systemic lupus erythematosus-1
DESCRIPTION
SeTRANSCRIPT
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By the end of the session the student will be enabled to:
Discuss with understanding the etiologyand pathophysiology of Systematic Lupus Erthematosus (SLE)
Demonstrate theoretical knowledge applied to nursing and collaborative care management of patients with SLE.
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• Chronic, progressive multisystem
inflammatory autoimmune disease periods
of exacerbations & remission
• Multifactorial origins
• Genetic
• Hormonal
• Environmental
• Immunologic
• Women are ten times more likely to
develop this than men
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Women more likely to develop this than men
Menarche - oral contraceptives
Typically affects skin joints and serous membranes
Genetic influence is suspect
Hormonal influence Higher risk amongst non
white population Genes from HLA complex
show strong associations with SLE
Hormones known to play a role in the development of SLE
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Environment• Sun exposure and burns
• ? Infectious agents Anti seizure drugs Procainamide (Pronestyl) Heart -decreases the speed of
electrical conduction through the heart muscle, prolongs the electrical phase during which the heart's muscle cells can be electrically stimulated, and prolongs the recovery period during which the heart muscle cells cannot be stimulated.
Hydralazine (apresoline) is a direct-acting smooth muscle relaxant used to treat hypertension by acting as a vasodilator primarily in arteries and arterioles.
Hydralazine (Apresoline)Anti Hypertensive
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Production of a large variety of auto
antibodies, erythrocytes, coagulation
proteins, lymphocytes, platelets and
many other self proteins
Autoimmune reactions directed against
the constituents of the cell nucleus.
Over aggressive autoimmune response
related to the actions of the B and T cells.
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Ranges in severity mild affecting all
body systems
Any organ can be affected by the
circulating immune complexes.
Most commonly affected are the skin ,
muscle, serous membranes, heart ,lung
linings, kidneys and nervous tissue
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Weight loss
Fever
Arthralgia (joint stiffness and pain)
Excessive fatigue
Palmar erythema Butterfly rash
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Severe rashes in those who are
photosensitive in sun exposed areas
Classic butterfly rash 50% of people
Persistent lesions round coin shaped
Ulcers of the oral and/or nasal
membranes
Alopecia
Dry, scaly and atrophied scalp
Photosensitivity
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Polyarthralgia, morning stiffness
Arthritis – may cause swan neck deformities, ulnar deviation andsubluxation.
Increased risk of bone loss and fracture
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Tachypnea and cough Restrictive lung disease Possible pleurisy Cardiac dysrhythmias from fibrosis of sino arterial and atrio
ventricular nodes Pericarditis may occur Hypertension Hypercholesterolemia Secondary anti phospholipid syndrome Antiphospholipid syndrome is a disorder in which your
immune system mistakenly produces antibodies against certain normal proteins in your blood. Antiphospholipidsyndrome can cause blood clots to form within your arteries or veins as well as pregnancy complications, such as miscarriages and stillbirths.
Hypercholesterolemia (also spelled hypercholesterolaemia) is the presence of high levels of cholesterol in the blood. It is a form of "hyperlipidemia.
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Lupus Nephritis (LN)
Mild proteinuria Glomerulonephritis
Primary goal: Slow the progression by
giving corticosteroids and immuno
suppressants
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Generalized or focal seizures
Peripheral neuropathy
Cognitive dysfunction – deposition of
immune complexes within the brain
tissue.
Presents as mood disorders, psychiatric
problems
Potential for stroke /aseptic meningitis
Headaches
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Anemia
Mild leukopenia
Thrombocytopenia
Either excessive bleeding or
blood clot development -Blood
clot development treated with
WARFARIN (coumadin)
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Increased susceptibility to infection
Defects in the ability to phagocytize
invading bacteria
Pneumonia most common infection
Fever serious indictor life
threatening problems
Avoid live vaccination (e.g. varicella)
although other vaccines are safe
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No specific test
H & P (Table 65-14)
Labs
+ANA (antinuclear antibodies)
Antibodies (e.g. anti-DNA)
Specific for SLE
Anti-double-stranded DNA
Anti-Smith
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Early diagnosis better prognosisManage exacerbation periodPrevent complications of treatmentSurvival depends on:
• Age
• Race
• Gender
• Socioeconomic status
• Co-morbidity
• Severity of disease
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NSAIDs - Polyarthralgias/PolyarthritisAntimalarial drugs (hydroxychloroquine
Plaquenil) → Fatigue/Skin & joint problemsNB: Funduscopic & visual field exams q6- 12 months → Retinopathy
Alternative: Antileprosy drug (e.g. Dapsone)
Anticoagulants (e.g. Coumadin/Heparin) for Clotting
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Corticosteroids (Methylprednisolone) → Polyarthritis & Cutaneous SLE
Steroid-sparing drugs (Methotrexate) with Folic Acid Immunosuppressive drugs (azathioprine Imuran &
cyclophosphamide Cytoxan to reduce long-term use of corticosteroids & organ-system
disease NSAIDs continue to be an important intervention, especially for
patients with mild polyarthralgias or polyarthritis. Antimalarial agents such as hydroxychloroquine (Plaquenil) often
are used to treat fatigue and moderate skin and joint problems. Steroid-sparing immunosuppressants such as methotrexate can
serve as an alternate treatment and are prescribed in combination with folic acid to decrease minor side effects of corticosteroids.
Immunosuppressive drugs such as azathioprine (Imuran) and cyclophosphamide (Cytoxan) may be prescribed to reduce the need for long-term corticosteroid therapy.
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Assess patient’s physical, psychologic, &
sociocultural problems with long-term
management of SLE
Subjective & Objective data (Table 65-16)
Specific considerations
Pain
Fatigue
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Fatigue
Acute pain
Impaired skin integrity
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Overall goals
Pain relief
Adhere to therapeutic regimen
Demonstrate awareness of & avoid
activities that cause disease exacerbation
Maintain optimal role function & a
positive self-image
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Accurate recording of severity of
symptoms & response to therapy
Assess• Fever pattern
• Joint inflammation
• Limitation of motion
• Location & degree of discomfort
• Fatigability
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36-year-old woman was admitted 8 years ago with polyarthritis, facial & palmar erythema, and general malaise.
She was diagnosed w/ probable systemic lupus erythematosus (SLE)
She was started on prednisone 100 mg/every other day
Within a few weeks of taking prednisone, she developed cushing’s syndrome
She has also had intermittent tonic - clonic(grand mal) seizures that are treated w/ Dilantin
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During the past year, her lab studies indicate early renal failure
She has had occasional UTIs that have responded to treatment
1. What common clinical manifestations of SLE does she have? Polyarthritis, facial and palmar erythema, and general malaise.
2. What psychosocial issues should you discuss w/ her? Concerns over her long-term prognosis, family planning, consultation about managing rash, and stress management.
3. What patient teaching should you do w/ her? Discuss the avoidance of triggers (e.g., sun exposure, stress)