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Immunology - Path > Allergy > Flashcards

Allergy Flashcards

1
Q

Define the following:

  1. Allergic disorder
  2. Allergen
A
  1. Allergic disorder: immunological process that results in immediate and reproducible symptoms after exposure to an allergen
  2. Allergen is usually a harmless substance that can trigger an IgE mediated immine response and may result in clinical symptoms
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2
Q

Describe what triggers a T cell helper 1 response and a t cell helper 2 response

A

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

  • Microbial PAMP –> Structural feature recognition –> leads to a Th1, Th17 immune response
  • Th2 response occurs with infection with helminthes, allergens and venoms

Huge overlap between the two systems that detect tissue damage and allergens which have extensive protease activity and the capacity to damage epithelial barriers

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3
Q

Describe the Th2 immune response when there is stressed or damaged epithelium as the sensor of the Th2 response:

  1. Sensor
  2. Signalling cytokines
  3. Lymphoyctes
  4. Effector cytokines
  5. Effector cells
  6. Immune response
A
  1. Sensors - stressed or damaged epithelium
  2. Signalling cytokines - ILalpha, IL-25, IL-13, TSLP
  3. Lymphocytes -
  • Th2 cells, Th8 cells, ILC2
  • Tfh2 cells
  1. Effector cytokines
  • IL-4, IL-5, IL-9, IL-13
  • IL-4, IL-21
  1. Effector cells
  • Eosinophils, basophils
  • B cells
  1. Immune response
  • Worm and allerge expulsion, mucous secretion
  • IgE, IgG4
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4
Q

Describe the Th2 immune response when the immune system is attacked by worms, allergens or venoms

  1. Sensor
  2. Signalling and effector cytokines/proteins
  3. Effector cells
  4. Immune response
A
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5
Q

Describe the following about Th2 immune responses

  1. What detects allergens, venoms and worms?
  2. What are secreted in response to stressed or damaged epithelial cells?
  3. Why are cytokines secreted by tissue lymphocytes to act on effector cells?
A
  1. Epithelial cells and mast cells detect allergens, venoms and worms
  2. 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-4, IL-9, IL-13
  3. Cytokines secreted by tissue lymphocytes act on effector cells (eosionphils, basophils, epithelial cells, B cells, sensory neurons endothelium and smooth muscle cells) in order to eliminate and expel pathogens allergens, and repair tissue damage
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6
Q

Describe the induction of Th2 immune responses

A
  • Not really well understood in humans
  • Defects in skin epithelial barrier e.g. atopic dermatitis are a significant risk factor for development of IgE antibodies
  • Skin dendritic cells (langerhans cells and dermal dc) promote secretion of TH2 cytokines much more efficiently than other DC subsets which suggest that DC subsets may prime TH2 immune responses in humans
  • IL-4 secretion is only induced following peptide-MHC presentation to TCR to either naive and/or memory Th2 cells
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7
Q

Describe the role of T regulatory cells derived from GI mucosa

A

T regulatory cells derived from GI mucosa inhibit IgE synthesis to keep immune system in balance

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8
Q

Describe some of the different allergic diseases that occur at the following ages:

  1. Infants
  2. Childhood
  3. Adults
A
  1. Infants
  • Atopic dermatitis
  • Food allergy (milk, egg, nuts)
  1. Childhood
  • Asthma (HDM, pets)
  • Allergic rhinitis (HDM, grass, tree pollens)
  1. Adults
  • Drug allergy
  • Bee allergy
  • Oral allergy syndrome
  • Occupational allergy
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9
Q

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

  1. IL-13
  2. Histamine
  3. IL-33
  4. IgE
  5. IL-5
A

3.IL-33

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10
Q

What are the theories for why allergic disorders have risen over the last 50 years?

