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y2 mechanisms of disease > Urticaria & Angiodema > Flashcards

Urticaria & Angiodema Flashcards

1
Q

What is the definition of urticaria?

A

a dermatological manifestation characterised by the sudden appearance of itchy hives (wheals), angioedema or both

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2
Q

What is meant by a ‘hive’?

A

superficial swelling with a pale centre surrounded by a red flare

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3
Q

What are the 3 typical features of a hive?

A
  1. central swelling surrounded by a reflex erythema
  2. associated itching (pruritus) and sometimes a burning sensation
  3. usually resolves in a few hours and always resolves by 24 hours
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4
Q

What is meant by erythema and what is it caused by?

A

redness of the skin caused by hyperemia (increased blood flow) in superficial capillaries

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5
Q

What are the 4 main characteristics of angioedema?

A
  1. sudden pronounced swelling of the lower dermis and subcutis
  2. sometimes pain rather than itching
  3. frequent involvement below mucous membranes
  4. up to 72 hours for resolution
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6
Q

What are the primary effector cells in urticaria and angioedema?

Where are they found?

A

Mast cells

Widely distributed in skin, mucosa and other areas of the body

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7
Q

What type of receptors are present on the surface of mast cells?

A

high affinity IgE receptors

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8
Q

What inflammatory mediators are released when a mast cell degranulates?

A

There is rapid release of histamine, leukotrienes, prostaglandins

There is delayed release (4-8 hr) of inflammatory cytokines

e.g. TNF, IL-4/5

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9
Q

What is the physiological outcome of mast cell degranulation?

A

Vasodilation and leakage of plasma in/below the skin

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10
Q

What happens for the first time when someone is exposed to an allergen?

A

The body makes large amounts of IgE antibody against the allergen

The IgE molecules attach themselves to mast cells

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11
Q

What happens when someone is exposed to an allergen for the second time?

A

IgE primed mast cells release granules and chemical mediators

These cause the characteristic symptoms of allergy

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12
Q

How can mast cell activation lead to the symptoms of urticaria?

A

The trigger can be heat, cold, exercise, undefined

Mast cells release mediators in response to drugs, peptides, etc.

Mediators cause symptom induction

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13
Q

What are the 2 types of acute urticaria?

A
  1. IgE-mediated urticaria

2. Non-IgE-mediated urticaria

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14
Q

What are the 4 typical triggers of IgE-mediated urticaria?

A
  1. drug allergy
  2. food allergy
  3. insect toxin allergy
  4. aeroallergies
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15
Q

What are the 4 typical triggers of non-IgE-mediated urticaria?

A
  1. infection
  2. medications (e.g. NSAIDs)
  3. Stress (exercise)
  4. idiopathic
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16
Q

What are the 3 ways of classifying urticaria?

A
  1. duration
  2. frequency
  3. cause
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17
Q

What is the difference between chronic and acute urticaria?

A

Chronic - daily symptoms for 6 weeks or more

Acute - symptoms for less than 6 weeks

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18
Q

What are the 2 types of chronic urticaria?

A
  1. spontaneous

2. inducible

19
Q

What is spontaneous urticaria?

A

There is no obvious external specific trigger

20
Q

What is inducible urticaria?

A

Symptoms are induced by a specific trigger

e.g. temperature, pressure

21
Q

What is the definition of chronic spontaneous urticaria (CSU)?

A

Spontaneous daily occurrence of itchy hives, angioedema or both, lasting for 6 weeks or more

22
Q

When taking a history of someone thought to have CSU, what are the 6 main areas that should be explored?

A
  1. timing/frequency/duration of attacks
  2. shape, size and distribution of lesions
  3. family and medical history - including allergies
  4. correlation to any triggers
  5. work/hobbies/smoking habits
  6. previous therapy and response to treatment
23
Q

Typically for how long will someone with CSU suffer for?

A

It is a chronic disease which typically lasts between 1 and 5 years

24
Q

What 4 factors suggest that CSU duration will be longer than 1-5 years?

A
  1. more severe disease
  2. concurrent angioedema
  3. concurrent inducible urticaria
  4. positive autologous serm skin test
25
Q

What is the most severe impact of CSU on a patient’s life?

A

It severely impacts quality of life

26
Q

In what ways does CSU typically affect a patient’s quality of life?

A
  1. unpredictability of attacks
  2. persistent lack of sleep
  3. fatigue
  4. disfigurement

Patients often have comorbidities such as depression and anxiety

27
Q

What is the basic mechanism behind treatments for CSU?

A

Reducing the effect of mast cell mediators on target organs

This prevents the symptoms or urticaria

28
Q

What are the 6 most common exacerbating factors in CSU?

A
  1. physical and emotional stress
  2. tight clothing and shoes
  3. NSAIDs
  4. Opiates
  5. Acute and chronic infection
  6. Pseudoallergens
29
Q

What is meant by a pseudoallergy?

A

A condition that has a similar presentation to a true allergy, but is due to different causes

Usually due to alterations in the metabolism of histamine

30
Q

What are examples of pseudoallergens?

A

colours, preservatives, aspirin

31
Q

What are the 4 stages in escalating treatments for CSU?

A
  1. standard dose non-sedating H1 antihistamine
  2. higher dose of H1 antihistamine or add second antihistamine
  3. consider anti-leukotriene or tranexamic acid if angioedema is present
  4. consider immunomodulant
32
Q

What is suggested to be the effect of increasing the dose of H1-antihistamines?

A
  1. reduction in mast cell activation

2. impact on cytokine and endothelial adhesion molecules

33
Q

What “generation” are H1 antihistamines?

A

Second generation

34
Q

What are the advantages in using second generation antihistamines?

A
  1. licensed and recommended in CSU
  2. trusted and in use for 25 years
  3. non-sedating
  4. very safe
35
Q

What are the disadvantages of using H1 antihistamines?

A

They have a restricted use in young children

36
Q

What are the advantages of using classical antihistamines?

A
  1. trusted and in use for over 50 years
  2. parenteral formulation
  3. cheap
  4. additional properties - anticholinergic
37
Q

What are the disadvantages of using classical antihistamines?

A
  1. sedating - impairs REM sleep
  2. harmful in overdose
  3. not recommended in CSU
38
Q

What is Omalizumab?

A

a monoclonal IgG antibody against IgE, with low immunogenicity

39
Q

What component of the mast cell plays a key role in the pathophysiology of CSU?

A

high-affinity IgE receptor plays role in activation of mast cells and symptoms associated with CSU

Total IgE levels in patients with CSU are higher

40
Q

How does Omalizumab work?

A

It inhibits binding of IgE to FceRI (IgE receptor) on the surface of mast cells and basophils

41
Q

How does Omalizumab inhibit binding of IgE to mast cells?

What does this lead to?

A

It binds to IgE and reduces free IgE levels

This leads to down-regulation of FceRI on mast cells

42
Q

When is Omalizumab used in treatment of CSU?

A

It is an add-on therapy that is used in patients with an inadequate response to HI antihistamine treatment

43
Q

What is the recommended dose of Omalizumab in patients with CSU?

A

300 mg every 4 weeks

y2 mechanisms of disease (36 decks)

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