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Urticaria and Angioedema

»	What percentage of the population experiences acute urticaria during their lifetime?
»	How is acute versus chronic urticaria defined?
»	What are the common causes of acute urticaria?
»	Are all urticarial reactions from medications allergic (IgE-mediated) in nature?
»	What is the cause of most chronic urticaria?
»	Is chronic urticaria primarily of allergic etiology?
»	How common are the physical urticarias?
»	What association has been described between autoantibodies and chronic urticaria?
»	What is the “triple response”? Name the components.
»	What is the mechanism of the axon reflex?
»	List five mediators that are capable of directly causing vasodilatation and increased vascular permeability in the skin.
»	Name three mediators that may cause vasodilatation and increased vascular permeability indirectly through action on the mast cell.
»	Which cells synthesize histamine releasing factors?
»	What cytokines/chemokines may also be increased in urticarial lesions?
»	In what form of physical urticaria are subjects at risk of drowning?
»	How quickly after the application of cold does whealing develop in acquired cold urticaria?
»	Only one form of urticaria has whealing that is sufficiently characteristic to suggest a specific diagnosis. Which one?
»	Where does cholinergic urticaria usually develop?
»	What are the precipitating events for cholinergic urticaria? By what mechanism do they produce the whealing?
»	How are the solar urticarias classified?
»	What is Darier’s sign?
»	How often does aspirin cause or exacerbate urticaria?
»	What is the prognosis of chronic urticaria?
»	Much has been discovered in recent years regarding the histopathology of chronic idiopathic urticaria. What three major types of cells may be encountered in increased numbers in these biopsies?
»	In contrast to chronic idiopathic urticaria, what are the typical histologic features of urticarial vasculitis?
»	Can clinical findings suggest the presence of urticarial vasculitis?
»	A number of clues in the patient’s history may suggest that a patient with recurrent angioedema has the hereditary form. Name some.
»	Why is C1 esterase deficiency not a part of the differential diagnosis of chronic urticaria?
»	Name the recommended screening laboratory test for hereditary angioedema.
»	What is the treatment of choice for HAE? How does it work?
»	How may a patient with HAE be treated prophylactically prior to elective surgery?
»	A 60-year-old patient presents with a new onset of attacks of nonpruritic angioedema and a depressed C4 level. What is the first diagnosis you consider?
»	Certain drugs have been identified as being particularly effective for a subset of patients with chronic urticaria or angioedema. What are these drugs, and when is a trial with them indicated?
»	What three mediator antagonists have been reported to be useful in symptomatic control of urticaria?

What is the treatment of choice for HAE? How does it work?

HAE is inherited in an autosomal dominant pattern. Attenuated androgens, such as danazol, induce synthesis of normal C1 esterase inhibitor by the liver in these patients. Patients with the functionally abnormal C1 esterase inhibitor also respond, since they too have one normal gene. Pooled C1 inhibitor (prophylaxis) and kallikrien inhibitors for acute attacks are available.