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EMS MOD > urticaria, angiodema and allergy > Flashcards

urticaria, angiodema and allergy Flashcards

1
Q

what is urticaria?

A

it is a dermatological manifestation that is characterised by the sudden appearance of itchy hives known as wheals, angiodema or both

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2
Q

what does a hive consist of?

A

three typical features

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3
Q

what are the three typical features of hives?

A

central swelling of variable size with surrounding reflex erythema
associated itching/pruritus, or a burning sensation
usually resolves within a few hours and always by 24 hours

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4
Q

what does angiodema consist of?

A

four typical characteristics

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5
Q

what are the four typical characteristics of angiodema?

A

sudden, pronounced swelling of the lower dermis and subcutis
sometimes pain rather than itch
frequent involvement below the mucous membrane
up to 72 hours for resolution

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6
Q

what are the primary effector cells in angiodema and urticaria?

A

mast cells

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7
Q

where are mast cells found?

A

they are widely distributed in the body, skin and mucosa

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8
Q

what is special about mast cells?

A

they have high affinity IgE receptors

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9
Q

what does degranulation of mast cells lead to?

A

the release of inflammatory mediators such as histamine, leukotrienes and prostaglandins
vasodilation and leakage of the plasma in or below the skin
delayed (4-8 hour) secretion of inflammatory cytokines - TNF and IL4/5
further inflammatory responses resulting in longer lasting lesions

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10
Q

what is the basis of the biology of mast cell activation?

A

there is a trigger - this could be allergy, temperature, exercise or undefined
the cutaneous mast cells release mediators in response to various factors such as drugs, peptides and vasoactive amines
these mediators result in symptom induction such as histamine and interleukins
this results in symptom manifestation

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11
Q

what are the induction methods and what manifestations do these lead to in mast cells?

A

there is activation leading to pruritus
there is vasodilation leading to erythema
there is extravasation leading to wheal
there is recruitment leading to infiltrate

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12
Q

how are mast cells activated with regards to antigens?

A

the IgE carrying and antigen will bind to the IgE Fc receptor on the mast cell
this results in signals for: cytokine gene activation, phopsolipase A2 activation and degranulation
degranulation results in granule contents being released
cytokine gene activation results in secreted cytokines
membrane phospholipids from activation

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13
Q

what is the initial mast cell response?

A

this is histamine, proteases, chemotactic factors (ECF and NCF) - initial response - primary mediators

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14
Q

what is the late phase response?

A

secondary mediators
these are the secreted cytokines
membrane phospholipids result in PAF and arachidonic acid (producing leukotrienes B, C and D4 and prostaglandins D2)

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15
Q

how can acute urticaria be divided?

A

into IgE mediated and non IgE Mediated causes

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16
Q

what are the non IgE mediated causes of urticaria?

A

stress - exercise
medications - NSAIDs
infection
idiopathic

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17
Q

what are the IgE causes of urticaria?

A

insect toxin, drug, aero and food allergies

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18
Q

how can urticaria be classified based on the symptoms?

A

on the frequency, the duration (acute or chronic) and the cause

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19
Q

what is the definition of chronic spontaneous urticaria or CSU?

A

it is the spontaneous daily or almost daily occurrence of itchy hives, angiodema or both lasting 6 weeks or more

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20
Q

what is acute urticaria?

A

symptoms less than 6 weeks

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21
Q

what is spontaneous compared to inducible?

A

inducible has symptoms induced by a specific trigger

no obvious external specific trigger in spontaneous

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22
Q

what are the divisions of spontaneous for chronic?

A

known causes such as an inducing autoimmune infection or unknown resulting in CSU

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23
Q

when can CIU be classified as idiopathic and what is it?

A

it is the skin lesions that are persistent for over 6 weeks with or without angiodema that are daily or episodic - inducible
can be idiopathic when there are exclusion of underlying aetiologies

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24
Q

how would you diagnose CSU?

A

a routine patient examination with a thorough history and examination that includes:
the shape, size, distribution and associated symptoms of the lesions
the timing, frequency and duration of attacks
FHx and PHMx including allergies
correlation to any triggers
work, hobbies, stress and smoking habits
previous therapies and responses to treatments

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25
Q

which is most common as a combination of symptoms?

A

hives only or hives and angiodema is most common from 30-70%

angiodema only in 0-20% of patients

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26
Q

what is the epidemiology of CU?

A

increasing
no apparent relationship between urticaria and education, income, occupation, ethnic background or place of residence
all age groups affected bu peak between 20-40 y/o
female:male is 2:1

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27
Q

what is the prevalence of CSU?

A

affects up to 1% of population at any given time and account for 2/3 of CU cases

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28
Q

what is the disease course of CU?

A

it is a chronic disease with a duration of around 1-5 years

29
Q

when is the disease course for CSU likely to be longer?

A

when the disease is more severe
when there is concurrent angiodema
when there is concurrent inducible urticaria
a positive autologous serum skin test

30
Q

what is the link between QoL and CSU?

A

CSU adversely affects QoL - many aspects contributing to QoL are found to be reduced in those patients with CSU and this is further impaired with angiodema

31
Q

what are the particular aspects of QoL that are impaired with CSU?

A

fatigue, unpredictability of attacks, lack of sleep persisting, disfigurement and comorbidities of depression and anxiety

32
Q

what is the onset and duration of symptoms like for CSU after diagnosis?

