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A2. CAH > Allergy > Flashcards

Allergy Flashcards

1
Q

What is allergy?

A

Allergy is an objective, reproducible reaction mediated via the body’s immune system, initiated by exposure to a defined stimulus at a dose tolerated by normal persons.

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2
Q

What is the difference between food allergy and food intolerance?

A

Food allergy is immune mediated but a food intolerance is NOT immune mediated

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3
Q

Simply, what are the 3 categories of food allergy in terms of the immunoglobulin involved?

A

IgE mediated – immediate, symptoms appear minutes to 2 hours after ingestion

Mixed IgE and NON-IgE mediated

Non-IgE mediated – 4 hours to days (T-cell mediated)

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4
Q

What is meant by food intolerance and what are the 3 categories of intolerance? Give an example of each.

A

Food intolerance is a reaction initiated by non-immunological mechanisms. The 3 categories are metabolic, pharmacologic and toxic.

Metabolic – CHO malabsorption (lactose intolerance)
Pharmacologic – Caffiene causing irritability, restlessness and palpitations
Toxic – Food poisoning (salmonella, fish toxins)

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5
Q

What is meant by atopy? Does it always lead to allergic disease? What are some examples of some atopic disease?

A

Atopy is the genetic predisposition to be sensitised as it produces IgE antibodies in response to ordinary exposures to common environmental allergies. This can lead to allergic disease but not necessarily.
Examples of atopic disease include asthma, allergic rhino-conjunctivitis, eczema, IgE mediated food allergy

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6
Q

What are 3 common triggers of an allergic response? (there are 6)

A 
Foods (nuts, shellfish etc.)
Stings (wasps and bees etc.)
Drugs (penicillin, NSAIDs, ACEi)
Radiographic contrast media
Blood Products
Latex
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7
Q

What are 5 of the major food groups that cause >90% of food allergies? (There are 8)

A 
Peanuts
Soy
Eggs
Milk
Fish
Wheat
Shellfish
Tree nuts
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8
Q

What type of hypersensitivity reaction is anaphylaxis?

A

Type 1 (IgE-mediated) Hypersensitivity Reaction. It is a result of the degranulation of IgE bound mast cells releasing various mediators causing systemic consequences

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9
Q

Explain the pathophysiology behind the 1st exposure of a person to an allergen in an IgE mediated food allergy

A

On 1st exposure
Allergens are introduced to the body through various routes: ingestion, inhalation, paraenteral, skin contact. When the person is first exposed to the allergen, they make IgE antibodies specific to the allergen which attach to the high affinity Fc receptors which are found on basophils and mast cells.

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10
Q

Explain the pathophysiology behind the 2nd exposure of a person a specific allergen allergen in an IgE mediated food allergy

A

On 2nd exposure
On subsequent exposure to the allergen, it will bind to the IgE antibodies on the mast cells and the basophils -> this will cause the degranulation of these mast cells -> Histamine, prostaglandin D2, leukotrienes, platelet-activating factor, tryptase*, nitric oxide, eosinophils and neutrophil chemotactic factors will all be released as a result of the degranulation-> this will cause varying effects on target organs

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11
Q

Following the degranulation of the mast cells and release of mediators into the systemic circulation, what are the 6 key effects of these mediators throughout the body?

A
  • Increased Vascular Permeability
  • Vasodilation
  • Myocardial Dysfunction
  • Altered Smooth Muscle Tone -> bronchospasm and uterine cramps
  • Activation of Sympathetic Nervous System -> tachy, increased mucus, anxiety
  • Increased Platelet Activation
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12
Q

What is the signs and symptoms of an IgE mediated food allergy?

A

Onset of around 2 hours
Systems involved: Cutaneous, Gastrointestintal, Respiratory, Cardiovascular

Cutaneous: Erythema, pruritis, urticaria, angioedema

Gastrointestinal:

  • Oral – Pruritis, Lip and Tongue Swelling
  • Lower – Nausea, colicky abdominal pain, vomiting, diarrhoea

Respiratory:

  • Upper – nasal congestion, rhinorrhoea, sneezing, hoarseness
  • Lower – cough, chest tightness, dyspnoea, wheeze, accessory muscle use

Cardiovascular: tachycardia (bradycardia), hypotension, dizziness, fainting, LOC

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13
Q

What is urticaria?

A

Blanching, raised, palpable wheals which can be linear, annular or arcuate on any skin area

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14
Q

What is angio-oedema?

A

Vascular permeability is increased in anaphylaxis which causes fluid to leak from blood vessels causing swelling. Can occur in the face, lips, tongue, lips, tongue and genital area but also in the throat which can also cause shortness of breath. 50% of the intravascular fluid will move to the extravascular space in minutes.

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15
Q

What is anaphylaxis?

A

Anaphylaxis is an acute, severe, life-threatening allergic reaction in pre-sensitised individuals, leading to a systemic response caused by release of immune and inflammatory mediators from basophils and mast cells. At least 2 organ systems are involved such as skin, upper and lower airways, cardiovascular, neurological, GI systems in this order of priority or in combination.

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16
Q

Who are the people that are in the High Risk group for having an anaphylactic attack? (6 points)

A 
History of Anaphylaxis
Multiple food and drug allergy
Poorly controlled asthma
Underlying lung disease
Beta-blockers/ACE inhibitors
Older age
17
Q

What are the 3 key points which are integral to the clinical presentation of anaphylaxis?

A
  1. Rapid Onset of Symptoms
  2. Compromise of one of ABC (Airways, Breathing, Circulation)
  3. Involvement of Skin/Mucosa
18
Q

What are the 6 points which are important to elicit in a history of an allergic reaction or an anaphylactic attack?

