Rheumatoid arthritis ppt by ann..

RHEUMATOID ARTHRITIS -

1. RHEUMATOID ARTHRITIS PRESENTED BY ANJALI RARICHAN M.PHARM 1 ST YEAR

2. CONTENTS DEFINITION OVERVIEW ETIOLOGY PATHOPHYSIOLOGY CLINICAL FEATURES DIAGNOSIS TREATMENT ALGORITHM

3. DEFINITION Rheumatoid arthritis (RA) is a chronic and usually progressive inflammatory disorder of unknown etiology characterized by polyarticular symmetrical joint involvement and systemic manifestations.

4. Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease that involves inflammation in the membrane lining of the joints and often affects internal organs. Most patients exhibit a chronic fluctuating course of disease that can result in progressive joint destruction, deformity, and disability. RA affects between 1 and 2 million Americans. It occurs three times more often in women, and peaks at age 35 to 50 years.

5. Rheumatoid arthritis is a chronic disease, characterized by periods of disease flares and remissions. The cause of rheumatoid arthritis is not known. In rheumatoid arthritis, multiple joints are usually, but not always, affected in a symmetrical pattern. Rheumatoid arthritis can affect people of all ages. Damage to joints can occur early and does not correlate with the severity of symptoms. The "rheumatoid factor" is an antibody that can be found in the blood of 80% of people with rheumatoid arthritis. Rheumatoid arthritis (RA) overview

6. The cause of rheumatoid arthritis is unknown.. It is believed that the tendency to develop rheumatoid arthritis may be genetically inherited (hereditary). It is suspected that certain infections or factors in the environment might trigger the immune system to attack the body's own tissues; resulting in inflammation in various organs of the body such as the lungs or eyes. Environmental factors also seem to play some role in causing rheumatoid arthritis. For example, scientists have reported that smoking tobacco increases the risk of developing rheumatoid arthritis. What causes rheumatoid arthritis? ETIOLOGY

7. The cause of RA is not fully understood but appears to be multifactorial. It is considered an autoimmune disease in which the body loses its ability to distinguish between synovial and foreign tissue. Other factors involved in RA are as follows: 1. Environmental influences , such as infections or trauma, are thought to trigger the development of RA.

8. 2. Genetic markers , such as human leukocyte antigen DR4 (HLA-DR4), have been associated with triggering the inflammatory process in RA. Such markers, however, are not considered diagnostic because 30 % of people with HLA-DR4 never develop RA. 3. Antigen-dependent activation of T lymphocytes leads to proliferation of the synovial lining, activation of proinflammatory cells from the bone marrow, cytokine and protease secretion, and autoantibody production .

9. 4. Anticitrullinated proteins and peptides are high specific for RA. 5. Tumor necrosis factor & (TNF-&), IL-1 , IL-6 , IL-8 , and growth factors propagate the inflammatory process , and agents found to alter these cytokines show promise in reducing pain and deformity. 6. Inflamed synovium is a hallmark of the pathophysiology of RA. Synovium proliferates abnormally, growing into the joint space and into the bone, forming a pannus. The pannus migrates to the articular cartilage and into the subchondral bone leading to destruction of cartilage, bone, tendons, and blood vessels.

10. Genetic and environmental factors play a part. Predisposing factors Gender. Women before the menopause are affected three times more often than men. After the menopause the frequency of onset is similar between the sexes, suggesting an etiological role for sex hormones. The use of the oral contraceptive pill has shown no affect on RA overall, as previously thought , but it may delay the onset of disease. Familial. The disease is familial with an increased incidence in first degree relatives and a high concordance amongst monozygotic twins (up to 15%) and dizygotic twins (3.5%). In occasional families it affects several generations.

11. 12 Genetic factors are estimated to account for up to 60% of disease susceptibility. There is a strong association between susceptibility to RA and certain HLA haplotypes . HLA-DR4, which occurs in 50–75% of patients , correlates with a poor prognosis, as does HLA-DRB1. Individuals with HLA-DRB1 combined with a positive rheumatoid factor are13 times greater risk for developing bone erosions in early disease. Genetic factors

12. 13 Joint involvement in RA Hands and wrists Shoulders Elbows Feet Knees Hips Cervical spine

13. PATHOPHYSIOLOGY

14. Chronic inflammation of the synovial tissue lining the joint capsule results in the proliferation of this tissue. The inflamed, proliferating synovium characteristic of rheumatoid arthritis is called pannus . This pannus invades the cartilage and eventually the bone surface, producing erosions of bone and cartilage and leading to destruction of the joint. The factors that initiate the inflammatory process are unknown.

15. The immune system is a complex network of checks and balances designed to discriminate self from non-self (foreign) tissues. It helps rid the body of infectious agents, tumour cells, and products associated with the breakdown of cells. In rheumatoid arthritis, this system no longer can differentiate self from non-self tissues and attacks the synovial tissue and other connective tissues.

16. Signs & Symptoms of RA Fatigue. Stiffness, especially in early morning and after sitting a long period of time . Not relieved by pain Low Grade Fever, Weakness. Muscle pain and pain with prolonged sitting. Symmetrical , affects joints on both sides of the body. Rheumatoid nodules. Deformity of your joints over time. Raynauds phenomenon. Pain

17. nodules

18. DIAGNOSIS

19. 1 . Rheumatoid factor (RF) is found in " 60% of patients with RA; however, as many as 5% of healthy individuals will have elevated titers of RF. If initially negative, the test can be repeated in 6 to 12 months. RF is not an accurate measure of disease progression. LABORATORY ASSESSMENT

20. 2. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) : They are markers of inflammation and are usually elevated in patients with RA. They can also help indicate the activity of the disease , but they do not indicate disease severity . 3. Anticyclic citrullinated peptide antibodies (ACPA) : T hese are found in most patients with RA and are useful in predicting erosive disease .

