lect 15.2 Flashcards
when would an oral food challenge be administered?
Clinical suspicion of food allergy but diagnosis uncertain based on SPT and / or
serum specific IgE
helps detemine if a patient has outgrown an allergy
what allergy is most and least common to outgrow
diary
shellfish
what kind of reaction occurs from biting not venomous insects
local reaction
extremely rare for systemic reaction
what kind of reaction comes froms stinging insects
type 1 hypersensitivity
what are the clinical interventions for type 1
enviroental interventino
- avoidance and masks
pharmacological intervention
immunological intervention
what are the pharmocological interventions for type 1
epinepherine- relxes SM, dec cAMP (prevent degranualation), inc vardiac output, reduces vascular permeability
anti histamins
cortisone- acts on first phase symptoms
what is hyposensitixation
immunological intervention for type 1 hypersensitivity
shifting from TH2 igE respnose to TH1 igG4 response
what does shifting from igE to igG lead to
turning on the inhibitory mast cell FcR to prvent degranulation
desensitization leading to inc igG4,
dec igE
dec basophil and mast cell activation
what is the function of T reg cells
they operate at the site of the immune response and are non specific
NOT SYSTEMICALLY
what are some other immunological interventions for typr 1
anti igE monoclonal antibody that binds to CIRCULATING igE
cytokines and anti cytokines and cytokine receptor antagonists
adhesion molecule antagonists
what are the adhesion molecule antagonsits used in typr 1 treatment
anti ICAM 1 treatment for asthma
what cytokines are ysed fro type 1 treatment
il 12
il 10
what are the anti cytokines used in type 1
anti il 4
what are the anti igE monoclinal antibodies drugs used
omalizumab
xolair
approved for asthma and food allergies
explain protective role of IgE
igE on mast cell binds to worm/ helminth antigen
leads to degranulation
extraceuular killing of the helminth
what antibodies used in type 2
igM - primary respsone
igG - secondary - class switch
what does type 2 hypersensitivity depend on
Ab binding on self antigen on cell
exposure requirements of tye2
previous exposure not required but increaes the change of reaction the more you are exposed
what type 2 reaction occurs if you have a tranfusion that isnt matched to your blood type
compliment medated hemolysiswh
why dont you react toyour own blood type or Rh
bc you have microbes in your gut that have the same antigens as in your blood, you wont produce Abs against these antigens
what is the result of Ag:Ab bidning of your own antigens in type 2
- Complement-mediated hemolysis
- Ab dependent cell-mediated
cytotoxicity (ADCC) - Anti-receptor Ab’s
- Hemolytic anemia
Ab dependent cell-mediated cytotoxicity (ADCC) in type 2
drug induced reactions
drug acts as a hapten on your cell that is then targetted by Abs
The FcR binds to NK cells leading to target cell apoptosis
what disease is implicated in anti-receptor antibodies
myasthenia gravis
explain myasthenia gravis
Antibodies develop that bind
to the acetylcholine receptor
on muscle cells
- prevents muscle activation
by ACh
- leads to muscle weakness
explain hemolytic disease of the newborn
fetal antigens normally go into the mothers blood and they incerase during delivery
if the kid has a Rh that doenst match mom, shell make antibodies against it that will bind to the RBC in the second pregnancy and clear the RBC of the kid by the spleen
BY HEMOLYSIS BY COMPLEMENT OR ABO incompatibitlity
maternal antibodies cirulate in the newborn for up to 6 mo and lead ot mild to severese anemia in the baby
bilirubin builds up form Hb rememnants and leadsot brain damage
what is used to treat hemolytic disease of newborn
Rhogam that binds to kids antigens perventing mom ab from binding and preventing B cell activation and memory cell formation
what is rheumatic fever
type 2
infection w step bact
lead to fomation of Ab against step but also against cardiac Ag (molecular mimmickery)
Ab deposition
rheumatic fever
