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CSP 3 > Allergy > Flashcards

Allergy Flashcards

1
Q

Define allergy.

A

An immune response against a foreign antigen (not autoimmune) which is unnecessary, and mediated by type 1 hypersensitivity.

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2
Q

What is type I hypersensitivity?

A

IgE-mediated hypersensitivity - antigen induces cross-linking of IgE bound to mast cells and basophils with release of vasoactive mediators.
Typical manifestations include anaphylaxis, hay fever, asthma, hives, food allergies, and eczema.

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3
Q

What is type II hypersensitivity?

A

IgG-mediated cytotoxic hypersensitivity – auto-antibody directed against cell surface antigens mediates (own) cell destruction via complement activation or antibody-dependent cell-mediated cytotoxicity.
Typical manifestations include blood transfusion reactions, and autoimmune haemolytic anaemia.

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4
Q

What is type III hypersensitivity?

A

Immune complex-mediated hypersensitivity – antigen-antibody complexes deposited in various tissues induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils.
Typical manifestations include SLE (nuclear antigens), RA (antibody complexes), and others such as “farmer’s lung” (antigen is often mould or hay dust).

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5
Q

What is type IV hypersensitivity?

A

Cell-mediated hypersensitivity – sensitised Th1 cells release cytokines that activate macrophages or cytotoxic T cells which mediate direct cellular damage. Typical manifestations include contact dermatitis, TB lesions and graft rejection.

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6
Q

What is type V hypersensitivity?

A

Stimulatory autoantibodies - antibodies are produced with the property of stimulating specific cell targets. The clearest example is Graves’ disease caused by antibodies that stimulate the TSH receptor, leading to overactivity of the thyroid gland.

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7
Q

Mast cells are stimulated by…? (4)

A

Surface IgE binding antigen
Complement activation: C5a, C3a
Nerves: axon reflex sensory nerves, Substance P
Direct stimulation

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8
Q

What is anaphylaxis?

A

Type 1 hypersensitivity reaction, with degranulation and
activation of mast cells and basophils. Histamine and
leukotrienes released.

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9
Q

What are the signs and symptoms of anaphylaxis? (7)

A 
Drop in blood pressure --> syncope
Bronchospasm --> wheeze
Urticaria (red itchy raised rash)
Angioedema (swelling with fluid in subcutaneous tissues) --> if in resp tract, gives stridor, death 
Abdominal pain
Vomiting
Diarrhoea
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10
Q

What is the diagnostic test for anaphylaxis?

A

Tryptase

C4 not consumed, but is in some angioedema

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11
Q

Name some food causes of anaphylaxis.

A

Peanuts & other legumes
True nuts – walnuts, cashew, almond, hazelnut.
Shellfish & fish
Egg, milk
Latex
Banana, avocado, kiwi, chestnut, potato, tomato
Ω gliadin

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12
Q

Name some drug causes of anaphylaxis. (4)

A

Antibiotics - beta-lactams and others
Neuromuscular blocking agents (suxamethonium) Peptide hormones (ACTH, insulin)
Monoclonal, polyclonal antibodies, antisera, plasma etc.

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13
Q

What else can cause anaphylaxis, apart from foods or drugs?

A

Arthropod venoms (bee, wasp stings etc)

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14
Q

Differentials for anaphylaxis.

A

MI, PE, hyperventilation, hypoglycaemia, vasovagal,

phaeochromocytoma, carcinoid, systemic mastocytosis. Also hereditary or idiopathic angioedema.

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15
Q

How can anaphylaxis and hereditary or idiopathic angioedema be differentiated using investigations?

A

Mast cell tryptase raised in anaphylaxis & mastocytosis. C4 complement component is low (consumption) in hereditary or idiopathic angioedema, & D-dimers high.

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16
Q

What is the acute treatment of anaphylaxis? (5)

A
  1. ABC approach –> Oxygen 100% (may need tracheostomy)
  2. 500 micrograms of 1:1000 Adrenaline IM
  3. IV fluid challenge (500-1000ml)
  4. 10mg chlorphenamine IM or slow IV
  5. 200mg hydrocortisone IM or slow IV

Admit and observe because of late phase (8 hours).
Note that there is no evidence that 4 and 5 work.

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17
Q

What is the long term treatment of anaphylaxis?

A

Identify antigen responsible (via history, skin prick tests, specific IgE tests) and then avoid antigen!
Can use prophylactic antihistamine if going into likely situation.
Carry adrenaline injection device.
Desensitisation is available for some antigens.

