Immune Slides

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    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

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    NURSING TREATMENT AND

    MANAGEMENT OF

    AUTOIMMUNE DISORDERS

    CORTICOSTEROID THERAPY

    CYTOTOXIC DRUGS EMOTIONAL SUPPORT

    EDUCATION

    RX SPECIFIC TO TYPE OFAUTOIMMUNE DISORDER

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    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

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    Pernicious Anemia

    Rheumatoid Arthritis

    Guillain-Barre

    Scleroderma

    Ulcerative colitis

    Myasthenia Gravis

    Multiple Sclerosis

    Systemic Lupus Erythmatosis

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    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

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    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

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    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 cellbreakdown

    ( leukemia, multiple myeloma, some types ofanemia, psoriasis)

    4. Altered renal tubular function - Pharmacological

    agents ( diuretics such as thiazides andfurosemide, saliciylates (low dose), ethanol

    5. Increase in alcohol intake

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    Metatarsophalangeal joint of big toe the

    most common site (90%)

    May cause renal stones and damage

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    RX

    Test of synovial fluid of joint involved

    Acute attack

    Colchicine

    Indomethethacin NSAID

    Corticosteroids

    After Acute Attack Subsides

    Urososuric Agents Benemid these correcthyperuricemia and dissolve deposited urate

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    If at risk for renal insufficiency or kidney

    stones

    Allopurinol, a xanthine oxidase inhibitor is

    also effective

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    FIBOMYALGIA

    Fibromyalgia is a common syndrome

    fatigue

    2% of population affected

    More common in women

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    Treatment

    No specific symptoms

    Trycyclic antidepressants

    Serotonin reuptake inhibitors

    Anticonvulsants

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    Osteoarthritis

    Degenerative Joint Disease

    Wear and Tear Syndrome

    Most common and most frequently

    over treated or under treated

    Idiopathic in nature

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    SYSTEMIC LUPUS

    ERYTHEMATOSUS (SLE) A result of disturbed immune regulation

    that causes an exaggerated production ofauto-antibodies.

    Chronic connective tissue diseaseinvolving multiple organ systems.

    Deposit of antigen or antibody complexes

    that affect the connective cells throughoutthe body.

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    CAUSES OF SLE

    Unknown

    Genetic

    Autoimmune

    Viral

    Drug induced: procainamide (Pronestyl) andhydralazine (Apresoline)

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    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, jointpain, renal complications

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    Diagnostic Tests

    Hematology

    Rheumatoid factor

    *LE cell preparation

    *Urine chemistry Blood chemistry

    *ANA

    *Skin Biopsy

    *Key findings

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    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