5- Allergy Flashcards
define allergy
- Hypersensitivity’s of the immune system to allergens
- Atopy is a term which describes a predisposition to having hypersensitise reactions to allergens
pathophysiology of allergy
Allergens are antigens (proteins) which the immune system recognises as foreign and potentially harmful, leading to an allergic response
Causes/risk factors for allergy
- Atopy
o Eczema
o Asthma
o Hayfever
o Allergic rhinitis
o Food allergies - Genetic
investigating allergy
3 methods
- skin prick testing
- RAST testing
- Food challenge testing (gold standard)
skin prick testing
- Assess’ sensitisation and not allergy (can be misleading- can often show many sensitisation and hard to explain to parent that their child can still safely eat foods)
- Protocol: patch of skin selected e.g. forearm. Allergen solutions selected e.g. peanuts, house dust mite and pollen. A drop of each allergen placed at marked points along patch of skin, along with a water control and histamine control. A fresh needle is used to make a tiny break in the skin at each site. After 15 mins, size of the wheals to each allergen are assessed and compared to the controls
RAST testing
- Assess’ sensitisation and not allergy
- Protocol: blood tests which measures total and allergen specific IgE quantities in patients blood sample. If patient atopic- often positive results for everything
Food challenge testing
Gold standard- tests allergy
often used if skin prick testing suggests allergy to confirm
- Protocol: performed in specialised unit with very close monitoring
- Starts with almost non-existent quantities diluted further in other foods e.g. mixing a tiny amount of peanuts into a bar of chocolate
- Children monitored very closely after each exposure
management of allergy
- Avoidance of established allergen
- Regular hoovering and changing of sheets and pillows in patients allergic to dust mites
- Stay indoors when pollen count high
- Prophylaxis antihistamines when contact is inevitable e.g. hayfever
- Epipen if at risk of anaphylaxis
- Immunotherapy in specialist centres: involves exposing patient to allergens over months
importance of excluding allergies
- Huge psychosocial burden if diagnosed
o Risk of anaphylaxis
o Responsibility of avoiding allergens and always carrying epipen - Can be a somatisation disorder rather than true allergy
o If wrongly diagnosed as an allergy can lead to restrictive or unhealthy eating
orign of allergies theory: skin sensitisation theory of allegry
The skin sensitisation theory is currently the leading theory on the origin of allergies. This theory suggests there are two main contributors to a child developing an allergy to a food:
1. There is a break in the infant’s skin (from eczema or a skin infection) that allows allergens, such as peanut proteins, from the environment to cross the skin and react with the immune system.
2. The child does not have contact with that allergen from the gastrointestinal tract, and there is an absence of GI exposure to the allergen.
The theory is that allergens entering through the skin are recognised by the immune system as being foreign and harmful proteins. The immune system reacts by becoming sensitised to that allergen, so that when it next encounters that allergen again it will launch a full immune response (an allergic reaction).
When a baby is weaned at around 6 months, if they are regularly eating foods that contain that allergen, their GI tract is regularly being exposed to that protein. The GI tract will recognise that allergen as a food and not a foreign or harmful protein, and inform the immune system that it is a safe thing to be exposed to.
The theory is that regular exposure to an allergen through food and preventing exposure to that allergen through the skin barrier can help prevent food allergies developing.
definitions
hypersensitivity conditions
Conditions
* Asthma
* Atopic eczema
* Allergic rhinitis
* Hayfever
* Food allergies
* Animal allergies
Hypersensitivity: Coombs and Gell classification
- Type 1: IgE antibodies to a specific allergen trigger mast cells and basophils to release histamines and other cytokines. This causes an immediate reaction. Typical food allergy reactions, where exposure to the allergen leads to an acute reaction, range from itching, facial swelling and urticaria to anaphylaxis.
- Type 2: IgG and IgM antibodies react to an allergen and activate the complement system, leading to direct damage to the local cells. Examples are haemolytic disease of the newborn and transfuse on reactions.
- Type 3: Immune complexes accumulate and cause damage to local tissues. Examples are autoimmune conditions such as systemic lupus erythematosus (SLE), rheumatoid arthritis
- Type 4: Cell mediated hypersensitivity reactions caused by T lymphocytes. T-cells are inappropriately activated, causing inflammation and damage to local tissues. Examples are organ transplant rejection and contact dermatitis.
