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Allergy Flashcards

1
Q

What is an allergic disorder?

A

Immunological process that results in immediate and reproducible symptoms after exposure to an allergen.

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2
Q

What is sensitisation?

A

Sensitisation is the detection of specific IgE either by skin prick testing or in vitro blood tests: OCCURS MORE OFTEN THAN ALLERGIC DISEASE

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3
Q

How does the body respond to allergens?

A

In clinical practice immunological process usually involves an IgE mediated type 1 hypersensitivity reaction

Allergen is usually a harmless substance that can trigger an IgE mediated immune response and may result in clinical symptoms

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4
Q

When is the Th1/ Th17 immune response elicited?

A

Microbial PAMP and structural feature recognition

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5
Q

What elicits a Th2 immune response?

A

Helminthes/ allergens/ Venoms

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6
Q

What can the immune system recognise?

A

Immune system recognizes enzymatic activities of allergens and multicellular parasites: no direct recognition as seen for example with bacteria, viruses and fungi

Considerable overlap in immune pathways that detect tissue damage and allergens which have extensive protease activity and the capacity to damage epithelial barriers.

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7
Q

Summarise Th2 immune responses

A

Epithelial cells and mast cells detect allergens, venoms, and worms

Stressed or damage epithelial cells secrete IL-25, IL-33 and TSLP to act on memory CD4 T cell subsets, innate lymphoid cells and other lymphoid cells to promote secretion of IL-4, IL-5, IL-9, IL-13

Cytokines secreted by tissue lymphocytes act on effector cells (eosinophils, basophils, epithelial cells, B cells, sensory neurons endothelium and smooth muscle cells) to eliminate and expel pathogens allergens, and repair tissue damage

Epithelial and mast cells can both detect and eliminate pathogens and allergens.

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8
Q

How is Th2 responses induced?

A

Not really well understood in humans

Defects in skin epithelial barrier ( atopic dermatitis) are a significant risk factor for development of IgE antibodies

Skin dendritic cells (DC) [Langerhans cells and dermal DC] promote secretion of Th2 cytokines much more efficiently than other DC subsets which suggest that different DC subsets may prime Th2 immune responses in humans

IL-4 secretion is only induced following peptide-MHC presentation to TCR to either naïve and/or memory Th2 cells

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9
Q

Which allergic diseases do children get?

A 
Atopic dermatitis 
Food allergy (milk, egg, nuts)
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10
Q

Which allergic diseases do children get?

A

Asthma
Allergic rhinitis

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11
Q

Which allergic diseases do adults get?

A

Drug allergy
Bee allergy
Oral allergy syndrome
Occupational allergy

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12
Q

Which one of the following proteins/cytokines is NOT a drug target for current drugs and/or biologics used to treat allergic disorders?

A. IL-13

B. Histamine

C. IL-33

D. IgE

E. IL-5

A

C. IL-33

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13
Q

What is the prevalence of asthma, allergic rhinitis, atopic dermatitis and food allergy in adults?

A

Asthma 10%

Allergic rhinitis 20%

Atopic dermatitis 5%

Food allergy 3.7%

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14
Q

How has the prevalence of allergic rhinitis changed over the 20th century?

A

Increased

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15
Q

Why have allergic disorders risen over the last 50 years?

A

Hygiene hypothesis: lack of childhood exposure to infectious agents increases susceptibility to allergic diseases by supressing natural development of immune system.

Lack of Vitamin D in infancy is a risk factor for development for food allergy

Dietary factors: reduced omega and linoleic fatty acids, delayed introduction of peanuts in children with egg allergy and atopic dermatitis

Rise in food allergy may be associated with high concentration of dietary advanced glycation end products and pro-glycating sugars which immune system mistakenly detects as causing tissue damage; fast food and soda

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16
Q

Which systems are affected in IgE responses?

A

Skin

Respiratory Tract

GI tract

Vasculature/ CNS

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17
Q

How are systems affected in IgE responses?

A

Occurs within minutes or up to 3 hours after exposure to allergen and symptoms can include:

Skin: angioedema (swelling of lips, tongues, eyelids) , urticaria ( wheals or ‘hives’), flushing and itch

Respiratory tract: cough, SOB wheeze, sneezing, nasal congestion and clear discharge, red itch watery eyes

Gastrointestinal tract: nausea, vomiting and diarrhoea

Vasculature and CNS: symptoms of hypotension (faint, dizzy, blackout) and a sense of impending doom

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18
Q

What are the clinical features of an allergic response?

A

At least 2 organ systems are usually involved.

Reproducible: occurs after every exposure

Allergic symptoms may be triggered by cofactors such as exercise, alcohol, and possibly infection.

Clinical history is used to select what allergens should be tested by skin prick and/or blood tests

Not always obvious e.g.:

House dust mite

Fungal skin colonisation

Red meat ingestion

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19
Q

Which symptoms are not associated with IgE allergic reactions?

A

Fatigue

Migraine

Recurrent episodes of abdominal pain, diarrhoea, constipation, bloating

Hyperactivity

Depression

Symptoms which vary over time, with antigen dose and source

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20
Q

What are the elective investigations of allergic diseases?

A

Skin prick and intradermal tests
Laboratory measurement of allergen specific IgE
Component-resolved diagnostics
Basophil activation test
Challenge test
Supervised exposure to the putative antigen

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21
Q

What investigations do you do during an acute episode?

A

Evidence of mast cell degranulation
Serial mast cell tryptase
Blood and/or urine histamine

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22
Q

What can specific IgE tests tell you?

A

Skin prick and blood test are used to detect presence/absence of IgE antibody against external proteins.

Diagnosis of allergic disease is made by the clinician; integrates data obtained from epidemiology, history, examination, SPT, laboratory, and challenge testing.

A positive IgE test only demonstrates sensitisation (risk of allergic disease) NOT CLINICAL ALLERGY. Detection of IgE is necessary but not sufficient to make a diagnosis of allergic disease.

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23
Q

What is the skin prick test?

A

Expose patient to standardised solution of allergen extract through a skin prick to the forearm.

Use standard skin test solutions and positive control (histamine) and negative control (diluent)

Measure local wheal and flare response to controls and allergens

Looking for crosslinking and degranulation

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24
Q

What’s a positive skin prick test?

A

A positive test is indicated by a wheal ≥ 3mm greater than the negative control.

Antihistamines should be discontinued for at least 48 hours beforehand

Skin prick testing is considered to be more sensitive and specific than blood tests to diagnose allergy in routine clinical practice

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25
Q

What are the advantages of the skin prick test?

A

Rapid (read after 15-20 minutes)

Cheap and easy to do

Excellent negative predictive value usually more than > 95%

Increasing size of wheals correlates with higher probability for allergy

Patient can see the response

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26
Q

What are the disadvantages of the skin prick test?

A

Requires experience to interpret

Risk of anaphylaxis: 1 in 3000

Poor positive predictive value: high false positive rate

Limited value in patients with dermatographism or extensive eczema

False negative results with labile commercial food extracts

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27
Q

What is the serum sprecific IgE blood test?

A

Allergen bound to sponge in a plastic cap and patient’s serum is added.

Specific IgE (if present) binds to allergen.

Anti-IgE antibody tagged with a fluorescent label is added.

Amount of IgE/Anti-IgE is measured by fluorescent light signal.

Blood test are very reliable but can be expensive.

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28
Q

Why should we use serum specific IgE tests?

A
  1. May help diagnosis of allergy
  2. Concentration of specific IgE predict who will outgrow allergy (should do oral food challenge)
  3. Higher values = more likely allergic disorder (triage patients who do not need oral food challenges)
  4. Very good NPV but not PPV
  5. Can be used to monitor response to anti-IgE therapy

Results of serum specific IgE do not predict severity of reaction

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29
Q

What are the indications for serum specific IgE tests?

A

Patients who can’t stop anti-histamines

Patients with dermatographism

Patients with extensive eczema

History of anaphylaxis

Borderline/equivocal skin prick test results

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30
Q

What is Component Resolved Diagnostics (CRD)?

A

Blood test to detect IgE to single protein components: abundance and stability of protein contribute to risk of allergic disease

Useful for diagnosis of peanut and hazelnut allergy: may reduce the needs for food challenges

IgE sensitisation to heat labile and proteolytic susceptible birch pollen homologue peanut and hazelnut allergen component target heat are usually associated with minor or no symptoms

IgE sensitisation to heat and proteolytic stable seed storage peanut and hazelnut allergen components are usually with severe allergic reactions

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31
Q

What are Indications for allergen component testing ?

A

A Detect primary sensitization
Confirm cross reactivity

B Define risk of serious reaction for stable allergens

C. Improve diagnostic sensitivity on addition of components which are poorly represented in whole food extracts

D Improve diagnostic sensitivity for unstable molecules in whole food extracts

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32
Q

Why is mast cell tryptase important?