A
  • Hygiene hypothesis - lack of childhood exposure to infectious agents increases susceptibility to allergic diseases by suppressing 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 sygars which immune system mistakenly detects as causing tissue damage, fast food and soda
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11
Q

What are the clinical features of IgE allergic responses in the following organs:

  1. Skin
  2. Respiratory tract
  3. GI tract
  4. Vasculature and CNS
A

IgE allergic responses occurs within minutes or up to 3 hours after exposure to allergen, symptoms can include:

  1. Skin
  • Angioedema (swelling of lips, tongues, eyelids)
  • Urticaria (wheals or ‘hives’)
  • flushing
  • Itching
  1. Respiratory tract:
  • cough
  • SOB
  • Wheeze
  • Sneezing
  • nasal congestion and clear discharge
  • red, itchy, watery eyes
  1. GI Tract
  • Nausea
  • Vomiting
  • Diarrhoea
  1. Vasculature and CNS
  • Symptoms of hypotension (faint, dizzy, blackout)
  • A sense of impending doom
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12
Q

Define an IgE allergic response

A
  • IgE allergic response occurs within minutes or up to 3 hours after exposure to an allergen
  • 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
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13
Q

What symptoms are not associated with IgE allergic reactions?

A
  • Fatigue
  • Migraine
  • Reccurent episodes of abdominal pain, diarrhoea, constipation, bloating
  • Hyperactivity
  • Depression
  • Symptoms that vary over time, with antigen dose and source
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14
Q

Describe investigations for allergic disease

  1. Elective
  2. During an active episode
A
  1. Elective investigations:​
  • 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
  1. During active episode
  • Evidence of mast cell degranulation
    • Serial mast cell tryptase
    • Blood and/or urine histamine
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15
Q

Describe some specific IgE sensitisation tests

  1. Skin prick and blood test
A

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

A positive IgE test only demonstrates sensitisation (risk of allergic disease) NOT CLINICAL ALLERGY

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16
Q

Describe the risk profile of serum IgE for prediction of allergic symptoms:

A
  • Concentration of IgE - higher levels more likely to be associated with symptoms
  • Molecular target within whole extract or even individual epitope can be linked to symptoms
  • Affinity (strength of binding) to target: higher affinity associated with risk
  • Capacity of IgE antibody to induce mast/basophil degranulation
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17
Q

Describe the skin-prick test

A
  • Expose patient to standardised solution of allergen extract through a skin prick to the forearm. also use a positive control (histamine) and a negative control (dilutent)
  • Measure local wheal and flare response to controls and allergens
  • A positive test is indicated by a wheal > 3mm greater than the negative control
  • Skin prick test is considered to be more sensitive and specific than blood tests to diagnose allerge in routine clinical practice
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18
Q

What are advantages and disadvantages of skin prick tests?

A

Advantages:

  • Rapid
  • Cheap and easy to do
  • Excellent negative predictieve value, usually more than 95%
  • Increasing size of wheals correlates with higher probability for allergy
  • Patient can see the response

Disadvantages:

  • 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 commerical food extracts
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19
Q

Describe serum specific 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 fluorecesent light signal
  • Blood test are very reliable but can be expensive

Results:

  • Higher values are more likely to be associated with allergic disorder and can be used to triage patients who do not need oral food challenges
  • Lots of false positives
  • Results of serum specific IgE do not predict severity of reaction
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20
Q

What are the indications of specific IgE blood tests over a skin prick test?

A
  • Patients who can’t stop anti-histamines
  • Patients with dermatographism
  • Patients with extensive eczema
  • History of anaphylaxis
  • Borderline/equivocal skin prick test results
21
Q

Describe Component reoslved diagnostics

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
    *
22
Q

What is mast cell tryptase?

A

Mast cell tryptase is a biomarker for anaphylaxis

  • Tryptase is a pre-formed protein found in mast cell granules
  • Systemic granulation of mast cells during anaphylaxis results in increase in serum tryptase
  • Peak concentration at 1-2 hours, returns to baseline 6-12 hours
  • However, reduced sensitivity for food induced anaphylaxis
23
Q

What could it mean is mast cell tryptase levels fail to return to baseline after anaphylaxis?

