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    Systemic Lupus Erythematosus (SLE) : Genetic Factors Environmental Factors

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    joyrena ochondra
    Systemic lupus erythematosus (SLE) is an autoimmune disease with no known cause. Genetic and environmental factors contribute to SLE, which results from the immune system attacking the body's own tissues and organs. The immune system produces antibodies that react against the body's own cells and tissues, causing inflammation and tissue damage. Common symptoms include joint pain, rash, fatigue, and fever. Complications can include damage to the skin, kidneys, heart, lungs, and nervous system if untreated. Women are affected more often than men, especially during their childbearing years.

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    Systemic Lupus Erythematosus (SLE) : Genetic Factors Environmental Factors

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    joyrena ochondra
    171 views5 pages
    Systemic lupus erythematosus (SLE) is an autoimmune disease with no known cause. Genetic and environmental factors contribute to SLE, which results from the immune system attacking the body's own tissues and organs. The immune system produces antibodies that react against the body's own cells and tissues, causing inflammation and tissue damage. Common symptoms include joint pain, rash, fatigue, and fever. Complications can include damage to the skin, kidneys, heart, lungs, and nervous system if untreated. Women are affected more often than men, especially during their childbearing years.

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    SLE PATHO

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    Systemic lupus erythematosus (SLE) is an autoimmune disease with no known cause. Genetic and environmental factors contribute to SLE, which results from the immune system attacking the body's own tissues and organs. The immune system produces antibodies that react against the body's own cells and tissues, causing inflammation and tissue damage. Common symptoms include joint pain, rash, fatigue, and fever. Complications can include damage to the skin, kidneys, heart, lungs, and nervous system if untreated. Women are affected more often than men, especially during their childbearing years.

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    © All Rights Reserved
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    Download as docx, pdf, or txt
    171 views5 pages

    Systemic Lupus Erythematosus (SLE) : Genetic Factors Environmental Factors

    Uploaded by

    joyrena ochondra
    Systemic lupus erythematosus (SLE) is an autoimmune disease with no known cause. Genetic and environmental factors contribute to SLE, which results from the immune system attacking the body's own tissues and organs. The immune system produces antibodies that react against the body's own cells and tissues, causing inflammation and tissue damage. Common symptoms include joint pain, rash, fatigue, and fever. Complications can include damage to the skin, kidneys, heart, lungs, and nervous system if untreated. Women are affected more often than men, especially during their childbearing years.

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    of 5

    Modifiable risk factors: Systemic Lupus Erythematosus Non-modifiable risk factors:

    Environmental Factors: Genetic Factors


    (SLE)
     UV light exposure, exposure  Monozygotic Twins
    from sunlight, and
     Epigenetics
    fluorescent light bulbs. Unknown cause
    Immunologic Factors
     Medication ( sulfa drugs,
    penicillin, or antibiotic Hormonal Factors
    drugs)
    Injury to the bodies own cell  Estrogen
     Viral Infections
     20x more common in women
     Emotional Stress during reproductive
    Damage cell protein in years( 15– and 45 yrs.
     Stress on the body( Surgery
    Old)
    and pregnancy
    their DNA
    Race
     Silica dust exposure
     African-Americans
    Lifestyle
    Injury to group of cells  Hispanics
     Cigarette Smoking,
     Asian-Americans

    Organ injury

    Apoptosis
    Cell Repair Flare ups
    (Programmed cell death)

    Exposure of apoptotic antibodies (nuclear


    antigens)
    Genetic factor
    Susceptibility genes Less effective clearance of nuclear antigens recognition of
    foreign bodies
    Build-up of nuclear antigens Creates ANA
    immune response

    B-cells swing by and starts


    antinuclear antibodies(ANA) Deposits in the tissue
    production

    Inflammation
    Anti-nuclear antibodies
    bind nuclear antigens

    Formation of antigen
    antibodies complexes

    Get into the blood and drift


    away

    Deposited or stick to the vessel


    wall in the different organs and
    tissue (skin, kidneys, joints, and
    heart)

    Deposited complies antibodies


    initiates local inflammatory reaction.
    Damage to activation of
    compliment system Type III
    Hypersens
    itivity
    Huge enzyme cascade reaction

    Cell membranes become permeable to


    fluid and molecules that let them go in
    and out causing cell to burst and die.

    Tissue damage Immune


    response

    Signs and
    Type III– Hypersensitivity
    symptoms:
    Activation
     Fever
     Weight loss
    Targets other cells (RBC,
     Joint Pain
    WBC, Phospholipids)
     Rash
     Fatigue
     Raynaud’s Phagocytosis and destruction
    phenomenon
     Chest pain
     SOB
    Type II Hypersensitivity reaction
    COMPLICATIONS:
     Skin Neurologic
    Malar rash Seizures
    Discoid rash Psychosis
    Photosensitivity
     Mucosa Hematologic
    Ulcers Thrombocytopenia
     Serosa Anemia
    Pleurisy Leukopenia
    Pericarditis Vasculitis
     Myocarditis Kidney
    Endocarditis Diffuse proliferative glomerulonephritis
     Joints Renal disorder
    Arthritis
    Bone tissue death (avascular necrosis) Pregnancy Complications (Preeclampsia)
    Increases the risk for cancer People with lupus are more vulnerable to infection

    Source: Brunner’s & Suddarth’s Textbook for Medical Surgical Nursing 14th edition
    https:// www.wikidoc.org/index.php/Systemic_lupus_erythematosus_pathophysiology

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