I - Allergy Flashcards
define allergy
immunological process that results in immediate and reproducible symptoms after exposure to an allergen
what type of reaction in allergy
type 1 hypersensitivity igE mediated
what is sensitisation
detection of specific IgE by skin prick testing or in vitro blood tests
does sensitisation or allergy occur more often
sensitisation +++
how does immune response to bacteria/virus/fungi differ from response to worms/venoms/proteases
immune reaction to worms/vemons respond to loss of tissue function, whereas bacterial immune reaction is due to response to direct pathogen
what are the signalling cytokines in Th2 immune response
IL25, IL33, TSLP
what are the effector cytokines in Th2 immune response
IL5, IL9, IL4, IL13
risk factor for development of IgE ABs
defects in skin epithelium (eczema)
describe pathway of Th2 immune response
damage epthelial cells secrete IL25/IL33 which act on tissue immune cells (DC, basophils etc)
induces Th2 cell immune response (IL4, IL5 etc)
and sensory neurons (itching)
when is IL4 induced in Th2 immune response
peptide MHC presentation to naive/memory Th2 cells
what causes immediate symptoms in allergy
release of inflamm mediators following allergen cross linking of IgE on surface of mast cells / basophils
what causes delayed symptoms in allergy
CD4 TH2 cell cytokine secretion and eosinophilic related tissue damage
what 4 factors promote IgE production
antigen dose
length of exposure
physical properties of allergen - eg assoicated w carrier proteins, linked to chitin, resistant to heat
route of exposure - resp/skin promotes IgE
what causes immune tolerance to food (prevent food allergy)
oral exposure to food
formation of anergic CD4 T cells lacking inflamm capacity to cause pathology
however they produce T reg cells that suppress tissue damage
what causes food allergy
skin / resp exposure to food, causing IgE sensitisation
describe the trends of the allergy epidemic
plateau of grass pollen / paeds asthma from 2000s ish to now
increase in red meat allergy recently
give 4 reasons why allergic disorders have risen over the last 150 years
hygiene hypothesis - decreased exposure = decreased natural immunity
increase in epithelial damaging agents due to industrialisation
loss of symbiotic relationship with bacteria
dietary changes
how do you diagnose allergy
HISTORY !!!
examination
allergen specific IgE test - eg skin prick / IgE blood test
functional allergen test
what allergies occur in infants
atopic dermatitis
food allergu
what allergies occur in childhood
asthma
allergic rhinitis
what allergies occur in adults
drug
bee
occupational
Sx of IgE allergies inc time frame
minutes or up to 2-4 hours post allergen exposure
angioedema, urticaria, itching, cough, SoB, sneeze, N&V, hypotension, sense of impending doom
how many organ systems are involved in an allergy
at least 2
what is a key feature of allergy that excludes allergy if its not present
reproducible - after EVERY exposure
is the presence of IgE sufficient for diagnosis of allergic disease
NO - it is necessary for diagnosis but not diagnostic in itself
does the result of skin prick test determine severity of reaction
NO
what is involved in the skin prick test
expose patient to standardised solution of allergen extract through a skin prick to forearm
positive control = histamine
negative control = saline
measure size of reaction to each
what is a positive result on skin prick test
wheal >3mm bigger than negative control
3 advantages of skin prick test
quick (15-20 mins)
cheap
negative predictive value >95%
3 disadvantages of skin prick test
requires experience to interpret
risk of anaphylaxis 1 in 3000
high false positive rate
benefits of intradermal tests vs skin prick
more sensitive
can be used to follow up venom / drug allergy if negative in SPT
cons of intradermal tests vs skin prick
less specific
labour intensive
greater risk of anaphylaxis
IgE AB blood test limitations
can detect IgE ABs with little clinical relevance
low abundance allergen leads to reduced sensitivity
limited clinical utility
when is component resolved diagnostics used
food allergy
insect allergy
guide immunotherapy
what % of peanut allergy persists after childhood
80%
what % of egg/milk allergy is outgrown
80%
when should blood sensitisation tests be done
Hx anaphylaxis
can’t stop antihistamines
no access to SPT
name a potential new blood biomarker for anaphyalxis
mast cell tryptase
what is the gold standard for food and drug allergy Dx
challenge test - increasing volume of allergen ingested and response watched
limitations of challenge tests
risk of anaphylaxis
difficult to interpret mild Sx
needs close medical supervision
defining features of anaphylaxis
acute onset of symptoms / signs (mins to hours)
severe / life threatening ABC problems
skin and mucosal signs
incidence of anaphylaxis
1.5 to 8/100,000
age peak for anaphylaxis
0-4yrs
4 mechanisms of anaphylaxis (inc type, cells and mediators)
IgE - mast cells/basophils - histamine/PAF
IgG - macrophages/neutrophils - histamine/PAF
complement - mast cells/macrophages - histamine/PAF
pharamcological - mast cells - leukotrienes/histamine
how can anaphylaxis be retrospectively diagnosed
serial serum tyrptase at 30 mins then 24hours
Mx of anaphylaxis
position - supine, legs raised
IM adrenaline
anti histamines after ABC
repeat IM adreanline & give IV fluids if no response
call for ITU help
what 3 receptors does andrenaline act on
alpha 1
beta 1
beta 2
safety netting for anaphyalxis
recognition of symptoms
avoidane of triggers
epi pen
