Allergic Diseases, Urticaria, Angioedema, and Eczematous Dermatoses

Type I hypersensitivity reaction

IgE-mediated immediate allergic reaction caused by mast cell degranulation

Mast cell degranulation

Release of histamine, prostaglandins, and leukotrienes after allergen–IgE cross-linking

Histamine effect

Increases vascular permeability and causes vasodilation leading to wheals

Urticaria

Transient superficial dermal edema presenting as itchy wheals lasting <24 hours

Angioedema

Deep dermal and subcutaneous swelling with normal skin color and soft consistency

Urticaria duration acute

Condition lasting less than 6 weeks

Urticaria duration chronic

Condition lasting more than 6 weeks

Idiopathic chronic urticaria

Urticaria with no identifiable cause in 30–50% of cases

Cold urticaria

Hives triggered by exposure to cold; confirmed by ice cube test

Cholinergic urticaria

Urticaria triggered by heat, exercise, sweating; mediated by acetylcholine

Dermographism

Urticaria induced by stroking or scratching the skin

Contact urticaria

Hives appearing at sites of direct allergen contact

Urticaria gigantea

Large urticarial lesions often with systemic symptoms like hypotension

Urticaria annularis

Annular patterns formed by merging wheals

Urticaria therapy first line

H1 antihistamines

Chronic urticaria advanced therapy

Omalizumab or Montelukast for refractory cases

Anaphylaxis

Severe systemic Type I reaction with hypotension, bronchospasm, and urticaria

Anaphylaxis first treatment

Adrenaline 0.5–1 ml subcutaneously, repeated every 15–20 minutes

Anaphylaxis IV adrenaline

Slow IV administration diluted 1:10 when SC ineffective

Anaphylaxis supportive therapy

Antihistamines, corticosteroids, IV fluids, aminophylline

Insect venom allergy

Type I reaction triggered by bee, wasp, or hornet stings

Uagne syndrome

Rare CNS-related toxic reaction after injection of crystalline suspensions

Hereditary angioedema

C1 esterase inhibitor deficiency causing recurrent non-histaminergic edema

HAE inheritance pattern

Autosomal dominant

HAE laboratory findings

Low C1 esterase inhibitor, low C4, low C2

HAE acute attack treatment

Purified C1 inhibitor or plasma infusion

HAE prophylaxis

Danazol to increase C1 inhibitor production

Urticarial vasculitis

Hives lasting >24 hours with leukocytoclastic vasculitis on histology

Urticarial vasculitis symptoms

Fever, arthralgia, malaise with persistent urticarial plaques

Urticarial vasculitis treatment

Prednisolone, antihistamines, dapsone

Eczema definition

Non-infectious inflammatory skin disease with erythema, vesicles, crusts, and lichenification

Endogenous eczema

Eczema driven by constitutional or genetic factors

Exogenous eczema

Eczema caused by external irritants or allergens

Contact dermatitis

Injury or inflammation of skin from allergen or irritant exposure

Allergic contact dermatitis

Type IV delayed-type hypersensitivity reaction to haptens

Irritant contact dermatitis

Non-immunologic reaction depending on chemical concentration and exposure time

Patch test

Dermatologic test for allergic contact dermatitis read after 72 hours

Spongiosis

Intercellular epidermal edema seen in eczematous dermatitis

Acute eczema features

Erythema, papules, vesicles, oozing, crusts

Chronic eczema features

Lichenification, hyperkeratosis, fissures, xerosis

Contact dermatitis therapy

Avoid trigger, topical steroids, emollients, antihistamines

Atopic dermatitis

Chronic relapsing pruritic eczema with age-dependent patterns and atopic background

