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7/28/2019 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