Complete run through of the MRCP Part I – Day 2 of 40

Wow. This is a long syllabus. It’s taken me three hours to put this next section together, which leaves me with little time for pretty pictures/mnemonics. Let’s crack page 83.


Occupational asthma

This accounts for one sixth of all cases of asthma. Forget asbestosis, silicosis or smelly mould fancier’s lung – occupational asthma is the most common occupational lung disease.

Common allergens include flour, grain, wood dust, animal bits and isocyanates.

The history is more useful for excluding occupational asthma rather than confirming it i.e. if you have symptoms which are worse at home then at work, you don’t have occupational asthma. However, if your symptoms are worse at work, you may or may not have occupational asthma.

To be sure, you need to do confirm a relationship between asthma and work exposure by performing Serial measurements of PEFR at home and at work. Measurements should be made every two hours from waking to sleeping for four weeks, keeping treatment constant and documenting times at work.

Rhinitis and asthma often co-exist, including when occupational.

Once the relationship is confirmed, the patient must not work in that environment. At all.


Other common allergies

1. Latex allergy

Affects medical workers, people with spina bifida and rubber workers. The allergen is either natural or synthetic rubber

Remember the fruit latex syndrome in 30-50% of those with latex allergy. This involves allergy to avocado, banana, chestnut, kiwi, peach, tomato, potato and bell pepper.

2. Insect strings 

Usually bee and wasp stings

3. Drug allergy

I had no idea there was guidance specifically for drug allergy – see

MRCPwise, it’s probably worth going through the table of Type I – IV hypersensitivities on page 45. The guidance tells you about risk factors for developing allergies as well as how to test for allergy semi-safely.

I also learnt from this guidance that intradermal tests are more sensitive but less specific than skin patch tests, and have a higher risk of causing anaphylaxis.

4. Food allergy

The Medical Masterclass focuses on nut allergies, which are the commonest food allergies. Peanuts account for >50% of all food allergies.

In children, failure to thrive, vomiting and eczema can all be explained by food allergy.

Distinguishing between intolerance and allergy can be tricky. Allergy happens within seconds of ingestion, and only minute quantities are needed. In contrast, intolerances take hours to develop, and a small quantity poses no problem.

Intolerance e.g. lactose intolerance produces bloating and diarrhoea. Allergies may provoke eczema, reflux, GORD as well as anaphylaxis.

A food diary, combined with skin prick testing/appropriate IgE tests can be helpful.


Angioedema and urticaria

I found the patient information to the British Association of Dermatologists helpful:

The weals of urticaria may be flesh-coloured, pink or red. They can be of different shapes and sizes, but usually look like nettle stings. An important feature of urticaria is that although the rash may persist for weeks, individual lesions usually disappear within a day, and often last only a matter of hours. However, they sometimes leave bruising especially in children. New weals may then appear in other areas. In ordinary urticaria, the weals can occur anywhere on the body, at any time.

The deeper swellings of angioedema occur most frequently on the eyelids, lips and sometimes in the mouth, but they may occur anywhere. They are not usually itchy, and tend to settle within a few days. If the hands and feet are affected, they may feel tight and painful.

Angioedema occurs beneath the dermis and affects the skin and mucosa, whereas urticarial occurs above the dermis and only affects the skin. Angioedema is painful and tense; urticarial is itchy.

Almost any medicine can cause ‘acute’ urticaria, but painkillers (especially aspirin and medicines like ibuprofen), antibiotics (especially penicillins) and vaccinations are most likely to be responsible. Angioedema, in particular, can be caused by a type of drug (ACE inhibitors) used to treat high blood pressure.

Where does C1 esterase deficiency come into it?

Hereditary angioedema causes provoked or unprovoked attacks lasting 2-5 days of laryngeal odema, subcutaneous swelling and abdominal pain. The tests you want initially is C4 level and if this is low, then C1 INH function and level of protein.

What about ACE inhibitors?

Any individual can get angioedema from ACE inhibitors, though it is more common in Afro-Carribeans. It can occur years after uneventful ACE inhibitor use, and is poorly responsive to antihistamines, corticosteroids or adrenaline. The episodes may persist for some months after stopping the ACE inhibitor. Switching to ARBs is usually successful.

What is the management of angioedema?

See In general, the acute attack usually needs nothing, although if there is airway compromise then manage as anaphylaxis. Chronic angioedema should be started with an antihistamine, although antihistamines don’t always work in angioedema.

And urticaria? 

First line is a non sedatating H1 antihistamine e.g. cetirizine plus three days of 50mg prednisolone.


Allergen sensitisation…

Step 1: Choose an allergen

Step 2: Get a B-cell to get excited by this allergen

Step 3: Invite this B-cell to mature into a plasma cell and secrete IgE specific to this antigen

Step 4: Stick the IgEs onto mast cells

You have now sensitized the patient!

Primary prevention of allergy prevents this sensitization from happening. This means allergen avoidance.

Secondary avoidance means preventing further sensitization once the process has started. This means leaving the job which triggers occupational asthma.

…and immunotherapy


  1. Hay fever that cannot be controlled with the usual management (unless asthmatic)
    To manage hay fever needs allergen avoidance, education and meds. Avoidance needs knowledge of the allergen, which can be found by skin prick tests
    Topical antihistamines for nasal symptoms are great, but only tackle nasal symptoms. Topical intranasal steroids are safe long term and more effective, but risk dryness, crusting and bleeding.
    Oral antihistamines are the mainstay, and work on neutrally mediated itch, sneezing and rhinorrhea. They don’t cover the blocked nose as well as intranasal steroids however.
    There are also nasal decongestants, and eye drops eg sodium cromoglicate

  2. Hypersensitivity to wasp and bee venom

What happens?

Administer gradually increasing quantities of specific allergens to patients with IgE-mediated conditions until a dose is reached that is effective in reducing disease severity from natural exposure.

How does it work?

Eventually, the allergen stimulates IgG rather than IgE production.


ACE inhibitors – they may trigger an anaphlyactoid reaction (anaphylactoid is basically anaphylaxis that is not IgE mediated)

Beta blockers – reduce the efficacy of adrenaline, which may be needed


Allergen avoidance

The main allergens are house dust mite, mould, pollen, pets and dust. Advice on avoidance is given at


Natural history of allergic diseases

Asthma stops in about 55% of children by the time they reach adulthood. This is more likely the earlier the asthma started.

Eczema stops in around a third of children when they reach adulthood.

Rhinitis tends to persist into adulthood.

There is a concept called the ‘allergic march’ – see


The tests

The skin prick test needs resuscitation facilities to hand, but is most useful for food allergy and rhinitis (include tree pollen, grass and weed)

Not great if: dark skin, dermatitis, dermatographism, unable to stop antihistamines for 48 hours before

Allergens introduced to skin through pricking. If positive, a wheal of at least 2/3mm develops. Negative predictive value is 95%, but positive predictive value is only 50%, which means a good history makes a big difference.

A skin test for A. fumigatus is done for ABPA, as well as total IgE.

RAST and ELISA are blood tests looking for specific IgEs. They are expensive, but are not affected by antihistamines or the condition of the skin.

Oral food challenge is the definitive but risky test for food allergy.

Patch testing – read at 48-72 hours, and is used for contact dermatitis and Type IV stuff in general.

Lactose intolerance is tested by the Lactose hydrogen breath test:

The patient ingests a standardised amount of lactose (2 g/kg, maximum 25 g) after an overnight fast with measurement of exhaled hydrogen over a 2- to 3-hour period. A positive test is an increase of >20 ppm of exhaled hydrogen after approximately 60 minutes. (BMJ Learning)


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