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Predisposing Factors: Precipitating Factors:

 Age  Environmental
 Gender UNKNOWN  Drug-Induced
 Hereditary ETIOLOGY  Infection
 Race
 Hormonal

Female producing estrogen First generation familial possession of Infectious agent’s n the body
influencing SLE DNA

Manifestation of heightened levels Similar activity and/or structure to

of estrogen during puberty and Genetic relational DNA passes down to our own systemic cells.
pregnancy next generation

Unknown cause of estrogen

influencing immune response of the Human Leukocyte Antigen Class 1 and 2
HLA system in chromosome 6 in chromosome 6 possess multiple genes
influenced in inheriting SLE.

occurrence of SLE

Human Leukocyte Antigen Class 1 and 2 in chromosome 6

possess multiple genes influenced in inheriting SLE.
Fewer or defective Tingible Body
Macrophages in the body

Defective clearance of early apoptotic cells Defect in mechanism of immune

complex clearance.
Secondary Necrosis of the cells Release of danger signals
Apoptotic chromatin
and nuclei attach to
Release of nuclear fragments as potential Endocytose of antigen material by dendrite surface.
autoantigens. dendritic cells

Defective B-cell
Impaired membrane integrity of dendritic Presented to T-cells activation by
cells autoantigens

Induced maturation of dendritic cells Activation of defective T-cells

Hyper reactivity of
defective B-cells
Production of defective helper T-
Production of self and
non-self antibodies and
B memory cells

Autoantibody Autoreactive cytotoxic T-cell activation Negative abnormal B-
productions cell contribution to
already deficient
immune system.
Inflammation of the affected system
Production of Anti-Nuclear Systemic Lupus Erythematosus
Antibodies (ANA) in renal

Antibodies bind with antigen

Production of ANA, anti-phospholipids, and other specific
Formation of immune
Anti- Lymphocytoto Antiphospholi
Leukocyte Infiltration erythrocyte xic antibody pid antibody
antibody activation activation
Proteinuria activation
Compliment protein cascade

Recruitment of inflammatory Formation of defective immune complex


Alteration in the permeability Hemolyti Hemolysis Direct WBC lysis

and structure of the c Anemia
glomerular basement
Reduced RBC Reduced WBC
count count
Induced Glomerular Injury

Management and If not treated: Management and Lymphopenia

treatment: -Lupus Nephritis treatment:
-Immunosuppressant -Acute or chronic -Iron and Vitamin C
agents renal impairment supplements If not treated:
-Mycophenolate -End-stage renal -Blood Transfusions -Hypoxemia
Mofetil and failure -Immunosuppressant -Chronic Pulmonary
intravenous agents Disease
Thrombocytopenia Platelet destruction
and reduction Cellular
Platelet aggregation
and clot formation

Anti-phospholipids bind with

vascular cells.
Loss of blood Vascular wall
supply to the bone inflammation
Formation of immune
Bone Necrosis Mononuclear cell
Vascular Inflammation
Myalgias Involved Joint
Arthritis collapse
Occurrence of
immunoglobulin and
compliment disposition

Management and If not treated:

treatment: -Further Occurrence of tissue damage
Malar Rash
-Analgesics deterioration of in the acute, subacute and
-Nonsteroidal anti- bones and joints. y chronic levels
inflammatory drugs Discoid Rash
-lifestyle changes
(including exercise and
weight control)
Management and treatment: If not treated:
-Nonsteroidal anti-inflammatory -Further obstruction of
drugs and antimalarials tissue.
-Prevent exposure to light or -Necrosis of the tissue.
other environmental factors. -Gangrene may occur.

Anti-phospholipids and Anti-phospholipids and Specific autoantibody Production of direct

other specific other specific activation in the neuronal tissue
autoantibody activation autoantibody activation neuronal tissue antibodies
in the cardiac linings in the pleural linings

Formation of defective immune complex. Immune Activation of Altered cerebral

disposition cerebral functioning
activation vasculature
Noninfective Noninfective
inflammation of inflammation of the Psychosis
pericardium, membrane around the Micro and Macro vascular Lupus
myocardium and lungs thrombosis Seizures

Cerebral edema and ischemia

Elevated intracranial pressure
Management and If not treated: Management and If not treated:
treatment: -Further inflammation treatment: -Progressive
-Immunosuppressive -Infection and -Immunosuppressive intracranial
drugs deterioration of drugs pressure.
-Non-steroidal anti- myocardial and -Non-steroidal anti- -Deterioration of
inflammatory drugs. pleural linings. inflammatory drugs. cerebral functions
-Lung Collapse -Multiple system
-Cardiac tamponade failure.
-Chronic constrictive
-Congestive Heart

Production of specific ANA in gastric cells Inflammatory response around the liver cells

Antibodies bind with self-antigen. Ineffective biliary cycle

Formation of immune complexes. Increased bilirubin in the body Jaundic

Upper and Lower gastrointestinal

Gastric irritability in Peritoneal

the stomach spasms
Increased gastric acid Ineffective defecation

Induced reflux of Management and If not treated:

Nausea and
gastric acid treatment: -Severe Diarrhea
-Laxatives to
promote effective
Management and If not treated: bowel movement
treatment: Stomach ulceration
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.