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SLE Pathophysiology and Risk Factors

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Systemic lupus erythematosus (SLE) is an autoimmune disease with no known cause. Genetic and environmental factors contribute to SLE, which results from the immune system attacking the body'…

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joyrena ochondra
  • Overview of SLE Pathophysiology
  • Antibody Formation Process
  • Tissue Damage and Symptoms
  • Complications of SLE

Modifiable risk factors: Systemic Lupus Erythematosus Non-modifiable risk factors:

Environmental Factors: Genetic Factors


(SLE)
 UV light exposure, exposure  Monozygotic Twins
from sunlight, and
 Epigenetics
fluorescent light bulbs. Unknown cause
Immunologic Factors
 Medication ( sulfa drugs,
penicillin, or antibiotic Hormonal Factors
drugs)
Injury to the bodies own cell  Estrogen
 Viral Infections
 20x more common in women
 Emotional Stress during reproductive
Damage cell protein in years( 15– and 45 yrs.
 Stress on the body( Surgery
Old)
and pregnancy
their DNA
Race
 Silica dust exposure
 African-Americans
Lifestyle
Injury to group of cells  Hispanics
 Cigarette Smoking,
 Asian-Americans

Organ injury

Apoptosis
Cell Repair Flare ups
(Programmed cell death)

Exposure of apoptotic antibodies (nuclear


antigens)
Genetic factor
Susceptibility genes Less effective clearance of nuclear antigens recognition of
foreign bodies
Build-up of nuclear antigens Creates ANA
immune response

B-cells swing by and starts


antinuclear antibodies(ANA) Deposits in the tissue
production

Inflammation
Anti-nuclear antibodies
bind nuclear antigens

Formation of antigen
antibodies complexes

Get into the blood and drift


away

Deposited or stick to the vessel


wall in the different organs and
tissue (skin, kidneys, joints, and
heart)

Deposited complies antibodies


initiates local inflammatory reaction.
Damage to activation of
compliment system Type III
Hypersens
itivity
Huge enzyme cascade reaction

Cell membranes become permeable to


fluid and molecules that let them go in
and out causing cell to burst and die.

Tissue damage Immune


response

Signs and
Type III– Hypersensitivity
symptoms:
Activation
 Fever
 Weight loss
Targets other cells (RBC,
 Joint Pain
WBC, Phospholipids)
 Rash
 Fatigue
 Raynaud’s Phagocytosis and destruction
phenomenon
 Chest pain
 SOB
Type II Hypersensitivity reaction
COMPLICATIONS:
 Skin Neurologic
Malar rash Seizures
Discoid rash Psychosis
Photosensitivity
 Mucosa Hematologic
Ulcers Thrombocytopenia
 Serosa Anemia
Pleurisy Leukopenia
Pericarditis Vasculitis
 Myocarditis Kidney
Endocarditis Diffuse proliferative glomerulonephritis
 Joints Renal disorder
Arthritis
Bone tissue death (avascular necrosis) Pregnancy Complications (Preeclampsia)
Increases the risk for cancer People with lupus are more vulnerable to infection

Source: Brunner’s & Suddarth’s Textbook for Medical Surgical Nursing 14th edition
https:// [Link]/[Link]/Systemic_lupus_erythematosus_pathophysiology

Genetic factor recognition of foreign bodies Susceptibility genes Less effective clearance of nuclear antigens Exposure of ap
Creates ANA immune response Build-up of nuclear antigens B-cells swing by and starts antinuclear antibodies(ANA) production D
Type III Hypersens itivity reaction Damage to activation of compliment system Huge enzyme cascade Cell membranes become perme
COMPLICATIONS: Skin Neurologic Malar rash

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