A

Tryptase: pre-formed protein found in mast cell granules

Systemic degranulation of mast cells during anaphylaxis results in increase in serum tryptase

Peak concentration at 1-2 hours; returns to baseline by 6-12 hours

Failure to return to baseline after anaphylaxis may be indicative of systemic mastocytosis

Useful if diagnosis of anaphylaxis is not clear (hypotension + rash during anaesthesia

Reduced sensitivity for food induced anaphylaxis

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33
Q

Why are challenge tests good?

A

Gold standard for food and drug allergy diagnosis

Increasing volumes of the offending food/drug are ingested

Double blind placebo or open challenge

Food challenges take place under close medical supervision. Very expensive in terms of clinical staff time.

Can be difficult to interpret mild symptoms

Risk of severe reaction

34
Q

What is the Basophil activation test?

A

Measurement of basophil response to allergen IgE cross linking

Activated basophils increase the expression of CD63, CD203, CD300 protein on cell surface

Increasing use in diagnosis of food and drug allergy: surrogate marker for challenge tests

Efforts to this standardise test to use n diagnostic laboratories to reduce need fro challenge tests

35
Q

A 15 year old with a history of asthma and hayfever who notices an urticarial and angioedema skin rash shortly after eating peanuts. What is the most appropriate initial diagnostic test?

A

Skin prick

36
Q

A 60 year old female with hypotension and skin rash under general anaesthesia What is the most appropriate test to diagnose anaphylaxis?

A

Serial mast cell tryptase

37
Q

What is anaphylaxis?

A

Anaphylaxis: a severe potentially systemic hypersensitivity reaction. Rapid onset, life threatening airway, breathing and circulatory problems which is usually but not always associated with skin and mucosal changes

Incidence: 1.5-8/100,000 persons years with studies from UK showing increase in hospital admissions over last 20 years

Estimated prevalence based on European studies is 0.3%

Skin (hives, itch, swollen lips, tongue, uvula) is most frequent organ involved (84%), then cardiovascular system (collapse, syncope, incontinence symptoms, drop in BP) in 72% cases and respiratory compromise (SOB, wheeze, stridor, fall in PEF, hypoxemia in 68%.

Respiratory symptoms occur more often in children and cardiovascular in adults

Acute onset of symptoms and/or signs (minutes to several hours)

38
Q

What is epi/ cause of anaphylaxis?

A

Prevalence of anaphylaxis 0.3% of population

More common in children aged 0-4 year than other age groups

Food more common in children, drug and venom diagnosed more often in adult

Idiopathic anaphylaxis seen in 20% cases: hidden causes include shrimp, wheat, and red meat

39
Q

Reactions that can mimic anaphylaxis

A

SKIN: Chronic urticaria and angioedema (ACE inhibitors)

THROAT SWELLING: C1 inhibitor deficiency

CARDIOVASCULAR: Myocardial infarction and PE

RESPIRATORY: Very severe asthma, vocal cord dysfunction, inhaled FB

NEUROPSYCHIATRIC: Anxiety or panic disorder

ENDOCRINE: carcinoid and phaechromocytoma

TOXIC: Scromboid toxicity (Histamine poisoning )

IMMUNE: Systemic mastocytosis

40
Q

Laboratory diagnosis of anaphylaxis

A

Serial measurement of serum tryptase (a highly specific marker for mast cell degranulation)

Samples taken 1 hour, 3 hours and 24 hours post episode of anaphylaxis

The rise in tryptase concentration is directly proportional to fall in BP

Persistent rise in tryptase 24 hours after allergic reaction suggestive of systemic mast cell disease

41
Q

What is the most important treatment of anaphylaxis and why?

A

Adrenaline

Mechanism of action adrenaline

α1 receptors: causes peripheral vasoconstriction, reverses low BP and mucosal oedema

β1 receptor: increase heart rate and contractility and BP

β2 receptor: relaxation bronchial sooth muscle and reduce release of inflammatory mediators

42
Q

What is the emergency management of anaphylaxis?

A

IM adrenaline into outer aspect of thigh and repeat if needed

Adjust body position: sit up, supine, lie on side

Oxygen 100%

Fluid replacement

Inhaled Bronchodilators

Hydrocortisone 100mg IV ( prevent late phase response)

Chlorpheniramine 10mg IV ( skin rash)

43
Q

What is the Further management of anaphylaxis?

