Hypersensitivity Disease 2 Flashcards
describe Type II hypersensitivity reactions
direct cell effects (cell surface antigens), onset in seconds/hours (if IgM/G pre-formed)
involves IgM or IgG antibodies to cell surface (or extracellular matrix)
normal adaptive immune response leads to the production of IgM/G antibodies that target;
self antigens (autoimmune diseases)
cross-reactive antigens (autoimmune diseases)
describe pathophysiological mechanisms of Type II
immunological mechanism; complement system activation opsonisation and phagocytosis ADCC via NK cells or eosinophils all resulting in cell death
other mechanisms;
anti-receptor antibodies disrupt the normal function of cell surface receptor
describe Goodpasture’s syndrome
type II hypersensitvity an autoimmune disease that affects the lungs and kidneys; pulmonary alveolar haemorrhage kidney disease (glomerulonephritis)
defined by the presence of auto-reactive antibodies to the alpha3 chain of type IV collagen present in the basement membranes of alveoli and glomeruli
complement system activation is overwhelming and so the ability to inhibit formation of MAC is overcome
thought to be result of environmental insult (smoking, infections, exposure to certain drugs) in a person with genetic susceptibility
treatment;
corticosteroids, cyclophosphamide
plasmapheresis
stop smoking
describe type III hypersensitivity
immune complex mediated (soluble antigens), onset hours (if IgG pre-formed)
in the presence of excess antigen, antibody binds forming small immune complexes. These are trapped in small blood vessels, joints and glomeruli
resulting in;
activation of complement system (cell lysis and opsonisation)
opsonisation (antibody-mediated phagocytosis)
infiltration and activation of neutrophils and macrophages (tissue damage)
describe acute hypersensitivity pneumonitis
Type III hypersensitivity - immune complexes deposited in the walls of alveoli and bronchioles
inhalation of antigen and deposited in lung
can be associated with;
dry cough/wheeze - inflammation of terminal bronchioles via phagocytes and complement system
pyrexia and malaise - inflammatory response
breathlessness - alveolitis via activated phagocytes and complement system (resulting in decreased efficiency of gas transfer)
examination normal
stimulated antibody formation antibodies form immune complexes with antigen resulting in complement activation; inflammation infiltration of inflammatory molecules tissue damage
describe causes of acute hypersensitivity pneumonitis
farmer's lung bird fancier's lung malt worker's lung cheese worker's lung maple bark stripper's lung
describe management of type III hypersensitivity
avoidance
decrease inflammation - corticosteroids
decrease production of antibody - immunosuppression
describe type IV hypersensitivity
delayed type hypersensitivity
onset - days
describe autoimmune disease of type IV hypersensitivity
type 1 diabetes
psoriasis
rheumatoid arthitis
describe non-autoimmune disease of type IV hypersensitivity
contact dermatitis
TB
leprosy
sarcoidosis;
multi-system granulomatous disease, idiopathic
underlying pathophysiology is type IV hypersensitivity to unknown allergen
failure to clear antigen via CD4+, CD8+ and B cells results in persistent stimulation and granuloma formation
cellular rejection of solid organ transplant
describe management of sarcoidosis
watchful waiting - many patients undergo spontaneous remission
NSAIDS - acute onset of disease
systemic corticosteroids - blocks T cell activation, blocks macrophage activation
describe ABCD of hypersensitivity
I - Allergic, Anaphylaxis, Atopy
II - antiBody
III - immune Complex
IV - Delayed
