1) Direct infection.
2) Immune mediated mechanism.
3) Physical injury.
4) Chemical injury.
1) Direct infection.
Eg
•) Neisseria Infection - Meningococcemia (meningococcal in blood) which damage to vessels and develop vasculitis in skin.
Clinical features::
-> Severe headache.
-> Conscious level.
-> Vasculitis lesion in skin.
•) Rickettsia
eg - Rocky Mount spotted fever.
•) Spirochetle.
eg - Syphilis , Treponema (secondary phage).
Clinical features -::
-> wide spread vasculitis.
•) Fungal infection - Specially person which suffering from Dibetic ketoacidosis
eg - Mucor mycosis.(zygomycosis).
•) Viral condition ( Herpes Zoster Varicella ).
2) Physical injury - like Irradiation.
3) Chemical injury - Toxins.
4) Immune mediated mechanism.
->>> Antigen-Antibody complex (Type 3 hypersensitivity reaction).
Antigen-Antibody complex go to blood vessels and activate local mast cell and mast cell secrete Histamine , and histamine do endothelial cell contraction - increase vascular permeability-> Compliment activate -> MAC (membrane attack complex) -> damage the blood vessels membrane.
i) Hepatitis A , B , C.
ii) Henoch schonlien purpura-> (IgA vasculitis).
IgA deposit in multiple system in mesengium.
iii) SLE (systemetic lupus erethromatus).
iv) Rheumatoid Arthritis->(more dominant synovial joints).
It may involve injury to any tissue of body . It is immune mediated not immune suppurative.
v) Serums sickness ->If we are suffering from Diptheria toxin -> so treatment by horse toxoids ( horse Antibody ) when this antibody come in our body it react with our antibody. And form Ab - Ab complex and destroy our cell and cause --> Vasculitis and Glomerular nephritis, etc.
vi) Drug hypersensitive vasculitis ->
Penicillin act on hapten by binding to serum protein or vessels wall constituents.
eg Streptokinase.
vii) ANCA(anti neutrophilic cytoplasmic antibody) -:associated mediated vasculitis-:
C- ANCA :-
Antibody against - Proteinase 3 & cause Polyangitis.
P- ANCA :-
Antibody against - Myeloperoxidase (normally which involves in O2 free radical generation.) -> ans cause Polyangitis & Chrug strauss syndrome.
Myeloperoxidase and proteinase 3 present in neutrophils, macrophages, & endothelial cell.
Q)How ANCA are produced ?
Ans-: If infection - produce cytokines ( TNF , CSF-GM colony stimulating factor granulocyte and monocytes, Endotoxin).
This cytokynes irritating Neutrophils.
And produce ANCA which will react with MPO and PR-3 and damage microcirculation and cause Vasculitis.
Normally MPO & PR-3 present in cytoplasm.
viii) Direct antibody toxicity (Anti endothelia cell antibody).
- person produce antibody directly react with endothelial cell or capillary or bone marrow of there own.
Eg - Good pasture syndrome ( Ab detected against the Bone marrow and Glomerular capillaries ) and cause Vasculitis.
ix) Cell mediated immunity.
x) Unknown cause.
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