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Y4 Paediatrics > 14 - Allergy and Immunology > Flashcards

14 - Allergy and Immunology Flashcards

1
Q

What is the definition of:

  • Allergy
  • Atopy
A

Allergy: hypersensitivity of the immune system to antigens, can be IgE or non-IgE mediated

Atopy: predisposition to having hypersensitivity reactions e.g eczema, asthma, hay fever, allergic rhinitis, food allergies

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2
Q

What is the definition of

  • Allergen
  • Sensitisation
A
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3
Q

What is the skin sensitisation theory?

A
  1. There is a break in the infant’s skin (from eczema or a skin infection) that allows allergens, such as peanut proteins, to cross the skin and react with the immune system
  2. The child does not have contact with that allergen from the GI 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)

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4
Q

What are some hypersensitivity medical conditions?

A

Allergic diseases occur when individuals make an abnormal immune response to harmless environmental stimuli

  • Asthma
  • Atopic eczema
  • Allergic rhinitis
  • Hayfever
  • Food allergies
  • Animal allergies
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5
Q

What are the 4 types of hypersensitivity reaction?

A

ABCD

Type 1: IgE antibodies trigger mast cells and basophils to release histamines and other cytokines. This causes an immediate reaction

Type 2: IgG and IgM antibodies react to an allergen and activate the complement system, leading to direct damage to the local cells

Type 3: Immune complexes accumulate and cause damage to local tissues, often autoimmune

Type 4: Cell mediated hypersensitivity reactions caused by T lymphocytes. T-cells are inappropriately activated, causing inflammation and damage to local tissues e.g contact dermatitis

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6
Q

Taking a history of an allergen is one of the most important aspects of diagnosis. What questions do you need to ask?

A

EATERS

  • Timing after exposure to the allergen
  • Previous and subsequent exposure and reaction to the allergen
  • Symptoms of rash, swelling, breathing difficulty, wheeze and cough
  • Previous personal and family history of atopic conditions and allergies
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7
Q

What investigations can be done to diagnose an allergy if the history is not solid enough?

A

Skin prick testing and RAST only look at sensitisation, may be sensitised but not allergic

  • Skin prick testing: assesses sensitisation
  • RAST testing: blood tests for total and specific IgE, assesses sensitisation
  • Food challenge testing: gold standard but expensive, done in special unit and gradually increase concentration of allergen
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8
Q

What is the difference between skin prick and skin patch testing?

A

Skin patch is for allergic contact dermatitis, Skin prick is for food allergies

Skin Prick

Drop of each allergen solution placed at marked points along with a water control and a histamine control. A fresh needle is used to make a tiny break in the skin at the site of each allergen.

After 15 minutes, the size of the wheals to each allergen are assessed and compared to the controls

Patch Testing

Could be be for latex, perfumes, cosmetics or plants. A patch containing the allergen is placed on the patient’s skin. The patch can either contain a specific allergen, or a grid of lots of allergens as a screening tool. After 2 – 3 days the skin reaction to the patch is assessed.

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9
Q

What is the difference between skin prick testing and RAST testing?

A

Level of sIgE/size of SPT correlates with likelihood of allergy but do not correspond with severity of allergy

RAST: detects IgE circulating in the blood.

Skin prick tests: detects IgE bound to skin mast cells

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10
Q

What is the issue with RAST testing?

A

If have an atopic condition like eczema or asthma it is likely to come back positive for everything you test

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11
Q

What are some actual symptoms of a food allergy?

A
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12
Q

What is the food allergy march?

A
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13
Q

What is the allergic march?

A
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14
Q

What effect does temperature have on the allergenicity of foods?

A

Also remember cross-reactive allergens e.g allergic to walnut may be allergic to brazil or cashew nuts

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15
Q

What are some of the mediators release during an allergic reaction and what do they cause?

A
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16
Q

What are the different categories of food allergy?

A

Allergy affects every organ, although skin and mucous membranes are most commonly involved as they are the‘frontier’ between the organism and the environment

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17
Q

How can you tell the difference between IgE and non-IgE mediated food allergies?

A

Think about timing of onset, duration and organ systems involved

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18
Q

How may Cow’s Milk Protein Allergy present?

A

Can be IgE or Non-IgE mediated symptoms

  • Often causes colic symptoms
  • GORD
  • Blood/Mucus in stool
  • Poor growth
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19
Q

What are some differentials for CMPA?

A
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20
Q

How common is CMPA and what is the prognosis with this?

