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YEAR 5: Immunopathology JK > Immuno: Allergy > Flashcards

Immuno: Allergy Flashcards

1
Q

Define allergic disorder.

A

Immunological process that results in immediate and reproducible symptoms after exposure to an allergen. Usually involves IgE-mediated type 1 hypersensitivity reaction.

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2
Q

Define sensitisation.

A

Detection of specific IgE either by skin prick testing or in vivo blood test

NOTE: this does NOT define allergic disease

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3
Q

Describe the difference between immune responses mediated by Th1 and Th2 cells.

A
  • Pathogens that have conserved structures (PAMPs) such as bacteria are recognised by Th1 and Th17 cells
  • Multicellular organisms (e.g. helminths) and allergens don’t have conserved structures but they release mediators that damage epithelial cells
  • Disturbance of epithelial cells is recognised by the Th2 cells
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4
Q

Outline the Th2-mediated immune response.

A
  • Damaged epithelium releases signalling molecules (e.g. TSLP)
  • These cytokines will act on Th2, Th9 and ILC2 cells, which then produce IL4, IL5 and IL13
  • These cytokines act on basophils and eosinophils which play a major role in the expulsion of allergens and parasites
  • TSLP and other cytokines can also activate follicular Th2 cells which release IL4
  • IL4 stimulates B cells to produce IgE and IgG4
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5
Q

What other allergic response can be initiated by parasites and allergens which is not mediated by Th2 cells?

A
  • Allergens can cross-link IgE leading to mast cell degranulation and the release of histamines, prostaglandins and leukotrienes
  • These mediators act on the epithelium causing increasing permeability, smooth muscle contraction and neuronal irritability (itching)
  • This response aims to expel the parasite/allergen and is implicated in asthma, eczema and hay fever
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6
Q

Describe the relationship between Langerhans cells and Th2 cells.

A

Langerhans cells promote the secretion of Th2 cytokines

NOTE: skin defects (i.e. epithelial barrier issues) are a significant risk factor for the development of IgE antibodies via Th2 responses

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7
Q

What induces the production of IL4?

A

Peptide presentation via MHC to TCR or Th2 cells

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8
Q

How is oral allergen exposure different from respiratory or skin exposure with regards to developing an allergic response?

A
  • Oral exposure promotes immune tolerance whereas skin and respiratory exposure promotes IgE sensitisation
  • When an allergen is ingested orally, Tregs in the GI mucosa will inhibit IgE synthesis to keep the immune system in balance
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9
Q

List the allergic diseases that present in the following age groups:

  1. Infants
  2. Children
  3. Adults
A
  1. Infants
    • Atopic dermatitis
    • Food allergy (milk, eggs, nuts)
  2. Children:
    • Asthma
    • Allergic rhinitis
  3. Adults:
    • Allergic rhinitis (MOST COMMON)
    • Drug allergy
    • Bee allergy
    • Occupational allergy
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10
Q

List some theories behind the increasing prevalence of allergic disorders.

A
  • Hygiene hypothesis
  • Lack of vitamin D in infancy (leads to food allergy)
  • Dietary factors (reduced omega and linleic fatty acids)
  • High concentration of dietary advanced glycation end-products and pro-glycating sugars which the immune system mistakenly recognises as causing tissue damage (e.g. soda)
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11
Q

List some clinical features of IgE-mediated allergic responses.

A
  • Angioedema
  • Urticaria
  • Flushing
  • Itching
  • Cough
  • SOB
  • Wheeze
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12
Q

State some examples of co-factors that could trigger an allergic response.

A
  • Exercise
  • Alcohol
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13
Q

List some elective investigations for allergic disease.

A
  • Skin prick and intradermal tests
  • Specific IgE measurement
  • Component resolved diagnostics
  • Basophil activation test
  • Challenge test
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14
Q

List some investigations that may be conducted during an acute allergic episode.

A
  • Serial mast cell tryptase
  • Blood/urine histamine
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15
Q

Does a postive specific IgE test demonstrate allergy?

A

No - it demonstrates sensitisation

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16
Q

What features of the specific IgE test are used to predic risk and likelihood of symptoms?

A
  • Concentration - higher levels means more symptoms
  • Affinity to the target - higher affinity means increased risk
  • Capacity of IgE antibody to induce mast cell degranulation
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17
Q

Describe how skin prick tests are conducted.

A
  • Expose a patient to a standardised solution of allergen extract through a skin prick on the forearm
  • Use standard skin test solutions with a positive control (histamine) and negative control (dilutent)
  • Measure the local wheal and flare response
  • Positive result: wheal >3mm greater than the negative control
  • Antihistamines should be discontinued for at least 48 hours before the test
18
Q

What are the advantages and disadvantages of skin prick testing?

A

Advantages:

  • Rapid (15-20 mins)
  • Cheap
  • High negative predictive value
  • Increasing size of wheals correlates with higher probability of allergy

Disadvantages:

  • Operator-dependent
  • Risk of anaphylaxis
  • Poor positive predictive value
  • Limited value in patients with dermatographism or extensive eczema
19
Q

Describe how specific IgE tests work.

A
  • Allergen is bound to a sponge and mixed with the patient’s serum
  • Specific IgE will bind to the allergens on the sponge (if present)
  • This is washed with anti-IgE antibody which is fluorescently labelled
  • Higher values are associated with allergic disorders

NOTE: good negative predictive value

20
Q

List some indications for specific IgE tests.

A
  • Patients who cannot stop antihistamines
  • Patients with dermatographism
  • Patients with extensive eczema
  • History of anaphylaxis
  • Borderline skin prick results
21
Q

What is component resolved diagnostics?

