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Systemic Lupus Erythematosus (SLE)

Description
Systemic Lupus Erythematosus is also called lupus or SLE, it is a disease where a
persons immune system attacks and injures the bodys own organs and tissues. Almost every
system of the body can be affected by SLE.
The bodys immune system is a network of cells and tissues responsible for clearing the
body of invading foreign organisms, like bacteria, viruses, and fungi. Anti-bodies are special
immune cells that recognize these foreign invaders, and begin a chain of events to destroy them.
In an autoimmune disorder like SLE, a persons antibodies begin to recognize the bodys own
tissues as foreign. Cells and chemicals of the immune system damage the tissues of the body.
The reaction that occurs in tissue is called inflammation. Inflammation includes swelling,
redness, increased blood flow, and tissue destruction. In SLE, some of the common anti-bodies
that normally fight diseases are thought to be out of control. These include antinuclear antibodies
and anti-DNA antibodies. Antinuclear antibodies are directed against the cells central structure
that contains genetic material. Anti-DNA antibodies are directed against the cells genetic
material. DNA is chemical substance that makes up the chromosomes and genes.
SLE can occur in both males and females of all ages, but 90% of patients are women. The
majority of these women are in their childbearing years. African Americans are more likely that
Caucasians to develop SLE.
Occasionally, medications can cause a syndrome of symptoms very similar to SLE. This
is called drug-induced lupus. Medications that may cause this syndrome include hydralazine
(used for high blood pressure) and procainamide (use for abnormal heartbeats). Drug-induced
lupus almost always disappears after the patient stops taking the medications that caused it.
Pathophysiology
SLE is an autoimmune disorder characterized by multisystem inflammation with the
generation of autoantibodies. Although the specific cause of SLE is unknown, multiple factors
are associated with the development of the disease, including genetic, epigenetic, ethnic,
immunoregulatory, hormonal, and environmental factors. Many immune disturbances, both
innates and acquired, occur in SLE.
In SLE, many genetic-susceptability factors, environmental triggers, antigen-antibody
responses, B-cell and T-cell interactions, and immune clearance processes interact to generate
and perpetuate autoimmunity. HLA = human leukocyte antigen; UV = ultraviolet light.
It is important to note that antibodies may be present for many years before the onset of
the first symptoms of SLE. One longstanding proposed mechanism for the development of
autoantibodies involves a defect in apoptosis that causes increased cell death and a disturbance in
immune tolerance. The redistribution of cellular antigens during necrosis/apoptosis leads to a
cell-surface display of plasma and nuclear antigens in the form of nucleosomes. Subsequently,
dysregulated lymphocytes begin targeting normally protected intracellular antigens. The

defective clearance of the apoptotic cell debris allows for the persistence of antigen and immune
complex production.
T cells have long been thought to play a central role in SLE pathogenesis, and T cells from
patients with lupus show defects in both signaling and effector function. These T cells secrete
less interleukin (IL) - 2, and one defect in signaling seems to be linked to an increase in calcium
influx, possibly due to changes in the CD3 signaling subunits. The following seem to be
adversely affected in T cells from patients with SLE: effector activity such as CD8 cytotoxicity;
T-regulatory, B-cell help; migration; and adhesion. However, the method by which each of these
deficits contributes to the exact clinical syndrome seen in an individual patient is still unknown.
These T-cell abnormalities are currently being explored as targets for therapy, as seen with the
recent approval of belimumab, which targets the B-lymphocyte stimulator (BLys) signaling
pathway.
Many clinical manifestations of SLE are mediated by circulating immune complexes that form
with antigens in various tissues or the direct effects of antibodies to cell surface components.
Immune complexes form in the microvasculature, leading to complement activation and
inflammation. Moreover, antibody-antigen complexes deposit on the basement membranes of
skin and kidneys. In active SLE, this process has been confirmed by demonstration of complexes
of nuclear antigens such as DNA, immunoglobulins, and complement proteins at these sites.
Autoantibodies have been found to be biomarkers for future neuropsychiatric events in SLE. A
prospective study (=10 years) of 1047 SLE patients demonstrated that individuals who had
evidence of lupus anticoagulant (LA) had an increased future risk of intracranial thrombosis and
that those with anti-ribosomal P antibodies had an increased future risk of lupus psychosis.
Serum antinuclear antibodies (ANAs) are found in nearly all individuals with active SLE.
Antibodies to native double-stranded DNA (dsDNA) are relatively specific for the diagnosis of
SLE. Whether polyclonal B-cell activation or a response to specific antigens exists is unclear, but
much of the pathology involves B cells, T cells, and dendritic cells. Cytotoxic T cells and
suppressor T cells (which would normally down-regulate immune responses) are decreased. The
generation of polyclonal T-cell cytolytic activity is impaired. Helper (CD4+) T cells are
increased. A lack of immune tolerance is observed in animal lupus models. Reports pointing to
important roles of interferon-alpha, transcription factors, and signaling variations also point to a
central role for neutrophils.
Management
It is depends on the organ systems affected by SLE and severity of the disease. Some
patients have a mild form of SLE. Their mild symptoms of inflammation can be treated with
non-steroidal anti-inflammatory drugs and aspirin. Severe skin rashes and joint problems may
respond to a group of medications usually used to treat malaria. More severely ill patients with
potentially life-threatening complications will require treatment with more potent drugs,

including steroid medications. Other treatments for SLE try to help specific symptoms. Clotting
disorders will require blood thinners.
Nursing Diagnosis
a. Disturbed body image related to presence of rash, lesions, alopecia and loss of strength.
Nursing Intervention
Nursing Intervention
-Assess the effect of the change on activities
of daily living, social activities, relationships
and work

Rationale
Changes in body image can reduce the
patients engagement in roles and
responsibilities.

-Assess the effect of changes body part on the


patients behavior.

Behavior changes may include ignoring the


altered structure or preoccupation with the
altered structure.

-Assess the patients feelings about the


change in body part or function.

Negative statements about the affected part


indicate an inability to integrate the change
into the self-concept

-Help the patient to talk about the positive or


negative feelings about the body change.

The patient should separate feelings about


the changes in her body from feelings
about her self-worth.

Hashimotos

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