Cjane Padilla

RHEUMATOID ARTHRITIS VS OSTEOARTHRITIS Arthritis Form of joint disorder involving inflammation of one or more joints Forms of Arthritis 1. Osteoarthritis – most common form 2. Rheumatoid arthritis 3. Psoriatic arthritis – related to auto-immune diseases Osteoarthritis Degradation of joints, articular cartilage and subchondral bone Diagnosed through X-Ray Osteoarthrosis – degenerative joint disease Pathophysiology Osteoarthritis begins with damage to articular cartilage through injury, excess joint loading, joint instability or injury causing abnormal loading. Cartilage damage leads to increase in metabolic activity of chondrocytes and cartilage swelling. This hypertropic phase is the first step to cartilage loss. There is increase in synthesis of matrix metalloproteinases (MMPs) as a response to inflammation causing collagen destruction. Chondrocytes undergo apoptosis (programmed cell death) resulting from nitric oxide induction and production of toxic metabolites. This process is a progressive cycle of cartilage destruction and chondrocyte loss. Pathogenic Factors 1. Abnormal stresses biophysical changes Collagen network fracture Proteoglycan unravelling a. Obesity b. Anatomic abnormalities c. Microfractures and bony remodelling d. Loss of joint stability e. Trauma 2. Abnormal Cartilage Biochemical changes Inhibitors reduced Proteolytic enzymes increased a. Aging b. Genetic and metabolic diseases c. Inflammation d. Immune system activity Clinical Manifestation 1. Sharp ache/burning pain 2. Loss of ability 3. Joint stiffness 4. Crepitus – cracking or grating sound in joints 5. Muscle spasms and contractions in the tendons 6. Heberden’s nodes – on the distal interphalangeal joints 7. Bouchard’s nodes – proximal interphalangeal joints 8. Bunions – subluxation of the big toe joint due to mal-alignment of the first metatarsal bone Pain Management 1. Nondrug therapy and in combination with drug therapy a. Nondrug therapy Rest Physical therapy Dietary modification, Assistive devices Patient education b. Analgesics Oral acetaminophen Topical capsaicin Glucosamine sulphate and chondroitin sulphate NSAID, COX2 inhibitors – may use different kinds depending on patient response Opioid analgesics Medications Commonly Used 1. Oral analgesics a. Acetaminophen b. Tramadol c. Acetaminophen/codeine d. Acetaminophen/oxycodone 2. Topical Analgesics a. Capsaicin 3. Nutritional Supplements a. Glucosamine sulphate/Chondroitin sulphate 4. NSAID a. Carboxylic acids – Aspirin, Salsalate, Diflunisal b. Acetic acids – Etodolac, Diclofenac, Indomethacin, Ketorolac, Nabumetone c. Propionic acids – Fenoprofen, Ibuprofen, Ketoprofen, Naproxen, Oxaprozin d. Fenamates – Mefenamic acid e. Oxicams – Piroxicam, Meloxicam f. Coxibs – Celecoxib NSAID – Adverse drug reactions 1. Gastric and duodenal ulcers Patients at high risk of GI complications but need NSAID are recommended to use COX2 selective inhibitor or non selective NSAID in combination with Proton-pump Inhibitor 2. Kidney diseases 3. Hepatitis 4. Hypersensitivity reactions – rashes 5. CNS complaints – drowsiness, dizziness, headache, depression, confusion, tinnitus Drug Interaction Lithium Warfarin Oral hypoglycemics High dose methotrexate Antihypertensives Angiotensin-converting enzyme inhibitors β-blockers Diuretics Topical Therapy 1. Capsaicin – extract of red peppers that causes release and ultimate depletion of substance P from nerve fibers 2. Diclofenac – local inhibition of COX2 enzymes 3. Rubefacients – have modest, short-term efficacy Methyl salicylates Trolamin salicylates Glucosamine and Chondroitin Dietary supplements that stimulate proteoglycan synthesis from articular cartilage CI: shellfish allergy SE: nausea Hyaluronate Injections Temporarily and modest ly increase synovial fluid viscosity and decrease pain Beneficial for osteoarthritis of the knee Short-term and poorly controlled SE: joint swelling, local skin reactions Evaluation of Therapeutic Outcomes 1. ROM (range of motion) for affected joints Flexio, extension, abduction, adduction 2. 50-feet walking 3. Baseline radiograph 4. Ask patients for adverse effects from medications 5. Baseline serum creatinine, hematology profiles, serum transaminases Rheumatoid Arthritis Autoimmune disease resulting in chronic, systemic, inflammatory disorder Primarily affects flexible joints Disabling and painful condition, can lead to loss of functioning and mobility Pathophysiology 1. Dysregulation of humoral and cell-mediated components of the immune system. 