ARTHRITIS BY balakrishna.

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INTRODUCTION 
Arthritis (from Greek arthro-, joint + -itis,

inflammation; plural: arthritides) is a group of conditions involving damage to the joints of the body. 
The major complaint by individuals who have arthritis

is pain. Pain is often a constant and daily feature of the disease. The pain may be localized to the back, neck, hip, knee or feet. 
There are over 100 different forms of arthritis

TYPES OF ARTHRITIS
RHEUMATOID

SPONDYLITIS

SEPTIC

ARTHRITIS

GOUT
OSTEO

JUVENILE IDIOPATHIC

RHEUMATOID ARTHRITIS .

DEFINITION:  It is a progressive and disabling autoimmune disorder of the synovial lining of the peripheral joints characterized by symmetrical inflammation leading to potentially deforming polyarthritis and a wide spectrum of extraarticular features.  Secondary changes can occur in the bone leading to pain. decreased functioning and even disability. .

Women are approximately 3 times more affected. . There is a strong association with H A-DR4( Human leucocyte antigen DR4. It can attack people of all ages but most common among people between 30 to 50 years. There are about 5 million people with RA in India alone.WHO ARE MOST AFFECTED!!! y RA affects over 21 million people y y y y world wide.

THE OTHER FACTORS INVOLVED IN (RA) ARE AS FOLLOWS: 1. 3.  It is considered as an autoimmune disease in which the body loses its ability to distinguish between synovial and foreign tissue. Environmental factors: such as bacterial and viral infections. 2. Genetic markers: human leukocyte antigen DR4( HLA-DR4) have been associated with triggering inflammatory response in RA. Tumor necrosis factor . IL-1.ETIOLOGY:  The cause of RA is¶nt fully known but appears to be multifactorial. . IL-6 and growth factors propogate the inflammatory process.

4) 5) Antigen.antibody complexes are formed. .PATHOPHYSIOLOGY: The pathogenesis of rheumatoid arthritis occurs via the following steps: 1) Autoimmune antigen presenting cells. 6) Due to phagocytosis mediators of inflammation like cytokines(TNF .IL6) introduced into synovial fluid 7) Pannus formation occurs. macrophages and the dendrite cells ingest. This pannus migrates to the articular cartilage and produce proteolytic enzymes which degrade the cartilage. IL-1. process and present the foreign protein antigen. 2) 3) Lead to the aggregation T-lymphocytes. This causes the infiltration of macrophages and polymorphs into the synovial fluid. This in turn initiates cellular immune response which stimulates differentiation of B-lymphocytes.

8) The cytokines activate osteoclasts which causes the demineralization of the bones. .

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often causing the involved joint to lose its shape and alignment. STAGE 2: Rapid division and growth cells or pannus which causes the synovium to thicken. .STAGES OF RHEUMATOID ARTHRITIS STAGE 1: swelling of the synovial lining causing pain. STAGE 3: The inflamed cells release enzymes that digest bone and cartilage. and swelling around the joint. redness. stiffness. more pain and loss of movement. warmth.

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SYMPTOMS: Malaise Weight loss Periarticular pain Stiffness of multiple joints Depression Dry eyes Fever Myalgias          Anorexia .SIGNS AND SYMPTOMS I.

SIGNS: PARENCHYMATOUS PLEURAL NODULES .

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OTHER SIGNS y Felty¶s syndrome y Pericarditis y Amyloidosis y Skin lesions y Cardiomyopathy .

c. ESR and C-Reactive Protein(CRP):Are markers of inflammation that are elevated in RA but indicate disease severity. The commonly found rheumatoid factors are IgM and IgG. b. a. .DIAGNOSIS I. d. LABORATORY ASSESSM:ENT Rheumatoid Factor: 60% of the people with (RA) will have increased RF. the antinuclear antibody(ANA): is present in 15% patients with RA. Anti-cyclic citrullinated peptide antibodies(anti-CCP): found in most patients with RA.

An MRI study detects proliferative pannus. RADIOGRAPHIC EXAMINATION: A radiograph is a good indicator of the extent of bone erosion and cartilage loss. .II.

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1996. et al. Annu Rev Immunol.RA Is Characterised by Synovitis and Joint Destruction NORMA Synovial membrane RA Inflamed synovial membrane Major cell types: T lymphocytes macrophages Minor cell types: fibroblasts plasma cells endothelium dendritic cells Pannus Cartilage Capsule Synovial fluid Major cell type: neutrophils Cartilage thinning Adapted from Feldmann M.14:397-440. .

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I. arthroplasty(knee replacement. crutches. h) Surgery : arthroscopy. b) Aerobic exercise programs c) Physical activity d) Use of assistive devices like cane. walkers. e) Accupunture f) Thermal therapy g) Patient education including tips on joint protection. osteotomy. NON PHARMACOLOGICAL TREATMENT: a) Diet control and in turn wieght loss. .

EXERCISES y Strengthening exercises .

STRECHING EXERCICES: .

AEROBIC EXERCICES: .

NON STEROIDAL ANTI-INFLAMMATORY AGENTS: NSAID¶S are used for the relief from pain in both rheumatoid and osteo arthritis. Arachidonic acid cyclo oxygenase 1&2 inhibited by NSAIDS prostaglandinG2 Prostacyclin prostaglandin E1 & E2 Thromboxanes INFLAMMATION .PHARMACOLOGICAL TREATMENT: 1.

 NSAID¶s act by direct inhibition of both COX 1 and 2. .. urticaria. COX 1 mainly functions as the physiologic enzyme producing prostaglandins critical for maintaining normal renal function. hepatic dysfunction. GI adverse reactions vary from superficial damage with minor symptoms of dyspepsia. abdominal pain. other ADR¶s include renal impairment. angiodema. gastric mucosa and homeostasis  COX 2 is mainly involved in the inflammation process.  ADR- gastrointestinal complications are the most important adverse reacs. hematological abnormalities. diarrhoea.

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. 3. y A dose of less than 4gms/day is adviced to avoid toxicity. y Hepatotoxicity can occur on taking doses above 4gms daily.2. ACETAMINOPHEN y First line of therapy in the treatment of osteoarthritis also used in the case of rheumatoid arthritis for the relief of pain.OTHER ORAL ANALGESICS y These are considered as a good choice when the patient¶s pain is unrelieved by NSAID¶s or if the patient cannot take NSAID¶s. y It is an excellent analgesic and antipyretic but has very little or no anti- inflammatory activity. y Commonly used oral analgesics are TRAMADOL(50-100mg/4-6hr) OPIATE analgesics like codiene and oxycodone.

4. Intra articular steroid administration effectively relieve pain . increase motility and reduce deformity. Dose is dependant upon the joint size with methyl prednisolone acetate 40mg or triamcinolone hexaacetonide 20mg appropriate for large joints. CORTICOSTEROIDS RHEUMATOID ARTHRITIS: They act by suppressing cytokines and produce rapid improvement of signs and symtoms. Oral prednisolone may be used for temporary relief until DMARD¶s become effective. .

MECHANISM OF ACTION: All DMARD¶s inhibit the action of or reduce the activity of inflammatory cytokines. ‡ Most likely combination is sulfasalazine and methothrexate. DRUG SPECIFIC FOR RHEUMATOID ARTHRITIS: a) ‡ DISEASE MODIFYING ANTI RHEUMATOID DRUGS(DMARDS) These drugs play a major role in the treatment of RA. ‡ Initially monotherapy is given if satisfactory response is not achieved then comination therapy is given. methothrexate. They have a slow onset if actionwith a response to treatment expected in 4-6 months. leflunomides andciclosporins inhibit T-cells .6.

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