A
  • Prevalence of 1-2%
  • All present before 12 months old
  • Most tolerant by 5 years. Earlier tolerance to baked milk. Small proportion remain allergic
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21
Q

What is Food protein enterocolitis syndrome?

A

Non-IgE mediated food hypersensitivity

  • Symptoms delayed 1-3 hours after contact
  • Profuse repetitive vomiting leading to shock
  • Occasional watery diarrhoea (affecting 25%)
  • Pallor and shock
  • Diagnosis frequently missed as appears like sepsis
  • WCC can be elevated; CRP normal
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22
Q

How is CMPA managed?

A
  • Breastfed: get mother to remove cow’s milk from diet
  • Formula: switch to amino-acid formula or hydrolysed formula
  • Every 6 months or so, infants can be tried on the first step of the milk ladder (e.g. malted milk biscuits) and then slowly progress up the ladder until they develop symptoms
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23
Q

How are food allergies managed in general?

A
  • Avoidance of that allergen or food
  • Prophylactic antihistamines when contact is inevitable
  • Patients at risk of anaphylactic reactions should be given an adrenaline auto-injector
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24
Q

What is the difference between CMPA, cow’s milk protein intolerance and lactose intolerance?

A

People with cow’s milk protein allergy do not have an allergy to lactose. Lactose is a sugar

Cow’s milk intolerance is not an allergic process and does not involve the immune system. Only GI symptoms

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25
Q

What may a child with allergic rhinitis have on examination?

A
  • Allergic crease
  • Allergic shiners
  • Swollen mid-face
  • Mouth breather
  • Swollen nasal turbinates
  • Dull retracted ear drums
  • Runny nose
  • Eviidence of concomitant asthma
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26
Q

What is lactose intolerance?

A

Deficit of lactase in the brush border of the GI tract so lactose malabsorption leading to symptoms when ingesting

Symptoms: abdominal pain, bloating, flatulence, nausea, diarrhoea

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27
Q

What is the definition of rhinitis and what symptoms are needed for the diagnosis?

A

Type 1 hypersensitivity IgE mediated reaction of the nasal mucosa to inhaled allergens

One or more of: nasal congestion, rhinorrhoea, sneezing and itching

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28
Q

How is allergic rhinitis diagnosed?

A
  • Diagnosis based on history
  • Skin prick for house dust mites, pollen
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29
Q

How is allergic rhinitis managed in children?

A
  • Allergen avoidance: hoovering and changing pillows regularly and allowing good ventilation of the home can help with house dust mite allergy.
  • Prophylactic antihistamines: intranasal better as quicker onset after a trigger
  • Regular intranasal corticosteroid: Beclomethasone, Fluticasone, Mometasone. Onset of action 6-8 hours after dose, may take 2 weeks for max effect
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30
Q

What antihistamines are used in allergic rhinitis?

A

Oral antihistamines are taken prior to exposure to reduce allergic symptoms:

  • Non-sedating: cetirizine, loratadine and fexofenadine
  • Sedating: chlorphenamine (Piriton) and promethazine

Nasal antihistamines are for acute after exposure

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31
Q

How do you explain to a parent/child how to use a nasal spray?

A
  • Hold the spray in the left hand when spraying into the right nostril and vice versa
  • Spray slightly outward, away from the nasal septum
  • Do NOT sniff at the same time as spraying, as this sends the mist straight to the back of the throat. Should not taste the spray at the back of the throat
32
Q

What is an allergy action plan?

A
33
Q

14-year-old male is referred by his GP. He was stung by a wasp and developed immediate symptoms. What determines whether this is a true allergic reaction or not?

A
34
Q

What is immunotherapy?

A
  • Administering the allergen to which the patient is sensitised gradually over months
  • For several allergic diseases
  • Commercially available in sublingual (grass, HDM) and subcutaneous (bee, wasp) forms
35
Q

What is anaphylaxis?

A

Life threatening emergency, type 1 hypersensitivity reaction allergic reaction from IgE cross linking triggering mast cell degranulation

36
Q

How may anaphylaxis present?

A
  • Urticaria
  • Itching
  • Angio-oedema, with swelling around lips and eyes
  • Abdominal pain
  • Shortness of breath
  • Wheeze
  • Swelling of the larynx, causing stridor
  • Tachycardia
  • Lightheadedness
  • Collapse
37
Q

What is the diagnostic criteria for anaphylaxis?

A

Need at least one of respiratory compromise or circulatory collapse!!

