Csb 336

Front 1

What does IgE stand for?

Back 1

Immunoglobin E.

- an antibody that is present in minute amounts in the body but plays a major role in allergic diseased. The IgE binds to llergens and triggers the release of substances from mast cells that cause inflammation.

Front 2

What is anaphylaxis and what is it charcterised by?

Back 2

Anaphylaxic is a severe, life threatening, genralised systemic hypersensiticity reaction.

Its characterised by life threatening upper airway obstruction, bronchocpasm and/or hypotension. Usually a sudden onset.

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Some authors reserve the term anaphylaxis only for Immunogloblin (IgE) dependent events and the term anaphylactoid to describe IgE-independent.

Front 3

What are the two main types of anphylaxis?

Back 3

IgE dependant and IgE independent.

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IgE dependant - actication of the mast cells and basophils is the key trigger for the majority of cases of antigen-induced immune-mediated allergic anaphylaxi.

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IgE independent - non-allergic anaphylaxis or anaphylactoid reaction. n identical clinical syndrome known as non-allergic anaphylaxis follows non-immunological mechanisms, with the release of identical inflammatoory mediatos.

Front 4

What is the pathophysology of IgE Dependant anphylaxis?

Back 4

Allergen-specific IgE molecules bind to mast cells and basophils via specilised receptors where they stay ready for a subsequent exposure. Upon challange, a specidic alleren release of mediators as well as cytokines happens which causes symotoms and signs of anaphylaxis.

Front 5

What is the pathophysology of IgE Independant anaphylaxis?

Back 5

- Certian allergens/substances including drugs can trigger the mast cell cascade directly without involving IgE as the initial mediator.

- Anaphylactoid reactions therefore do not require prior sensitisation as they are direct mass cell releasers and may produce anaphylaxis like reactions in a dose-dependent manner.

Front 6

What are the effects of mast cell activation of different tissues? From the mast-cell activation and granule release.

Back 6

- The GI tract - increase fluid secreation and increased peristalsis. Expulsion of GI tract contents (Vomiting and diarrhoea)

- The airways - Decrease diametre, increased mucus secretion. Causing congestion and blockage of airways (wheezing, coughingand phlegm). Swelling and mucus secreation in nasal airways.

- The Blood Vessels - Increased blood flow, increased permeability. This increased fluid in tissues causing increased flow of lymph to pymoh nodes, increased cells and protein in tissues, increasing effector response in tissues.

Front 7

What are some causations of anaphylaxis (IgE Mediated)?

Back 7

- foods (peanuts, tree nuts and crustaceans), medications (antibiotics), venoms, latex, allergen vaccines, howmones, animal or human proteins, colorants (insect derived, such as carmine), enzymes, polysaccharides, asprin and other non-steroidal- anti-inflamatory drugs (probably), exersise (possible, in food and medication-dependent events)

Front 8

What are some causations of anaphylaxis (IgE independent)?

Back 8

Multimediator compement activation - activation of contct system. Radiocontrast media, non-spevific degranulation of mast cells and basophils. Opiods and muscle relaxants, idiopathic, physical factors, exersise, temprature (cold, heat), immune aggregants, IV immunoglobulin and dextraan (possible), cytotoxic. Transfusion reactions to cellular elements (IgG, IgM), psychogenit, factitious and undifferentiated somatoform idiopathic anaphylaxis.

Front 9

What is the pthophysiology of anaphylaxis?

Back 9

Mast cell leukocyte cytokine cascade. Release of stored mediators from basophils and mast cells - histamine, cytokines and chemokines.

- systhesis of new mediators - leukotrienes, tumor necrosis actor and prostaglandins.

Front 10

What are some clinical presontations of IgE independent?

Back 10

Mucocutaneous- rhinitis, conjunctiva erythema and trearing, flushing, itch, uritcaria and agioedema.

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Respiratory/chest- dysphagia and stridor due to upper airway angioedma, throat and/or chrst tightness, dyspnoea, cough and wheeze.

Front 11

gWhat are some clinical presontations of severe anaphylaxis?

Back 11

Cardiovasculr - palpitations, tachycardis, bradycardia, ECG changes (due to the hypotension and the heart not proplerly perfused), hypotension and cardiac arrest.

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Neurological - vascular headache, dizziness, collapse, confusion, and ALOC.

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Abdo - nausea, vomiting, abdo pain, pelvic pain, diarrhoea. Remember that skin and mucosal chnges in isolation do not constitute an anaphylactic reaction.

Front 12

What is the most common type of anaphylactic reaction in children?

Back 12

Most often is caused by food. Bronchiospasm is a common symptom, and there is usually a backgound of atory and asthma.

Front 13

What types of anaphylaxis are more common in adults?

Back 13

Venom- and drug induced. Hypotension is more likely to occure.

Front 14

What are the three grades of genralised hypersensitivity?

Back 14

1) Mild - skin and subcutanious only.

2) Moderate - features suggesting respiratory, cardiovascular or GI involvement.

3) Severe - Hypoxia, hypotension or neurologic compremise.

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Moderate to severe grades with multisystem correlated with the need for adrenaling and represented true anaphylaxis.

Front 15

What are some differential diagnosis for severe allergic reactions?

Back 15

Tissue swelling - idiopathic urticaria, isolated angiodema, ACE inhibitor-induced, acquired or herediatry C1 esterase inhibitor deficiency.

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Conditions mimmicing upper airway oedma - dystonic reactions mimicking symptoms of a swolen toung. Acute oesphageal reflux (sudden onset of painful throat swelling).

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Acute respiratory distress - asthma, panic disorders, globus, laryngospasm, vocal cord dysfunction.

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Other causes of collapse - vasovagal episodes, systemic inflammatory response syndrome, shock (septic, cardiogenic, haemorrhagic)

Front 16

What does adrenaline do in anaphylaxis?

Back 16

Its an alpha receptor agonist - it reverses peripherl vasodilation and reduces angioedema and ueitcaria. It pushed blood back to the organs. The beta 1 adernergic stimulation has a positive intropic (squeezes of heart increase) and chronotropic effect on cardiac muscle. The beta 2 adrenergic stimulation leads to bronchodilation. The mast cells also have beta 2 adrenergic receptors and therefore it stabilises the mast cells by inhibiting activation of histaming. (Still got IgE binding to Mast cells and the adrenaline stabilises the mast cells). Antihistamines are avoided because they take time to have effect.