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Systemic Lupus Erythematosus Pathophysiology
Systemic Lupus Erythematosus Pathophysiology
Predisposing Factors:
Age
Gender
Hereditary
Race
Hormonal
Female producing estrogen
Manifestation of heightened levels
of estrogen during puberty and
pregnancy
Unknown cause of estrogen
influencing immune response of the
HLA system in chromosome 6
Precipitating Factors:
Environmental
Drug-Induced
Infection
UNKNOWN
ETIOLOGY
Presented to T-cells
Apoptotic chromatin
and nuclei attach to
dendrite surface.
Defective B-cell
activation by
autoantigens
Hyper reactivity of
defective B-cells
Production of self and
non-self antibodies and
B memory cells
Various
Autoantibody
productions
Production of Anti-Nuclear
Antibodies (ANA) in renal
Formation of immune
complexes
Leukocyte Infiltration
Proteinuria
Lymphocytoto
xic antibody
activation
Antiphospholi
pid antibody
activation
Antierythrocyte
antibody
activation
If not treated:
-Lupus Nephritis
-Acute or chronic
renal impairment
-End-stage renal
failure
Hemolysis
Reduced RBC
count
Management and
treatment:
-Iron and Vitamin C
supplements
-Blood Transfusions
-Immunosuppressant
agents
Lymphopenia
If not treated:
-Hypoxemia
-Chronic Pulmonary
Disease
Platelet destruction
and reduction
Thrombocytopenia
Platelet aggregation
and clot formation
Cellular
membrane
component
damage
Bone Necrosis
Myalgias
Arthritis
Management and
treatment:
-Analgesics
-Nonsteroidal antiinflammatory drugs
-lifestyle changes
(including exercise and
weight control)
Vascular wall
inflammation
Mononuclear cell
infiltration
Involved Joint
collapse
If not treated:
-Further
deterioration of
bones and joints.
Formation of immune
complex
Vascular Inflammation
Occurrence of
immunoglobulin and
compliment disposition
Malar Rash
Photosensitivit
y
Discoid Rash
Anti-phospholipids and
other specific
autoantibody activation
in the cardiac linings
Anti-phospholipids and
other specific
autoantibody activation
in the pleural linings
Noninfective
inflammation of
pericardium,
myocardium and
endocardium
Noninfective
inflammation of the
membrane around the
lungs
If not treated:
-Further obstruction of
tissue.
-Necrosis of the tissue.
-Gangrene may occur.
Specific autoantibody
activation in the
neuronal tissue
Immune
disposition
activation
Activation of
cerebral
vasculature
Production of direct
neuronal tissue
antibodies
Altered cerebral
functioning
Psychosis
Lupus
Headache
Seizures
Management and
treatment:
-Immunosuppressive
drugs
-Non-steroidal antiinflammatory drugs.
If not treated:
-Further inflammation
-Infection and
deterioration of
myocardial and
pleural linings.
-Lung Collapse
-Cardiac tamponade
-Chronic constrictive
pericarditis.
-Congestive Heart
Failure.
Management and
treatment:
-Immunosuppressive
drugs
-Non-steroidal antiinflammatory drugs.
Gastric irritability in
the stomach
Peritoneal
spasms
Abdominal
Pain
Jaundic
e
If not treated:
-Progressive
intracranial
pressure.
-Deterioration of
cerebral functions
-Multiple system
failure.
Induced reflux of
gastric acid
Management and
treatment:
-Immunosuppressive
drugs
-Antiemetic:
metacropamide
Ineffective defecation
Nausea and
Vomiting
If not treated:
Stomach ulceration
Management and
treatment:
-Immunosuppressive
drugs
-Laxatives to
promote effective
bowel movement
If not treated:
-Severe Diarrhea
NARRATIVE PATHOPHYSIOLOGY
The pathophysiology of SLE has not been defined fully, although many genes that affect
immune function, particularly the human leukocyte antigen (HLA), may augment susceptibility
to clinical disease. Most monozygotic (identical) twins are discordant for clinical SLE, strongly
suggesting that additional factors, probably environmental, trigger the widespread development
of autoimmunity in susceptible individuals.
Certain medications (eg, phenytoin, hydralazine, procainamide, and isoniazid) may
produce drug-induced lupus, but this disorder differs from classic SLE in its autoantibody profile
(eg, antihistone antibody positive) and in sparing the kidneys and central nervous system (CNS).
Once triggered, SLE's autoimmune reaction affects many sites through multiple mechanisms
such as deposition of immune complexes, effects of cytokines and other chemical
neuromodulators, direct attack by autoantibodies or activated leukocytes, and others.
Non-neurologic sites of damage include the renal glomeruli, joints, pleural or pericardial
serosa, integument, cardiac or vascular endothelium, cardiac valves, and the oral and
conjunctival mucosa. Multiple sites may be involved within the nervous system.
One 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 apoptosis leads to a cell-surface display of plasma and
nuclear antigens in the form of nucleosomes. Thus, dysregulated (intolerant) lymphocytes begin
targeting normally protected intracellular antigens.
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 based on the presence of
complexes of nuclear antigens such as DNA, immunoglobulins, and complement proteins at
these sites. Serum antinuclear antibodies (ANAs) are found in virtually all individuals with
active SLE, and antibodies to native double-stranded DNA (dsDNA) are relatively specific for
the diagnosis of SLE.