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BCS Lectures > Toni and Dave Hutchinson > Flashcards

Toni and Dave Hutchinson Flashcards

1
Q

Definition of allergy

A

a hypersensitivity reaction initiated by immunologic
mechanisms (Antibody- or Cell-mediated). In the majority of
cases allergy is IgE-mediated.

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2
Q

Definition of hypersensitivity?

A

causes objectively reproducible symptoms or
signs , initiated by exposure to a defined stimulus that is
tolerated by normal subjects.

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3
Q

Definition of atopy

A

genetic predisposition to become sensitized and
produce IgE antibodies on exposure to common
environmental allergens

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4
Q

Examples of nnon allergic food hypersensitivity?

A
  • Toxic/Pharmacologic (Bacterial poisoning, etc)

- Non-toxic / Intolerance (Lactase deficiency, etc)

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5
Q

Examples of IgE mediated food allergy?

A
  • Urticaria - Angioedema
  • Anaphylaxis
  • Oral Allergy Syndrome
  • Immediate gastrointestinal allergy
  • Atopic dermatitis
  • Asthma - Rhinitis
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6
Q

Examples of non IgE mediated food allergy

A
  • Protein-Induced Enterocolitis/proctocolitis
  • Celiac disease
  • Dermatitis herpetiformis
  • Food-induced Pulmonary Hemosiderosis
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7
Q

Immunotherapy for allergic asthma?

A

Omalizumab - monoclonal IgE antibody

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8
Q

Diagnostic pathway for allergies?

A
  1. History
  2. Physical examination - e.g. wheezing, urticaria, increase HR etc.
  3. Allergy tests
    - Skin prick (Prick, intradermal, APT)
    - Blood test for IgE (RAST, CAP)
    - Challenges (Open, DBPCFC)
    - Other (BHR, epitopes)
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9
Q

What do we need to know about a food allergy?

A

When and where ? (age of patient, environment)

What food ? (ingredients, preparation, quantity)

What symptoms ? (timing, onset, duration, reproducibility)

What associated factors ? (exercise, drugs)

What treatment ? (medication, response)

What management plan ? (avoidance, re-exposure)

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10
Q

What does the IgE (CAP/RAST) test check?

A

Multiple allergens against patients serum

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11
Q

When should you consider serum specific IgE test?

A
  1. Skin disorder (dermagraphism)
  2. Unable to discontinue medication (antihistamines)
  3. Suggestive history
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12
Q

When can you not do skin prick test

A

When you are on antihistamines

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13
Q

What is considered a positive value in the IgE serum test?

A

Results expressed in kUa/L (positive > 0.35 kUa/L)

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14
Q

What is the gold standard for challenge testing?

A

double-blind placebo-controlled challenges (DBPCC)

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15
Q

Natural history of food allergis?

A

80-90% outgrown by age 5

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16
Q

What is Hymenoptera venom allergy

A

bumble bee sting

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17
Q

What is Hymenoptera venom allergy

A

bumble bee sting

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18
Q

Relevance of investigations for allergies (BMJ)

A
  1. Serum tryptase
    - More specific to mast cells
    - Usually undetectable in healthy individuals
    - Not useful in food-induced anaphylaxis with local reaction
  2. In vitro IgE testing
    Putting known allergen in with patient’s serum IgE
    - Tagging other IgE molecules with immunofluorescence to see if they have bound
  3. Skin test
    - >3mm diameter and greater than control
    - Low diagnostic value for food allergy testing
    - If negative do the challenge test
  4. Challenge test
    - Expose patient to increasing amount of offending allergen
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19
Q

Relationship between NSAIDs and allergic reactions?

A

Regardless of COX selectivity pattern, NSAIDs may function as haptens capable of inducing allergic sensitization. Unlike anaphylaxis, anaphylactoid reactions are most likely related to inhibition of COX-l by NSAIDS. Thus, an anaphylactoid reaction caused by a particular COX-1 inhibiting NSAID will occur with a chemically unrelated NSAID which also inhibits COX-1 enzymes. Selective COX-2 inhibitors appear to be safe in patients with a history of NSAID-related anaphylactoid reactions but can function as haptens, with resulting sensitization and anaphylaxis upon next exposure.

