Allergies Flashcards

1
Q

What is hypersensitivity?

A

Hypersensitivity – the antigen-specific immune response that are either inappropriate or excessive and result in harm to host.

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2
Q

What happens in the first and second encounter for someone allergic to something?

A

Sensitisation phase – first encounter with the antigen.

Effector phase – clinical pathology upon re-exposure to the same antigen.

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3
Q

What are the 4 types of hypersensitivity reactions?

A
  1. Type I – or immediate <30mins allergies – environmental non-infectious antigens or allergens. Mediated by IgE
  2. Type II – or antibody mediated (5-12hours). IgG or IgM mediated directed against tissue antigens
  3. Type III – or immune complexes mediates (3-8 hours). IgG or IgM mediated and is directed at soluble antigens
  4. Type IV – or cell mediated (24-48hours). Cell mediated.

Type II, III and IV are usually directed against environmental infectious agents and self-antigens

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4
Q

Discuss epidemiology of allergies

A

Increasing worldwide prevalence >50% of children in UK. 13million <45 years olds have 2 or more allergies. 1 in 50 children have a peanut allergy. Life threatening reactions (anaphylactic shock) – systemic reaction to allergens which is a medical emergency.

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5
Q

What is the Hygiene hypothesis?

A

Not really known but Hygiene hypothesis. The less infections you have during your childhood the less likely you are to develop allergies. Definitive genetic component – atopy – the predisposition to develop classic allergies i.e. to produce IgE inappropriately.

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6
Q

What component does environment and socioeconomic status play in

A

In developing countries with children living in farms they generally: have large family sizes, rural homes with livestock, low antibiotic use, more diverse microflora, high parasitic burden, high orofaecal burden, and poor sanitation. Children growing up in westernised countries generally: have small family sizes, affluent urban homes, low variability in microflora, high antibiotic use, low parasitic burden, low orofaecal burden and good sanitation.

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7
Q

What phenotype do we use to describe people who do/don’t have allergies?

A

TH2 phenotype is how we describe those with allergies whilst TH1 is those without allergies.

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8
Q

What is clinical cross reactivity?

A

Being allergic to one allergen can icnrease your risk of allergies to certain other similar allergens and so we must be careful, they are also useful to know to work out what a trigger could have been

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9
Q

Describe some common clinical cross reactivity examples

A
Cow's milk  - Goat's milk
Shellfish - other shellfish
Fish - other fish
Tree nut - other tree nuts
Peanut - tree nuts
Soy - other ;egumes
Latex - fruits (kiwi, banana and avocado)
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10
Q

Describe Mast cells and their role in allergies

A

IgE dependant mechanism activating mast cells. Large nucleus, large cytoplasm and lots of granules. Play role in acute phases of inflammation. Located next to vessels and mucosal tissues. Cause a problem when activated inappropriately.

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11
Q

Describe the effects of the common mast cell mediators - histamine, leuktrienes, prostaglandins and cytokines

A

Histamine, leukotrienes and prostaglandins all do the same thing - Increase vascular permeability and cause smooth muscle contraction.

Cytokines - recruits and activates immune cells, promotes inflammation and activates the endothelium

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12
Q

Describe the mechanism by which an allergic reaction occurs?

A

Mechanism of immune reaction – Plasma cells detect the antigen and inappropriately begins to produce Antigen specific IgE to this antigen this IgE then binds to high affinity receptors on mast cells arming them. On second exposure to the allergen the antigen forms cross links between the IgE antibodies on the mast cells and this stimulates the mast cells to degranulate.

These granules contain histamine and chemokines and the mast cells are stimulated to synthesise new mediators such as leukotrienes and prostaglandins. These all cause increased vascular permeability, vasodilation and bronchial constriction (and other specific reactions dependant on the organ triggered).

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13
Q

What clinical use do the cell products of mast cells have?

A

We can use the serum levels of mast cell products as a diagnostic mechanism.

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14
Q

Describe some skin manifestations of allergic reations

A

Mast cells in the epidermis release their granules causing increased vascular permeability and vasodilation causing Urticaria or Hives.

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15
Q

Describe manifestations when allergic reaction triggered in deep dermis

A

When triggered in the deep dermis – causes Angioedema, lip, eyes, tongue, and upper respiratory airways. Which can lead to respiratory arrest.

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16
Q

Discuss some systemic manifestations of allergic reactions

A

Systemic manifestations  anaphylaxis – hypotension, cardiovascular collapse, generalised urticaria, angioedema and breathing problems.

17
Q

How are systemic allergic reactions treated?

A

Treatment with Adrenaline
Reverses peripheral vasodilation, reduced oedema and alleviates hypotension. Reverses airway obstruction/bronchospasm. Increases the force of myocardial contraction and inhibits mast cell activation.

DO NOT DELAY THIS TREATMENT

18
Q

What is a very important point to remember about treatment of allergies with adrenaline

A

Timesaver not a lifesaver – because the reaction may come back as it is biphasic. Intramuscular injection is preferred route of administration, better than sub cutaneous. Multiple doses may be required. Proper use of epipen is extremely important (only 16% knew how to use)

19
Q

How are allergies diagnosed?

A
  1. Clinical history – atopy, allergens, seasonality and route of exposure
  2. Blood tests – serum allergen-specific IgE and serum mast cell tryptase, histamine (systemic degranulation)
  3. Skin prick test – wheal and flare reaction above 3mm
  4. Challenge tests – slight risk of anaphylaxis in highly sensitised patients (food and drug)
20
Q

How do we manage people with sever allergies?

A

Allergen avoidance/elimination
Education – of symptoms, epipen in school and social activities etc.
Medical alert identification i.e. penicillin wrist bands

21
Q

What pharmacological interventions are there for allergies?

A

Antihistamines, corticosteroid, Anti-IgE, IgG and epipen

22
Q

What is allergen desensitisation?

A

Allergen desensitisation – patients with high risk of systemic attacks – specialist hospital based unit with resuscitation equipment. Involves the administration of increasing doses of allergen extracts over a period of years. Given to patients by injection of drops/tablets under the tongue. 90% effective in patients with bee and wasp venom anaphylaxis.