compared with MMP production in OA cartilage.
  • 25.  Intriguing is the role of growth factors such as TGF-beta and others, which do not simply repair the tissue damage induced by catabolic factors, but play an important role in OA pathogenesis
  • 26. DIAGNOSIS No blood test for the diagnosis of osteoarthritis Blood tests are performed to exclude diseases that can cause secondary osteoarthritis. X-rays: Loss of joint cartilage, narrowing of the joint space between adjacent bones, and bone spur formation.
  • 27.  Arthrocentesis (Joint aspiration): Sterile needle is used to remove joint fluid for analysis. Joint fluid analysis is useful in excluding gout, infection, an d other causes of arthritis.
  • 28.  Arthroscopy: A surgical technique whereby a doctor inserts a viewing tube into the joint space to detect the abnormalities of and damage to the cartilage and ligaments.
  • 29.  Careful analysis of the location, duration, and character of the joint symptoms and the appearance of the joints. Bony enlargement of the joints from spur formations: Presence of Heberdens nodes, Bouchards nodes
  • 30. TREATMENT & MANAGEMENT Non-Pharmacological Pharmacological
  • 31. NON-PHARMACOLOGICAL Diet control with weight reduction. Avoiding activities that exert excessive stress on the joint cartilage Rest, exercise, physical and occupational therapy, and mechanical support devices.
  • 32.  Exercise: Strengthens the muscular support around the joints. Prevents the joints from "freezing up" and improves and maintains joint mobility. Helps with weight reduction and promotes endurance.
  • 33. PHARMACLOGICAL Topical analgesics NSAIDS Opioid analgesics Intra-articular injection Surgical Treatment
  • 34. TOPICAL ANALGESICS:CapsiacinFor patients who cannot tolerate systemic therapy.Pain reliefRecommended 4 times dailyLong term adherence: twice daily
  • 35. NSAIDS1. Paracetamol: First choice Divided doses, at regular intervals, with the total daily dose not exceeding 4 g. Should be used with caution in patients who have liver disease and those with a history of excessive alcohol consumption.
  • 36. 2.Cyclo-oxygenase-2-specific inhibitors Aspirin, Acetaminophen, Coxibs, Oxicams Choice between NSAIDs and COX- 2 inhibitors should be made after carefully assessing the risk of serious upper-GI complications and discussing with patients the risk of serious thrombotic cardiovascular events.
  • 37.  For patients with impaired renal function, NSAIDs and COX-2 inhibitors should only be prescribed after very careful consideration. Plasma sodium, potassium and creatinine levels, blood pressure and the presence of oedema should be checked at baseline and regular intervals.
  • 38. OPIOID ANALGESICS Combination of codeine and paracetamol provides better analgesia than paracetamol alone. Nausea, vomiting, dizziness and constipation lead to discontinuation of this combination in up to a third of patients.
  • 39.  Tramadol (centrally acting synthetic opioid) inhibits the reuptake of serotonin and noradrenaline. Generally well tolerated, but is contraindicated in seizure disorders, as it lowers the seizure threshold, and in combination with selective serotonin reuptake inhibitors because of the risk of serotoninergic syndrome.
  • 40. Glucosamine and chondroitin: Glucosamine sulfate (GS) and chondroitin sulfate (CS) are derivatives of glycosaminoglycans found in articular cartilage. Oral GS confirm a 20%–25% reduction in pain in patients with mild to moderate primary knee OA but not so effective in severe cases. GS is contraindicated in seafood allergy. Topical application of GS and CS may be effective in reducing pain from knee OA
  • 41. INTRA-ARTICULAR INJECTION1. Viscosupplementation (Hyaluronate Injections): Hyaluronic acid helps in reconstitution of synovial fluid temporarily improving its elasticity and viscosity and enhancing joint function Given as a weekly intra-articular injection for 3 weeks
  • 42. 2.Glucocorticoids: A modest and short-lived reduction in pain. Some patients have a dramatic and sustained response. Iatrogenic infection is rare if aseptic technique is used. Common side effects include flushing (40%), worsening hyperglycaemia and post-injection flare (thought to be inflammation in response to glucocorticoid crystals). Single joint not be injected more than three times a year.
  • 43. SURGICAL TREATMENT Patients must be medically fit and able to participate in a rehabilitation program postoperatively. Total joint arthroplasty relieves pain and improves function over at least 10 years. Total joint arthroplasties do deteriorate over time, and may require revision. Revision arthroplasty is a more complicated procedure, so arthroplasty may be best postponed in younger patients with OA.
  • 44. HAPPY JOINTSHAPPY HEALTH

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