Miscellaneous Lesions Flashcards
Angioedema description and forms
- deeper swelling of the skin involving subcutaneous tissues; often involves the eyes, lips, and tongue
- may or may not accompany urticaria
- hereditary or acquired forms
Hereditary angioedema description, onset and triggers
• hereditary angioedema (does not occur with urticaria)
■ onset in childhood; 80% have positive family history
■ recurrent attacks; 25% die from laryngeal edema
■ triggers minor trauma, emotional upset, temperature changes
Types of acquired angioedema
■ acute allergic angioedema (allergens include food, drugs, contrast media, insect venom, latex)
■ non-allergic drug reaction (drugs include ACEI)
■ acquired C1 inhibitor deficiency
Angioedema treatment
■ prophylaxis with danazol or stanozolol for hereditary angioedema
■ epinephrine pen to temporize until patient reaches hospital in acute attack
Urticaria description and pathophysiology
- also known as “hives”
- transient, red, pruritic well-demarcated wheals
- each individual lesion lasts less than 24 h
- second most common type of drug reaction
- results from release of histamine from mast cells in dermis
- can also result after physical contact with allergen
DDx for urticaria
DAM HIVES
Drugs and foods
Allergic
Malignancy
Hereditary Infection Vasculitis Emotions Stings
Acute urticaria
> 2/3 of cases
Attacks last <6 wk
Individual lesions last <24 h
Acute urticaria etiology
Drugs; especially ASA, NSAIDs
Foods: nuts, shellfish, eggs, fruit
Idiopathic (vast majority)
Infection
Insect stings (bees, wasps, hornets)
Percutaneous absorption: cosmetics, work exposures
Stress
Systemic diseases: SLE, endocrinopathy, neoplasm
Chronic urticaria
<1/3 of cases
Attacks last >6 wk
Individual lesion lasts <24 h
Chronic urticaria etiology
IgE-dependent: trigger associated
- Idiopathic (90% of chronic urticaria patients)
- Aeroallergens
- Drugs (antibiotics, hormones, local anesthetics)
- Foods and additives
- Insect stings
- Parasitic infections
- Physical contact (animal saliva, plant resins, latex, metals, lotions, soap)
Direct mast cell release
- Opiates, muscle relaxants, radio-contrast agents
Complement-mediated
- Serum sickness, transfusion reactions
- Infections, viral/bacterial (>80% of urticaria in pediatric patients)
- Urticarial vasculitis
Arachidonic acid metabolism
- ASA, NSAIDs
Physical
- Dermatographism (friction, rubbing skin), cold (ice cube, cold water), cholinergic (hot shower, exercise), solar, pressure (shoulder strap, buttocks), aquagenic (exposure to water) adrenergic (stress), heat
Other
- Mastocytosis, urticaria pigmentosa
Approach to urticaria
- Thorough Hx and P/E
- Acute: no immediate investigations needed; consider referral for allergy testing
- Chronic: further investigations required: CBC and differential, urinalysis, ESR, TSH, LFTs to help identify underlying cause
- Vasculitic: biopsy of lesion and referral to dermatology
Wheal
- Typically erythematous flat-topped, palpable lesions varying in size with circumscribed dermal edema
- Individual lesion lasts <24 h
- Associated with mast cell release of histamine
- May be pruritic
Mastocytosis (Urticaria Pigmentosa)
Rare disease due to excessive infiltration of the skin by mast cells. It manifests as many reddish-brown elevated plaques and macules. Friction to a lesion produces a wheal surrounded by intense erythema (Darier’s sign), due to mast cell degranulation; this occurs within minutes
Urticarial vasculitis description and intervention
Individual lesions last >24 h
Often painful, less likely pruritic, heals with bruise type lesions
Requires biopsy
Urticarial vasculitis etiology
Idiopathic Infections Hepatitis Autoimmune diseases SLE Drug hypersensitivity Cimetidine and diltiazem