Atopic diathesis

Genetic tendency toward eczema, asthma, and allergic rhinitis

Atopic dermatitis hallmark

Severe pruritus caused by xerosis and barrier dysfunction

Infantile AD distribution

Face, cheeks, scalp, extensor surfaces

Childhood AD distribution

Flexural areas of elbows, knees

Adult AD distribution

Neck, hands, eyelids, flexural surfaces

Atopic triad

Atopic dermatitis, allergic rhinitis, asthma

Atopic dermatitis triggers

Heat, sweating, irritants, allergens, infections, low humidity

AAD essential diagnostic features

Pruritus, typical morphology, chronic or relapsing course

AAD supportive features

Early onset, atopy, xerosis

AD exclusion conditions

Scabies, psoriasis, seborrheic dermatitis, cutaneous lymphoma

Atopic dermatitis therapy core

Regular emollient use to restore barrier function

Topical therapy AD

Topical corticosteroids or calcineurin inhibitors

Calcineurin inhibitors in AD

Tacrolimus or pimecrolimus for steroid-sensitive areas

AD systemic therapy

Antihistamines, short-term corticosteroids, phototherapy

Eczema herpeticum

HSV infection superimposed on atopic dermatitis

Diaper dermatitis

Irritant dermatitis from urine/feces occlusion in infants

Diaper dermatitis features

Redness, maceration, possible Candida superinfection

Diaper dermatitis therapy

Zinc paste, antifungals, mild corticosteroids

Nummular eczema

Round or oval coin-shaped eczematous plaques, often on legs

Dyshidrotic eczema

Vesicles on palms and soles with intense itching

Dyshidrotic eczema triggers

Stress, sweating, allergens, infections

Lichen simplex chronicus

Localized thickened plaques caused by chronic scratching

Lichen simplex therapy

Potent topical steroids, antihistamines, behavioral modification

Acute urticaria hallmark

Fleeting wheals resolving within 24 hours

Angioedema skin color

Typically normal skin color despite swelling

Type IV hypersensitivity

Delayed T-cell mediated immune response

Hives pathophysiology

Superficial dermal vasodilation and plasma leakage

Angioedema pathophysiology

Deep dermal and subcutaneous edema

Rule of “I” in urticaria

Ingestion, inhalation, instillation, injection, insertion, insect sting, infestation, infection

Prick test

Immediate hypersensitivity test read after 15–20 minutes

H1 antihistamines role

Block histamine receptors to reduce itching and wheals

H2 antihistamines use

Adjunct therapy in chronic urticaria

Montelukast usage

Leukotriene receptor blocker for chronic urticaria

Omalizumab mechanism

Anti-IgE monoclonal antibody reducing mast cell activation

Irritant dermatitis risk factor

Dry skin with reduced barrier function

Airborne contact dermatitis

Face and neck dermatitis triggered by airborne allergens

Subacute eczema signs

Erythema, scaling, mild crusts without acute vesiculation

Lichenification

Dermal thickening with accentuated skin markings from chronic rubbing

Excoriations

Scratch marks caused by intense pruritus

Hot water urticaria

Urticaria triggered by warm water exposure

Aquagenic urticaria

Hives triggered by water contact regardless of temperature

Solar urticaria

Urticaria induced by sun exposure

Hypotension in anaphylaxis

Caused by massive vasodilation and plasma leakage

Aminophylline role

Relieves bronchospasm during anaphylaxis

5% glucose or saline in anaphylaxis

Restores intravascular volume in shock

Complement activation in HAE

Uncontrolled due to absence of C1 inhibitor

Spongiosis significance

Histologic hallmark of eczematous dermatitis

Flexural dermatitis hallmark

Key diagnostic pattern in atopic dermatitis

Xerosis in AD

Dry skin due to impaired skin barrier function

Palmar hyperlinearity

Increased skin lines associated with atopy

Keratosis pilaris

Perifollicular keratotic papules associated with atopic skin

Ichthyosis association

Dry scaly skin linked to atopic dermatitis

Periorbital changes in AD

Darkening, Dennie-Morgan folds, eyelid dermatitis

Perioral dermatitis

Perioral erythema and papules associated with atopy

Secondary infection in eczema

Bacterial, viral, or fungal superinfection worsening dermatitis

Topical steroid misuse

Risk of skin atrophy, striae, rebound dermatitis

Irritant threshold

Individual variation in susceptibility to irritants

Haptens

Small molecules that become allergenic when bound to skin proteins