A
  • A blood test to detect IgE to single protein components (useful for peanut and hazelnut allergy)
  • IgE sensitisaton to heat and proteolytic labile proteins = minor symptoms
  • IgE sensitisation to heat and protolytic stable protein = major symptoms
22
Q

List some indications for allergy component testing.

A
  • Detect primary sensitisation
  • Confirm cross-reactivity
  • Define risk of serious reaction for stable allergens
23
Q

What is mast cell tryptase used for?

A
  • Tryptase is pre-formed protein found in mast cell granules
  • Systemic degranulation during anaphylaxis results in increased serum tryptase
  • Therefore, it is a biomarker for anaphylaxis
24
Q

When does mast cell tryptase reach peak levels and return to baseline levels?

A
  • Peak = 1-2 hours
  • Baseline = 6-12 hours

NOTE: if it fails to return to baseline, it may suggest systemic mastocytosis

25
Q

When might mast cell trypase be measured?

A

If the diagnosis of anaphylaxis is unclear (e.g. hypotension and rash during anaesthesia)

NOTE: it has lower sensitivity for food-induced anaphylaxis

26
Q

What is the gold standard test for diagnosing food and drug allergy?

A

Challenge test

27
Q

Describe how challenge tests are carried out.

A
  • Increasing volumes of the offending food/drug are ingested
  • Observe a reaction
  • Done under close medical supervision
  • Risk of severe reaction
28
Q

What is a basophil activation test?

A
  • Measurement of basophil response to allergen IgE cross-linking
  • Activated basophils show increased expression of CD63, CD203 and CD300
  • This is increasingly used in food and drug allergy
29
Q

Define anaphylaxis.

A

A severe, potentially life-threatening systemic hypersensitivity reaction characterised by rapid-onset airway, breathing and circulatory problems which are often associated with skin and mucosal changes.

NOTE: skin is the most frequent organ involved

30
Q

List some mechanisms of anaphylaxis.

A
  • IgE - mast cells and basophils - histamine and PAF (triggered by food, venom, ticks, penicillin)
  • IgG - macrophages and neutrophils - histamine and PAG (triggered by blood product transfusions)
  • Complement - mast cells and macrophages - histamine and PAF (triggered by lipid excipients, liposomes, dialysis membranes)
  • Pharmacological - mast cells - histamine and luekotrienes (triggered by NSAIDs)
31
Q

List some reactions that can mimic anaphylaxis.

A
  • Skin - chronic urticaria and angioedmea (ACE inhibitors)
  • Throat swelling - C1 inhibitor deficiency
  • CVS - MI and PE
  • Resp - severe asthma, inhaled foreign body
  • Neuropsych - anxiety/panic disorder
  • Endocrine - carcinoid, phaeochromocytoma
  • Toxic - scromboid toxicity (histamine poisoning)
  • Immune - systemic mastocytosis
32
Q

Describe the mechanism of action of adrenaline in treating anaphylaxis.

A
  • Alpha 1 - peripheral vasoconstriction, reverses low BP and mucosal oedema
  • Beta 1 - increases HR, contractility and BP
  • Beta 2 - relaxes bronchial smooth muscle, reduces release of inflammatory mediators
33
Q

Which supportive treatments are given alongside adrenaline in the management of anaphylaxis?

A
  1. Adult body position
  2. 100% O2
  3. Fluid replacement
  4. Inhaled bronchodilators
  5. Hydrocortisone 100 mg IV
  6. Chlorpheniramine 10 mg IV
34
Q

List some measures that may be taken in the ongoing management of a patient who has experienced an episode of anaphylaxis.

A
  • Referral to allergy clinic
  • Investigate cause
  • Written information on recognition of symptoms, trigger avoidance and indications for self-treatment with EpiPen
  • Prescription of emergency kit to manage anaphylaxis
  • Copy of management plan for patients, parents and school staff and GP
  • Immunotherapy (if indicated)
  • Refer to dietician (if food-induced)
  • Advise getting MedicAlert bracelet
  • Utilise patient support groups (Anaphylaxis Campaign)
35
Q

Which commonly used drug can cause angioedema?

A

ACE inhibitors

NOTE: this can happen at any point when taking ACE inhibitors (i.e. even several years after being on ACE inhibitors)

36
Q

What is the key difference between food allergy and food intolerance?

A

The mechanism behind food intolerance is NOT immunological

37
Q

List some types of food intolerance.

A
  • Food poisoning
  • Enzyme deficiency (e.g. lactose intolerance)
38
Q

List some types of food allergy.

A
  • IgE mediated - anaphylaxis
  • Mixed IgE and cell-mediated - atopic dermatitis
  • Non-IgE mediated - coeliac disease
  • Cell-mediated - contact dermatitis
39
Q

Which investigations are usually used to confirm the diagnosis in patients with a clinical history suggestive of food allergy?

A

Skin prick test or specific IgE blood test

40
Q

List some IgE-mediated food allergy syndromes.

A
  • Anaphylaxis (e.g. peanut)
  • Food-associated exercise-induced anaphylaxis (ingestion of food leads to anaphylaxis if the individual exercises within 4-6 hours of ingestion (e.g. wheat, shellfish))
  • Delayed food-induced anaphylaxis to beef/pork/lamb (symptoms occur 3-6 hours after ingestion, induced by tick bites)
  • Oral allergy syndrome (limited to oral cavity with swelling and itching, occurs after pollen allergy is established, caused by cross-reaction of IgE antibody to pollen with stone fruits (e.g. apples), vegetables and nuts)

YEAR 5: Immunopathology JK (13 decks)

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