Sudden onset

38
Q

What are some of the mediators involved in anaphylaxis?

A

Tryptase, Histamine, PAF

Difference between allergy and anaphylaxis is anaphylaxis has airway, breathing or circulatory compromise!!!

39
Q

Children cannot communicate signs of anaphylaxis so how can you usually tell?

A
  • Rapid onset coughing or choking
  • Stridor
  • Urticaria
  • Profuse vomiting
  • Rapid onset unresponsiveness
40
Q

What is the management of anaphylaxis in general terms?

A

Acute and Long Term

41
Q

What is the acute management of anaphylaxis? (important card)

A
  • ABCDE and call for help
  • Removal of trigger
  • Lie patient flat with legs up
  • Monitoring
  • IM adrenaline repeated after 5 mins if needed
  • High flow oxygen
  • IV fluid bolus
  • Nebulised salbutamol OR adrenaline if bronchospasm
  • If refractory give cetirizine and hydrocortisone
42
Q

What dose of IM adrenaline is given to children in anaphylaxis?

A

Use 1:1000

43
Q

What fluid is used for bolus in anaphylaxis and at what dose?

A

0.9% saline or Hartmans or 5% Dextrose

44
Q

What monitoring is done throughout acute anaphylaxis?

A
  • Pulse
  • BP
  • SpO2
  • ECG

If cardiorespiratory arrest start CPR

45
Q

What is given for refractory anaphylaxis after initial management?

A

Contact ICU and do this if 2 doses of IM adrenaline have failed

  • IV adrenaline infusion
  • IV hydrocortisone
  • IV anti-histamine
46
Q

What antihistamine is given in refractory anaphylaxis and at what dose?

A

PO Cetirizine is preferred as non-sedating

47
Q

What dose of nebuliser adrenaline is given if upper airway obstruction (stridor) in anaphylaxis?

A

5ml of 1mg/ml (1:1000) adrenaline

48
Q

What investigations are done following an anaphylactic reaction?

A
  • Admit to Child Short Stay Unit for monitoring and consult with allergy consultant
  • If diagnosis uncertain do mast cell tryptase 2 hours later, no later than 4 hours after
  • Take 3 samples
49
Q

What is the most to least common cause of anaphylaxis in children?

A
50
Q

What do you need to warn parents and children of following an anaphylactic reaction?

A

Biphasic reaction

Second anaphylactic reaction without rexposure to allergen that usually happens around 8-10 hours later, up to 72 hours later

Treated in same way as anaphylaxis, that is why they need admission after emergency treatment

51
Q

What information is given to children and their families after anaphylactic reaction?

A
  • Adrenaline Auto Injector and how to use it
  • Education on allergen avoidance
  • Education on signs of anaphylaxis
  • Basic life support
52
Q

Adrenaline autoinjectors are given to all children following anaphylaxis. Which children without a history of anaphylaxis should also have an auto injector?

A

Do a risk assessment after an allergic reaction

  • Asthma requiring inhaled steroids
  • Poor access to medical treatment (e.g. rural locations)
  • Nut or insect sting allergies are higher risk
  • Significant co-morbidities, such as cardiovascular disease
53
Q

How do you instruct a parent on how to use an EpiPen?

A
  • Prepare the device by removing the safety cap on the non-needle end
  • Grip the device in a fist with the needle end pointing downwards. Do not put your thumb over the end
  • Administer the injection by firmly jabbing the device into the outer portion of the mid 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
54
Q

What is required for discharge of a child who has had an anaphylactic reaction?

A

Usually 6 hour observation minimal

55
Q

What is the diagnosis?

A

Post-prandial exercise-induced anaphylaxis

56
Q

What is urticaria?

A

Superficial swelling of the skin (epidermis and mucous membranes) that results in a red, raised, itchy rash

Angio-oedema is a deeper form with swelling in the dermis and subcut tissues

Can be acute or chronic if >6 weeks daily

57
Q

What are some causes of urticaria in children?

A

Always beware of anaphylaxis associated with this!!

Acute

[Chronic**](https://dermnetnz.org/topics/chronic-urticaria/) **(rare in children)

  • Chronic idiopathic urticaria
  • Chronic inducible urticaria
  • Autoimmune urticaria e.g SLE
58
Q

How is urticaria in children managed?

A

AVOID TRIGGERS

  • Likely to be self-limiting without treatment
  • Use fan and calamine to calm itch
  • If chronic non sedating antihistamine e.g Fexofenadine daily for 6/52
  • If severe short course (up to 7 days) of an oral corticosteroid
59
Q

What are some secondary care treatments for urticaria?