A

CONSERVATIVE Onward Referral: Referral to an allergy/immunology clinic, Investigate the cause of anaphylaxis, Refer patients with food induced anaphylaxis to a qualified dietician, Review patients to ensure that they understand their disease and can use their Epipen

CONSERVATIVE Education: Recognition of symptoms, Avoidance of identifiable triggers, Indications for self treatment with an Epipen, Copy of management plan and training for patient, carers, school staff and GP, Advise patients to acquire a Medic Alert bracelet, Utilise patient support groups ie Anaphylaxis Campaign

MEDICAL: Prescription of emergency kit to manage anaphylaxis, Venom immunotherapy and drug desensitisation as appropriate

44
Q

What is in a Emergency community anaphylaxis kit?

A

Epipen: preloaded adrenaline syringe

Contains 300ug adrenaline for adult patients and 150ug adrenaline for children
AND
Prednisolone 20mg OD

Antihistamine tablet
Cetirizine 10mg OD

Must call for ambulance and attend A&E after using emergency kit

45
Q

24 year female with rapid onset of a skin rash, breathless, loss of consciousness shortly after eating shellfish. What is the most appropriate initial treatment?

A. Intramuscular adrenaline

B. Intravenous adrenaline

C. Intravenous fluids

D. Intravenous hydrocortisone

E. Nebulised salbutamol

A

A: Intramuscular adrenaline

46
Q

A 55 year old man who attends A&E with angioedema involving lips and tongue which has developed over previous hours. He has a history of hypertension and is taking an ACE inhibitor and calcium channel blocker. Clinical examination show a pulse of 75bpm, blood pressure 150/90, respiratory rate of 18/min and oxygen saturation 78% on air. What is the most likely diagnosis?

A. C1 inhibitor deficiency

B. Acute anxiety attack

C. Systemic Mastocytosis

D. Idiopathic Anaphylaxis

E. ACE inhibitor induced angioedema

A

E: ACE inhibitor induced angioedema

47
Q

Summarise food allergies

A

Food allergy: adverse health effect arising from specific immune response that occurs reproducibly on exposure to a given food

Food intolerance: non immune reactions which include metabolic, pharmacological and unknown mechanisms

Food allergy likely affect up to 5% of adults and 8% of children

48
Q

What are the adverse reaction to foods?

A

Food intolerance

Food aversion

Food allergy

49
Q

describe the adverse reaction to foods?

A

1) Food intolerance Food poisoning (bacterial, scromboid toxin) Enzyme deficiencies (lactase) Pharmacological (caffeine, tyramine )
2) Food aversion Fads, eating disorders

3) Food allergy IgE mediated reactions (anaphylaxis, OAS)
Mixed IgE and cell mediated (atopic dermatitis)
Non IgE mediated (coeliac disease)
Cell mediated (contact dermatitis)

50
Q

Which allergies can be outgrown and what is related to food allergies?

A

Most children outgrow milk and egg allergy but rarely outgrow peanut and tree nut allergy

Moderate/severe atopic dermatitis is an important risk factor for food allergy (indication for allergy testing even in absence of clinical history)

51
Q

What might you find in the clinical history of food allergy?

A

What does the patient mean by allergy.

Distinguish between IgE and non IgE mediated symptoms.

Dose, how food is prepared and co-factors can influence clinical symptoms

Does the patient have any history of atopic disease

Enquire about previous investigations for food allergy ie SPT, IgE blood tests and complementary medical tests

Has elimination of food made any difference to symptoms

Consider other differential diagnoses (food intolerance, eating disorders, coeliac disease)

52
Q

What investigations would you do for food allergy?

A

Clinical history is used to estimate prior probability of allergy, identify culprit foods and decide what diagnostic allergen tests are used to achieve a post test probability of allergy

A positive SPT/specific IgE blood test is useful to confirm a clinical history of food allergy.

A negative SPT/specific IgE blood test essentially excludes IgE mediated allergy (Negative predictive value NPV = 95%).

Fruit and vegetable skin prick test solutions are labile and it often better to useful use actual fruit or vegetable.

Testing for individual allergen protein component can distinguish between IgE sensitisation and IgE mediated allergy

53
Q

What is the management of food allergy?

