PATHOPHYSIOLOGY SLE

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

UNKNOWN
ETIOLOGY

First generation familial possession of

influencing SLE DNA
Genetic relational DNA passes down to
next generation

Human Leukocyte Antigen Class 1 and 2

in chromosome 6 possess multiple genes
influenced in inheriting SLE.
Spontaneous
occurrence of SLE
activation.

Human Leukocyte Antigen Class 1 and 2 in

chromosome 6 possess multiple genes influenced
in inheriting SLE.

Precipitating Factors:
Environmental
Drug-Induced
Infection

Infectious agents n the body

Similar activity and/or structure to
our own systemic cells.

Fewer or defective Tingible Body

Macrophages in the body
Defective clearance of early apoptotic cells
Secondary Necrosis of the cells

Defect in mechanism of immune

complex clearance.
Release of danger signals

Release of nuclear fragments as potential

autoantigens.

Endocytose of antigen material by

dendritic cells

Impaired membrane integrity of dendritic

cells

Presented to T-cells

Induced maturation of dendritic cells

Activation of defective T-cells

Production of defective helper Tcells

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

Autoreactive cytotoxic T-cell activation

Inflammation of the affected system

Negative abnormal Bcell contribution to

already deficient
immune system.

Production of Anti-Nuclear
Antibodies (ANA) in renal

Systemic Lupus Erythematosus

Antibodies bind with antigen

Production of ANA, anti-phospholipids, and other specific

autoantibodies.

Formation of immune
complexes
Leukocyte Infiltration
Proteinuria

Compliment protein cascade

Recruitment of inflammatory
cells
Alteration in the permeability
and structure of the
glomerular basement

Lymphocytoto
xic antibody
activation

Antiphospholi
pid antibody
activation

Formation of defective immune complex

Hemolyti
c Anemia

Induced Glomerular Injury

Management and
treatment:
-Immunosuppressant
agents
-Mycophenolate
Mofetil and
intravenous
Cyclophosphamide

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

Direct WBC lysis

Reduced WBC
count

Lymphopenia

If not treated:
-Hypoxemia
-Chronic Pulmonary
Disease

Platelet destruction
and reduction

Thrombocytopenia

Platelet aggregation
and clot formation

Cellular
membrane
component
damage

Anti-phospholipids bind with

vascular cells.
Loss of blood
supply to the bone

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

Occurrence of tissue damage

in the acute, subacute and
chronic levels

Management and treatment:

-Nonsteroidal anti-inflammatory
drugs and antimalarials
-Prevent exposure to light or
other environmental factors.

Anti-phospholipids and
other specific
autoantibody activation
in the cardiac linings

Anti-phospholipids and
other specific
autoantibody activation
in the pleural linings

Formation of defective immune complex.

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

Micro and Macro vascular

thrombosis

Cerebral edema and ischemia

Serositis
Elevated intracranial pressure

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.

Production of specific ANA in gastric cells

Antibodies bind with self-antigen.
Formation of immune complexes.

Management and
treatment:
-Immunosuppressive
drugs
-Non-steroidal antiinflammatory drugs.

Inflammatory response around the liver cells

Ineffective biliary cycle
Increased bilirubin in the body

Upper and Lower gastrointestinal

inflammation

Gastric irritability in
the stomach

Peritoneal
spasms

Abdominal
Pain

Jaundic
e

If not treated:
-Progressive
intracranial
pressure.
-Deterioration of
cerebral functions
-Multiple system
failure.

Increased gastric acid

content

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