NSAIDs may also trigger cell activation by altering arachidonic acid metabolism. Activation of complement, the complement peptides (anaphylatoxins) such as C3a and C5a, and their direct action on mast cells and basophils may lead to mediator release, producing symptoms indistinguishable from the classic IgE-mediated reaction

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20
Q

Outline the process of sensitisation in anaphylaxis

A

Sensitisation:
Allergens carried to LNDs by APC’s and present allergen to T helper cells
Expression of costimulatory molecules
Differentiates into Th2 cell via IL4, 5, 10
Th2 release IL4 causing class switching of B cells to IgE
IL5 release = eosinophils
IgE attach to Fc receptors on mast cells AND BASOPHILS

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21
Q

Outline the process of cross-linking in anaphylaxis

A

2nd exposure to antigen crosslinks IgE
Activation of mast cells
Histamine, prostaglandin D2, leukotrienes, platelet-activating factor, tryptase, nitric oxide, and eosinophil and neutrophil chemotactic factors have diverse effects on target organs and lead to the clinical manifestations of anaphylaxis.

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22
Q

Outline the early phase reaction in anaphylaxis

A

Vasodilation
Urticaria (hives)
Edemia
Bronchoconstriction

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23
Q

Outline the late/delayed phase reaction in anaphylaxis

A

Occurs due to release of arachadonic acid metabolites e.g. leukotrines

IL4, 5, 10 and leukotrienes (LTB4 and LTC4)
Damage to epithelium
Attraction of more immune cells

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24
Q

Disease LOB anaphylaxis see notes

A

see notes

25
Q

Difference between food addictive allergic reaction and normal food allergy?

A

Food additives directly activate mast cells
Most common food additive allergies:
Sulfites
Food colourings

26
Q

Factors affecting skin prick test results

A
  1. Medication
    - antihistamines , corticosteroids
  2. Quality of the allergen extracts
    - standardization issues, stability
  3. Method and Area of the skin tested
    - back > forearm, anteccubital fossa > wrist, ulnar > radial
  4. Age and origin of subject
    - increase with age, African > Caucasian
  5. Pathologic conditions
    - Atopic dermatitis, chronic renal failure
27
Q

Significance of IgE when diagnosing an allergy?

A

Elevated levels simply reflect an atopic tendency

• Not a screening test for Allergy
(normal total, but positive Specific IgE)

• High total IgE levels often seen in patients with:

  • eczema
  • asthma
28
Q

Levels of accuracy of SPT and IgE resutls

A

• High sensitivity and negative predictive accuracy ~ 95%
- negative test (< 3mm / 0.35kUA/L) almost excludes IgE-mediated allergy

• Poor specificity and positive predictive accuracy ~ 50%

  • positive test (≥ 3mm / 0.35kUA/L ) diagnostic if strongly suggestive history
  • test only highly suspected allergens , avoid “panels”

• Specificity and positive predictive accuracy increase with
increasing SPT wheal size and sIgE level
- usually no need for further tests in those with a strongly positive test

29
Q

Use of component resolved diagnostics

A

• High sensitivity and negative predictive accuracy ~ 95%
- negative test (< 3mm / 0.35kUA/L) almost excludes IgE-mediated allergy

• Poor specificity and positive predictive accuracy ~ 50%

  • positive test (≥ 3mm / 0.35kUA/L ) diagnostic if strongly suggestive history
  • test only highly suspected allergens , avoid “panels”

• Specificity and positive predictive accuracy increase with
increasing SPT wheal size and sIgE level
- usually no need for further tests in those with a strongly positive test

30
Q

CRD in the diagnosis of peanut allerg y

A

 MAAS 8-year follow up (n=1029)
 5.1 % sensitised by SPT and 9.3% by sIgE
 1.9% peanut-allergic proven by DBPCFC
 All peanut-tolerant subjects sensitised to grass
 Cross-reacting allergens (e.g. Ara h 5) in extracts
 Ara h 2 sensitisation predicts clinical peanut allergy

31
Q

Significance of serum tryptase?

