Arthritis

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Arthritis

  1. 1. AARTHRITIS AND AANALGESICS
  2. 2. GOUTYGOUTY ARTHRITISARTHRITIS
  3. 3. Gouty arthritis A systemic disease caused by deposition of uric acid crystals in the joint and body tissues
  4. 4. ETIOLOGY Primary  Innate defect of 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. 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
  6. 6. 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
  7. 7. 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
  8. 8. Gouty arthritis ASSESSMENT FINDINGS 5. Fever, malaise 6. Body weakness and headache 7. Renal stones
  9. 9. Gouty arthritis DIAGNOSTIC TEST Elevated levels of uric acid in the blood (+) monosodium urate crystals Dramatic response to colchicine
  10. 10. INOSINIC ACID HYPOXANTHINE XANTHINE URIC ACID XANTHIN E OXIDASE XANTHIN E OXIDASE ALLANTOIN URATE OXIDASE METABOLISM PATHWAYMETABOLISM PATHWAY
  11. 11. PATHOPHYSIOLOGY MONOSODIUM URATE CRYSTALS INFLAMMATION TOPH ICOMPLICATIONS •ACUTE TUBULAR OBSTRUCTION •UROLITHIASIS •CHRONIC URATE NEPHROPATHY
  12. 12. ACUTE GOUTY ARTHRITIS  Differentials  Pseudogout (Ca pyrophosphate dihydrate crystals)  Septic arthritis
  13. 13. 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
  14. 14. THERAPY FOR ACUTE GOUT COLCHICINE  PO  1mg  0.5 q 2hrs  relief/ GIT discomfort  Total : 8mg  IV NEVER GIVEN IM OR SQ!
  15. 15. 2. Indomethacin as effective as colchicine but less GI toxicity S/E: GI ulcer and bleeding headache and dizziness (unique) other NSAIDs are also effective
  16. 16. 3. Corticosteroids - for resistant patients
  17. 17. THERAPY FOR ACUTE GOUT CORTICOSTEROIDS  Intra – articular injections (Methylprednisolone acetate)  Systemic corticosteroid therapy  C/I NSAIDS, colchicine  Oral prednisone  IM corticotropin  IM Triamcinolone acetonide  IV methylprednisolone Taper dose!
  18. 18. 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
  19. 19. 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
  20. 20. Gout
  21. 21. Gout
  22. 22. NONDRUG  Avoid purines!  Control weight  Avoid alcohol Goodbye meat, organ meats, seafood, beans, peas, asparagus…
  23. 23. CHRONIC TOPACEOUS GOUT May remain undetected and untreated for years Development of tophi in pinna of external ear Allopurinol and probenecid
  24. 24. OSTEOARTHRITISOSTEOARTHRITIS
  25. 25. 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
  26. 26. AGING ∀↓ tendon, ligament, muscle strength ∀↓ 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
  27. 27. RISK FACTORS Advanced age Female gender  Muscle weakness Obesity Joint trauma Heredity Congenital defects Repetitive stress
  28. 28. SIGNS AND SYMPTOMS Deep, localized joint pain with rest or immobility Lasts < 30 minutes Mild inflammation Crepitus upon joint movement
  29. 29. DIAGNOSIS Physical examination  Joint tenderness, diminished motion range, crepitus, abnormalities in joint shape Radiography  Narrowing of joint space  (+) Osteophytes
  30. 30. TREATMENT NONDRUG  Weight reduction  Aerobic exercises and physical therapy  Devices  Avoid prolonged standing, kneeling, and squatting  Thermal therapy
  31. 31. Pharmacologic: 1. Acetaminophen - first-line drug for pain in OA - dose: 325-650 mg 4x daily S/E: hepatotoxicity 2. NSAIDS
  32. 32. 3. Capsaicin - extract of red peppers - MOA: release and depletion of substance P from nerve fibers -S/E: burning at site of application
  33. 33. 4. Glucosamine and chondroitin dietary supplements - shown to alleviate pain, slows down loss of cartilage 5. Corticosteroids - systemic steroids not recommended - intraarticular steroids for local inflammation
  34. 34. 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
  35. 35. RHEUMATOIDRHEUMATOID ARTHRITISARTHRITIS
  36. 36. PATHOPHYSIOLOGY TNF - a TNF - a IL - 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
  37. 37. PROGNOSIS High RF titer Elevated ESR > 20 joints Early age onset Extra – articular involvement
  38. 38. Rheumatoid arthritis A type of chronic systemic inflammatory arthritis and connective tissue disorder affecting more women (ages 35-45) than men
  39. 39. TREATMENT : NONDRUG Joint protection Exercises Rest PT and OT Support groups
  40. 40. First-line 1. Methotrexate - MOA: DHF reductase inhibitor; inhibits cytokine production and purine synthesis - relatively rapid onset (2 to 3 weeks)
  41. 41. - S/E: GI (stomatitis, nausea, vomiting, diarrhea), hematologic (leukopenia, thrombocytopenia), pulmonary (fibrosis, pneumonitis), hepatic (elevated enzymes, cirrhosis) Teratogenic leucovorin
  42. 42. 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
  43. 43. 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
  44. 44. S/E: GI (nausea, vomiting, diarrhea), derma (rash, stomatitis), renal (proteinuria), hematologic (anemia, leukopenia) dimercaprol
  45. 45. 2. Azathioprine - purine analog converted to 6- mercaptopurine which inhibits DNA and RNA synthesis -S/E: bone marrow suppression, hepatotoxicity, oncogenic
  46. 46. 3. Penicillamine Analog of AA 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
  47. 47. 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
  48. 48. 3. Adalimumab (Humira) - anti-TNF antibody - S/E: local injection site reaction, infection 4. Anakinra (Kineret) - IL-1 receptor antagonist
  49. 49. Treatment 1.NSAIDS Analgesic and anti-inflammatory but does not slow disease progression 2.Disease-modifying anti-rheumatic drugs (DMARDs) Started within the first 3 months of symptom onset
  50. 50. SUCCESS is to have made aSUCCESS is to have made a life breathe easier becauselife breathe easier because you have livedyou have lived.

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