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Atopy
the genetic tendency to develop a hypersensitivity reaction to common environmental substances (allergens)
- High degree of heritability & concordance
- among twins
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popularity: urticaria, asthma, allergic rhinitis
- Allergic
- rhinitis > urticaria > asthma
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rish inc for Atopy with...
a + GHx ((esp if both parent are atopic)
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aeroallergens
◦Seasonal pollens (grass pollens, ragweed)
◦Outdoor molds (airborne fungi)
◦Indoor allergens (indoor fungi, animal dander, dust mites, insects)
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hay fever - clinical aspect
◦Sneezing, rhinorrhea (clear secretions), nasal congestion, itching in the nose & palate
- ◦Less common signs: conjunctivitis
- (allergen must be blown into the eyes), fatigue, arthralgia, myalgia, cognitive
- changes (esp in children) - these are mostly cytokine-mediated effects
◦Other: obstruction of sinus ostia causing acute (bacterial) sinusitis
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hay fever - mng
- ◦Avoidance of the allergen is the best
- intervention
◦First-line therapy: antihistamines - first generation formulas reduce motor skills, second generation compounds are better
- ◦Immune therapy: anti-IgE (omalizumab) -
- effective but $$
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hives
pruritic (itchy), erythematous (red) & blanching (loose color with pressure) skin papules (slightly raised bumps!)
◦Shape: round or oval with pale raised centers (wheals)
◦Size: varies from several millimeters to a few centimeters
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itching is cause by
- ◦immediate release of histamine, leukotrienes
- & PGs from mast cells (vasodilitation, leakage of plasma from venules)
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Angioedema
involves non-pitting edema of lips, tongue, eyelids, hands, feet or genitalia
◦May involve the oropharynx & larynx
◦No report of itching but may feel burning or pressure (stretching)
- ◦Swelling involves a delayed reaction caused by inflammatory cytokines released in
- subcutaneous or submucosal tissues
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Chronic recurrent hives or angioedema over 6 weeks - clinical aspect
◦Food – requires chronic exposure (i.e., wheat)
◦Physical – triggered by scratching, exercise, exposure of skin to heat, ice, vibration, pressure, UV radiation, chronic infections (sinusitis, dental abscess, H. pylori)
◦Immune-mediated – during flares of autoimmune diseases such as rheumatoid arthritis, Hashimoto’s thyroiditis
◦Complement-mediated - Hereditary Angioneurotic Edema
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Acute hypersensitivity rxn - clinical aspect and tx
5-30 minutes after ingesting a drug or food or insect bite, but may also be idiopathic
Treatment
- ◦Acute cases are self-limited; antihistamines
- can prevent recurrent attacks
- ◦Antileukotriene
- medications or corticosteroids may become
- necessary for severe or chronic cases
Treatment
- ◦Acute cases are self-limited; antihistamines
- can prevent recurrent attacks
- ◦Antileukotriene medications or corticosteroids may become
- necessary for severe or chronic cases
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Hereditary Angioneurotic Edema
- ◦An autosomal dominant
- trait
◦Involves a deficiency of C1 esterase inhibitor - a regulatory protein that controls and limits complement activation, fibrinolysis & bradykinin production – it is this latter process that causes capillary leakage and edema
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Hereditary Angioneurotic Edema - clinical features
◦Mild attacks may begin in infancy but become severe at puberty
- ◦Swelling is spontaneous or precipitated
- by pressure, trauma, stress
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Hereditary Angioneurotic Edema - tx
no tx
◦Epinephrine is only modestly effective
- ◦Other approaches may include
- antihistamines, attenuated androgens, transfusion with FFP
- Acute attacks may require nasotracheal
- intubation
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Systemic Anaphylaxis
Immediate and life-threatening hypersensitivity reaction
- Allergy mediators are found in multiple organs
- Skin: urticaria, angioedema, flushing
- Respiratory:laryngeal edema, bronchospasm
- CV:hypotension, arrhythmia,
- GI:nausea, vomiting, gastrointestinal spasms
- Most common allergens are drugs, insect venoms, foods, radiocontrast media & latex
- ◦Allergen exposure must lead to sensitization before an immediate hypersensitivity can occur
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