A

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

24
Q

Describe challenge tests for food and drug allergy

A
  • Gold standard for food and drug allergy diagnosis
  • Increasing volumes of the offending food/drug are ingested
  • 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
25
Q

Describe the basophil activation test

A
  • Measurement of basophil response to allergen IgE cross linking
  • Activated neutrophils 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 standardise test to use in diagnostic laboratories to reduce need for challenge tests, which can be dangerous
26
Q

EMQ

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 diagnosis?

  1. Component allergen test
  2. Skin prick test
  3. IgE blood test
  4. mast cell tryptase
  5. Food challenge
A
  1. Skin prick test
27
Q

EMQ

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

  1. Skin prick
  2. Drug challenge
  3. Blood histamine
  4. Serial mast cell tryptase
  5. Urine prostaglandin D2
A
  1. Serial mast cell tryptase
28
Q
  1. Define anaphylaxis
  2. What is the incidence of anaphylaxis?
  3. What are the signs and symptoms of anaphylaxis?
  4. What age group is anaphylaxis most common in?
A
  1. Anapylaxis is a potentially severe sytsemic hypersensitivity reaction. Rapid onset, life threatening airway, breathing and circulatory problems which is usually not be always associated with skin and mucosal changes
  2. Incidence is 1.5-8/100,000 persons a year. Prevalemce is 0.3% across Europe
  3. Signs and symptoms:
  • Skin - hives, itch, swollen lips, tongue and uvula) most common
  • Cardiovascular system - collapse, syncope, incontinence symptoms, drop in BP
  • 72% of cases - respiratory compromise - SOB, wheeze, stridor, fall in PEF and hypoxia in 68%
  1. More common in children aged 0-4 years

Food more commn in children, drug and venom diagnosed more often in adults

29
Q

What are the 4 ‘types’ of anaphylaxis and examples of each?

A
  1. IgE - Food, insect venom, ticks, penicillin
  2. IgG - Biologicals, blood and IgG transfusions
  3. Complement - Lipid excipients, liposomes, dialysis membranes and PEG
  4. Pharmacological - NSAID including aspirin, opiates, neuromuscular and quinolones drug
30
Q

Describe the cells involved and mediators for the 4 different types of anaphylaxis:

  1. IgE
  2. IgG
  3. Complement
  4. Pharmacological
A
  1. IgE
  • Cells: Mast cells and basophils
  • Mediators: Histamine and PAF

2.IgG

  • Cells: macrophages and neutrophils
  • Mediators: histamine and PAF
  1. Complement
  • Cells: mast cells and macrophages
  • Mediators: PAF and histamine
  1. Pharmalogical
  • Cells: mast cells
  • Mediators: leukotrienes and histamine
31
Q

Name a condition that mimic anaphylaxis in the following groups:

  1. Skin
  2. Throat swelling
  3. Cardiovascular
  4. Respiratory
  5. Neuropsychiatric
  6. Endocrine
  7. Toxic
  8. Immune
A
  1. Skin = Chronic urticaria and angioedema (ACE inhibitors)
  2. Throat swelling - C1 inhibitor deficiency
  3. Cardiovascular - Myocardial infarction and PE
  4. Respiratory - Very severe asthma, vocal cord dysfunction, inhaled FB
  5. Neuropsychiatric - anxiety or panic disorders
  6. Endocrine - carcinoid and phaeos
  7. Toxic - scromboid toxicity (histamine posioning)
  8. Immune - systemic mastocytosis
32
Q

Describe laboratory diagnosis of analphylaxis

A
  • Serial measurement of serum tryptase ( a highly specific markers for mast cell degranulation)
  • Samples taken at 1hr, 3 hr and 24 hours post episode
  • 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
33
Q

What does serum tryptase show?

A

A highly specific marker for mast cell degranulation

34
Q
  1. What is the main treatmet for anaphylaxis?
  2. How does it work on the following receptors

a) a1
b) b1
c) b2

A
  1. Adrenaline is most important treatment for anaphylaxis
  2. Mechanism of action
    a) a1 = causes peripheral vasoconstriction, reverses low BP and mucosal oedema
    b) b2 = increase heart rate and contractility and BP
    c) b2 = relaxation of bronchial smooth muscle and reduce release of inflammatory mediators
35
Q

Describe the emergency management of anaphylaxis

A
  • IM adrenaline into outer aspect of thigh and repeat and 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)
36
Q

What is further management of anaphylaxis, after the emergency treatment?

