Immuno: Case Studies in Immunology Pt.1 Flashcards
Define anaphylaxis.
A systemic hypersensitivity reaction in which the response is so overwhelming that it can be life-threatening
Describe the mechanism of type I hypersensitivity reactions.
- Cross-linking of IgE on mast cells by an antigen causes degranulation
- The release of various mediators including histamines and leukotrienes results in increased vascular permeability, smooth muscle contraction, inflammation and increased mucus production
List some clinical features of anaphylaxis.
- Conjunctival injection
- Rhinorrhoea
- Angioedema
- Urticaria
- Wheeze/bronchoconstriction
- Laryngeal obstruction/stridor
- Hypotension
- Cardiac arrhythmias
- Vomiting, diarrhoea, abdominal pain
What is the most common clinical feature of anaphylaxis?
Urticaria
Outline the management of anaphylaxis.
- ABCDE approach
- Respiratory support if necessary
- Oxygen by mask
- IM adrenaline (0.5 mg)
- IV antihistamine (10 mg chlorpheniramine)
- IV corticosteroid (200 mg hydrocortisone)
- IV fluids
- Nebulised bronchodiliators
NOTE: steroids take about 30 mins to start working but they are important in preventing rebound anaphylaxis
Describe the mechanism of action of adrenaline in anaphylaxis.
- It stimulates beta-2 receptors causing constriction of arterial smooth muscle
- This leads to increased blood pressure, limits vascular leakage and has a bronchodilator effect
Define positive trypase test
> 1.2 x baseline +2
List some common causes of anaphylaxis.
- Foods: peanuts, fish, shellfish, milk, eggs, soy
- Insect stings: bee venom, wasp venom
- Chemicals, drugs and other foreign proteins: penicillin, IV anaesthetic, latex
What is latex?
Milky fluid produced by rubber trees (Hevea brasiliensis)
What are the two types of latex allergy and how do they typically present?
Type I Hypersensitivity
- Acute onset of classical allergic symptoms soon after exposure (e.g. wheeze, urticaria, angioedema)
- Spectrum of severity
- Occupational exposure can lead to symptoms similar to asthma (e.g. lab workers)
Type IV Hypersensitivity
- Causes contact dermatitis (very itchy, well demarcated rash)
- Usually affecting the hands and feet (due to gloves and footwear)
- Symptoms begin 24-48 hours after exposure
- Not responsive to antihistamines
Which patient groups are particularly susceptible to type I hypersensitivity reactions to latex?
- Patients undergoing multiple urological procedures
- Preterm infants
- Patients with indwlling latex devices (e.g. ventriculoperitoneal shunt)
What can a type I hypersensitivity reaction to latex cross-react with?
- Avocado
- Apricot
- Banana
- Passion fruit
- Papaya
NOTE: basically quite a lot of fruit
Name and describe three types of test for hypersensitivity.
- Specific IgE - this is a blood test that is preferentially used in patients with a history of anaphylaxis
- Skin prick testing
- Patch testing - patch is pasted onto the skin for 24-48 hours and eczema will be seen if there is a reaction
Describe the appearance of biopsy of urticarial tissue in anaphylaxis.
- Infiltrating T cells
- Granulomas
Which subset of patients should be referred to an allergist/immunologist?
All patients after anaphylaxis
For which types of allergies doees desensitisation work?
Insect venom and some sero-allergens (e.g. grass pollen)
List some disorders associted with recurrent meningococcal meningitis.
- Complement deficiency (increases risk of encapsulated organisms)
- Antibody deficiency (causes recurrent bacterial infections)
- Neurological (disturbance of blood-brain barrier (e.g. hydrocephalus, occult skull fracture))
Inherited and aquired immunodeficiency
Which investigation are typically usd to investigate complement deficiency?
- CH50
- AP50
- C3 and C4
What does AP50 and CH50 test?
- AP50 - tests the alternative pathway
- CH50 - tests the classical pathway
Functional tests for compliment
Deficiency in both = defect in final pathway C5-C9
What are the main aspects of management of complement deficiency?
- Vaccination (meningococcus, pneumococcus, Hib)
- Daily prophylactic penicillin
Investigations in SLE
Screen all lupus patient for APS antibodies
What is lupus anticoagulant test
(for APS)
Prolonged APTT that does not correct with normal pooled plasma but corrects with phospholipids
APTT relies on phospholipids
because they have antibodies to phospholipids - prolonged - lab artefact
Main interferon in SLE
Type 1 interferon
treated with antifrolumab
General pathogenesis of SLE
Abberent cell removal
Overactive B cells
Leads to abnormal B cell reaction of nuclear proteins
Describe the mechanism of action of serum sickness.
- Penicillin binds to cell surface proteins
- This acts as a neo-antigen, which stimulates a very strong IgG response
- This means that the individual is sensitised to penicillin
- Subsequent exposure leads to the formation of immune complexes with the penicillin and the production of more IgG antibodies
- Immune complexes deposit in joints, kidneys and skin causing arthralgia, glomeruloephritis and a vasculitic rash
How can serum sickness due to penicillin be investigated?
- Low serum C3 + C4 (suggests classical pathway activation)
- Specific IgG to penicillin
- Biopsy of skin or kidneys (showing infiltration of macrophages and neutrophils, deposition of IgG, IgM and complement)
