This document discusses several potential mechanisms that can lead to autoimmune diseases, including the release of sequestered antigens, molecular mimicry, superantigen infection, and mutations in genes regulating the immune response. It also provides an overview of different types of hypersensitivity reactions (types I-IV) and lists some common organ-specific and non-organ-specific autoimmune diseases. Finally, it briefly touches on epidemiology, etiology, clinical features, investigations, and management of systemic lupus erythematosus.

1. • Injury  antigen penetrate  antigen activates T cells in
nodes  T cells attach BOTH eyes
1. RELEASE OF SEQUESTERED
ANTIGEN
• Drugs : Hydralazine, penicillin2. ALTERATION OF SELF
• Antigen = mimic cardiac muscles
• Ie : RF, IE, post strep GN
3. MOLECULAR MIMICRY
• Uncontrollable massive T-helper cells expansion
• Loss of specificity [defense of antigen]
4. SUPERANTIGEN INFECTION
• Presence of signal 2 [x peripheral T-cell tolerance]
• Signal 2 : infection  activation
5. INFECTION OF APC
• ALPS
• fas/fas ligand mut  no apoptosis of lymphocytes  ON!
6. MUTATION IN GENES
REGULATING IMMUNE RESPONSE
‘Leaky ‘
tolerance
Autoimmune
reactivity
Autoimmune
dz

2. • Antigen + antibody
• Antibody agglutinate to form button
• PROB : if [Ab] highfalse –ve,
therefore try at different [ ]  dilute
AGGLUTINATION ASSAYS
INDIRECT
IMMUNOFLOURESCENCE
ELISA

3. TYPE II HS
[Ab mediated
cytotoxicity]
MECHANISM LAB TEST
TYPE III HS
[immune complex
deposition]
MECHANISM LAB TEST
TYPE IV HS
[delayed HS]

4. AUTOIMMUNE DISEASE
ORGAN SPECIFIC
AUTOIMMUNE
THYROIDITIS
IDDM
PERNICIOUS
ANAEMIA
A.I
ADRENALITIS
A.I HEPATITIS
NON-ORGAN
SPECIFIC
RHEUMATOID
DZ
CTD
PRIMARY
VASCULITIS
OTHERS

5. TISSUE
MUSCLES
roduce force and
cause motion
NERVOUS
Transmit info
EPITHELIAL
protect organisms
from
microorganisms,
injury, and fluid loss.
CONNECTIVE
gives shape to
organs and holds
them in place

6. CTD
SLE
-multisystem
-ANA=ANF!
Schleroderma
-skin + internal organ
-CREST syndrome
Myocitis
-increase muscle
enzymes
-worry malignancy
Mixed CTD
Overlapped CTD
Typical autoAb profile
Milder than SLE,scleroD
Sjoren’s Syndrome -salivary + eyes (Sicca)
Vasculitides Tx same as CTD

7. SPECTRUM
APS
-thrombosis
Latent lupus
Neonatal
lupus
End stage
lupus
Drug-induced
lupus
EPIDEMIOLOGY
F:M = 9:1
Dz of young
women [20-
30 yo]
Black>white
Genetics ass.
C4A null alleles
AETIOLOGY
Unknown but
multifactoral
Genetics
-If
HLAB8,DR2,D
R3 +ve 
10% risk
immunologic
al
drugs
Infection :
EBV
Sex hormones
CRITERIA
A RASH POINTS
AN MD
-Malar rash
-Discoid rash
-
photosensitivity
-oral/nasophra
Ulcer
-arthritis
-serositis
-renal d/o
-neuro d/o
-haematolgic
-immuno. d/o
ANA test +ve
INVESTIGATION
FBC- anaemia
High ESR, N
CRP
Serum
autoAb:
-ANA
-anti-dsDNA
-RF
Anti
cardiolipin
[APS]
Histology
Urine cast :
RBC, Protien
TREATMENT
Gluco
corticoid
NSAID
Immuno
supressant
-anti malaria
Remitting relapse!
Different complaint. Urm...
UV light

8. EPIDEMIOLOGY
F:M = 4:1
30-50 yo
Affect SKIN +
INTERNAL ORGAN +
Reynaud’s
Tightening + thickening of
skin
CLINICAL
FEATURES
60%
Limited systemic
sclerosis:
Face. Hand. Feet.
CREST syndrome
40%
Systemic :
Diffuse skin
involvement + organ
fibrosis
INVESTIGATION
FBC :
Anaemia
Raised ESR
Serum auto Ab
-ANA
-Anti topoisomerase
-anti centromere
NOT ALL PX!
Radiology
Oesophageal
monometry
MANAGEMENT
If symptomatic
-ACE inhibitor
PROGNOSIS
10 year survival
-70% : limited
-55% diffuse

9. DEFINITION +
EPI
Inflam and
necrosis of skeletal
muscle fibre + rash
Peak : childhood +
5/6th decade
CLINICAL
FEATURES
Photosensitive
rash
SKIN CHANGES :
-heliotrope
periorbital rash
-gottren’s papule
-erythema on
nailbed
Symmetrical
progressive muscle
weakness
INVESTIGATION
Muscle test/exam
 wasting
Muscle enzymes
[CPK,LDH,AST,
aldolase]
EMG
Muscle biopsy
 Lymphatic
infiltrate +
necrosis
ANF / others
MANAGEMENT
Oral prednisolone
Immunosupressive
therapy
Screen for
malignancy
PROGNOSIS
50% affected
children die within
2 years
Adult better
prognosis
15-30% elderly px
 ass. cancer
Inclusion body myositis?

10. DEFINITION
Inflammation
within the
BV,disrupting the
internal elastic
lamina
May involve :
-many/single organ
-different vessels’
size + type
CLASSIFICATION
CAUSES :
-PRIMARY
-SECONDARY
VESSELS’ SIZE:
-LARGE
-MEDIUM
-SMALL
DIAGNOSIS
Serology : ANCA
Biopsy
-affected organ/
blind
-granulomata?
Angiography : large
V
TREATMENT
Large : steroids
Medium/Small :
steroids + IV
cyclophosphamides
Immunosuppressive
: azathioprine
[steroid sparing tx]
Vasculitis?

11. SECONDARY VASCULITIS
INFECTION
SBE
CF
DRUGS NEOPLASIA RADIATION CRYOGLOBULI
NAEMIA
Meltzer’s triad
-Purpura
-Arthralgia
-Weakness
CTD