A

Conservative

Education: Avoidance, Education about food labelling, interaction with restaurants, school, Anaphylaxis guidelines

Diet advice: Nutritional input for dietary balance, growth in children

Reassurance: Acknowledge anxiety, potential bullying: mental health support if needed

Ensure allergic asthma is well controlled

Prevention

Breast feeding: strong family of allergy, LEAP study: early rather than delayed introduction of peanut in high risk children (moderate/severe AD and egg allergy) significantly reduces development of peanut IgE sensitisation and allergy

54
Q

What is the IgE mediated food allergy syndromes?

A

Anaphylaxis:
Peanut, tree nut shellfish, fish, milk and eggs are most common

Natural history dependent on food

Food associated exercise induced anaphylaxis
Food induces anaphylaxis if individual exercises within 4-6 hours of ingestion

Common food triggers are wheat, shellfish, celery

Delayed food-induced anaphylaxis to beef, pork, lamb
Symptoms occur 3-6 hours after eating red meat and gelatin

IgE antibody to oligosaccharide alpha-gal (α1, 3-galactose) found in gut bacteria

Induced by tick bites which should be avoided

55
Q

What is oral allergy syndrome?

A

Limited to oral cavity, swelling and itch: only 1-2% cases progresses to anaphylaxis

Sensitisation to inhalant pollen protein lead to cross reactive IgE to food

Onset after pollen allergy established: affect adults > young children

Respiratory exposure to pollen (birch) results in IgE directed to homologous proteins in stone fruits (apple, pear) vegetables (carrot) and nuts (peanut, hazelnut)

Cooked fruits, vegetables and nut cause no symptoms: heat labile allergens detected by component allergen tests

56
Q

A 35 year old man with tree pollen hayfever and immediate lip tingling and swelling immediately after eating apples. What is the most likely explanation for IgE hypersensitivity ?

A. IgG4 subclass deficiency

B. Cross reactive IgE sensitisation between hay fever and apple allergens

C. Apple-hay fever immune complex disease

D. Increased Th17 immune response to apple allergen

E. Food aversion disorder

A

B: Cross reactive IgE sensitisation between hay fever and apple allergens

57
Q

What is Type 1 and Type 2 inflammatory allergic reactions?

A
58
Q

What is involved in Th2 immune responses? (Label the picture below)

A
59
Q

What is involved in a Th2 reaction?

A
60
Q

What can cause reactions?

A

Defects in skin are RFs for IgE antibodies

Il-4 plays a crucial role in memory cells/ basophils/ mast cells

61
Q

Which 3 allergic diseases saw a sequential rise?

A
62
Q

Exam style Question on Innate lymphoid cells:

  1. Where are innate lymphoid cells found?
  2. What do Innate Lymphoi cells respond to?
  3. How are CD4 innate lymphoid cells classified?
  4. What does ILC2 secrete?
  5. Which diseases is ILC2 implicated in?
  6. What does Amphiregulin do?
A
63
Q

Exam style question:

What is an eosinophil?

What does it do?

What is the key cytokine for development?

What are eosinophils implicated in?

A
64
Q

Exam question:

What are the 2 types of mast cells?

What is mast cell degranulation triggered by?

What is the role of mast cells?

What are the key mast cell receptors?

Do opiates and quinolones involve basophils/ IgE?

A

Opiates and quinolones directly stimulate mast cells.

65
Q

How does mast cell degranuation occur?

A
66
Q

What factors promote IgE production?

A
67
Q

Summarise the Th2 Immune response

A
68
Q

Why does allergic rhinitis exist?

A
69
Q

How do microbes protect against asthma?

A
70
Q

How can you diagnose allergies?

A
71
Q

Why is IgE sensitisation important?

A
72
Q

How and when are intradermal tests used?

A
73
Q

What are sensitisation tests?

A
74
Q

What is the risk profile of specific IgE blood tests?

A
75
Q

What are the indications for blood sensitisation tests?

A
76
Q

Summarise component resolved/ molecular testing?

A
77
Q

What tests can you use for nuts, wheata, egg/ mil and fish/ shellfish?

A
78
Q

Summarise the diagnosis of anaphylaxis

A
79
Q
A
80
Q

60 year old hypotension and rash: test to diagnose anaphylaxis?

A

Seriel mast cell tryptase

81
Q

What can you identify from specific IgE testing?

A

We can identify:

  1. Risk Profile
  2. Concentration of IgE (positive correlation with symptoms)
  3. Affinity of IgE (Positive correlation with risk)
  4. Ability of IgE to induce degranulation
  5. Identification of molecular target

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