of 28 /28

Systemic Lupus Erythematosus-1

  • Author
    bs81

  • View
    4

  • Download
    0

Embed Size (px)

DESCRIPTION

Se

Text of Systemic Lupus Erythematosus-1

  • 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.

  • 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

  • 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

  • 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

  • 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.

  • 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

  • Weight loss

    Fever

    Arthralgia (joint stiffness and pain)

    Excessive fatigue

    Palmar erythema Butterfly rash

  • 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

  • Polyarthralgia, morning stiffness

    Arthritis may cause swan neck deformities, ulnar deviation andsubluxation.

    Increased risk of bone loss and fracture

  • 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.

  • Lupus Nephritis (LN)

    Mild proteinuria Glomerulonephritis

    Primary goal: Slow the progression by

    giving corticosteroids and immuno

    suppressants

  • 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

  • Anemia

    Mild leukopenia

    Thrombocytopenia

    Either excessive bleeding or

    blood clot development -Blood

    clot development treated with

    WARFARIN (coumadin)

  • 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

  • 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

  • Early diagnosis better prognosisManage exacerbation periodPrevent complications of treatmentSurvival depends on:

    Age

    Race

    Gender

    Socioeconomic status

    Co-morbidity

    Severity of disease

  • 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

  • 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.

  • Assess patients physical, psychologic, &

    sociocultural problems with long-term

    management of SLE

    Subjective & Objective data (Table 65-16)

    Specific considerations

    Pain

    Fatigue

  • Fatigue

    Acute pain

    Impaired skin integrity

  • 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

  • Accurate recording of severity of

    symptoms & response to therapy

    Assess Fever pattern

    Joint inflammation

    Limitation of motion

    Location & degree of discomfort

    Fatigability

  • 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 cushings syndrome

    She has also had intermittent tonic - clonic(grand mal) seizures that are treated w/ Dilantin

  • 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)