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Arthritis
Rheumatoid arthritis is a chronic systemic inflammatory arthritis that affects more women than men between ages 35-45. It is characterized by inflammation of the synovium that leads to cartilage degradation and bone damage. Treatment involves non-drug approaches as well as disease-modifying anti-rheumatic drugs (DMARDs) like methotrexate which are started early to slow disease progression. Biologic agents that target cytokines like TNF have also shown effectiveness. The goal of treatment is to reduce pain and inflammation and prevent long-term joint damage.
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Arthritis
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- 3. Gouty arthritis A systemicdisease caused by deposition of uric acid crystals in the joint and body tissues
- 4. ETIOLOGY Primary Innate defectof purine metabolism or uric acid excretion HYPERURICEMIA Overproduction (10%, >800mg/dL) Impaired renal clearance (90%, <600mg/dL) HGPRT (Hypoxanthine Guanine phosphoribosyltransferase) deficiency PRPP (Phosphoribosyl – 1 pyrophosphate) excess
- 5. ETILOGY Secondary Hematological causes CRF Drug – induced ASA and Salicylates (<2g/day) Cytotoxic drugs Diuretics (except spironolactone) Ethambutol and Nicotinic acid Cyclosporine, INH, L – dopa Ethanol Miscellaneous disorders
- 8. INCIDENCE Higher in men(95%) Onset is at 47 y/o Marked by >7mg/dL serum uric acid Genetic predisposition (10 – 60%) Risk factors Obesity Heavy alcoholics
- 9. Gouty arthritis ASSESSMENT FINDINGS 1.Severe pain in the involved joints, initially the big toe 2. Swelling and inflammation of the joint 3. TOPHI- yellowish-whitish, irregular deposits in the skin that break open and reveal a gritty appearance 4. PODAGRA-big toe
- 10. Gouty arthritis ASSESSMENT FINDINGS 5.Fever, malaise 6. Body weakness and headache 7. Renal stones
- 11. Gouty arthritis DIAGNOSTIC TEST Elevatedlevels of uric acid in the blood (+) monosodium urate crystals Dramatic response to colchicine
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- 14. PATHOPHYSIOLOGY MONOSODIUM URATE CRYSTALS INFLAMMATION TOPH ICOMPLICATIONS •ACUTE TUBULAROBSTRUCTION •UROLITHIASIS •CHRONIC URATE NEPHROPATHY
- 16. ACUTE GOUTY ARTHRITIS Differentials Pseudogout (Ca pyrophosphate dihydrate crystals) Septic arthritis
- 17. TREATMENT 1. Colchicine Initiate within 12 – 36 hrs after attack DOC for ACUTE attack MOA: impairs leukocyte migration and disrupts urate deposition and subsequent inflammation - S/E: GI toxicity, BM toxicity
- 18. THERAPY FOR ACUTEGOUT COLCHICINE PO 1mg 0.5 q 2hrs relief/ GIT discomfort Total : 8mg IV NEVER GIVEN IM OR SQ!
- 19. 2. Indomethacin as effectiveas colchicine but less GI toxicity S/E: GI ulcer and bleeding headache and dizziness (unique) other NSAIDs are also effective
- 20. 3. Corticosteroids - forresistant patients
- 21. THERAPY FOR ACUTEGOUT CORTICOSTEROIDS Intra – articular injections (Methylprednisolone acetate) Systemic corticosteroid therapy C/I NSAIDS, colchicine Oral prednisone IM corticotropin IM Triamcinolone acetonide IV methylprednisolone Taper dose!
