Lague, Inah Krizia O.

BSN 3D
Systemic Lupus Erythematous
Predisposing Factors: Precipitating Factors:
Age Environmental
Gender UNKNOWN Drug-Induced
Hereditary ETIOLOGY Infection
Race
Hormonal

Female producing estrogen First generation familial possession of Infectious agent’s n the body
influencing SLE DNA

Manifestation of heightened levels Similar activity and/or structure to

of estrogen during puberty and Genetic relational DNA passes down to our own systemic cells.
pregnancy next generation

Unknown cause of estrogen

influencing immune response of the Human Leukocyte Antigen Class 1 and 2
HLA system in chromosome 6 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.
 Fewer or defective Tangible Body
Macrophages in the body

Defective clearance of early apoptotic cells Defect in mechanism of immune

complex clearance.
Secondary Necrosis of the cells Release of danger signals
Apoptotic chromatin
and nuclei attach to
Release of nuclear fragments as potential Endocytosis of antigen material dendrite surface.
autoantigens. by dendritic cells

Defective B-cell
Impaired membrane integrity of dendritic Presented to T-cells activation by
cells autoantigens

Induced maturation of dendritic cells Activation of defective T-cells

Hyper reactivity of
defective B-cells
Production of defective helper T-
cells
Production of self and
non-self antibodies and
B memory cells

Various
Autoantibody Autoreactive cytotoxic T-cell activation Negative abnormal B-
productions cell contribution to
already deficient
immune system.
Inflammation of the affected system
 SYSTEMIC LUPUS
Production of Anti-Nuclear
ERYTHEMATOUS
Antibodies (ANA) in renal (SLE)
cells

Antibodies bind with antigen

Production of ANA, anti-phospholipids, and other specific
autoantibodies.
Formation of immune
complexes
Anti- Lymphocytoto Antiphospholi
Leukocyte Infiltration erythrocyte xic antibody pid antibody
antibody activation activation
Proteinuria activation
Compliment protein cascade

Recruitment of inflammatory Formation of defective immune complex

cells

Alteration in the permeability Hemolyti Hemolysis Direct WBC lysis

and structure of the c Anemia
glomerular basement
Reduced RBC Reduced WBC
count count
Induced Glomerular Injury

Lymphopenia
 Thrombocytopenia Platelet destruction
and reduction Cellular
membrane
component
damage
Platelet aggregation
and clot formation

Anti-phospholipids bind with

vascular cells.
Loss of blood Vascular wall
supply to the bone inflammation
Formation of immune
complex
Bone Necrosis Mononuclear cell
infiltration
Vascular Inflammation
Myalgias Involved Joint
Arthritis collapse
Occurrence of
immunoglobulin and
compliment disposition

Occurrence of tissue damage

Malar Rash
Photosensitivit in the acute, subacute and
y chronic levels
Discoid Rash
Anti-phospholipids and Anti-phospholipids and Specific autoantibody Production of direct
other specific other specific activation in the neuronal tissue
autoantibody activation autoantibody activation neuronal tissue antibodies
in the cardiac linings in the pleural linings

Formation of defective immune complex. Immune Activation of Altered cerebral

disposition cerebral functioning
activation vasculature
Noninfective Noninfective
inflammation of inflammation of the Psychosis
pericardium, membrane around the Micro and Macro vascular Lupus
Headache
myocardium and lungs thrombosis Seizures
endocardium

Cerebral edema and ischemia

Serositis
Elevated intracranial pressure
 Diagnostic Test Categories of Treatment Management
 ANA (antinuclear  Recognize flare-ups
antibody)titer o Conservative  Schedule rest & activity
 Maintain integrity of
 Inc. ESR and C o Aggressive immune system
reactive protein  Lessen stress
o  Avoid environmental
 Decrease C3 and triggers
C4  Stop drugs that induces
attacks
 CBC  Plasmapheresis

 Coomb’s test Pharmacologic Management:

NSAIDS and Aspirin
Hydroxychloroquine
Glucocorticosteroids
Immunosuppressive
Production of specific ANA in gastric cells Inflammatory response around the liver cells therapy
(Cyclophosphamide)
Gamma globulin
Antibodies bind with self-antigen. Ineffective biliary cycle

Formation of immune complexes. Increased bilirubin in the body Jaundic

e
Upper and Lower gastrointestinal
inflammation

Gastric irritability in Peritoneal

Abdominal
the stomach spasms
Pain
Increased gastric acid Ineffective defecation
content

Induced reflux of
Nausea and
gastric acid
Vomiting
Acute Glomerulonephritis
Etiology

Post-streptococcal infection  Streptococcal

(group-A, beta hemolytic) Infection of the
Respiratory
 Impetigo
 IgA neropathy
 Lipid Nephrosis
Release of material from the organism,
into the circulation (antigen)

Formation of antibody

Immune complex reaction in the

glomerular capillary

Inflammatory response

Proliferation of epithelial cells lining

glomerolus & cells between
endothelium & epithelium of capillary
membrane
 Swelling capillary membrane &
infiltration with leukocytes

↑ Permeability of base membrane

Occlusion of the capillaries of the

glomeruli vasospasm of afferent
arterioles

↓ Glomerular filtration rate

↓ Ability to form filtrate from

glomeruli plasma flow

Retention of H2O & Na; hypovolemia; Diagnostic Test

circulatory congestion
 Blood testing: elevated
antistreptolysin- O titers,
electrolytes,BUN
and creatinine, low serum
protein, elevated anti-Dnase
B titers

 Kidney biopsy

 Urinalysis: presence
of RBC, WBC, mixed call
casts & protein.
 Edema
Hypertension
↓ urinary output
Urine dark in color
Anorexia
Irritability lethargy ACUTE
Oliguria
Hematuria GLOMERULO-
Proteinuria NEPHRITIS
Bibasilar crackles

Management Nursing Management

Treatment of - Check V/S and electrolyte

primary disease values.
- Monitor I/O and weigh OD
Antibiotics, - Assess serum creatinine,
anticoagulants, BUN and urine creatinine
vasodilators, clearance levels daily.
corticosteroids - Report signs of ARF.
- Monitor for ascites and
Fluid restrictions edema.
- Provide a high-caloric diet
Dialysis that’s low in protein, sodium,
potassium and fluids.
Plasmapheresis - Provide good skin care and
oral hygiene.
- Take diuretics in the
morning.
- Prevent secondary infection.