A

• Enzyme: ‘marker’ of Mast cell activation - degranulation

  • acute activation : anaphylaxis
  • ongoing activation: systemic mastocytosis
32
Q

Half life of serum tryptase?

A

Short half life (normalises after 12-24 hours)

33
Q

Use of serum tryptase in suspected anaphylaxis

A

In suspected anaphylaxis:

  • 1st sample between 15 min – 3hours after onset of reaction
  • 2nd sample after 24-28hours to check baseline levels

• High levels in 1st & normal in 2nd sample indicate anaphylaxis

34
Q

Lung function tests for allergies?

A
  1. Spirometery

2. Bronchodilation

35
Q

Management of allergic disease?

A
  • Individualized management plan (Tailor measured)
  • Allergen avoidance/ environmental control
  • Pharmacological treatment (e.g. antihistamines, adrenaline)
  • Specific Immunotherapy (e.g. Rhinitis, Hymenoptera venom)
36
Q

Risk factors for fatal anaphylaxis?

A
  1. age related,
  2. concomitant
    diseases (asthma),
  3. concurrent medication (β-blockers)
37
Q

Why would people on b blockers not respond to epinepherine

A

beta-blockers who develop anaphylaxis are likely to be resistant to the therapeutic effects of epinephrine used to treat the anaphylaxis

38
Q

Indications for adrenaline

A
  1. In cardiac arrest, adrenaline is routinely administered as part of the Advanced Life Support (ALS) treatment algorithm.
  2. In anaphylaxis, adrenaline is a vital part of immediate management.
  3. Adrenaline may be injected directly into tissues to induce local
    vasoconstriction. For example, it is used during endoscopy to control
    mucosal bleeding, and it is sometimes mixed with local anaesthetic
    drugs (e.g. lidocaine) to prolong local anaesthesia.
39
Q

MOA of adrenaline

A
  • Adrenaline is a potent agonist of the α1, α2, β1 and β2
    adrenoceptors, and correspondingly has a multitude of sympathetic
    (‘fight or flight’) effects.
  • These include: vasoconstriction of vessels
    supplying skin, mucosa and abdominal viscera (mainly α1-mediated);
    increases in heart rate, force of contraction and myocardial excitability
    (β1); and vasodilatation of vessels supplying the heart and muscles (β2).
    These explain its use in cardiac arrest, where the redistribution of
    blood flow in favour of the heart is desirable, at least theoretically,
    and may improve the chances of restoring an organised rhythm.
  • Additional effects of adrenaline, mediated by β2 receptors, are
    bronchodilatation and suppression of inflammatory mediator
    release from mast cells.
40
Q

Adverse affects of adrenaline

A
  1. Adrenaline induved HTN post cardiac arrest
  2. Anxiety, tremor, headache and palpitations post anaphylaxis
  3. Angina, myocardial infarction and
    arrhythmias, particularly in patients with existing heart disease.
41
Q

CI for adrenaline use

A

ombination
adrenaline–anaesthetic preparations should not be used in areas
supplied by an end-artery (i.e. with poor collateral supply), such as
fingers and toes, where vasoconstriction can cause tissue necrosis.

42
Q

Important durg interractions :Adrenaline. Also give the reason for this interraction

A

In patients receiving treatment with a β-blocker, adrenaline may
induce widespread vasoconstriction, because its α1-mediated
vasoconstricting effect is not opposed by β2-mediated vasodilatation.

43
Q

Clinical criteria for diagnosing anaphylaxis

A
  1. SUDDEN onset of an illness (minutes to several hours) with involvement of the skin,mucosal tissue, or both (e.g. hives, itching or flushing, swollen lips-tongue-uvula)
  2. And at least one of the following:
    - Sudden respiratory symptoms and signs
    - Sudden reduced BP or symptoms of end organ dysfunction (hypotonia, collapse, incontinence)

OR

Two or more of the following that can occur suddenly after exposure to a likely allergen or other trigger for that patient (minutes to several hours)