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18
Q

What are anaphylactoid reactions?

A

Direct or indirect activation of mast cells without IgE.

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19
Q

Drug causes of anaphylactoid reactions. (5)

A

Opiates, vancomycin, anaesthetic agents, NSAIDs, radiocontrast agents.

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20
Q

Food cause of anaphylactoid reactions.

A

Strawberries

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21
Q

Physical stimuli causes of anaphylactoid reactions. (3)

A

Exercise (but this my involve IgE to omega-gliadin), cold, trauma.

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22
Q

Immune complex reactions (type III hypersensitivity) causes of anaphylactoid reactions.

A

Reactions to blood products, IVIG, antisera, antibodies.

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23
Q

How are anaphylactoid reactions diagnosed?

A

All tryptase positive.

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24
Q

How are anaphylactoid reactions treated?

A

Same treatment as anaphylaxis

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25
Q

What are scromboid reactions?

How are they differentiated from other reactions with investigations?

A

Massive ingestion of histamine from decayed mackerel & other oily fish.
Mast cells not involved, so tryptase negative.

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26
Q

What is urticaria?

A

Raised itchy erythematous rash i.e. wheals (“hives”) that can be acute or chronic (>1 month). It is inflammation within dermis.
There are a variety of causes, only some of which are allergic, in sense of IgE-mediated responses to external harmless antigens.
Mast cells, histamine, and leukotrienes are almost always involved.

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27
Q

What are the allergic causes of urticaria?

A

USUALLY ACUTE
The same antigens that cause anaphylaxis, anaphylactoid and scromboid reactions - basically drugs, foods, and arthropod venoms.
Also local injection of antigens, e.g cat scratch and insect bites (papular urticaria, lasts several days).
Also direct contact e.g. lying on grass, latex gloves.

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28
Q

What are the infective causes of urticaria?

A

Acute viral infections, H pylori, prodromal Hep B, Lyme disease, cat-scratch fever, acute or chronic bacterial infections, parasitic infections.
These may be acute or chronic. Probably immune complexes.

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29
Q

What are the autoimmune causes of urticaria?

A

Autoantibodies to Fc-epsilon receptors on mast cells/basophils may be responsible for much chronic urticaria.
SLE (through autoantibodies to mast cells or immune complexes, or cryoglobulins)
VASCULITIS (painful rather than itchy, leave bruise & iron pigmentation when lesions resolve due to extravasation) - e.g. due to serum/blood products injected, via immune complexes & type III hypersensitivity.

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30
Q

What is cold urticaria?

A

Caused by cryoglobulinaemia. SLE and other autoimmune diseases, leukaemias and lymphomas, infections, idiopathic. Also mycoplasma infections, which
cause haemolytic anaemia. All these can cause Raynaud’s phenomenon.
There is an inherited form of cold urticaria due to C1AS1 gene mutation.

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31
Q

What are the physical causes of urticaria?

A

Sunlight, heat, pressure (including dermographism), vibration. Probably direct stimulation of mast
cells &/or nerves.

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32
Q

What is exercise urticaria?

A

May be associated with IgE to omega gliadin: typical history of exercise within hours of a meal containing gluten causing urticaria, even anaphylaxis.

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33
Q

What are the hormonal causes of urticaria?

A

E.g. associated with luteal phase of menstrual cycle (progesterone)
Other steroids can cause urticaria.

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34
Q

What are the autonomic causes of urticaria?

A

Cholinergic urticaria, associated with heat and sweating. Smaller wheals.
Adrenergic urticaria due to stress.

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35
Q

Give an example of a mast cell disorders that can cause urticaria.

A

Urticaria pigmentosa

36
Q

What deficiencies can cause urticaria?

A

Fe, B12 & folate deficiency

37
Q

How is urticaria treated?

A

Antihistamines - cetirizine, fexofenidine, loratidinde (all non-sedating). Chlorpheniramine is sedating. Take up to 4x BNF-recommended dose.

Can add ranitidine (H2 antagonist), montelukast (inhibits
leukotriene synthesis) if not totally effective.

If this fails, progress to omalizumab – a monoclonal that binds to IgE.

Lymphomas, autoimmune diseases will need their own
treatment.

38
Q

What is angioedema?

A

Swelling of subcutaneous tissues: inflammation.

39
Q

What is allergic angioedema?