Evaluating a child with a suspected food allergy
1) Medical history
2) Physical examiantion
3) Screening tests
- skin prick tests
- blood specific IgE
4) Diagnosis verification with controlled oral food challenge
5) Interpretation of tests
medical history
physical examination
Screening tests
IgE mediated food allergy
- Skin prick tests
- blood specific IgE
Non-IgE
- elimination diet
diagnosis verification
allergy tests detect
sensitisation and not allergy
BUT
- patient often translate their result into clinical allergy
test are good at confirming…
Non allergy
- the higher the IgE the higher the Positive predicitve value
level of IgE does not correlate to
allergy severity
anaphylaxis background
- Type 1 sensitivity reaction
- The key feature that differentiates anaphylaxis from a non-anaphylactic allergic reaction is compromise of the airway, breathing or circulation.
- Examples: cows milk and nut
pathophysiology of anaphylaxis
- Immunoglobulin E (IgE) stimulates mast cells to rapidly release histamine- mast cell degranulation
- Causes rapid onset of symptoms with airway, breathing and circulation compromise
presentation of anaphylaxis
Patients present with a history of exposure to an allergen (although it can be idiopathic). There will be rapid onset of allergic symptoms:
- Urticaria
- Itching
- Angio-oedema, with swelling around lips and eyes
- Abdominal pain
Additional symptoms that indicate anaphylaxis are: - Shortness of breath
- Wheeze
- Swelling of the larynx, causing stridor
- Tachycardia
- Lightheadedness
- Collapse
investigations for anaphylaxis
- Usually after treatment
- Can be confirmed by measuring serum mast cell tryptase within 6 hours
management of anaphylaxis
- A- secure airway
- B- give oxygen and salbutamol
- C- provide IV bolus of fluids
- D- lie patient flat to help with cerebral perfusion
- E- look for flushing, urticaria and angio-oedema
Once anaphylaxis established
- Intramuscular adrenaline- repeat after 5 mins if require
- Antihistamines- chlorphenamine or cetririzine
- Steroids – hydrocortisone
Beware of biphasic reaction
dose of intramuscular adrenaline for anaphylaxis
trade names for adrenaline auto-injector
Epipen, Jext and Emerade are trade names for adrenalin auto-injector devices.
Indications for an Adrenalin Auto-Injector
They are given to all children and adolescents with anaphylactic reactions. They may also be considered in children with generalised allergic reactions (without anaphylaxis) with certain risk factors:
* Asthma requiring inhaled steroids
* Poor access to medical treatment (e.g. rural locations)
* Adolescents, who are at higher risk
* Nut or insect sting allergies are higher risk
* Significant co-morbidities, such as cardiovascular disease
How to Use an Adrenalin Auto-Injector
- The first step is to confirm the diagnosis of anaphylaxis.
- Prepare the device by removing the safety cap on the non-needle end. There is a blue cap on EpiPen and a yellow cap on Jext.
- Grip the device in a fist with the needle end pointing downwards. The needle end is orange on EpiPen and black on Jext. Do not put your thumb over the end, because if the device is upside down you will inject your thumb with adrenalin and could risk losing it.
- Administer the injection by firmly jabbing the device into the outer portion of the mid anterolateral thigh until the device clicks. This can be done through clothing. EpiPen advise holding it in place for 3 seconds and Jext advise 10 seconds before removing the device.
- Remove the device and gently massage the area for 10 seconds.
- Phone an emergency ambulance. A second dose may be given (with a new pen) after 5 minutes if required.
