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Sle Concept Map Part 1

1) Systemic lupus erythematosus (SLE) is influenced by a combination of predisposing genetic and environmental factors. 2) SLE occurs when a combination of genetic, hormonal, and environmental factors lead to defects in the immune system's ability to clear cellular debris and regulate autoreactive immune cells. 3) This impaired clearance and dysregulated immune response results in the production of autoantibodies that attack the body's own tissues and organs, causing the signs and symptoms of SLE.

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0% found this document useful (0 votes)
2K views1 page

Sle Concept Map Part 1

1) Systemic lupus erythematosus (SLE) is influenced by a combination of predisposing genetic and environmental factors. 2) SLE occurs when a combination of genetic, hormonal, and environmental factors lead to defects in the immune system's ability to clear cellular debris and regulate autoreactive immune cells. 3) This impaired clearance and dysregulated immune response results in the production of autoantibodies that attack the body's own tissues and organs, causing the signs and symptoms of SLE.

Uploaded by

Vane Ucat
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PATHOPHYSIOLOGY

PREDISPOSING FACTOR PRECIPITATING FACTOR


Age, gender, heredity, race, UNKNOWN Environment, drugs, infection,
hormones, history
ETIOLOGY lifestyle

Female producing estrogen 1st generation familial Influencing agents in the body
possession of influencing SLE
DNA

Increase level of estrogen Similar activity/structure to our


Genetic relational DNA passes own systemic cell
down to ext generation

Unknown cause of estrogen


influencing immune response Human leukocyte antigen class
of the human leukocyte system 1 &2 in chromosome 6
in chromosome 6 possesses multiple genes
influencing in inheriting SLE

Occurrence of SLE activation

Fewer or defective tangible Human leukocyte antigen class


body macrophages in the body 1 &2 in chromosome 6 posses Defect in mechanism of
multiple genes influenced in immune complex clearance
inheriting SLE
Defective clearance of early
apoptotic cell Apoptic chromatin and nuclei
Release of danger signs attach to dendrite

Secondary necrosis of cell

Endocytose of antigen material Defective B cell activation by


by dendritic cell autoantigen
Release of nuclear fragments
as potential auto antigens
Presented to T cells Hyperactivity of defective B cell

Impaired membrane integrity


of dendrite cell
Activation of defective T cell Production of self and non-self
antibodies and B memory cells

Induced maturation of
dendritic cell Production of defective T cells
Negative abnormal B cell
contribution to already
deficient immune system

SYSTEMIC LUPUS
ERYTHEMATOSU
S

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