Urticaria (acute, chronic) Flashcards

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1
Q

Define urticaria.

A

Urticaria (also called hives) are erythematous, blanching, oedematous, non-painful, pruritic lesions that typically last less than 24 hours and leave no residual markings upon resolution.

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2
Q

What % of urticaria is associated with angio-oedema?

A

Approximately 40% of episodes of urticaria have associated angio-oedema. Angio-oedema is swelling involving the deeper layers of the sub-dermis and can occur in both the acute and chronic setting.

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3
Q

How common is urticaria?

A
  • Lifetime incidence of acute urticaria is 20%
  • 30% will go on to have prolonged symptoms
  • Acute urticaria is more common in children and adolescents
  • Chronic urticaria typically affects adults (and women are more affected 1.5:1)
  • ACE-i related angio-oedema is more common in black ethnic groups
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4
Q

What is the difference between acute and chronic urticaria?

A

Acute - Episodes that occur over a period of <6 weeks are generally considered acute, can be caused by a specific stimulus (usually hypersensitivity reaction), and are self-limiting.

Chronic - Episodes of hives that occur daily or almost daily over a period of >6 weeks are classified as chronic and appear to be “spontaneous”. They have a complex aetiology.

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5
Q

What is a common cause of acute urticaria in children?

A

Hypersensitivity reaction or underlying viral infections are a common cause of acute urticaria, particularly in children.

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6
Q

Summarise briefly the differences in investigations/management of acute and chronic urticaria.

A

Acute

  • Self resolving
  • Diagnosis based on history and physical examination
  • Antihistamines are mainstay therapy

Chronic

  • Diagnosis may require laboratory testing, depending on history
  • Referral to a specialist may be needed
  • Antihistamines are mainstay therapy

*For those who don’t respond to mainstay therapy options include omalizumab and immunomodulatory medications.

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7
Q

Angio-oedema in which locations is dangerous?

A

Angio-oedema involving the face or neck can potentially compromise the airway and requires prompt airway management

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8
Q

What is the pathophysiology of urticaria?

A

MAST cells are tfound everywhere including in dermis, sub-dermis, mucosal surfaces

  • Soluble antigen (IgE mediated) –> mast cell activation –> degranulation –> release of vasoactive mediators including histamine, leukotriene C4, prostaglandin D2
  • Vasoactive mediators –> 1) vasodilation, 2) increased vascular permeability –> oedema and pruritus
  • Delayed release of cytokines (TNF, IL-4, IL-5) causes longer-lasting lesions

Biopsies of lesions contain CD4+ lymphocytes, eosinophils, basophils and neutrophils and sometimes immune complex depoosition

Urticaria is confined to the DERMAL layer; angio-oedema involves the SUB-DERMAL and MUCOSAL sites

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9
Q

What type of hypersensitivity reaction is urticaria? Which immunoglobulins are involved? What is the antigen?

A
  • This is a type 1 hypersensitivity reaction
  • IgE mediated
  • Soluble antigen
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10
Q

What are the risk factors for urticaria?

A
  • FH
  • Exposure to trigger (drug/food)
  • Recent viral infection - in children; non-IgE
  • Insect bite
  • Female sex
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11
Q

What are the most common causes of acute urticaria?

A

Allergy (IgE mediated reaction)

  • Drugs - penicilins, sulfonamides, muscle relaxants, diuretics, NSAIDs
  • Foods - milk, eggs, peanuts, tree nute, finfish, shell fish
  • Insect bites

Other (non-IgE mediated mechanisms)

  • Drugs - NSAIDs, opioids, vancomycin
  • Radiocontrast dye
  • Acute viral infection (in children)
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12
Q

What are the most common causes of chronic urticaria?

A
  • 40% are thought to be autoimmune causes - IgG autoantibodies to high-affinity receptor for IgE or thyroid antibodies
  • Idiopathic
  • Strong emotional situations

Only 10% of those with chronic urticaria have an identifiable cause.

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13
Q

What are the clinical features of urticaria?

A
  • Erythematouc oedematous lesions
  • Pruritus
  • Resolution in 24hrs with no residual markings
  • Swelling of face, tongue, lips
  • Blanching lesions (non-blanching = vasculitis)
  • Stridor - if severe laryngeal angio-oedema causing airway obstruction
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14
Q

What investigations would you do for urticaria?

A
  • Usually diagnosed from history and physical examination
  • Ask patient to keep a food diary if suspected trigger is food then re-introduce slowly.

Consider these for chronic urticaria:

  • FBC with differential
  • Complete metabolic panel
  • Urinalysis - renal dysfunction in vasculitis -> proteinuria and WBC
  • ESR and CRP - raised
  • IgE receptor antibody and related tests - +ve in AI related chronic U
  • TSH
  • Antithyroid antibody - Hashimoto’s thyroiditis
  • ANA - rheumatological conditions
  • Skin biopsy - check for vasculitis
  • C4 lecels - low in angio-oedema
  • C1-esterase inhibitor level or function - low in hereditary AO
  • C1q levels - low levels in acquired angio-oedema (normal in hereditary)
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15
Q

How do you manage urticaria?

A
  1. Trigger identification and avoidance
  2. H1 receptor antagonists (antihistamines) e.g. cetirizine or loratadine
  3. Systemic corticosteroids - if severe
  4. Adrenaline (0.3mg IM every 1-2hrs as required) - if severe or causing airway compromise
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