A
  • Referral to allergy/immunology clinic to investiagte cause
  • Prescription of emergency kit
  • Management plan to all areas including school, clubs and home
37
Q

What can be found in an emergency community anpahylaxis kit?

A
  • Epipen: preloaded adrenaline syringe - contains 300ug adrenaline for adult patients and 150ug adrenaline for children
  • AND prednisolone 20mg OD
  • Antihistamine - cetirizine 10mg OD
  • Must call for ambulance and attend A&E after using emergency kit
38
Q

EMQ

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

  1. Intramuscular adrenaline
  2. Intravenous adrenaline
  3. Intravenous fluids
  4. Intravenous hydrocortisone
  5. Nebulised salbutamol
A
  1. Intramuscular adrenaline
39
Q

EMQ

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?

  1. C1 inhibitor deficiency
  2. Acute anxiety attack
  3. Systemic Mastocytosis
  4. Idiopathic anaphylaxis
  5. ACE inhibitor induced angioedema
A
  1. ACE induced angioedema
40
Q
A
41
Q

Define each of the following:

  1. Food allergy
  2. Food intolerance
A
  1. Food allergy - adverse health effect arising from specific immune response that occurs reproducibly on exposure to a given food
  2. Food intolerance - non immune reactions which include metabolic, pharmalogical and unknown mechanisms
42
Q

Describe the different adverse reactions to food in the following groups:

  1. Food intolerance
  2. Food aversion
  3. Food allergy
A
  1. Food intolerance
  • Food poisoning - bacterial, scromboid toxin
  • Enzyme deficiencies (lactase)
  • Pharmalogical (caffeine, tyramine)
  1. Food aversion
  • Fads
  • eating disorders
  1. Food allergy:
  • IgE mediated reactions e.g. anaphylaxis, oral allergy syndrome
  • Mixed IgE and cell mediated - atopic dermatitis
  • Non IgE mediated - coeliac disease
  • Cell mediated - contact dermatitis
43
Q

In the US, which food allergy is most prevalent in:

  1. Children
  2. Adults
A
  1. Chidren - milk
  2. Adults - shellfish
44
Q

What blood tests confirms a clinical history of food allergy?

A

A positive SPT/Specific IgE blood test

A negative specific IgE blood test essentially excludes IgE mediated allergy

45
Q

Can a skin prick test be used to confirm presence of an allergy?

A

A positive skin test or food specific IgE blood test indicated sensitisation and not necessarily allergy

Increasing high food-specific IgE levels or larger skin tests wheal size indicate a higher chance of allergy

46
Q

What is the gold standard for the diagnosis of food allergy?

A

Double blinf oral food challenge

47
Q

Describe the management/treatment of food allergy

A
  • Avoidance of allergy
  • Emergency management
  • Prevention
48
Q

What are the 4 IgE mediated food allergy syndromes and what can cause them?

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 and lamb
    • Symptoms occur 3-6 hours after eating red meat and gelatin
    • IgE antibody to oligosaccharide alpha-gal found in gut bacteria
    • Induced by tick bites which should be avoided
  • Oral allergy syndrome:
    • Limited to oral cavity, swelling and itch and very few develop to anaphylaxis
    • Sensitisation to inhalant pollen protein lead to cross reactive IgE to food
49
Q

EMQ

A 35 year olf man with tree pollen hayfever and immediate lip tingling and swelling immediately after eating apples

What is the most likely explanation for IgE hypersensitivity?

  1. IgG4 subclass deficiency
  2. Cross reactive IgE sensitisation between hayfever and apple allergens
  3. Apple-hay fever immune complex diseases
  4. Increased Th17 immune response to apple allergen
  5. Food aversion disorders
A
  1. Cross reactive IgE sensitisation between hayfever and apple allergens

Immunology - Path (9 decks)

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