- 22. Prophylactic Therapy/Chronic gout 1. Allopurinol(Zyloprim) - xanthine analog - xanthine oxidase inhibitor - major metabolite: oxypurinol - indicated for patients with renal failure, leukemias -S/E: rash, leucopenia, GI toxicity, acute gouty attack with initiation
- 23. 2. Uricosurics - probenecid,sulfinpyrazone - inh. renal tubular reabsorption of uric acid - maintain adequate urine flow, alkalinize urine with NaHCO3 -S/E: GI irritation, rash, acute gout, renal stones
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- 26. NONDRUG Avoid purines! Control weight Avoid alcohol Goodbye meat, organ meats, seafood, beans, peas, asparagus…
- 27. CHRONIC TOPACEOUS GOUT May remain undetectedand untreated for years Development of tophi in pinna of external ear Allopurinol and probenecid
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- 29. DEFINITION and ETIOLOGY OSTEOARTHRITIS(OA) “Degenerative Joint Disease” Chronic cartilage degeneration Most common form of arthritis >55 y/o, M = F, F> M if > 55y/o
- 30. AGING ∀↓ tendon, ligament, musclestrength ∀↓ chondrocytes ∀↓ proteoglycan production AGING ∀↓ tendon, ligament, muscle strength ∀↓ chondrocytes ∀↓ proteoglycan production CHONDROCYTES ∀↓ healing and remodelling cartilage matrix degeneration ∀↓ proteoglycans CHONDROCYTES ∀↓ healing and remodelling cartilage matrix degeneration ∀↓ proteoglycans ↑ IL – 1 and Proinflammatory cytokines ↑ IL – 1 and Proinflammatory cytokines PAIN Osteophytes Synovitis Bursitis Tendonitis PAIN Osteophytes Synovitis Bursitis Tendonitis
- 31. RISK FACTORS Advanced age Femalegender Muscle weakness Obesity Joint trauma Heredity Congenital defects Repetitive stress
- 32. SIGNS AND SYMPTOMS Deep,localized joint pain with rest or immobility Lasts < 30 minutes Mild inflammation Crepitus upon joint movement
- 33. DIAGNOSIS Physical examination Jointtenderness, diminished motion range, crepitus, abnormalities in joint shape Radiography Narrowing of joint space (+) Osteophytes
- 36. TREATMENT NONDRUG Weight reduction Aerobic exercises and physical therapy Devices Avoid prolonged standing, kneeling, and squatting Thermal therapy
- 37. Pharmacologic: 1. Acetaminophen - first-linedrug for pain in OA - dose: 325-650 mg 4x daily S/E: hepatotoxicity 2. NSAIDS
- 38. 3. Capsaicin - extractof red peppers - MOA: release and depletion of substance P from nerve fibers -S/E: burning at site of application
- 39. 4. Glucosamine andchondroitin dietary supplements - shown to alleviate pain, slows down loss of cartilage 5. Corticosteroids - systemic steroids not recommended - intraarticular steroids for local inflammation
- 40. 6. Hyaluronate injection(Na hyaluronate, hylan G-F 20) - reported to decrease pain 7. Narcotic analgesics - for unresponsive patients and those with contraindications to acetaminophen or NSAIDs
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- 42. PATHOPHYSIOLOGY TNF - a TNF - aIL - 1IL - 1 IL - 6IL - 6 GFGF INFLAMME D SYNOVIUM INFLAMME D SYNOVIUM PANNUSPANNUS PROTEOLYTIC ENZYMES CARTILAGE DEGRADATION CARTILAGE DEGRADATION BONE DEMINERALIZATION BONE DEMINERALIZATION OSTEOCLAST ACTIVATION
- 44. PROGNOSIS High RF titer ElevatedESR > 20 joints Early age onset Extra – articular involvement
- 46. Rheumatoid arthritis A typeof chronic systemic inflammatory arthritis and connective tissue disorder affecting more women (ages 35-45) than men
- 47. TREATMENT : NONDRUG Jointprotection Exercises Rest PT and OT Support groups
- 48. First-line 1. Methotrexate - MOA:DHF reductase inhibitor; inhibits cytokine production and purine synthesis - relatively rapid onset (2 to 3 weeks)
- 49. - S/E: GI(stomatitis, nausea, vomiting, diarrhea), hematologic (leukopenia, thrombocytopenia), pulmonary (fibrosis, pneumonitis), hepatic (elevated enzymes, cirrhosis) Teratogenic leucovorin
- 50. 2. Leflunomide (Arava) -inhibits pyrimidine synthesis - S/E: liver toxicity, teratogenic 3. Hydroxychloroquine Inhibit NA synthesis - S/E: diarrhea, blurring of vision, rash 4. Sulfasalazine - S/E: rash, leukopenia
- 51. Less frequently used 1.Gold preparations - aurothioglucose (suspension in oil), gold sodium thiomalate (aqueous solution)- IM - auranofin- oral but less effective than IM Taken up by macrophages,supressing phagocytosis,then lysosomal activity
- 52. S/E: GI (nausea,vomiting, diarrhea), derma (rash, stomatitis), renal (proteinuria), hematologic (anemia, leukopenia) dimercaprol
- 53. 2. Azathioprine - purineanalog converted to 6- mercaptopurine which inhibits DNA and RNA synthesis -S/E: bone marrow suppression, hepatotoxicity, oncogenic
- 54. 3. Penicillamine Analog ofAA cysteine -S/E: rash, metallic taste, hypogeusia (blunting of taste),stomatitis, proteinuria 4. Cyclosporine - decreases production of cytokines - S/E: hypertension, hyperglycemia, nephrotoxicity, tremor, GI intolerance, hirsutism, gingival hyperplasia
- 55. Biologic agents 1. Etanercept(Enbrel) - TNF receptor; binds to and inactivates TNF 2. Infliximab (Remicade) - anti-TNF antibody - combination with MTX is superior than MTX alone - S/E: infections
- 56. 3. Adalimumab (Humira) -anti-TNF antibody - S/E: local injection site reaction, infection 4. Anakinra (Kineret) - IL-1 receptor antagonist
- 57. Treatment 1.NSAIDS Analgesic and anti-inflammatorybut does not slow disease progression 2.Disease-modifying anti-rheumatic drugs (DMARDs) Started within the first 3 months of symptom onset
- 58. SUCCESS is tohave made aSUCCESS is to have made a life breathe easier becauselife breathe easier because you have livedyou have lived.