Systemic lupus erythematosis

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2. INTRODUCTION 3. DEFINITION SLE is a chronic multisystem inflammatory disease of autoimmune in origin 4. INCIDENCE More women are affected than men 5. ETIOLOGY Viral infection Genetic factors bacterial infection drugs, (Sulpha drugs hydralazine procainamide) Purperium Exposure to sunlight, sun burns Hormones 6. PATHOPHYSIOLOGY 7. CLINICAL MANIFESTATIONS Skin Butterfly-shaped rash Discoid lesions are ring-shaped Discoid lesions may also result in erythematous, scaly plaques 8. ARTHRITIS: Generally bilateral and symmetric,. Can resemble RA Unlike RA, the arthritis is non erosive;. Tendon involvement is common 9. CARDIAC Pericarditis. Pleural effusion. Myocarditis. Endocarditis. Coronary arteritisless common. 10. PULMONARY: Pleuritis. Pleural effusion. Lupus pneumonitis. Pulmonary hemorrhage. Pulmonary embolism. 11. GASTROINTESTINAL. Oral ulcers. Acute or sub acute abdominal pain. Pancreatitis. Spontaneous bacterial peritonitis. Bowel infarction. 12. RENAL: Nephritis. Focal segmental glomerulonephritis Proliferative Membranous nephritis 13. CENTRAL NERVOUS SYSTEM: Neuropsychiatric disorders. Depression Psychosis. Transient ischemic attacks/stroke. Epilepsy. Migraine headache. Myleopathy. Guillain-Barre syndrome. Chorea and other movement disorders. 14. HEMATOLOGIC: Hemolytic anemia. Leucopenia. Thrombocytopenia 15. CONSTITUTIONAL: Fever. Weight loss. Fatigue. 16. DIAGNOSTIC EVALUATION CBC ESR Complement levels Urinalysis 24-hour urine for protein and creatinine clearance. Chest x-ray Computed tomography (CT) scan or MRI. 17. MANAGEMENT Pharmacologic NSAIDsto reduce pain and inflammation. Antimalarialsto decrease disease activity. Corticosteroidsto reduce inflammatory process. Immunosuppressiveto suppress immune process 18. NON PHARMACOLOGIC Avoid direct exposure to sunlight to reduce the chance of exacerbation. Behavior modification to prevent exacerbations and to reduce symptoms. Joint protection and energy conservation. 19. OTHER MANAGEMENT Close follow-up for evaluation of cardiac, neurologic, renal, and other body systems. Referral to specialists for systemic manifestations. 20. NURSING ASSESSMENT Obtain clinical history, review systems, and perform physical examination for characteristic findings. Assess for signs and symptoms of infection and other side effects to medications. Assess patient's and family's ability to cope with impact of prolonged disease. 21. NURSING DIAGNOSES Fatigue related to chronic inflammation and altered immunity as evidenced by lack of energy inability to maintain usual routine Acute pain related to inflammatory process and inadequate comfort measures as evidenced by complaints of joint pain lack of relief from pain relieving measures ,reduction of activity to avoid exacerbation of pain 22. Impaired skin integrity related to photosensitivity ,skin rash ,and alopecia as evidenced by rash anywhere on body butterfly rash on face hairless areas of ulceration on fingertips, complaints of urticaria and photosensitivity Knowledge deficit related to lack of exposure to and unfamiliarity with information resources as evidenced by questions about SLE misinterpretation of information and inaccurate follow -through of instruction 23. NURSING INTERVENTIONS REDUCING PAIN Administer and teach self-administration of medications use of hot or cold applications, relaxation techniques 24. INCREASING CONTROL OVER DISEASE PROCESS Instruct patient to avoid factors that may exacerbate disease. Avoid exposure to sunlight and ultraviolet light. Use sunscreen with sun protection factor (SPF)of 15 or greater. Avoid prolonged sun exposure. Wear protective, lightweight clothing, long sleeves, hats. Avoid use of tanning beds. Avoid exposure to drugs and chemicals. Avoid exposure to hair spray Avoid exposure to hair-coloring agents. 25. MEDICATIONS Teach self-administration of pharmacologic agents to reduce disease activity. Encourage good nutrition, sleep habits, exercise, rest, and relaxation to improve general health and to help prevent infection. Encourage ventilation of feelings, counseling, or referrals to social work, occupational therapy, as needed. 26. MAINTAINING SKIN AND MUCOUS MEMBRANE INTEGRITY Apply topical corticosteroids to skin lesions as ordered. Suggest alternative hairstyles, scarves, and wigs to cover significant areas of alopecia. Encourage good oral hygiene and inspect mouth for oral ulcers. Avoid hot or spicy foods that may irritate oral ulcers. Apply topical agents or analgesics to reduce pain and to promote eating. 27. REDUCING FATIGUE Advise patient that fatigue level will fluctuate with disease activity. Encourage patient to modify schedule to include several rest periods during the day, pace activity and exercise according to body's tolerance, use energy conservation techniques in daily activities. Teach relaxation techniques, such as deep breathing, progressive muscle relaxation, and imagery to reduce emotional stress that causes fatigue. 