cows milk protein allergy
- Allergy to milk proteins casein and whey
- Commonest cause odffood allergy death
- Typically affects infanta and young children under 3 years- immune mediated response
- Different to lactose intolerance and cows milk intolerance
cows milk protien allergy vs cows milk intoleance
- Peoples with cows milk protein allergy do not have a reaction to lactose (Lactose is a sugar not a protein)
- Lactose intolerance is not allergic- may get similar GI symptoms but no allergic features
SIDE NOTE: proteins are what generally cause anaphylaxis
Pathophysiology behind Cows milk protein allergy
- Hypersensitivity to protein (casein and whey) in cows milk
Types
- IgE mediated -> rapid reaction
- Non- IgE mediated -> slow reaction
RF
- Atopy
- Fx of atopy
Pathophysiology behind Cows milk protein allergy
- Hypersensitivity to protein (casein and whey) in cows milk
Types
- IgE mediated -> rapid reaction
- Non- IgE mediated -> slow reaction
RF
- Atopy
- Fx of atopy
presentation of cows milk protein allergy
<1 yo
- Comes apparent when weaned from breast milk to food containing milk
- Can also occur if mother is consuming dairy whilst breastfed
GI
- Bloating
- Abdominal pain
- D and V
Allergic
- Urticarial rash
- Angio-oedema
- Cough or wheeze
- Sneezing
- Watery eyes
- Eczema
- Rarely anaphylaxis can occur
investigation for cows milk protien allergy
- Full history and examination
- Blood test looking for specific IgE antibodies to cows milk (sensitive test with low specificity (false positives)
- Skin prick testing may help
management of cows milk protein allergy
1) Avoiding cows milk
- Breast feeding mothers should avoid dairy
- Replace formula with special hydrolysed formulas of cows milk allergy -> contain broken down proteins which don’t trigger immune response
- Replace formula with amino acid formula- more expensive, good for children with severe allergys
-
2) Every 6 months infants can be tried on the first step of the milk ladder e.g. malted milk biscuits and slowly progress up it until dthey develop symptoms
prognosis for cows milk allergy
- Most out grow by 3 years
- Earlier tolerance to baked milk
urticaria background
- Also known as hives
- A superficial swelling of the skin (epidermis and mucous membranes) that results in a red (initially with a pale centre), raised, and intensely itchy rash.
- Can be localised or widespread
- May be associated with angioedema and flushing
- Classification
o Acute
o Chronic
pathophysiology behind urticaria
- Causes by release of histamine and other pro-inflammatory chemicals (leukotrienes, prostaglandins) by mast cells
- Acute: allergic reaction
- Chronic: autoimmune (Autoantibodies target mast cells)
RF for acute urticaria
(mast cell release of histamine)
o Allergies to food
o Contact with chemicals, latex, nettles
o Medication
o Viral infections
o Insect bites
RF for chronic urticaria
(autoimmune)
o Chronic idiopathic urticaria: describes recurrent episodes without a clear cause
o Chronic inducible urticaria: induced by certain triggers:
Sunlight
Temp change
Exercise
Strong emotions
o Autoimmune urticaria
E.g. SLE
presentation of urticaria
- Pruritus
- Vascular permeability
- Oedema
- Rash: erythematous swelling of various shapes and sizes, classically have central pallor with erythematous flare
management of urticaria
- Antihistamines e.g. Fexofenadine (chronic), cetrixzine (acute)
- Oral steroids (Prednisone)may be considered for short course for severe flare
- Third line:
o Anti-leukotrienes e.g. Montelukast
o Omalizumab- target IgE
o Cyclosporin
acute rhinitis background
- IgE mediated Type 1 hypersensitivity reaction
- Can significantly affect sleep, mood, hobbies, work and quality of life
pathophysiology behind allergic rhinitis
- Environmental allergens cause an allergic inflammatory response in nasal mucosa
pathophysiology behind allergic rhinitis
- Environmental allergens cause an allergic inflammatory response in nasal mucosa
causes of allergic rhinitis
Allergic rhinitis can be
- Seasonal e.g. hay fever
- Perennial (year round) e.g. house dust mite allergy
- Occupation e.g. associated with school or work
Risk facotrs
- Atopy- therefore can be genetic
Common triggers
- Tree pollen or grass
- House dust mites
- Pets
- Mould
presentation of acute rhinitis
- Runny, blocked and itchy nose
- Sneezing
- Itchy, red and swollen eyes
investigations for acute rhinitis
- Diagnosis based on history
- Skin prick testing can be useful particularly when testing for pollen, animals and house dust mite allergy
management of acute rhinitis
Avoid trigger
- Dust mite allergy: changing pillow reg, allow good ventilation, hoovering
- Hay fever: stay indoors, wash clothes, don’t touch eyes
- Pets: minimise contact
Medication:
Oral antihistamines
- Non sedating: cetirizine, loratadine and fexofenadine
- Sedating: chlorphenamine (piriton) and promethazine
Nasal corticosteroids e.g. fluticasone and mometasone
Nasal antihistamines