A
  • Anti-leukotrienes such as montelukast
  • Omalizumab, which targets IgE
  • CIclosporin
60
Q

need to do primary immunodeficiency when on infectious disease module

A
61
Q

Why does food pollen syndrome only cause mouth issues and not a full allergic reaction?

A

Stomach acid breaks down the allergen so no longer allergenic

62
Q

When should you be concerned about recurrent infections in children?

A

Normal to have around 4-8 respiratory infections a year

63
Q

What investigations should be done for recurrent infections in children and why?

A
  • FBC: low neutrophils suggest phagocytic disorder and low lymphocytes suggest T cell disorder
  • Immunoglobulins: suggest a B cell disorders
  • Complement proteins: abnormalities suggest a complement disorder
  • Antibody responses to vaccines, specifically pneumococcal and haemophilus
  • HIV test if clinically relevant
  • Chest xray for scarring from previous chest infections
  • Sweat test for cystic fibrosis
  • CT chest for bronchiectasis
64
Q

What are the different categories of primary immunodeficiency?

A
  • B cell
  • T cell
  • Combined
  • Complement
65
Q

What is SCID and how does it present?

A

No immune system, number of different genetic disorders that result in absent or dysfunctioning T and B cells

Presentation

Will present in first few months of life with:

  • Persistent severe diarrhoea
  • Failure to thrive
  • Opportunistic infections e.g severe chickenpox, PCP, CMV
  • Unwell after live vaccinations e.g BCG, MMR and nasal flu vaccine
66
Q

How is SCID managed?

A
  • Stem cell transplant
  • Avoid live vaccines
  • Sterile environment
  • IVIG therapy for infections
67
Q

What are the different types of B cell immunodeficiency?

A

B Cells produce antibodies (immunoglobulins) so deficiency is called hypogammaglobulinemia

  • Selective Immunoglobulin A Deficiency (most common)
  • Common Variable Immunodeficiency
  • X-linked Agammaglobulinaemia (Bruton’s)
68
Q

How does selective IgA deficiency (B cell immunodeficiency) present?

A

Low levels of IgA and normal levels of IgG and IgM

IgA is in saliva, respiratory tract secretions, GI tract secretions, tears and sweat and protects against opportunistic infections of these mucous membranes

Patients have a tendency to recurrent mucous membrane infections, such as LRTIs, and autoimmune conditions.

69
Q

Selective IgA deficiency is often asymptomatic or never diagnosed. Where may it be opportunistically diagnosed?

A

When testing for coeliac disease as need to test for total IgA

70
Q

What is CVID and how does it present and how is it managed?

A
  • Deficiency in IgG and IgA, with or without deficiency in IgM
  • Recurrent respiratory tract infections, leading to chronic lung disease
  • Patients are unable to develop immunity to infections or vaccinations
  • Prone to immune disorders such as RA, Hodgkin’s lymphoma
  • Treat with regular immunoglobulin infusions
71
Q

How does Bruton’s X Linked Recessive Agammaglobulinaemia present?

A
  • Abnormal B cell development so deficiency in all classes of immunoglobulins
  • Similar presentation to CVID
72
Q

What are some examples of T cell immunodeficiency?

A
  • Di George Syndrome
  • Purine Nucleoside Phosphorylase Deficiency
  • Wiskott-Aldrich Syndrome
  • AIDS
  • Ataxic Telengectasia
73
Q

What is Di George Syndrome?

A

22q11.2 deletion syndrome

CATCH-22 mnemonic:

  • C – Congenital heart disease
  • A – Abnormal facies (characteristic facial appearance)
  • T – Thymus gland incompletely developed
  • C – Cleft palate
  • H – Hypoparathyroidism and resulting Hypocalcaemia
  • 22nd chromosome affected
74
Q

What is the issue with complement immunodeficiency?

A
  • Vulnerability to encapsulated bacteria, leading to recurrent infections with these organisms
  • Vaccination against encapsulated organisms is very important
75
Q

What is the most common complement deficiency and how does it present?

A

C1 Esterase Inhibitor Deficiency (Hereditary Angioedema)

  • Bradykinin is part of the inflammatory response by promoting blood vessel dilatation and increased vascular permeability, leading to angioedema
  • C1 esterase inhibits bradykinin so absence of C1 esterase causes angioedema to intermittently occur in response to minor triggers like stress and viral infections

Y4 Paediatrics (31 decks)

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