MANOVA analysis, accounting homework help

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Question Description

Need powerpoints on SLE

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TeacherLarissa
School: University of Maryland

here you gobyee

Dr. Ashiono E. M

OUTLINE









Definition
Epidemiology
Pathophysiology
Classification and diagnosis
Clinical Features
Lupus related syndromes
Treatment
Prognosis

DEFINITION
• Inflammatory autoimmune disorder affecting
multiple organ systems characterized by the
production of autoantibodies directed against
cell nuclei and cytoplasmic antigens reflecting
a global loss of self-tolerance.
• SLE can affect any organ system, but it
mainly involves the skin, joints, kidneys, blood
cells, and nervous system ”

EPIDEMIOLOGY
• Prevalence influenced by age, gender, race,
and genetics





Prevalence: 1:2000
Peak incidence 14-45 years
Black > White (1:250 vs. 1:1000)
Female predominance :4 : 1 before puberty to 8 :
1 afterward.
• HLA DR3 association, Family History

• Severity is equal in male and female
• Disease onset before 8 yr of age is unusual,
although lupus has been diagnosed even in
the 1st yr of life

Epidem Cont:
• Genetic (HLA-B8, HLA-DR2, and HLADR3)
• Abnormal immune response

• Environmental
• UV
• Viruses
• Hormones (Estrogen)

• Congenital complement deficiencies
also predispose to SLE

Pathogenesis – immunologic
abnormalities
• Central concept:
• Tolerance to self violated→→Autoantibodies
produced
• Dysregulation of apoptosis in lupus may lead to the
persistence of self-reactive lymphocytes that
normally undergo apoptosis
• Abnormalities in macrophages and other cells of
the innate immune system
• Abnormal activation of interferon and toll-like

Mechanism of autoantibody production and tissue
injury in lupus

B Cells in SLE
• Auto antigen specific B cells are found in
everyone

• Anergy and apoptosis prevents activation
In SLE : these B cells activate and produce
autoantibodies due to loss of self tolerance
Immune complex formation→→complement
consumption

T cells in SLE
• Probable central role in B cell activation
• Autoreactive T cell activation: failure of
• Thymic deletion
• Peripheral T cell anergy
• T suppresor cells function

• Futile activation results in impaired cellular
immunity

Mechanisms of tissue damage in SLE
• Immune complex deposition in tissues and
vessels initiates inflammation leading to
damage
• Autoantibodies
• Cell mediated cytotoxicity

CLINICAL FEATURES: Mucocutaneous








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