2. Immunogloblins (Igs) activate the complement system. 3. Enhance chemotaxis, phagocytosis, and release of lymphokines by mononuclear cells then to T lymphocytes. 4. Rheumatoid factor – antibody found in blood 5. Antigen is recognised on the lymphocyte surface causing activation of T cells producing cytotoxins and B cells producing plasma cells 6. Macrophages release prostaglandins and cytotoxins. 7. Antibodies combined with complement accumulate polymorphonuclear leukocytes that release cytotoxins, oxygen-free radicals and hydroxyl radicals promoting damage to synovium and bone. 8. Histamines, kinins, and prostaglandins are released at inflammation sites, increasing blood flow and permeability for granulocytes. 9. Pannus formation in cartilage and bone surface. 10. Erosion of bone and cartilage, joint destruction. Etiology 1. Genetic 2. Smoking 3. Herpes virus infection – trigger autoimmune disease a. Epstein barr b. Human herpes virus 6 4. Vitamin D deficiency Clinical Manifestations 1. Affect small joints of hands, wrists and feet, elbows, shoulders, hips, knees, ankles. 2. Joint stiffness especially in the morning. 3. Tissue feels soft and spongy. May appear erythematous and warm. 4. Chronic joint deformities. 5. Extra-articular involvement of the rheumatoid nodules, vasculitis, pleural effusions, pulmonary fibrosis, ocular manifestations, pericarditis, bone marrow suppression, and lymphadenopathy. Criteria for Classification 1. Morning stiffness – lasting an hour before improvement 2. Arthritis of 3 or more joint areas – simultaneous swelling 3. Arthritis of hand joints 4. Symmetric arthritis – involvement of same joint areas on both sides of the body 5. Rheumatoid nodules – subcutaneous nodules, over bony prominences, or extensor surfaces or juxtaarticular regions 6. Serum rheumatoid factor 7. Radiographic changes Pharmacologic Treatment DMARD – diseae- modifying anti-rheumatic drug Methotrexate Hydroxychloroquine Sulfasalazine Leflunomide Combination drugs First Line DMARD 1. Methotrexate (MTX) – inhibits cytokine production and purine biosynthesis Teratogenic ADR: GI, hematologic, pulmonary and hepatic CI: pregnancy and nursing women, chronic liver disease, immunodeficiency, blood disorders Dose: 7.5 – 15mg / week Monitoring tests: CBC with platelet, albumin 2. Leflunomide – inhibit pyrimidine synthesis, reducing lymphocyte proliferation and modulation of inflammation Efficacy similar to MTX Dose: 100mg for 3 days, 10-20mg daily Monitoring tests: CBC with platelet 3. Hydroxychloroquine – lacks myelosuppressive , hepatic and renal toxicity Delayed onset of therapeutic effect, up to 6 weeks Dose: 200 – 300mg twice daily, decrease to 200mg once daily after 1-2 months Monitoring tests: Baseline- color fundus photography, ophthalmoscopy, Amsler grid 4. Sulfasalazine – use is limited by adverse effects Anti-rheumatic effect seen in 2 months Take with food and start with low, divided doses to minimize adverse effects Dose: 500mg-1g twice daily Monitoring tests: CBC with platelet 5. Azathioprine Dose: 50-150mg daily Monitoring tests: CBC with platelet, AST 6. Pennicillamine Dose: 125-250mg daily, maximum of 750mg/day Monitoring tests: UA, CBC with platelet 7. Gold salts a. Gold Thiomalate Dose: 25-50mg weekly, IM Monitoring tests: UA, CBC with platelet b. Auranofin Dose: 3mg once or twice daily Monitoring tests: UA, CBC with platelet 8. Minocycline 9. Cyclosporine Dose: 2.5mg/kg/day Monitoring tests: BP 10. Cyclophosphamide Dose: 1-2mg/kg/day Monitoring tests: UA, CBC with platelet 11. Corticosteroids Dose: IM, IV, IA Monitoring tests: Glucose, BP 12. Anti-TNF (tumor necrosis factor) – binds to and inactivates TNF preventing it from interacting with cell surface TNF receptors thereby activating cells a. Etanercept SE: pancytopenia, neurologic demyelinating syndrome Dose: 50mg SC/week Monitoring tests: Tuberculin skin test b. Infliximab SE: risk of URTI, lupus-like syndrome Dose: 3mg/kg IV at 0,2,6 weeks, then every 8 weeks Monitoring tests: Tuberculin skin test c. Adalimumab SE: local injection site reaction Dose: 40mg SC every 2weeks Monitoring test: tuberculin skin test 13. IL-1 (interleukin) receptor antagonist – inhibit release of chemostatic factor and adhesion molecules a. Anakinra SE: