hypersensitivity Flashcards
what can trigger hypersensitivity
infection
environmental substances
self antigen
hypersensitivity due to influenza
exaggerated immune resposne to damaged epithelium in resp tract
cytokine storm –> hypotension and coagulation
hypersensitivity due to dust
can get to lower extremities of resp tract –> area rich in adaptive immune cells
if IgE mediated = allergy symptoms
if IgG mediated = farmers lung
hapten hypersensitivity
haptens are small molecules that bind to proteins and elicit immune response
small environmental antigens can diffuse into skin and act like these
delayed hypersensitivity
T1 hypersensitivity
IgE, eosinophils
degranulation of mast cells
immediate sensitivity, allergy
atopy
genetic tendency to produce IgE to normally innocuous environmental allergens
allergy
clinical expression of atopy
urticaria
angioedema
asthma
dermatitis, eczema
T1: degranulating cells
release of mediators cause allergy
mast cells release after IgE and allergen interact
T1: IgE required, how is it produced
IgE is produced by B cells when they are co-stimulated with IL-4
mast cell mediators
stored: histamine, heparin
new: prostaglandins, leukotrienes
T1: drug Rx
B2 agonists epinephrine antihistamines specific receptor antagonists corticosteroids
T1: how do B2 agonists work
mimic effects of sympathetic nervous system
prevent smooth muscle bronchial contraction in asthma
T1: how does epinephrine work
lifesaving in anaphylaxis
stimulates alpha and beta adrenergic receptors, decreased vascular permeability, inc BP and reverses airway obstruction
T1: how do antihistamines work
block specific histamine receptors
T1: how do specific receptor antagonists work
block effects of leukotrienes
TII hypersensitivity
IgM or IgG react with antigen present on surface of cells
antigen can be self or exogenous - distinction between hypersensitivity and autoimmunity can be blurred
e.g. ABO blood group reaction
TII: how is damage caused
when antibody binds damage arises through:
- complement activation
- Fc binding and stimulation of phagocytes
- antibody dependent cellular toxicity
- effects on target cell: inhibitory, stimulatory
TII: immune mediated haemolysis
alloimmune haemolysis
autoimmune haemolysis
drug induced haemolysis
TII: good pasture’s syndrome
IgG binds glycoprotein in basement membrane of lungs and glomeruli
TII: Grave’s disease
antibodies affecting cell function
hyperthyroidism
thyroid stimulated when autoantibodies bind to TSH receptor
TIII hypersensitivity
IgG antibody reaction to self or exogenous antigen
abnormal deposition of antigen-antibody immune complexes in the tissues
normal immune complex formation
- kept soluble in blood by activated complement components
- travel in blood to liver, spleen
- phagocytes take up complexes
- complexes destroyed once phagocyte has taken up antigen
normal immune complex clearance
complement breaks down large complexes
complement receptor 1 transfers complexes to phagocytes
pathological immune complexes: antigen factors
chronic persistence
abnormal ratio of antigen to antibody
rate of complex formation
pathological immune complexes: host factors
antibody defects
complement defects
Fc or phagocyte defects
TIII: serum sickness
systemic illness
complexes distributed widely throughout many tissues
TIII: arthus reaction
localised disorder
complexes formed in tissues
TIII: clinical disorders
extrinsic allergic alveolitis e.g. Farmer’s lung
post-strep glomerulonephritis
TIII: immune complex disease in kidney
cause of renal failure
glomerulonephritis
TIII: Rx
antigen elimination
removal complexes
immunosuppressive Rx
TIV hypersensitivity
delayed hypersensitivity (2-3days) mediated by Th1 and Th17 cells and the cytokines they secrete
TIV pathophys
- initiated when macrophages recognise danger signals and initiate inflammatory response
- dendritic cell presents antigen to T cell
- TNF secreted by T cells and macrophages