A

If allergic then will be accompanied by urticaria. Part of

anaphylaxis, anaphylactoid syndromes etc. Same aetiology and treatments as the “allergic” urticaria.

40
Q

What are the three types of hereditary angioedema?

A

Type 1 = deficiency of C1 esterase inhibitor, which exercises restraint on the classical complement pathway and on the bradykinin pathway.
Type 2 = mutation of the C1 esterase inhibitor
Type 3 = mutation of Factor XII gene, which initiates bradykinin pathway as well as intrinsic clotting pathway.

41
Q

What can cause acquired C1 esterase inhibitor deficiency?

A

Autoimmune disease, haematological malignancy, cryoglobulins, infections (Hep B and C, H pylori).

42
Q

What is meant by idiopathic angioedema?

How is it treated?

A

Normal C1 esterase inhibitor level

Tranexamic acid

43
Q

How is C1 inhibitor deficiency treated?

A

Anabolic steroids, (tranexamic acid), C1 inhibitor iv or s/c.
Icatibant s/c inhibits bradykinin pathway.

44
Q

Allergic conjunctivitis/rhinitis/sinusitis - how is it mediated?

A

Type 1 hypersensitivity, IgE mediated

45
Q

Allergic conjunctivitis/rhinitis/sinusitis - what are the common antigens?

A

Grass pollens, tree pollens, animal danders, house dust mite

46
Q

Allergic conjunctivitis/rhinitis/sinusitis - what are the common antigens?

A

Grass pollens, tree pollens, animal danders, house dust mite

47
Q

How are allergic conjunctivitis/rhinitis/sinusitis diagnosed?

A

History i.e. if seasonal: pollens, hayfever

Skin prick tests and specific IgE to confirm

48
Q

How are allergic conjunctivitis/rhinitis/sinusitis treated?

A

Topical or systemic anti-histamines
Topical mast cell stabilisers eg disodium chromoglycate
Topical steroids
Antigen exclusion

49
Q

Other causes of rhinitis and sinusitis?

A

Viral and bacterial infections: common. Leprosy (rare).
Vaso-motor rhinitis
Non-allergic rhinitis with eosinophilia (NARES)
Drug induced: alpha agonist sprays, cocaine abuse.
Irritant fumes & solvents
Vasculitis, Wegener’s granulomatosis.
Septal deviation, foreign bodies.
Late pregnancy (oestrogens)
CSF leak

50
Q

How is asthma treated?

A

Topical beta-2 agonists, topical steroids, nebulised
theophylline etc., systemic steroids.
Ventilation in extremis.

51
Q

How does the mechanism of childhood asthma and late onset asthma differ?

A

Allergy more important in childhood asthma

52
Q

Define atopy.

A

The genetic predisposition to make IgE antibody against

common environmental antigens. Associated with hayfever, childhood asthma, and atopic dermatitis.

53
Q

What is atopic dermatitis?

A

Dry, cracked very itchy raised lichenified weeping lesions. Initially may be on extensor surfaces, then flexures, also cheeks.

54
Q

What is the pathology of atopic dermatitis?

A

Genetic component as with atopy. Also filaggrin mutation. IgE often raised 1000ku/l (NR <81). Langerhans cells in skin express Fcε, and eosinophils and mast cells in affected skin are increased.

55
Q

Aspirin sensitivity - how does it present?

A

Can cause angioedema, like other NSAIDS

56
Q

What foods have salicylates?

A

Tea, coffee, herbs & spices, black pepper, sharp green apples, cherries, strawberries, dried fruit, tomatoes, fruit juices, cider, wine, peppermints and liquorice.

57
Q

What is the triad of aspirin sensitivity?

A

Asthma, nasal polyps, sinusitis

58
Q

Treatment of aspirin sensitivity?

A

Polyps may need surgery, or topical steroids.

Avoid aspirin, and salicylates in food.

59
Q

Food allergy/oral allergy syndrome - what is it?

A

Itching and local swelling in oropharynx within minutes of eating food. Rarely may progress to urticaria & angioedema of face, and even anaphylaxis.

60
Q

What is food allergy mediated by?

A

Specific IgE: type I hypersensitivity.

61
Q

Antigens found in fresh fruit and vegetables, and cross-react with pollens, so patients frequently have hay-fever. Give examples.