  • Sudden skin or mucosal S+S
  • Sudden resp. symptoms
  • Sudden reduced BP or symptoms of end organ dysfunction
  • Sudden GI symptoms (crampy abdo pain, vomiting)

OR

Reduced BP after exposure to known allergen for that patient (minutes to several hours)

44
Q

1st line Tx for anaphylaxis

A

Epipen

45
Q

ROA for Epipen

A

IM - mid anterlateral thigh

46
Q

Dose or epi for body weight

A

BW < 25 kg: 0.15mg, > 25 kg: 0.3 mg

47
Q

Actions of epinepherine on a1

A
  1. Vasoconstriction in blood vessels and gut and piloerector muscle
48
Q

Actions of epinepherine on B2

A
  1. Mast cell inhibition
  2. Bronchial SM relax
  3. Increase renin from kidney
  4. Vasodilation in skeletal muscle
49
Q

Actions of epinepherine on ab2

A
  1. Liver glycogenolysis

2. GI tract decreases motility

50
Q

Actions of epinepherine on B1

A
  1. Increased rate and force of heart
51
Q

Actions of epinepherine on a

A

Eye mydriasis

52
Q

Describe Type I hypersensitivity reactions

A
  • Anaphylactic and atopic
  • Antigen crosslinking to IgE on pre-sensitized mast cells and basophils triggering relase of vasoactive amines
  • Delayed phase results from mast cells and basophils release CKs that induce cellular inflamm
53
Q

What is a “true food allergy”

A
  1. “ True Food allergy” - IgE mediated de-granulation of mast cells
cow's milk protein
egg white
wheat
soya bean
codfish
peanuts

NB: ‘Oral allergy syndrome’ is due to cross reacting ‘pan-allergens’ which are found in various members of the plant family (fruits, vegetables, nuts etc). They are heat labile and destroyed by digestion, hence symptoms are usually limited to the oral cavity.

54
Q

What is a false food allergy

A
  1. “False food allergy”- direct stimulation of mast cells or histamine ingestion e.g. Scromboid fish poisoning (scrombotoxicosis) – Histamine is released by bacterial action (spoilage) on scromboid fish (e.g tuna). When fish (containing histamine) is consumed, symptoms that mimic an allergic reaction are produced.
55
Q

What is food intolerance

A

Adverse reaction to food, with no histamine related symptoms

56
Q

Investigations for food poisoning

A

Stool microscopy for WBCs and RBCs
Positive in invasive or inflammatory diarrhoea (e.g. Ecoli o157:H7 which is an invasive organism)
Dark-field microscopy can be done to identify Vibrio cholerae.
Stool microscopy for WBCs and RBCs should be done in patients presenting with blood in stool, fever, suspected invasive pathogens (such as Escherichia coli O157:H7), when other diagnoses are considered (such as inflammatory bowel disease,

Stool culture
Isolation of speecific pathogen
Salmonella, Shigella, and Campylobacterorganisms becomes mandatory in any patient with grossly bloody stools
; if a stool sample shows positive results for WBCs or blo od, or if patient has fever or symptoms persisting for longer than 3 to 4 days.
Stool serologic testing and toxin testing can help diagnose the type of Shiga-toxin producing bacteria, and also which toxin is being produced.

Stool O+P
Micrscopic examination of stool for ova and parasites

FBC
high WBC with most inflammatory/invasive pathogen associated diarrhoea;
low WBC are associated with typhoid fever and some viruses; anaemia; high Hb and haematocrit could reflect haemoconcentration

57
Q

Signs and symptoms of dehydration

A
  1. Dry mouth
  2. Sunken eyes
  3. Extreme thirst
  4. Dizziness
  5. Confusion
  6. Soft spot on top of skull
  7. No tears when crying
  8. Sunken cheeks
  9. No wet diapers for three hours
58
Q

Distinguish toxigenic food poisoning from food-borne infection

A

. Foodborne illness is an infection or intoxication that results from eating food contaminated with viable (live) microorganisms or their toxins.

Foodborne illness also includes allergic reactions and other conditions where foods act as a carrier of the allergen. Food poisoning is a form of foodborne illness and is caused by the ingestion of preformed toxins

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