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Immunology > Lecture 7: Atopy and Allergy > Flashcards

Lecture 7: Atopy and Allergy Flashcards

1
Q

what is the atopy?

A

A genetic predisposition to produce IgE after antigen exposure. This leads to a tendency toward developing hypersensitivity reactions, especially allergic rhinitis, eczema, and asthma (atopic triad).
• Genetic tendency to make IgE reactions
• Clinically manifest as rhinitis, asthma or hayfever
• Laboratory – high total IgE
• Measurement of total IgE rarely useful – history rather than lab tests will help determine if symptoms are allergic

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2
Q

atopy is characterized laboratory by

A

high total IgE

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3
Q

how common are allergies?

A

asthma-21%
hay fever-35%
eczema-23%

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4
Q

how common are food allergies?

A
  • Wycombe study – 30% think they are allergic to foods (adult population)
  • 1-2% adults have IgE-mediated food allergy
  • Approx 5% children have food allergy
  • Milk & egg common in pre-schoolers
  • Majority resolve
  • Peanut allergy – now approx 1:50 children
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5
Q

what is the dermographism?

A

The formation of urticaria (wheals) after minor pressure is applied to the skin, likely mediated by local histamine release. An increased incidence has been reported during pregnancy (especially in the second half), at the onset of menopause, in atopic children, and in patients with Behçet disease.

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6
Q

what is the white dermographism?

A

a physical finding of transiently blanched skin after skin stroking.
Caused by capillary vasoconstriction.
Normal variant, but more common in patients with atopic dermatitis.

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7
Q

what is the urticaria?

A

A condition of well-circumscribed, raised, pruritic, and erythematous plaques with a round, oval, or serpiginous shape. Can be up to several centimeters in diameter (wheals). Often worsen over minutes to hours and disappear after a few hours. Can appear as part of an allergic reaction soon after exposure to an antigen (e.g., following latex or drug exposure). Can occasionally occur without allergen exposure (e.g., pseudoallergy).
caused by mast cell activation in the superficial dermis
• Seen in 80% of allergic reactions
• However most urticaria is non-allergic
• 25% of population will have urticaria
• 1% at least will have chronic urticaria
• Children – most commonly results from viral infection
• Adults – most common cause chronic spontaneous urticaria
• Causes huge anxiety

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8
Q

what is the pseudoallergy?

A

A condition characterized by symptoms of a type I hypersensitivity reaction that are not the result of an IgE-mediated process. Typical mechanisms include direct mast cell degranulation, complement-mediated mast cell degranulation (anaphylactoid reactions), and an increase in the production of certain cytokines (e.g., increased leukotriene production in aspirin-exacerbated respiratory disease).
In contrast to true anaphylactic reactions, no sensitization to allergens is required → First contact can already lead to anaphylactic shock.

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9
Q

what are the common causes of pseudoallergy?

A

adiocontrast media, narcotics, vancomycin, NSAIDs

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10
Q

what is the angioedema

A

self-limited, localized swelling of the dermis, subcutaneous tissues, and/or submucosal tissues caused by fluid leakage into the interstitial tissue. Mediated by vasoactive substances and can be classified as either mast cell-mediated (often secondary to allergic reactions and NSAIDs), bradykinin-mediated (due to ACE inhibitor use or enzyme deficiencies), or idiopathic. Life-threatening laryngeal edema may occur and requires immediate airway protection.

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11
Q

what is the difference of angioedema and urticaria?

A

• Usually due to histamine release from mast cells
• Urticaria = superficial release in epidermis
• Angioedema = histamine release in subcutis
• Histamine effects: vasodilation
increased vascular permeability, itching

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12
Q

Chronic urticaria +/- angioedema is NOT caused by an allergy. True/False

A

True

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13
Q

Allergy causes acute (within 1 hour) urticaria & angioedema
True/False

A

True

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14
Q

what is the chronic spontaneous urticaria?

A

Chronic urticaria is the daily or episodic occurrence of weals, angioedema, or both, for 6 weeks or more [1,2]. Chronic urticaria can persist for 1–5 years, sometimes longer
Chronic spontaneous urticaria refers to chronic urticaria that has no specific cause or trigger. Weals are present on most days of the week for 6 weeks or more.
Chronic spontaneous urticaria was previously referred to as chronic idiopathic urticaria. This term is no longer used as many cases have an autoimmune basis

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15
Q

allergy vs sensitization

A
  • Allergy = history of allergic reactions to the substance.
  • History substantiated by the demonstration of allergen-specific IgE (skin prick test or blood)
  • Sensitization = allergen-specific IgE present in the absence of clinical symptoms.
  • Tolerance maintained by regular exposure
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16
Q

are there clinical symptoms in sensitization?

A

No
Sensitization = allergen-specific IgE present in theabsence of clinical symptoms.
• Weakly-positive skin tests/specific IgE blood tests rarely clinically relevant
• People with eczema have grossly elevated total IgE – causes false positive specific IgE
• Cutting out food to which person is sensitized can actually cause allergy
• Causes huge anxiety

17
Q

how the allergy is diagnosed?

A
  • History
  • Skin Prick Tests
  • (Allergen-specific IgE)
  • Food/exposure & symptom diary
  • Food Challenge
  • Double Blind Placebo Controlled Challenge
18
Q

how not to diagnose an allergy?

A
  • IgG testing
  • Vega testing
  • Kinesiology
  • Hair analysis
  • Broad testing of specific IgE is not advised
19
Q

what is the anaphylaxis?

A

A potentially life-threatening type I hypersensitivity reaction that manifests with a variable combination of rash, mucosal swelling, respiratory compromise, hypotension, and/or gastrointestinal symptoms within minutes to hours of exposure to an offending agent.