A 
of patients that are diagnosed with CSU:
50% will still have symptoms after 6 months
30% after 3 years
10% after 5 years 
8% after 25 years
33
Q

what are the six main impacts of CSU?

A

self perception, daily living, metal status, treatment induced restrictions, social functions, leisure

34
Q

what are the factors in self perception?

A

loneliness, anxiety, unhygienic and conspicuousness

35
Q

what are the factors in daily living?

A

physical activities, chores, eating, sleeping and concentration

36
Q

what are the factors for mental status?

A

tired, stressed, overwhelmed and anxious

37
Q

what are the factors for social functions?

A

impact on relationships and sexuality

38
Q

what are the factors for leisure?

A

avoiding sun exposure, limited hobbies and clothing

39
Q

what are the factors for treatment induced restrictions?

A

financial burdens, EDAs impact and discomfort

40
Q

what is the aim of therapy for urticaria?

A

to relieve quickly and completely the symptoms

41
Q

what does the treatment encorporate?

A

symptomatic treatment to reduce the effects of basophil or mast cell mediators such as histamine on the target organ leading to symptoms of urticaria - affecting the reaction after activation

42
Q

what are the exacerbating factors in CSU?

A

physical and emotional stress, NSAIDs, tight clothing and shoes, opiates, acute and chronic infection and pseudoallergens

43
Q

what are pseudo allergens?

A

they are colours, preservatives and aspirin
natural salicytates in fresh food and drinks
biogenic amines
tomato extract, beer, cider, wine, walnuts, cheese, avocado etc

44
Q

what is an example of treatment?

A

H1 antihistamines

45
Q

what are the benefits of using modern second generation H1s?

A

they are well tolerated by most patients, are non or minimally sedating and are free of anticholinergic effects

46
Q

what did the Cochrane review of antihistamines show?

A

in 73 studies that the antihistamines were more effective than placebos - no single most effective and many were studies in small number of trials

47
Q

What are the issues with the modern second generation antihistamines?

A

they fail to control symptoms in up to 50% of patients with CSU in licensed doses

48
Q

what happens when there is a failure to control symptoms of CSU at licensed doses?

A

guidelines state a four fold increase in dose however 1/3 will still remain symptomatic

49
Q

what is the reason for increasing the doses so much in patients who do not respond to the licensed dose?

A

it does not only block the histamine mediated effects but also mast cell activation and has an impact on various cytokine and endothelial adhesion molecules

50
Q

what is the process of using second gen H1s?

A

identification of the triggers, education around avoidance of them, then firstly the standard dose, then a higher dose or adding a second H1, then a second line target such as an anti-leukotriene or tranexamic acid in angiodema and then immunomodulant

51
Q

what are the benefits of using a classical antihistamine?

A

they are trsuted as have been used for over 50 years, they have a parenteral formulation, they have additional properties that are anticholinergic and are cheap

52
Q

what are the disadvantages of using classical antihistamines?

A

sedating so impair REM sleep, they are harmful in overdose and they are no recommended in CSU

53
Q

what are the advantages of using second or third generation antihistamines?

A

they are trusted as have been used for 10-25 years, they are non sedating, very safe and licensed and recommended in CSU

54
Q

what are the disadvantages of using 2nd/3rd gen H1s?

A

they have restricted use in young children

55
Q

what are the types of first gen H1s? give examples?

A 
alkylamines - chlorphenamine 
ethanolamines - diphenhydramines
piperazines - hydroxyzine
piperidines - azatadine 
phenothiazines - promethazine 
ethylendiamines
56
Q

what are types of second generation H1s?

A

piperazines such as cetirizine

piperidines such as loratadine

57
Q

what are types and examples of third gen H1s?

A

piperazines such as levocetirizine

piperidines such as desloratadine

58
Q

what is omalizumab?

A

it is a humanised monoclonal IgG that is against the IgE that has low immunogenicity

59
Q

what is meant by humanisation?

A

it is a murine anti-IgE and therefore was needed to reduce the human anti-mouse AB response

60
Q

how was omalizumab made?

A

portions of the murine CDRs (complementary defining regions) were grafted onto a human IgG1 kappa framework (95% is this and 5% is the mouse sequence)

61
Q

why is there so little mouse sequence?

A

so that it is hidden from the immune system when omalizumab binds to IgE

62
Q

what is a use of omalizumab?

A

in CSU

63
Q

why is IgE used as a target is patients with CSU?

A

it may alleviate the symptoms
the high affinity IgE receptor on mast cells plays a key role in the activation of these cells and the pathophysiology of CSU
total IgE levels in patients with CSU are typically higher than in healthy individuals

64
Q

how does omalizumab work?

A

it binds to the C3 domain of the IgE so trimers or hexamers are formed preventing the IgE from finding to the Fc receptor on the mast cell or basophils
it will also reduce free IgE levels by binding to them leading to down regulation of the receptor on the mast and basophil cells

65
Q

what are the key symptoms of CSU?

A

reflex erythema, angiodema itch and hives

66
Q

when is omalizumab indicated?

A

as an add on therapy for adults and adolescents over 12y/o for CSU when the H1 therapy is inadequate
the only licensed add on therapy

67
Q

what is recommended dose of omalizumab?

A

300mg every 4 weeks

68
Q

what are the effects of adding on omalizumab?

A

itch reduced, increased QoL

data from three randomised controlled trials where n = 975

EMS MOD (28 decks)

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