Hypersensitivity Flashcards
true allergy or atopy
Type 1 Hypersensitivity
IgE antibody-mast cell mediated in response to antigen
Type 1 Hypersensitivity
sensitization phase
Type 1 Hypersensitivity
first exposure to allergen protein that binds haptens
no reaction
IgE to the allergen is produced long term by the plasma cells and binds to ______ on mast cells
Fc epsilon R1 IgE receptors
elicitation phase
hypersensitivity reaction upon repeat exposure
occurs only after sensitization
allergen cross links the IgE on the mast cell _______
Fc epsilon R1
immediate hypersensitivity is mediated by
vasoactive amines and lipid mediators
late phase hypersensitivity is mediated by
cytokines
mast cells are located in
all connective tissue
Fc epsilon R1
high affinity receptor on mast cells and basophils
ITAM phosphorylation causes
release of preformed mediators
arachidonic acid metabolism secreting lipid mediatiors
activation of cytokine transcription genes to secrete cytokines
histamine is released
upon mast cell degranulation
effect: histamine
vasodilation, increased vascular permeability, smooth muscle contraction, mucous production
proteases are released upon
degranulation
proteases cause
tissue damage
prostaglandins are released
arachidonic acid metabolism
prostaglandins cause
vasodilation
leukotrienes are released
arachidonic acid metabolism
leukotrienes cause
prolonged smooth muscle contraction
synthesized THF-a causes
endothelial cell activation
inflammation
neutrophil activation
synthesized IL-4 causes
IgE class switching by B cells
synthesized IL-5 causes
eosinophil generation and activation
antihistamines
reduce the potential for histamine to bind and cause symptoms
H1 antagonists: first gen
antihistamines that cause sedation, short acting
first gen H1 antagonists: drug names
diphenhydramine, hydroxyzine, doxepin, cyproheptadine
H1 antagonists: 2nd gen
antihistamines that are long acting, little to no sedation
H1 antagonists: 2nd gen drug names
cetrirzine, levocetirizine, loratadine, desloratadine, fexofenadine
H2 antagonists
receptors mostly in gut
indigestion/heartburn
H2 antagonists: drug names
ranitidine and famotidine
1st line in anaphylaxis
epinephrine
montelukast, zafirlukast
leukotriene receptor antagonists
relax bronchial smooth muscle
administration: corticosteroids
inhaled, topical, oral, IV, IM
allergy shots are
desensitization
repeated increasing dose of allergens to help the system overcome the allergy
desensitization
cromolyn
inhibits mast cell degranulation
mepolizumab
reslizumab
benralizumab
anti IL-5 therapy
duplimab
anti IL-4, IL-13 therapy
clinical use: duplimab
atopic dermatitis in adults
asthma
antibodies can be directed against cells or extracellular matrix components
Type II
antibodies/antigens can bind and be directly deposited in blood vessels
Type III
complement and Tc mediated recruitment and activation of leukocytes
Type II
opsonization and phagocytosis of cells
Type II
cell function abnormalities by competitive inhibition or activation
Type II
complement activation released C3a and C5a
Type II
Type II activates
neutrophils
neutrophils generate ______ through ROS and lysosomal enzymes
inflammation/injury
associated with strep infection
Type II
mycarditis
Type II
anemia/thrombocytopenia
Type II
autoimmune hemolytic anemia: target
erythrocyte membrane proteins
autoimmune hemolytic anemia: pathophys
opsonization and phagocytosis of erythrocytes
autoimmune hemolytic anemia: effect
hemolytic anemia
autoimmune (idiopathic) thrombocytopenia purpura: target
platelet membrane proteins
autoimmune (idiopathic) thrombocytopenia purpura: pathophy
opsonization and phagocytosis of platelets
autoimmune (idiopathic) thrombocytopenia purpura: effect
bleeding
goodpasture syndrome: target
NC protein in kidney glomeruli and lung alveolar basement membranes
goodpasture syndrome: pathophys
complements and Fc receptor mediated inflammation
goodpasture syndrome: effect
nephritis
lung hemorrhage
grave’s disease: target
TSH receptor
grave’s disease: pathophy
antibody mediated stimulation of TSH receptors
grave’s disease: effect
hyperthyroidism
myasthenia gravis: target
Ach receptor
myasthenia gravis: pathophys
antibody competitively inhibits Ach binding which leads to down regulation of receptors
myasthenia gravis: effects
muscle weakness
paralysis
pemphigus vulgaris: target
desmoglein- protein in intercellular junction of epidermal cells which holds cells together
pemphigus vulgaris: pathophys
antibody mediated activation of proteases cause disruption of intercellular adhesions
pemphigus vulgaris: effect
bullae (large fluid filled blisters)
pernicious anemia: target
intrinsic factor of gastric parietal cells
pernicious anemia: pathophys
neutralization of intrinsic factor leads to decreased absorption of vitamin B12
pernicious anemia: effect
anemia
rheumatic fever: target
streptococcal cell wall antigen; antibody cross reacts with myocardium
rheumatic fever: pathophys
inflammation
macrophage activation
rheumatic fever: effect
myocardities
arthritis
Type III hypersensitivity diseases
SLE
polyarteritis nodosa
post-streptococcal glomerulonephritis
serum sickness
arthus reaction
antibody specificity: SLE
DNA, nucleoproteins, other
manifestation: SLE
nephritis, arthritis, vasculitis
antibody specificity: polyarteritis nodosa
mostly unknown, hep B surface antigen
manifestation: polyarteritis nodosa
vasculitis
antibody specificity: post-streptococcal glomerulonephritis
streptococcal cell wall antigens
manifestation: post-streptococcal glomerulonephritis
nephritis
antibody specificity: serum sickness
protein antigens
manifestation: serum sickness
systemic vasculitis
nephritis
arthritis
antibody specificity: arthus reaction
protein antigens
manifestation: arthus reaction
cutaneous vasculitis
arthus reaction
formation of complexes at the site of antigen injection
disease caused by deposition of circulating antibody/antigen complexes in blood vessels
Type III
activation of complement and inflammatory cascade by circulating complexes
Type III
Type II and III treatment
corticosteroids
plasmapheresis
IVIg
Anti CD20 antibody (rituximab)
local autoimmune reaction with T cells directed against cellular antigens within that local tissue
Type IV
persistent reaction to chemicals
poison ivy, chemicals, metals, triggers
Type IV
response to superantigens
Type IV
Type IV hypersensitivity disease
myelin proteins
demyelination in the CNS, sensory and motor dysfunction
multiple sclerosis
Type IV hypersensitivity disease
unknown antigens
inflammation of synovium and erosion of cartilage and bone in joints
rheumatoid arthritis
Type IV hypersensitivity disease
pancreatic islet antigens
impaired glucose metabolism, vascular diseaase
Type 1 DM
Type IV hypersensitivity disease
unknown
inflammation of the bowel wall; abdominal pain, diarrhea, intestinal bloating
IBD
chron’s
Type IV hypersensitivity disease
modified skin proteins
delayed type hypersensitivity rash
contact sensitivity
poison ivy
metal allergy
Type IV hypersensitivity disease
microbial proteins
chronic granulomatous inflammation
tuberculosis
Type IV hypersensitivity disease
viral. encoded proteins
cytotoxic T cells cause death, hepatic dysfunction, fibrosis
hep B and C
Type IV hypersensitivity disease
microbial super antigens
cytokine release causing fever and shock
Type IV hypersensitivity disease
Type IV hypersensitivity disease treatment
anti-inflammatories: corticosteroids
Decrease T cell response of effects: TNF-a, IL receptor antagonists, anti-CD20