Immunology and allergy Flashcards

1
Q

What is allergy

A

An immunological hypersensitivity that can leads to a variety of different diseases via different pathological mechanisms (IgE or non IgE mediated) with different approaches in diagnosis, therapy and prevention

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2
Q

What is the difference between sensitivity and hypersensitivity

A

sensitivity is normal response to stimulus, hypersensitivity is exaggerated

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3
Q

What is sensitisation?

A

production of IgE antibodies after repeated exposure to an allergen

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4
Q

What is atopy?

A

A personal or famillial tendancy to produce IgE in response to exposure to potential allergens. Associates with eczema, asthma, allergic rhinitis and food allergy.

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5
Q

other than food and drug allergy, how may allergy present? (4)

A
  • Insect allergy (local inflammation or anaphylaxis due to bee or wasp sting)
  • Allergic rhinitis
  • Eczema
  • Allergic asthma
  • Allergic conjunctivitis
  • Urticaria/ hives (macropapular itchy rash due to allergen)
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6
Q

What is the allergic march?

A

How prevalence of types of allergies change with change with age- Food allergies, asthma and eczema are most common in young but can decrease with age, rhinitis and conjunctivitis tend to affect older ppl more.

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7
Q

What is the difference between food allergy and intolerance?

A

Intolerance is adverse reactions to food, allergy is immune response

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8
Q

Give 2 mechanisms/ reasons/ examples for food intolerance caused by food characteristics and 2 caused by host characteristics

A
Food: 
- pharmacological (caffeine) 
- Toxic (scromboid fish toxin from spoiled oily fish causes excess histamine production)
Host:
- metabolic (lactose intolerance)
- psychological (food aversion)
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9
Q

Describe the difference in symptoms onset between IgE and non IgE mediated allergy?

A

IgE mediated: Immediate (5-30 mins)

Non: Delayed (hrs to days)

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10
Q

Describe the common food groups associated with IgE and non IgE mediated allergy?

A

IgE mediated: milk, eggs, peanuts, tree nuts, fish and shellfish, fruit and vegetables (PFS).
Non: Milk and soya, wheat, rice and oats

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11
Q

Describe the age of onset and resolution of IgE and non IgE mediated allergy?

A

IgE mediated: onset varies by age of contact. PFS in adolescence and milk by 1 yr. Milk and egg may resolve early, others persist into adulthood.
Non: Most start in infancy and early childhood, all milk by 1 yr. They resolve earlier than IgE, most by school age.

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12
Q

Name and describe the 4 specific disorders that IgE mediated food allergy presents with

A
  • Urticarial/ angiodema: acute hives and swelling w/ N+ V, due to any food
  • Anaphylaxis: multiorgan dysfunction w/ cardio and resp symptoms, mainly w/ nuts, fish, milk, egg
  • Food associated exercise induced anaphylaxis: food triggers anaphylaxis only if ingestion is followed by exercise within 2 hrs
  • Pollen food syndrome (PFS): itching and swelling of lips, mouth, tongue, throat after eating raw veg and nuts- associated with hayfever and unprogressing
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13
Q

State and describe 4 specific presentations of non IgE mediated food allergy?

A
  • protocolitis: bright red blood in stool of otherwise asymptomatic infant (usually milk allergy)
  • enterocolitis: feed refusal, vomiting, loose stools, abdo cramps, constipation (usually due to milk, eggs, wheat allergy)
  • eosinophillic oesphagitis: reflux symptoms, dysphagia, food impaction, usually due to milk, eggs, wheat
  • Food induced enterocolitis syndrome (FPIES): infants with profuse vomiting followed by pallor, lethargy, shock etc. often mistaken for infection but due to milk, soya, rice, wheat, meat
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14
Q

Why does food pollen syndrome occur?

A

It occurs due to cross reactivity of veg/ fruit pollen and hayfever pollens. The allergen is generally denatured in the stomach, preventing systemic symptoms

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15
Q

Why is milk in baked biscuits or boiled eggs less likely to cause an allergic response than cold milk or raw eggs (eg in mayo) in milk and egg allergies respectively? wordy

A

heat denatures the proteins to make them less allergenic

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16
Q

Describe 3 investigations to help diagnose a food allergy?

A
  • skin prick test
  • serum assays for IgE
  • food exclusion tests
  • oral food challenges (rare)
17
Q

Give 5 interventions for management of food allergy

A
  • Anticipatory allergy testing for cross reaction of other similar allergens
  • dietician for dietary exclusion
  • prescription of emergency medicine PRN (adrenalin)
  • early food introductions in infants - giving allergenic foods early reduces risk of later allergy, also weaning onto baked milk etc in known allergies can help
  • Desensitisation to food allergens- induce tolerance/ desensitisation by introducing foods slowly. Used for eggs and milk and can be for nuts but not widely available.
18
Q

Briefly describe the 4 types of hypersensitivity reactions

A
1= immediate, IgE mediated reaction to non- infectious agent (allergy)
2= antibodies reacting with antigens on cell bodies (Myasthesia gravis)
3= formation and subsequent reaction of antibody- antigen complexes in solution (SLE, RA)
4= cell mediated/ delayed reactions due to macrophages, lymphocytes etc (hashiomotos)
19
Q

Does the sensitisation phase (first encounter antigen/ agent) of a hypersensitivity reaction lead to a pathological reaction?