28. PRESERVING URINARY ELIMINATION Assist with monitoring of urinary status as indicated by degree of renal involvement. Monitor intake and output and urine specific gravity. Measure urine protein, micro albumin, or obtain24- hour creatinine clearance, as ordered. Check test results of serum blood urea nitrogen (BUN) and creatinine. 29. PATIENT EDUCATION AND HEALTH MAINTENANCE Stress that close follow-up is mandatory, even in times of remission, to detect early progression of organ involvement and to alter drug therapy. Advise on the use of special cosmetics to cover skin lesions.Advise about reproduction. Avoid pregnancy during time of severe disease activity. Immunomodulators may have teratogenic effects. Use of some drugs for treatment of SLE can result instability. 30. COMPLICATIONS Renal failure. Permanent neurologic impairment. Infection. 31. GOUT 32. INTRODUCTION 33. DEFINITION Gout is a disorder of purine metabolism characterized by elevated uric acid levels and deposition of urate in joints and other tissues 34. INCIDENCE more commonly in men, middle aged men are more affected 35. ETIOLOGY Common causes Under excretion of uric acid Medications and chemicals 36. COMMON CAUSES Inherited enzyme defects. Certain disease conditions: Myelo proliferative disorders. Lymphoproliferative disorders. Cancer chemotherapy. Hemolytic anemias. Psoriasis. 37. UNDER EXCRETION OF URIC ACID (90% OF CASES) Renal disease. Endocrine disorders 38. MEDICATIONS AND CHEMICALS: Diuretics. Ethanol (alcohol). Low-dose aspirin. Pyrazinamide anti tuberculosis agent. Lead. Volume depletion statesnephrogenic diabetes insipidus. 39. PATHOPHYSIOLOGY Uric acid is the major end product of purine catabolism and is primarily excreted by the kidneys hyperuricemia may be result of of increased purine synthesis decreased renal excretion or both, Gout results from an overabundant accumulation and subsequent deposition of uric acid in the body. 40. CLINICAL MANIFESTATIONS ACUTE GOUTY ARTHRITIS Generally affects one jointoften first metatarso-phalangeal joint Other joints can be affected, such as ankle, knee; upper extremities are less commonly involved. Pain, warmth, erythema, and swelling of tissue surrounding the affected joint. Fever may occur. Onset of symptoms is sudden; intensity is severe. Duration of symptoms is self-limiting; lasts approxi-mately 3 to 10 days without treatment 41. CHRONIC TOPHACEOUS GOUT Occurs if acute gout is inadequately treated or if it goes untreated. Characterized by development of tophi or deposits of uric acid in and around joints, cartilage, and soft tissues. Arthritis is more prolonged in nature with discrete attacks less common. 42. RENAL DISEASE Caused by hyperuricemia (persistent elevation of uric acid in the blood). Kidney stones are composed of uric acid. Deposition of uric acid in kidney tissue. 43. DIAGNOSTIC EVALUATION Synovial fluid analysis. Identification of monosodium urate crystals under polarized microscopy. Synovial WBC count can range from 2,000 to 100,000/mm3. Culture of synovial fluid to rule out infection. 24-hour urine for uric acid to determine overproduction of uric acid versus under excretion. ESRelevated. X-rays of affected joints show changes consistent with diagnosis of gout. 44. PHARMACOLOGIC MANAGEMENT NSAIDsfor acute attacks to relieve pain and swelling. Colchicinesfor prevention of acute attacks and their treatment. Oral at onset of an attack, taken hourly until pain relief or first signs of toxicity (nausea, vomiting ,cramping, diarrhea 45. CORTICOSTEROIDS. Intra-articular if attack confined to one joint. Oralin short tapering course if other treatments are contraindicated or if attack involves many joints. 46. URATE-LOWERING AGENTS Uricosuric drugs, such as probenecid (Benamid), inter-fere with tubular reabsorption of uric acid. Allopurinol (Zyloprim)interferes with conversion of hypoxanthine and xanthine to uric acid. 47. NONPHARMACOLOGIC Avoidance of obesity. Avoidance of alcohol. Low-purine diet gives only a minor decrease in serum uric acid levels. 48. NURSING ASSESSMENT Obtain history for factors predisposing to gout. Perform physical examination. Inspect involved joint. Observe for tophi: a) Pinna of ear. b) Olecranon bursa c) Achilles tendon. Assess pain and pain relief pattern if attack is acute 49. NURSING INTERVENTIONS RELIEVING PAIN Administer and teach self-administration of pain relieving medications as prescribed. Encourage adequate fluid intake to assist with excretion of uric acid and to decrease likelihood of stone formation. Instruct patient to take prescribed medications consis-tently because interruptions in therapy can precipitate acute attacks. 50. FACILITATING MOBILITY Elevate and protect affected joint during acute attack. As