A

What was ingested? (peanut butter sandwich vs mixed nuts)

Amount ingested? (nut touched lip vs whole packet of nuts)

How was it cooked? (egg within cake vs licking raw egg batter)

Timing of exposure to onset/offset

Treatment needed

Previous exposures

19
Q

What are some common clinical features of a patient presenting with anaphylaxis?

A 
Difficult/noisy breathing
Swelling of the tongue
Swelling/tightness in throat/Difficulty swallowing
Difficulty in talking or hoarse voice
Wheeze or persistent cough
Persistent dizziness or collapse
Pale and floppy infant/young child
20
Q

What is an investigation that can be used in the diagnosis of anaphylaxis?

A

Anaphylaxis is a clinical diagnosis.

A raised mast cell tryptase can be a useful clue in the diagnosis of anaphylaxis. This test should only be conducted if the diagnosis is unclear and is confused with life-threatening cardiac or respiratory collapse. This serum tryptase returns to normal hours after anaphylaxis AND normal serum tryptase does not rule out anaphylaxis.

21
Q

What is are the key points in the management of a patient experiencing an ANAPHYLACTIC ATTACK? **

A

IM ADRENALINE!!! (epipen is crucial) – into antero-lateral thigh and repeat in 5 mins if no improvement.

A: Airway Obstruction

  • Nebulised Adrenaline – only used if upper airway obstruction is present
  • Early intubation or laryngeal mask – if airway oedema is not responding to nebulised adrenaline
  • If complete obstruction: bag mask ventilation with high flow O2

B: Breathing
- High Flow O2

C: Circulation

  • Posture: prevent exacerbating collapse – keep patient supine or at 45 degrees if any breathing difficulty
  • IV access with large gauge cannula – saline fluid bolus as a volume expander and may consider adrenaline infusion.
  • If no pulse is detected: begin resuscitation
22
Q

What are the key points in the management of a patient experiencing a GENERALISED ALLERGIC REACTION?

A 
Anti-histamines*
Cool Compress
Observation
Identify trigger
Allergy Action Plan*
Education and Referral
23
Q

What are some investigations that can be made in follow-up management after the stabilisation of the patient or in the context of a relatively minor allergic reaction?

A

Skin Prick Test – Allergen scratched on back and wheal is measured at 15 mins. +ve. >3mm wheal is positive result. The larger the wheal the more likely an IgE mediated reaction will occur. It does NOT tell you the severity of the reaction itself. Correlation with Hx is critical.

Serum Specific IgE – detects free antigen specific IgE in serum. Results are usually concordant with the skin prick test.

Food Challenges – Gold standard for allergy diagnosis. This confirms the diagnosis of a food allergy. This can also test the tolerance/resolution of food allergy.

24
Q

What are the types of non-IgE mediated food allergy conditions?

A 
Mainly GI, skin symptoms/signs
Food Protein Induced Enterocolitis Syndrome
Food Protein Induced Enteropathy
Food Protein Induced Proctocolitis
Esosionophilic Oesophagitis
25
Q

What are the differences in Age, Allergen and Presentation between the three Food Protein Induced Food Allergies?

A

FPIES – Occurs from weeks to months of age, Triggered by Cow milk, soy milk and rice. Clinically this is the worst reaction with an acutely well baby with potential CVS collapse.

Food Protein Induced Enteropathy – Occurs in early infancy. Triggered by cows milk. Clnically this is the 2nd most acute behind FPIES with an unwell baby with vomiting, diarrhoea, abdominal distension.

Food Protein Induced Proctocolitis – Occurs in early infancy, Triggered by cow milk, soy milk, BF (50-60%). Clinically this is well baby but has bloody streaks in the stools.

26
Q

What is the onset of a non-IgE mediated food allergy condition?

A

Intermediate Reaction – 2-24 hours

Delayed reaction - >24 hours

27
Q

What are the investigations carried out in a non-IgE mediated food allergy condition?

A

Patch Testing

Food Challenge

28
Q

What is Food Protein Induced Eneterocolitis Syndrome (FPIES)? What are the triggers for FPIES? How do you manage FPIES?

A

It is uncommon but seen exclusively in infants and young children. But most children outgrow FPIES by 3-4 years of age.

Most common triggers are cow’s milk (dairy) and soy but almost any food can cause FPIES.

Clinical Features: Acutely unwell baby. Characterised by profuse vomiting (sometimes diarrhoea) which happens most commonly 2-4 hours after ingestion of allergen. Along with this there is a redistribution of body fluid which leads to hypotension, pallor and floppiness.

Acute management: IV fluid resuscitation. IM adrenaline is NOT used to treat this reaction

29
Q

How do you diagnose a non-IgE mediated Food Allergy?

A

History
Oral Food Challenge
NO skin prick test or serum IgE testing because there is not IgE reaction to ellicit

30
Q

How do you manage a diagnosed non-IgE mediated food allergy?

A
  1. Avoid allergen (e.g cows milk)
  2. Challenge to alternative (e.g soy milk)
  3. Ensure diet is adequate otherwise
  4. Rechallenge if appropriate in 6-12 months
31
Q

What is eosinophillic oesophagitis? What are its presenting features? How do you manage this condition in terms of investigations and treatment?

A

It is a type of non-IgE mediated FA which is the eosinophillic infiltration of oesophageal mucosa. Usually caused by dairy, wheat, egg and soy.

It presents variably with regurgitation/vomiting, slow eater/food refusal, failure to thrive, difficulty swallowing, food impaction, epigastric pain.

Investigation is gastroscopy and histology of biopsies.

Management is food avoidance and swallowed aerosolised corticosteroids

A2. CAH (47 decks)

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