20
Q

what is the treatment of anaphylaxis?

A

1) Withdrawal of offending agent if possible (e.g., in drug reactions)
2) Airway: examination of airway and intubation if obstruction seems imminent
3) Epinephrine IM
4) Antihistamines
- -H1 antihistamine (e.g., diphenhydramine) IV for urticaria
- -H2 antihistamine (e.g., ranitidine) IV
5) Methylprednisolone
6) Positioning: The patient should be placed in a recumbent/supine position with elevation of the lower extremities.
7) O2 by facemask
8) If the patient is hypotensive: volume replacement – normal saline 1–2 L IV rapid bolus
9) Bronchospasm and no benefit of epinephrine: nebulized albuterol (salbutamol)
10) Continuous monitoring of blood pressure, heart rate, heart function, and pulse oximetry; urine output should also be monitored in hypotensive patients receiving resuscitation.

21
Q

allergic reaction severity is affected by?

A 
–	Dose of allergen
–	Asthma/chest status
–	Exacerbating factors- exercise, NSAIDs, alcohol
–	ACE inhibitors; beta-blockers
–	Prompt treatment/emergency plan
22
Q

what medications should be discontinued in patients with allergies?

A

ACE antagonists
beta-blockers
NSAIDs

23
Q

what are the causes of angioedema?

A
  • Allergic – usually venom, food or drugs
  • Spontaneous / Physical
  • Drugs
  • C1inhibitor deficiency: Hereditary, Acquired
  • Vasculitis
  • Idiopathic
24
Q

what is the hereditary angioedema?

A

An autosomal dominant inherited condition in which a C1 inhibitor deficiency or dysfunction leads to a buildup of bradykinin, a potent vasodilator that also increases vascular permeability, resulting in edema in various tissues in the body. Can be triggered by trauma, surgery, dental procedures, infections, and drugs.
–Unregulated activation of kallikrein → ↑ bradykinin → angioedema

25
Q

what are the triggers of hereditary angioedema?

A

trauma, surgery, dental procedure, menstruation, infections (e.g., Helicobacter pylori), or pharmacotherapeutic agents (e.g., ACE inhibitors, estrogens)

26
Q

what is the acquired angioedema?

A

acquired C1 inhibitor deficiency
Presents in older age (in or after the fourth decade of life)
Often associated with lymphoproliferative diseases and B-cell malignancies

27
Q

what are the causes of C1 inhibitor deficiency?

A 
Hereditary
Type I - too little protein
Type II- Dysfunctional protein
Acquired
•	Consumption
•	Autoantibody
Need to measure C1inh, C1q and C4
28
Q

what are the diagnostic tests that need to be performed in hereditary angioedema?

A
  • -CH50 assay screening test
  • -↑ Bradykinin levels
  • -Low C4 levels
29
Q

what is the C1 esterase inhibitor?

A

An enzyme that inactivates proteases involved in the complement cascade (C1r, C1s, and MASP), kallikrein, and coagulation factors XIa and XIIa. A deficiency of C1 esterase inhibitor results in hereditary angioedema.

30
Q

bradykinin is metabolized by

A

ACE

31
Q

what is the treatment of C1 inhibitor deficiency angioedema?

A

• Anti-histamines and steroids do not work
• Adrenaline ineffective
• Treat with C1 inhibitor or block bradykinin (icatibant)
Acute: purified C1-INH concentrate, a bradykinin-B2-receptor antagonist (icatibant), kallikrein inhibitor (ecallantide); FFP if other therapies are unavailable
Prophylaxis: long-term prophylaxis with attenuated androgens (e.g., danazol) or plasma-derived C1-INH concentrate

32
Q

what is the icatibant?

A

A bradykinin B2-receptor antagonist used to treat acute attacks of hereditary angioedema (i.e., due to C1 inhibitor deficiency, which leads to excessive release of bradykinin). Icatibant is applied subcutaneously. Side effects include injection site reactions, fever, rash, and dizziness.

33
Q

episodes fo spontaneous urticaria can be treated by?

A
  • Alcohol
  • Stress
  • Exercise (in some people)
  • NSAIDs
  • Codeine
  • Hormonal factors – always check TFTs
34
Q

what is the management of chronic spontaneous urticaria?

A
  • Reassurance
  • Awareness of triggers
  • Anti-histamines
  • Steroids work – but side effects excessive
  • Do not need adrenaline pen
35
Q
  • 27-year-old woman
  • 2-year history of urticaria
  • Now occurring x3 per week
  • In the last 6 months, has been waking up with a swollen lip and or tongue at least weekly
  • Eats dinner at 6 pm, goes to bed well at 12. Symptoms present when she wakes
  • No regular medications
  • No OTC
  • No herbal remedies/echinacea
  • Can eat all common allergens
  • Does occur the day after alcohol ingestion, but can occur without alcohol
A
  • Typical history of chronic spontaneous urticaria and angioedema
  • > 6 week history
  • Regular symptoms – don’t have to be daily
  • May have Ab to IgE receptor on mast cells
  • Natural history will eventually resolve
36
Q

what is the atypical urticaria?

A
  • Lesions > 24 hrs
  • Bruising
  • Must exclude vasculitis
37
Q

what is the approach to the diagnosis of a patient with urticaria?

A

Acute urticaria +/- angioedema and other allergic symptoms
Chronic urticaria +/- angioedema
• Chronic spontaneous urticaria & angioedema
• Chronic inducible urticaria
• Angioedema only – rule out C1 inhibitor deficiency
• Atypical urticaria – consider vasculitis

Immunology (9 decks)

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