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Diseases
Immune system :
Distinguish foreign antigens
from self component of body
tissues.
Autoimmune response : Activating
lymphocyte and producing
autoantibody against selfantigens.
Autoimmune disease :
result from tissue injury
cause by T-cell or antibodies
that react against selfantigens
Classification of Autoimmune
diseases
1.Tissue or organ specific disease
Autoantibody against a single
organ or tissue
Systemic Lupus
Erythematosus
(SLE )
Chronic systemic
autoimmune disease
characterized by loss of
self-tolerance and
production of
autoantibodies
1. MALAR RASH
2. DISCOID RASH
3. PHOTOSENSITIVITY SKIN
RASH
4.ORAL OR NASOPHARYNGEAL
ULCERATION
5. SEROSITIS. PLEURITIS OR
PERICARDITIS
6. NON-EROSIVE ARTHRITIS
7. RENAL DISORDER
Persistant proteinuria
>0.5 g/day OR
>3+ OR
Cellular castes
8.
NEUROLOGICAL
DISORDER
SEIZURES OR
PSYCHOSIS
9. HEMATOLOGICAL DISORDER
Hemolytic anemia (AIHA)
Leukopenia <4000/mm3, on 2 or
more occasions
Lymphopenia <1500/mm3, on 2 or
more occasions
Thrombocytopenia <100000/mm3
ANAs
indirect immunofluorescence
positive in >95% patient with SLE
but it is not specific
Anti double-stranded DNA (40-60%)
and Anti Smith (Sm) (20-30%)
High specificity in diagnosis of SLE
LE cell test
positive ~80% of SLE
LE cell is any phagocytic
(neutrophil or macrophage)
phagocytize round
hamatoxylin bodies
Found in pleural or synovial fluid
or in tissue section
LE cell
Pathological Abnormallities in
SLE
Kidney :
immune complex deposit
in renal structure
increase thickness and
rigidity of the GBM of
peripheral capillary loops
"wire loops" are common
Wire
loop
Skin :
Liquefactive degeneration
(vacuolization) of the basal layer
of the epidermis
Edema and perivascular
mononuclear in dermis
Deposition of immunoglobulin
along the dermal-epidermal
junction
Pericarditis
Nonbacterial endocarditis
(Libman-Sacks endocarditis)
cause by vegetations
affected to the valve leaflet
Mesangial become thickened
obliterate serosal cavity
Spleen :
Capsular thickening
Follicular hyperplasia
Thickening and perivascular
fibrosis Onion-skin
appearance
is pathognomonic
Sjogrens
syndrome
An autoimmune disease
characterized by destruction
of the lacrimal and salivary
glands
Result in dry eyes
(keratoconjunctivitis sicca)
and dry mouth (xerostomia)
Including respiratory and
gastrointestinal tracts
Pathogenesis
Anti ribonucleoprotein Ab
Anti SSA (Ro)
Anti SSB (La)
Perivascular lymphocytic
infiltration
Enlargement of salivary &
lacrimal glands (Mikulicz
syndrome)
Ductal epithelial
hyperplasia
Systemic
sclerosis
(scleroderma)
An autoimmune disease
characterized by fibroblast
stimulation and deposition
of collagen in skin and
internal organs
Classified
disease
1. Systemic sclerosis
- Widespread skin involvement
- Early internal organs involvement
- Anti DNA topoisomerase1 Ab (Scl-70)
2. Localized scleroderma
- skin involvement of face and hands
- Late internal organs involvement
- Anti centromere Ab
MINOR CRITERIA:
1. SCLERODACTYLY:
Skin changes limited to the fingers
Pathological Abnormality in
Scleroderma
Skin :
Early stages
Skin have a doughy
consistency
perivascular infiltrates
containing CD4+T cells
swelling and
degeneration of collagen
fibers
Thickening of basal
laminar, endothelial cell
-damage and partial
occlusion of capillaries
and small arteries
DOUGHY SKIN
FISH MOUTH
Edematous phase
Progressive fibrosis of
dermis
Increase of compact
collagen in dermis
Thinning of epidermis
Atrophy of dermal
appendages
Hyaline thickening of
walls of dermal
arterioles & capillaries
Patient with CREST may
have diffuse
subcutaneous
calcification
Advanced stages
Clawlike appearance
of fingers
Loss of blood supply
may lead to cutaneous
ulceration & atrophic
changes in the
terminal phalanges
Alimentary tract :
Progressive atrophy and
collagenous fibrous
replacemant of muscle
Lower 2/3 of esophagus
develops a rubber-hose
inflexibility
Lungs :
Pulmonary hypertension
& interstitial fibrosis
Pulmonary hypertension
(vascular changes,
pulmonary vasospasm)
Scleroderma lung
Rheumatoid
Arthritis
Chronic inflammatory
disease affects primarily
the joints, may involve
extra-articular tissue
Associated with anti-IgG
autoantibodies called
rheumatoid factors
Pathogenesis
Proliferative changes in the
synovial membrane
infiltrated with
lymphocytes, plasma cell
and macrophages
Destructive erosion of joint
cartilage and bone cartilage
Joint space become
obliterated
3. SWELLING OF
WRIST,MCP OR PIP
for at least 6 wks.
4. SYMMETRICAL JOINT
SWELLING.
for at least 6 wks.
6. SERUM RHEUMATOID
FACTOR POSITIVE
7. RHEUMATOID NODULES
Inflammatory
Myopathies
Heliotro
ph
Grottons sign
Polymyosit
is
THE END