AUTOIMMUNE DISORDERS

INFLUENCED BY GENETIC, HORMONAL, VIRAL OR ENVIRONMENTAL FACTORS FORMATIONS OF ANTIBODIES AGAINST SELF-TISSUES MAY INVOLVE T-CELLS AND B-CELLS OR BOTH ORGAN SPECIFIC ALSO NON-ORGAN SPECIFIC

NURSING TREATMENT AND MANAGEMENT OF AUTOIMMUNE DISORDERS

CORTICOSTEROID THERAPY CYTOTOXIC DRUGS EMOTIONAL SUPPORT EDUCATION RX SPECIFIC TO TYPE OF AUTOIMMUNE DISORDER

CHRONIC FATIGUE SYNDROME

LASTING FATIGUE 6 MONTS OR MORE MAY FOLLOW COLD, FLU, MONO MUSCLE WEAKNESS / JOINT DISEASE HEADACHE, LOSS OF CONSCIOUS ETIOLOGY UNCLEAR TREATED SOMETIMES WITH ANTI-VIRAL AGENTS, ANTIDEPRESSANTS, NSAIDS NO CURE

Pernicious Anemia Rheumatoid Arthritis Guillain-Barre Scleroderma Ulcerative colitis Myasthenia Gravis Multiple Sclerosis Systemic Lupus Erythmatosis

SCLERODERMA
Cause unknown 18 20 people per million, per year (rare) Remissions and exacerbations Starts with skin involvement Then skin undergoes fibrotic changes loss of elasticity and movement Becomes non-functional

GOUT
A heterogenous group of conditions related to a genetic defect in purine metabolism that results in hyper uricemia. Over secretion of of uric acid Or a renal defect resulting in decreased excretion of uric acid or a combination of both occur

Faulty Uric Acid Metabolism

1. Severe dieting or malnutrition 2. Excessive diet of foods high in purines (shellfish, organ meats) 3. Secondary to increase in cell turnover and cell breakdown ( leukemia, multiple myeloma, some types of anemia, psoriasis) 4. Altered renal tubular function - Pharmacological agents ( diuretics such as thiazides and furosemide, saliciylates (low dose), ethanol 5. Increase in alcohol intake

 Metatarsophalangeal joint of big toe the most common site (90%) May cause renal stones and damage

RX
Test of synovial fluid of joint involved Acute attack Colchicine Indomethethacin NSAID Corticosteroids After Acute Attack Subsides Urososuric Agents Benemid these correct hyperuricemia and dissolve deposited urate

 If at risk for renal insufficiency or kidney stones Allopurinol, a xanthine oxidase inhibitor is also effective

FIBOMYALGIA
Fibromyalgia is a common syndrome fatigue 2% of population affected More common in women

Treatment
No specific symptoms Trycyclic antidepressants Serotonin reuptake inhibitors Anticonvulsants

Osteoarthritis
Degenerative Joint Disease Wear and Tear Syndrome Most common and most frequently over treated or under treated Idiopathic in nature

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)

A result of disturbed immune regulation that causes an exaggerated production of auto-antibodies. Chronic connective tissue disease involving multiple organ systems. Deposit of antigen or antibody complexes that affect the connective cells throughout the body.

CAUSES OF SLE
Unknown Genetic Autoimmune Viral

Drug induced: procainamide (Pronestyl) and hydralazine (Apresoline)

Home Care Instructions

Stop smoking Lupus foundation Identify ways to reduce stress S & S Renal failure Avoid people with infections Monitor self for infection, fatigue, joint pain, renal complications

Diagnostic Tests
Hematology Rheumatoid factor *LE cell preparation *Urine chemistry Blood chemistry *ANA *Skin Biopsy

*Key findings

Complications of SLE
Necrosis of glomerular capillaries Inflammation of cerebral and ocular blood vessels Necrosis of lymph nodes Vasculitis of GI tract and pleura Degeneration of the skins basal layer Heart failure Seizures Depression Infection Peripheral neuropathy