The MRCP Part I has a syllabus, which consists of pages 82 to 121 of this document.
That’s 41 pages, and the exam is on 10th September 2013.
Going at just over a page a day for the next 40ish days, I’ll find out about each topic and then summarise them as a blog post, and throw in some SBAs.
I’m totally relying on this, so I can assure you it’s in my interests to be as comprehensive yet memorable as possible.
The syllabus has three knowledge levels:
A Establishing a diagnosis
B Establishing a diagnosis and Knowledge of relevant investigations
C Establishing a diagnosis and Knowledge of relevant investigations and management and Knowledge of prognosis and likely response to therapy
Let’s start at page 82:
Anaphylaxis (Level C)
A severe, life threatening, generalised or systemic hypersensitivity reaction
Usually this involves an allergen binding to some IgE that is itself bound to mast cells or basophils. When the IgE is bound, inflammatory mediators are released from mast cells or basophils. This includes histamine, amongst others. Histamine and other inflammatory mediators cause vasodilation, oedema and increased capillary permeability.
1. Insect stings, especially bee and wasp.
2. Lots of foods, especially nuts (peanuts account for >50% of food related anaphylaxis).
3. Medication wise, antibiotics, NSAIDs, muscle relaxants and aspirin are the most commonly involved.
4. Contrast agents.To establish a diagnosis:
According to the ALS course, anaphylaxis is likely if a patient who is exposed to a trigger:
1. develops a sudden illness which rapidly progresses
2. with skin changes (flushing, urticarial, angioedema)
3. life threatening ABC problems
Q. How do you distinguish simple urticaria from anaphylaxis?
A. The presence or absence of life threatening ABC problems. Also bear in mind that up to 20% of anaphylaxis cases will have minimal or absent skin changes.
Q. What exactly does urticaria look like?
Tips for treatment:
The position you put the patient in depends on what is going to kill them first. If they are massively hypotensive, consider lying them flat and raising the legs. If they are short of breath, they may prefer sitting up. Unconscious but breathing patients should be placed in the recovery position.
Cystalloids are preferred, as there is a risk of further anaphylaxis with colloids.
IM injection site
The best site is the anterolateral aspect of the middle third of the thighs.
If cardiac arrest occurs after anaphylaxis, start normal ALS. In addition, consider steroids, antihistamines and large volumes of fluids.
Don’t mess around unless you are experienced. You can worsen laryngeal edema with ham fisted intubation attempts. Intubation becomes more and more difficult as time progresses, so ask a senior anaesthetist to consider early intubation.
These only take place once the patient is stable.
Mast cell tryptase taken:
1. As soon as possible after the patient is stable
2. 1-2 hours after symtoms began
3. 24 hours or later for a baselines
Observe all patients for at least 6 hours, and sometimes longer for high risk patients e.g. asthma, previous biphasic response. Continue steroids and antihistamines for 3 days, and educate the patient about EpiPen use.
The risk of death is increased in asthmatics. You may need to start treating asthmatic patients with anaphylaxis for asthma concurrently.
If an untreated patient hasn’t died within six hours of the exposure, it probably is not anaphylaxis. Food allergy takes about 30 minutes to kill, insect stings about 15 minutes and IV meds less than 5 minutes.
If the patient is beta blocked, you should use glucagon instead of adrenaline.
Tomorrow: Page 83 – Allergies in general and a bit of oncology