SYSTEMIC LUPUS ERYTHEMATOSIS

INTRODUCTION 

DEFINITION

SLE is a chronic multisystem inflammatory disease of autoimmune in origin

INCIDENCE

More women are affected than men

ETIOLOGY

Viral infection Genetic factors bacterial infection drugs, (Sulpha drugs hydralazine

procainamide) Purperium Exposure to sunlight, sun burns Hormones

PATHOPHYSIOLOGY

CLINICAL MANIFESTATIONS

Skin Butterfly-shaped rash Discoid lesions are ring-shaped Discoid lesions may also result in

erythematous, scaly plaques

ARTHRITIS:

Generally bilateral and symmetric,. Can resemble RA Unlike RA, the arthritis is non erosive;. Tendon involvement is common

CARDIAC

Pericarditis. Pleural effusion. Myocarditis. Endocarditis. Coronary arteritis—less common.

PULMONARY:

Pleuritis. Pleural effusion. Lupus pneumonitis. Pulmonary hemorrhage. Pulmonary embolism.

GASTROINTESTINAL.

Oral ulcers. Acute or sub acute abdominal pain. Pancreatitis. Spontaneous bacterial peritonitis. Bowel infarction.

RENAL:

Nephritis. Focal segmental glomerulonephritis Proliferative Membranous nephritis

CENTRAL NERVOUS SYSTEM:

Neuropsychiatric disorders. Depression Psychosis. Transient ischemic attacks/stroke. Epilepsy. Migraine headache. Myleopathy. Guillain-Barre syndrome. Chorea and other movement disorders.

HEMATOLOGIC:

Hemolytic anemia. Leucopenia. Thrombocytopenia

CONSTITUTIONAL:

Fever. Weight loss. Fatigue.

DIAGNOSTIC EVALUATION

CBC ESR Complement levels Urinalysis 24-hour urine for protein and creatinine clearance. Chest x-ray Computed tomography (CT) scan or MRI.

MANAGEMENT

Pharmacologic NSAIDs—to reduce pain and inflammation. Antimalarials—to decrease disease activity. Corticosteroids—to reduce inflammatory

process. Immunosuppressive—to suppress immune

process

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.

OTHER MANAGEMENT

Close follow-up for evaluation of cardiac, neurologic, renal, and other body systems.

Referral to specialists for systemic manifestations.

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.

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

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

NURSING INTERVENTIONS REDUCING PAIN

Administer and teach self-administration of medications

use of hot or cold applications, relaxation techniques

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.

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.

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 andto promote eating.

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.

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.

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.

COMPLICATIONS

Renal failure. Permanent neurologic impairment. Infection.

GOUT

INTRODUCTION

DEFINITION

Gout is a disorder of purine metabolism characterized by elevated uric acid levels and deposition of urate in joints and other tissues

INCIDENCE

more commonly in men, middle aged men are more affected

ETIOLOGY

Common causes Under excretion of uric acid Medications and chemicals

COMMON CAUSES

Inherited enzyme defects. Certain disease conditions: Myelo proliferative disorders. Lymphoproliferative disorders. Cancer chemotherapy. Hemolytic anemias. Psoriasis.

UNDER EXCRETION OF URIC ACID (90% OF CASES)

Renal disease. Endocrine disorders

MEDICATIONS AND CHEMICALS:

Diuretics. Ethanol (alcohol). Low-dose aspirin. Pyrazinamide— anti tuberculosis agent. Lead. Volume depletion states—nephrogenic

diabetes insipidus.

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.

CLINICAL MANIFESTATIONS ACUTE GOUTY ARTHRITIS

Generally affects one joint—often 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

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.

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.

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.

ESR—elevated. X-rays of affected joints show changes

consistent with diagnosis of gout.

PHARMACOLOGIC MANAGEMENT

NSAIDs—for acute attacks to relieve pain and swelling.

Colchicines—for 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

CORTICOSTEROIDS.

Intra-articular if attack confined to one joint. Oral—in short tapering course if other

treatmentsare contraindicated or if attack involves many joints.

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.

NONPHARMACOLOGIC

Avoidance of obesity. Avoidance of alcohol. Low-purine diet gives only a minor decrease

in serum uric acid levels.

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

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.

FACILITATING MOBILITY

Elevate and protect affected joint during acute attack.

Assist with activities of daily living. Encourage exercise and maintenance of

routine activity in chronic gout, except during acute attacks.

Protect draining tophi by covering and applying anti biotic ointment as needed.

PATIENT EDUCATION

Instruct patient and family about nature of disease.

Encourage to avoid alcohol. Avoid rapid weight loss by fasting or crash Avoid medications known to increase uric

acid levels. Advise prompt treatment of acute attack Instruct in signs and symptoms of allopurinol

hyper sensitivity Review foods containing purine

COMPLICATIONS

Uric acid kidney stone. Urate nephropathy. deforming arthritis

SIDE EFFECTS OF TREATMENT

Include skin rash hypersensitivity syndrome renal failure bone marrow depression

EVIDENCE BASED RESEARCH

CONCLUSION

BIBLIOGRAPHY

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