arthritis
DESCRIPTION
TRANSCRIPT
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AARTHRITIS AND AANALGESICS
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GOUTY GOUTY ARTHRITIS ARTHRITIS
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Gouty arthritis
A systemic disease caused by deposition of uric acid crystals in the joint and body tissues
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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
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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
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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
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Gouty arthritis
ASSESSMENT FINDINGS1. Severe pain in the involved joints, initially the big toe2. Swelling and inflammation of the joint3. TOPHI- yellowish-whitish, irregular deposits in the skin that break open and reveal a gritty appearance4. PODAGRA-big toe
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Gouty arthritis
ASSESSMENT FINDINGS
5. Fever, malaise
6. Body weakness and headache
7. Renal stones
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Gouty arthritis
DIAGNOSTIC TEST
Elevated levels of uric acid in the blood
(+) monosodium urate crystals
Dramatic response to colchicine
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INOSINIC ACID
HYPOXANTHINE
XANTHINE
URIC ACID
XANTHINE
OXIDASE
XANTHINE
OXIDASE
ALLANTOIN URATE OXIDASE
METABOLISM PATHWAYMETABOLISM PATHWAY
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PATHOPHYSIOLOGY
MONOSODIUM URATE CRYSTALS INFLAMMATION
TOPHICOMPLICATIONS
•ACUTE TUBULAR OBSTRUCTION•UROLITHIASIS•CHRONIC URATE NEPHROPATHY
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ACUTE GOUTY ARTHRITIS
Differentials Pseudogout (Ca pyrophosphate dihydrate crystals) Septic arthritis
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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
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THERAPY FOR ACUTE GOUT
COLCHICINE PO
1mg 0.5 q 2hrs relief/ GIT discomfort Total : 8mg
IV NEVER GIVEN IM OR
SQ!
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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
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3. Corticosteroids
- for resistant patients
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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!
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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
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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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Gout
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Gout
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NONDRUG Avoid purines! Control weight Avoid alcohol
Goodbye meat, organ meats,
seafood, beans, peas,
asparagus…
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CHRONIC TOPACEOUS GOUT
May remain undetected and untreated for years
Development of tophi in pinna of external ear
Allopurinol and probenecid
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OSTEOARTHRITISOSTEOARTHRITIS
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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
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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 andProinflammatory cytokines IL – 1 andProinflammatory cytokines
PAIN Osteophytes
SynovitisBursitis
Tendonitis
PAIN Osteophytes
SynovitisBursitis
Tendonitis
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RISK FACTORSAdvanced ageFemale gender Muscle weaknessObesityJoint traumaHeredityCongenital defectsRepetitive stress
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SIGNS AND SYMPTOMS
Deep, localized joint pain with rest or immobility
Lasts < 30 minutes
Mild inflammation
Crepitus upon joint movement
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DIAGNOSIS
Physical examination Joint tenderness, diminished motion range,
crepitus, abnormalities in joint shape
Radiography Narrowing of joint space (+) Osteophytes
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TREATMENT
NONDRUG Weight reduction Aerobic exercises and physical therapy Devices Avoid prolonged standing, kneeling, and
squatting Thermal therapy
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Pharmacologic:
1. Acetaminophen
- first-line drug for pain in OA
- dose: 325-650 mg 4x daily
S/E: hepatotoxicity
2. NSAIDS
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3. Capsaicin
- extract of red peppers
- MOA: release and depletion of substance P from nerve fibers
-S/E: burning at site of application
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4. Glucosamine and chondroitin dietary supplements- shown to alleviate pain, slows down loss of cartilage5. Corticosteroids- systemic steroids not recommended- intraarticular steroids for local inflammation
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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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RHEUMATOIDRHEUMATOIDARTHRITISARTHRITIS
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PATHOPHYSIOLOGYTNF -
a
TNF - a
IL - 1IL - 1
IL - 6IL - 6GFGF
INFLAMMED
SYNOVIUM
INFLAMMED
SYNOVIUM
PANNUSPANNUS
PROTEOLYTIC ENZYMES
CARTILAGE DEGRADATION
CARTILAGE DEGRADATION
BONE DEMINERALIZATION
BONE DEMINERALIZATION
OSTEOCLAST ACTIVATION
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PROGNOSIS
High RF titer
Elevated ESR
> 20 joints
Early age onset
Extra – articular involvement
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Rheumatoid arthritis
A type of chronic systemic inflammatory arthritis and connective tissue disorder affecting more women (ages 35-45) than men
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TREATMENT : NONDRUG
Joint protection
Exercises
Rest
PT and OT
Support groups
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First-line
1. Methotrexate
- MOA: DHF reductase inhibitor; inhibits cytokine production and purine synthesis
- relatively rapid onset (2 to 3 weeks)
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- S/E: GI (stomatitis, nausea, vomiting, diarrhea),
hematologic (leukopenia, thrombocytopenia),
pulmonary (fibrosis, pneumonitis),
hepatic (elevated enzymes, cirrhosis)
Teratogenic
leucovorin
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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
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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
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S/E: GI (nausea, vomiting, diarrhea),
derma (rash, stomatitis), renal (proteinuria),
hematologic (anemia, leukopenia)
dimercaprol
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2. Azathioprine
- purine analog converted to 6-mercaptopurine which inhibits DNA and RNA synthesis
-S/E: bone marrow suppression, hepatotoxicity, oncogenic
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3. PenicillamineAnalog of AA cysteine-S/E: rash, metallic taste, hypogeusia (blunting of taste),stomatitis, proteinuria4. Cyclosporine- decreases production of cytokines- S/E: hypertension, hyperglycemia, nephrotoxicity, tremor, GI intolerance, hirsutism, gingival hyperplasia
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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
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3. Adalimumab (Humira)
- anti-TNF antibody
- S/E: local injection site reaction, infection
4. Anakinra (Kineret)
- IL-1 receptor antagonist
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Treatment1.NSAIDSAnalgesic and anti-inflammatory but does not slow disease progression2.Disease-modifying anti-rheumatic drugs (DMARDs)Started within the first 3 months of symptom onset
Treatment1.NSAIDSAnalgesic and anti-inflammatory but does not slow disease progression2.Disease-modifying anti-rheumatic drugs (DMARDs)Started within the first 3 months of symptom onset
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