PATHOPHYSIOLOGY SLE

UNKNOWNETIOLOGY

Predisposing Factors: Age Gender Hereditary Race Hormonal

Precipitating Factors: Environmental Drug-Induced Infection

Female producing estrogen

Manifestation of heightened levels of estrogen during puberty and

pregnancy

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.

Infectious agent’s n the body

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

Unknown cause of estrogen influencing immune response of the

HLA system in chromosome 6

Spontaneous occurrence of SLE

activation.

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

Secondary Necrosis of the cells

Release of nuclear fragments as potential autoantigens.

Impaired membrane integrity of dendritic cells

Induced maturation of dendritic cells

Release of danger signals

Endocytose of antigen material by dendritic cells

Presented to T-cells

Activation of defective T-cells

Production of defective helper T-cells

Defect in mechanism of immune complex clearance.

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

Negative abnormal B-cell contribution to already deficient immune system.

Autoreactive cytotoxic T-cell activationVarious

Autoantibody productions

Inflammation of the affected system

Systemic Lupus Erythematosus

Production of ANA, anti-phospholipids, and other specific autoantibodies.

Production of Anti-Nuclear Antibodies (ANA) in renal

Antibodies bind with antigen

Formation of immune complexes

Leukocyte Infiltration

Compliment protein cascade

Recruitment of inflammatory cells

Alteration in the permeability and structure of the glomerular basement

Induced Glomerular Injury

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

If not treated:-Lupus Nephritis-Acute or chronic renal impairment-End-stage renal failure

Proteinuria

Anti-erythrocyte antibody activation

Lymphocytotoxic antibody activation

Antiphospholipid antibody activation

Formation of defective immune complex

Hemolysis

Reduced RBC count

Direct WBC lysis

Reduced WBC count

Hemolytic Anemia

Lymphopenia

If not treated:-Hypoxemia-Chronic Pulmonary Disease

Management and treatment:-Iron and Vitamin C supplements-Blood Transfusions-Immunosuppressant agents

Anti-phospholipids bind with vascular cells.

Cellular membrane component damage

Platelet destruction and reduction

Platelet aggregation and clot formation

Thrombocytopenia

Formation of immune complex

Vascular Inflammation

Occurrence of immunoglobulin and

compliment disposition

Vascular wall inflammation

Mononuclear cell infiltration

Loss of blood supply to the bone

Bone Necrosis

Involved Joint collapse

MyalgiasArthritis

Occurrence of tissue damage in the acute, subacute and

chronic levels

Malar RashPhotosensitivit

yDiscoid Rash

Management and treatment:-Analgesics-Nonsteroidal anti-inflammatory drugs-lifestyle changes (including exercise and weight control)

If not treated:-Further deterioration of bones and joints.

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

If not treated:-Further obstruction of tissue.-Necrosis of the tissue.-Gangrene may occur.

Production of direct neuronal tissue

antibodies

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

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

Specific autoantibody activation in the neuronal tissue

Formation of defective immune complex. Immune disposition activation

Activation of cerebral vasculature

Noninfective inflammation of pericardium, myocardium and endocardium

Noninfective inflammation of the membrane around the lungs

Micro and Macro vascular thrombosis

Cerebral edema and ischemia

Elevated intracranial pressure

Altered cerebral functioning

Serositis

PsychosisLupus

HeadacheSeizures

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 anti-inflammatory drugs.

Management and treatment:-Immunosuppressive drugs-Non-steroidal anti-inflammatory drugs.

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

Production of specific ANA in gastric cells

Antibodies bind with self-antigen.

Formation of immune complexes.

Upper and Lower gastrointestinal inflammation

Inflammatory response around the liver cells

Ineffective biliary cycle

Increased bilirubin in the body Jaundice

Gastric irritability in the stomach

Peritoneal spasms

Abdominal Pain

Increased gastric acid content

Ineffective defecation

Induced reflux of gastric acid

Nausea and Vomiting

Management and treatment:-Immunosuppressive drugs-Antiemetic: metacropamide

If not treated:Stomach ulceration

Management and treatment:-Immunosuppressive drugs-Laxatives to promote effective bowel movement

If not treated:-Severe Diarrhea