2. • a group of disorders characterized by the formation of weals
• Nettle rash
• Dermal oedema
• Histamine
• autoimmune aetiology: lymphocytes
3. Clinical features:
• The skin itches or stings
• Weals develop
• always clear spontaneously within a few hours, even though new
lesions may continue to develop.
• angioedema :especially around the eyes and lips and in the mouth
and pharynx
• may form part of a systemic anaphylactic reaction.
4. Clinical forms:
• Acute urticaria:
• Attacks last only a few hours or days
• Contact, ingestion (food, drug), infection.
• Mast cell degranulation (IgE, direct)
• Atopy > susceptible
• Chronic urticaria:
• > 6w
• a single causative factor is rarely found
• caused by an autoimmune process or one of the physical stimuli
6. • The physical urticarias
• Dermographism
• Pressure (delayed)
• Cholinergic urticaria: small white weals with a red halo on the upper trunk.
• Cold: contact with cold objects or blasts of cold air
• Water.
• Sunlight.
• Heat
• Chronic spontaneous/idiopathic urticaria : is diagnosed when no
other trigger can be identified
• Hereditary angioedema:
• very rare AD
• C1 esterase inhibitor is lacking or defective.
• sudden attacks of angioedema, which can be life‐threatening.
• The gut (spasms of abdominal pain).
8. Treatment of urticaria:
• If a possible trigger can be elicited from the history, it should be avoided.
• Aspirin and aspirin‐like substances should be avoided by anyone prone to
urticaria
• H1‐receptor antihistamines: sedating and non sedating effect (e.g.
desloratadine, levocetirizine, fexofenadine).
• H2‐receptor antagonist (cimetidine, ranitidine
• other agents: such as montelukast, systemic steroids, ciclosporin, and
adrenaline
• biologic agent omalizumab (anti-IgE)
• Angioedema: may require parenteral therapy with adrenaline,
antihistamines and steroids.
• Anaphylaxis: adrenaline is required.
• Hereditary angioedema: Danazol , Purified enzyme preparations
10. • Aetiology: idiopathic, HSV,orf, hepatitis, mumps.
Mycoplasma, Cancers, radiotherapy, Connective tissue
diseases, drugs
• Examination:
• The classic lesion is the ‘iris’ or ‘target’ lesion
• about 3 weeks.
• Extensor surfaces of the arms and legs.
• Mucous membranes
• palms and soles
• Skin lesions may blister (bullous erythema multiforme).
• Treatment: self‐limiting, and treatment is not usually required.
11. Target lesions of erythema multiforme Erosions on the lips in erythema multiforme
13. • major systemic disturbance
• acute onset
• severe inflammation of conjunctivae, mouth and
genitalia
• Patients occasionally die of severe bronchopulmonary
involvement or renal
• failure.
• Treatment:
• fluid balance and nutrition
• role of systemic steroids is controversial
17. •most of the skin becomes red, inflamed and oedematous
•There may be some scaling.
•four most important causes:
• Psoriasis.
• Eczema/dermatitis.
• Drug reactions.
• Lymphomas (especially cutaneous T‐cell lymphoma).
•management depends on the underlying disease process