21. Radiographic examination : T his can reveal the extent of bone erosion and cartilage loss. An MRI can detect proliferative pannus.

22. Rheumatoid Arthritis Symptom criteria Morning stiffness Arthritis of 3 or more joints Arthritis of hand joints Symmetric arthritis Rheumatoid nodules Serum rheumatoid factor Radiographic changes A person shall be said to have rheumatoid arthritis if he or she has satisfied 4 of 7 criteria, with criteria 1-4 present for at least 6 weeks

23. Diagnosis and clinical evaluation : In 2010, EULAR (European League Against Rheumatism) established a score-based algorithm criteria aimed at diagnoses before joint damage occurs. Definitive RA is defined as a score # 6/10 based on four domains: 1 . Joint involvement (e.g., number and location of involved joints) 2. Serology (e.g., RF, ACPA) 3. Acute phase reactants (e.g., CRP, ESR) 4. Duration of symptoms

24. TREATMENTS

25. Treatment objectives The goals in the management of RA are: 1. To prevent or control joint damage 2. To prevent loss of function 3. To decrease pain 4. To maintain the patient’s quality of life 5. To avoid or minimize adverse effects of treatment. 6 . Preservation of muscle and joint function. 7 . Return to a desirable and productive life.

26. ALGORITHM OF TREATMENT OF RA Methotrexate Or other DMARD ± NSAID Prednisone within first 3 months   Poor response Other DMARD mono Rx (MTX if not used above) Combo DMARD Rx Biologic DMARD Mono or combo with DMARD Poor response Try other combination, triple drug (DMARD + Biologic), add low dose of Prednisone for long term, consider second line DMARD.

27. Non pharmacological Treatment Diet Exercise Acupuncture Herbal Medicines Massage Stress Reduction Techniques – prayer, meditation, hypnosis, yoga .

28. Nutrition The most commonly observed vitamin and mineral deficiencies in patients with RA are: folic acid vitamin C vitamin D vitamin B 6 vitamin B 12 vitamin E calcium magnesium zinc selenium

29. Exercise Being overweight strains joints and leads to further inflammation. 4 times a week for 30 minutes Walking Light jogging Water aerobics Cycling Yoga Tai chi stretching

30. Medications There are four types of medications used to treat RA: Non-steroidal anti-inflammatory drugs (NSAIDs) Disease-modifying anti-rheumatic drugs(DMARDS). Corticosteroids Biologic Response Modifiers (“ Bioligics ”) (Arthritis Foundation, 2012; Gulanick & Myers 2011) Pharmacological treatment

31. Non-steroidal anti-inflammatory drugs (NSAIDs) Examples General Use Side Effects Nursing Considerations Aspirin, ibuprofen, naproxen, COX-2 inhibitors, propionic acid, phenylacetic acid anti-inflammatory: Used in the management inflammatory conditions Antipyretic: used to control fever Analgesic: Control mild to moderate pain Nausea Vomiting Diarrhea Constipation Dizziness Drowsiness Edema Kidney failure Liver failure Prolonged bleeding Ulcers Use cautiously in patients with Rx of bleeding disorders Encourage pt to avoid concurrent use of alcohol NSAIDs may decrease response to diuretics or antihypertensive therapy

32. Corticosteroids Examples General Use Side Effects Nursing Considerations Cortisone, hydrocortisone, prednisone, betamethasone,dexa-methasone Used in the management inflammatory conditions W hen NSAIDS may be contraindicated Promptly improve symptoms of RA Increased appetite Weight gain Water/salt retention Increased blood pressure Thinning of skin Depression Mood swings Muscle weakness Osteoporosis Delayed wound healing Onset/worsening of diabetes Take medications as directed (adrenal suppression) Used with caution in diabetic patients Encourage diet high in protein, calcium, potassium and low in sodium and carbohydrates Discuss body image Discuss risk for infection

33. Disease-modifying anti-rheumatic drugs(DMARDS ) Examples General Use Side Effects Nursing Considerations Methotrexate (the gold standard) , gold salts, cyclosporine, sulfasalazine, azathioprine immunosuppressive activity Reduce inflammation of rheumatoid arthritis Slows down joint destruction Preserves joint function Dizziness, drowsiness, headache Pulmonary fibrosis Pneumonitis Anorexia Nausea Hepatotoxicity Stomatitis Infertility Alopecia Skin ulceration Aplastic anemia Thrombocytopenia Leukopenia Nephropathy fever photosensitivity May take several weeks to months before they become effective Discuss teratogenicity, should be taken off drug several months prior to conception Discuss body image

34. Biologic Response Modifiers (“Biologics”) Examples General Use Side Effects Nursing Considerations Etanercept , anakinra , abatacipt , adalimumab , Infliximab ( Remicade ) Used in the management inflammatory conditions W hen NSAIDS may be contraindicated Promptly improve symptoms of RA Increased appetite Weight gain Water/salt retention Increased blood pressure Thinning of skin Depression Mood swings Muscle weakness Osteoporosis Delayed wound healing Onset/worsening of diabetes Take medications as directed (adrenal suppression) Encourage diet high in protein, calcium, potassium and low in sodium and carbohydrates Discuss body image Discuss risk for infection

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