A

No- effector phase does

20
Q

Describe the mechanism for type 1 hypersensitivity reactions?

A
  1. TH2 activation on sensitisation causes B cells to produce IgE specific to that antigen
  2. Antigen specific IgE waits on mast cells for allergen to be re introduced
  3. on cross linking of allergen and IgE the mast cells degranulate
  4. Granules contents (histamine, chemokines, prostaglandins etc) vasodilate, increase vascular permeability, attract phagocytes and cause smooth muscle contraction
21
Q

Describe 4 agents released in mast cell granules and the effect they have?

A
  • Tryptase: remodels CT matrix
  • Histamine: increase vascular permeability and smooth muscle contraction
  • Leukotrienes: smooth muscle contraction, mucus secretion, increase vascular permeability
  • Platelet activating factor: attract leukocytes, neutrophils, eosinophils and platelets
22
Q

What is the effect of mast cell degranulation in epidermis and deep dermis?

A

Epidermis: rashes called urticaria, if this is prolonged = eczema
Deep dermis: swelling of lips, eyes, tongue and upper resp tract

23
Q

What are the 5 types of allergic reactions?

A
  • systemic anaphylaxis (drugs, venoums, nuts etc in blood)
  • acute urticaria (skin contact of hairs, bites)
  • allergic rhinitis (inhaled pollons, dust mite faeces)
  • asthma (inhaled agent- often dust mite faeces, pollons, danders)
  • food allergy (oral intake of nuts, shellfish, milk, eggs etc, usually leads to diarrhoea, vomiting, pruritus, urticaria and rarely anaphylaxis)
24
Q

Why is it thoughts that allergies are most common in the developed world?

A
  • excessive sanitation, high antibiotic use, low helmithin burden, low contact to unclean animals
  • thought to lead to changes in normal flora, which increases allergy risk (biodiveristy hypothesis)
25
Q

Give 4 ways type 1 hypersensitivities can be treated?

A
  • Desensitisation (give increasing doses of allergen over a number of years, works 90% for bee venom, some sucsess in nuts- thought to shift response from TH2 to TH1 and IgA release)
  • Anti IgE
  • Anti histamines
  • leukotriene receptor antagonists
  • corticosteroids
26
Q

What type of antibodies are involved in type 2 hypersensitivity reactions?

A

IgG or IgM

27
Q

What type of hypersensitivity reaction is a haemolytic transfusion reaction?

A

Type 2 because it is immune response against a cell bound antigen (RHO groups on RBCs)

28
Q

What causes haemolytic disease of a new born?

A

If a Rh+ father and Rh- mother have a baby and it is Rh+, the Rh+ antigens can cross into the mother during delivery and sensitise her. If she has another Rh+ baby, anti- Rh+ antibodies will cross the placenta and damage the foetuses blood cells causing a jaundice baby with high reticulocyte count.

29
Q

How is haemolytic disease of new born prevented?

A

Giving RhoGram or ‘anti-D’ to Rh- mothers during her first and subsequent births to Rh+ children. It works by destroying any rhesus antigens before her immune system can be sensitised to them

30
Q

What type of hypersensitivity is Graves disease?

A

Type 2- antibodies react to TSH receptor on thyroid cells, causes activation of TSH receptor-> hyperthyroidism

31
Q

How are type 2 hypersensitivities treated?

A
  • steroids
  • plasmapheresis (take out antibodies and replace with fresh- short term releif)
  • immunoglobulin injections (IgG degradation)
  • correct metabolism (Give TSH inhibitors in graves)
  • replacement therapies (Achesterase inhibitors in MG)
32
Q

How long do type 1,2,3 and 4 hypersensitivity reactions take to develop?

A
1= <30 mins
2= 5-12 hrs
3= 3-8 hrs
4= 24-72 hrs
33
Q

Describe how a type 3 hypersensitivity reaction occurs?

A

Antigen antibody complex in solution binds with C3b/C5a (classical pathway) and this causes neutrophil chemotaxis. These will adhere to the surface and degranulate, damaging tissues.

34
Q

Give 3 examples of type 3 hypersensitivity reactions

A

RA- antigens against rheumatic factor.
Glomerularnephritis
Systemic lupus erythematous- antigens against dsDNA

35
Q

Give 3 examples of type 4 hypersensitivity

A

eczema, nickel, poision ivy, tuberculin skin test, TB, sarcoidosis, hashimotos disease, T1 diabetes

36
Q

How are type 3 and 4 hypersensitivities treated?

A

Anti inflammatory drugs (NSAIDs and steroids) and monoclonal antibodies