A

Birch pollen allergy + hazelnut, apple, pear, carrot.
Birch pollen allergy + plums, peaches, cherries, almonds.
Ragweed allergy + melon, banana.
Grass pollen allergy + tomato, melon.
Mugwort pollen allergy + celery, carrot, spices.

62
Q

How is food oral allergy syndrome treated?

A

Avoid foods

63
Q

What are the symptoms of food allergy (beyond oral allergy)?

A

Abdo pain, diarrhoea, vomiting
Urticaria & angioedema
Bronchospasm and angioedema

Should follow ingestion of food in minutes - an
hour or two.

64
Q

How is food allergy diagnosed?

A

History
Skin prick tests (milk, egg, fish, peanut, true nuts)
Specific IgE less sensitive

65
Q

How is food allergy treated?

A

Avoidance. Steroids for eosinophilic enteritis.

66
Q

Latex allergy - how is it mediated?

A

IgE mediated against proteins in latex (a plant product).

Plasticisers in gloves etc can cause type IV hypersensitivity with contact dermatitis.

67
Q

Symptoms of latex allergy?

A

Contact urticaria, rhino-conjunctivitis, asthma, angioedema, anaphylaxis.

68
Q

How is latex allergy diagnosed and treated?

A

Skin prick tests and specific IgE tests against recombinant antigens
Treatment = avoidance

69
Q

Pathology of drug allergies?

A

A range of reactions e.g. type I – IV hypersensitivity, direct activation of mast cells & complement pathway etc.

70
Q

How do you test for drug allergies? How to treat?

A

For IgE against penicillin, test for antibodies, skin prick tests
Desensitisation

71
Q

Symptoms of antibodies to insulin?

A

Local urticarial, induration, may get some general anaphylactic type symptoms.

72
Q

What is DRESS syndrome?

A

Drug reaction with eosinophils & systemic
symptoms.
E.g. after several weeks –> fever, rash, lymphadenopathy

73
Q

How is anaesthetic drug allergy tested?

A

Measure tryptase! Save serum.

74
Q

What is extrinsic allergic alveolitis?

A

Type III Hypersensitivity e.g. due to inhaled foreign antigens, occupational exposure, animal, fungi, bacterial, plant, chemical.

Symptoms start about 6 hours after exposure & often worst at 24-48 hours –> fever, cough, shortness of breath. Chronic exposure leads to worsening interstitial pulmonary disease.

75
Q

Allergic bronchopulmonary aspergillosis - what is it?

A

Type III & type I reaction to Aspergillus. Wheeze, cough, fever, haemoptysis. Bronchiectasis may develop. High IgG & IgE to Aspergillus.

76
Q

Serum sickness - what is it?

A

Type III hypersensitivity
Infused human serum or serum products eg IVIG, monoclonal antibodies, and any drug that can bind to patients’ own proteins, altering the (eg penicillin).

Fever, poly-arthritis, vasculitis, lymphadenopathy, urticarial.
7-14 days after primary exposure, 1-3 days after secondary exposure.

77
Q

What can cause contact hypersensitivity (type IV hypersensitivity)?

A 
Nickel “allergy”
Topical drug applications
Aniline dyes in leather
Chromium from cement
Latex &amp; rubber material
Hair dyes, fragrances, cosmetics.
Plants: ivy, sumac, chrysanthemum.
Exposure to sunlight may be required to trigger sensitivity
78
Q

Special tests?

A 
First take a good history!
Skin prick tests.
Specific IgE in vitro tests.
Autoantibody screen etc.
Patch testing.
Tryptase
D-dimers
Complement: C3 &amp; C4, C1q, C2, autoantibodies to C1q.
79
Q

Tryptase is the diagnostic test for…?

A

Anaphylaxis

80
Q

D-dimer is high in…?

A

Hereditary or idiopathic angioedema

81
Q

C1 esterase inhibitor deficiency in…?

A

Hereditary angioedema

82
Q

Skin prick test for…?

A

Anaphylaxis
Allergic conjunctivitis, rhinitis, sinusitis
Food allergy (milk, egg, fish, peanut, true nuts)
Latex allergy
Drug allergy

83
Q

Specific IgE test for…?

A

Anaphylaxis
Allergic conjunctivitis, rhinitis, sinusitis
Latex allergy

84
Q

C4 low in…?

A

Hereditary or idiopathic angioedema

85
Q

Cryoglobulins test for…?

A

Acquired C1 esterase inhibitor deficiency

Autoimmune urticaria

CSP 3 (13 decks)

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