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Allergy and Hypersensitivuty - Coggle Diagram
Allergy and Hypersensitivuty
Types
A
Gell and Coombs Classification
Type 1
IgE
Allergy immediate
Type 2
Antibody mediated
IgG / IgM vs cells
Type 3
Immune complexes
Type 4
T cell mediated
Drugs
Allergy
Type 1 hypersensitivity
immediate reacion
Mast cell and bsaophul drivern
IgE
Phases
Phase 1
Sensitisiation
Sensitisiation
Antigen presenting cell takes us allergen
Presents to Th2 cells
IL4 and IL13 activate B cell - produce IgE ab
Phase 2
Re-exposure
IgE specific to allergen attached to mast cells
Cross linking
Activate mast cell
Degranulation of mast cell
Histamine - urticaria, oedema, anaphylaxis
Cytokines / chemokines - sustained inflammatory response
Mast Cell MEdiators and Efects
Histamine
Itch
Flushing
bronchoconstriction
Leukotrienes
Prostglandin
Tryptase
Specific marker for anaphylaxis
Early vs Late Phase Allergic Response
Early
Minutes
Wheeze
Urticaria
Hypotension
Late
Hours
Persistent inflammation
Asthma
Steroids target the late phase
Clinical Spectrum of Allergy
Skin
Urticaria
Angiooedema - airways
Flushing
Puritis
Absence of rash does not exclude anaphylaxis
Respiratory
Wheeze
Stridor
Throat tightness
Hoarse
Hoarseess - airwy involvement
GI
Vomiting
Abdo pain
Diarrhoea
GI only pres can still be anaphylaxis but not in isolation???
VSD
Hypotension
Collapse
Tachycardia
Presyncope / syncope
Bradycardia
Anaphylaxis
Defin
Severe, life threathnbing
Common pitfalls
No rash
Normal blood pressure initially
GI predominant symptoms
Mistaken for panic attack
Drug Allergy
Contrast
Vaccines
Physiologic
Exercise induce
Diagnosis
Clinical - objective signs of systemic involvement
Lab aid: Tryptase
Management
ABCDE
Call for help
Raise legs - depends on presence or resp symptoms
Bronchospasm - raise up
Medical
First line Medical Tx 1️⃣
IM adrenaline
0.5mg
Latera. thigh
Repeat every 5 min if needed
α effects - vasoconstriction
β1 increases cardia output
β2 bronchodilation and mast cell stabilisation
tx airway, beathing and circulation
Other
O2
IV fluids
Hitsmine - skin
Steroids - late phase prevention
Remove trigger
Adrenaline Auto-injectors
Indications
Confirmed anaphylaxis
High-risk allergy eg Nuts
No indication
Intolerance
Isolated mild symptoms
Other co-morbidity: Asthma
Social circumstances
Higher doses
beta blockers
Obese
Allergy vs Intolerance
Allergy
Immune-mediated
Not dose related
Anaphylaxis possible
Intolerance
Not immune mediated
Dose related
Anaphylaxis not possible
Mislabelled Allergy
Broader spectrum abx
Increased resistance
Longer hopsital stays
Worse outcomes
Impaired QoL
Type I Allergic Hypersensitivity Testing
Sensitisation tests
Specific IgE (Blood)
AKA TRAST
Atopic: Higher levels of total IgE
Skin Prick Test SPT
Negative control
Positive control: Histamine
Do not correlate to clinical significance
Intradermal testing
Select drugs / venoms
Serum tryptase
Acute and baseline
Marker of anaphylaxis
Neg does not outrule
High baseline tryptase at higher risk of developing anaphylaxis
Drug / food provocation 🥇
Gold standard
Not done in positive sensitisation tests
Type II Hypersensitivity
Antibody mediated
Complement Mediated
IgG/IgM against cells
Examples
Atoimmune haemolytic anaemia
ITP
Testing
Direct Antiglobulin test (DAT / Coombs)
Disease specific autoantibodies
Full blood count
Peripheral blood film
Type III Hypersensitivity
Immune complex deposition
Complement activation
Examples
Serum sickness
Vasculitis
Mechanism
Formation of circulation antigen-ab IgG/IgM immune complexes
Inadequate clearance
Deposition in tissues
BLood vessels
Kidneys
Joints
Skin
Complement activation - inflammation and tissue damae
SLE as prototype
Autoantibodies form immune complexes
Deposition leads to
Lupus nephritis
Vasculitis
Arthritis
Cutaneous lupus
Investigations
Complement levels
decreaed (consumption) of C3 C4
Inflammatory markers: ESR / CRP
Anti-dsDNA
Elevated
Urinalysis
Proteinuria
Haematuria
Tissue biopsy with immunofluourescence
immune complex deposition
Not typically needed for diagnosis
Type IV
T cell mediated
Delayed 48-72hrs
Examples
Contact dermatitis
Drug rashes ( maculopapular)
TB skin test
Investigations
Clinica hx
timing is key
Patch testing 🥇
Delayed reading - 24hrs, 48hrs, 72hrs
Useful for penicillin
Diagnostic yield low for other drugs
Good for contact derm / nicil allergy
Biopsy
Rarely needed
Urticaria and Angioedema Overview
Definitions
Urticaria
Superficial dermal oedema (wheels)
Angioedema
Deeper / dermal / submucosal swelling
Key mediator
Mast cell activation - histamine release
Mechanism
Mast cell degranulation
Histamine activates H1 receptors
Increased vascular permeability
Wheel and flare response
Most Urticaria is NOT IgE mediated
Angioedema
Mast cell mediated
Kinin related - bradykinin
ACE inhibitors angioedema
C1 inhibitor deficiency
Chronic Spontaneous Urticaria CSU
Definition
Urticaria +/- angioedema lasting > 6 weeks with no external trigger
Pathophys
Autoimmune 40-50%
IgG against IgE itself / FcεRI receptor
Leads to spontaneous mast cell activation
Majority of flares in morning or evening - more mast cell activity
No risk of progression to anaphylaxis - benign condition
Take Home
Urticaria =/= Allergy
CSU is usually autoimmune
Avoid over investigation
Hx is most important
Investigations
Minimal
Bloods
FBC
CRP
+/- TSH - can be assocaited with AI thyroid disease
No outine allergy test
Treatment
Stepwise
Non sedating antihx up to 4x
Add on therapy - leukotriene antag
Biologic: Omalizumab
Ciclosporin
Symptomatic treatment except ciclosporin
