Urticaria and angiooedema Flashcards
(116 cards)
1
Q
Urticaria lesions typically last more than 24 hours.
A
False – Lesions usually resolve within 24 hours; >24h suggests urticarial vasculitis.
2
Q
Pruritus is a characteristic symptom of urticaria.
A
True – Itching is a hallmark symptom.
3
Q
Chronic urticaria is defined as episodes occurring daily for >6 weeks.
A
True – >6 weeks of near-daily hives defines chronic urticaria.
4
Q
Histamine is the only mediator involved in urticaria.
A
False – Leukotrienes, prostaglandins, cytokines also involved.
5
Q
Urticaria always presents with angioedema.
A
False – Angioedema only occurs in ~40% of chronic urticaria.
6
Q
Urticaria is due to mast cell degranulation in the dermis.
A
True – Superficial dermal mast cell degranulation.
7
Q
Antihistamines are the first-line treatment for chronic urticaria.
A
True – 2nd-gen H1 antihistamines are first-line.
8
Q
Urticaria caused by physical triggers is called inducible urticaria.
A
True – Physical stimuli trigger inducible forms.
9
Q
A skin biopsy is always needed to diagnose urticaria.
A
False – Biopsy is only needed if atypical features present.
10
Q
Urticaria is associated with autoimmune thyroid disease.
A
True – Common in autoimmune urticaria.
11
Q
Most CSU is idiopathic.
A
True – No clear cause in most cases.
12
Q
Autologous serum skin testing can be positive in autoimmune CSU.
A
True – Indicates functional IgG autoantibodies.
13
Q
Omalizumab is an approved treatment for CSU.
A
True – Anti-IgE biologic approved for CSU.
14
Q
Anti-TPO antibodies are absent in CSU.
A
False – Anti-TPO Ab may be present.
15
Q
NSAIDs can exacerbate urticaria in sensitive individuals.
A
True – Common exacerbator of CSU.
16
Q
Urticaria in CSU never occurs during sleep.
A
False – Can occur at any time including sleep.
17
Q
Systemic corticosteroids are first-line therapy in CSU.
A
False – Reserved for short courses in flares.
18
Q
Elevated D-dimer can be seen in severe CSU.
A
True – Linked to disease activity.
19
Q
Cyclosporine can be used for antihistamine-refractory CSU.
A
True – Immunosuppressant for refractory cases.
20
Q
Urticaria is always caused by IgE-mediated mechanisms.
A
False – Autoimmune/non-IgE pathways also involved.
21
Q
Cold urticaria can cause anaphylaxis.
A
True – Systemic reactions possible.
22
Q
Heat urticaria is a common subtype.
A
False – It’s rare.
23
Q
Delayed pressure urticaria presents immediately after pressure.
A
False – Onset typically delayed 4–6 hours.
24
Q
Cholinergic urticaria is triggered by sweating and heat.
A
True – Often triggered by heat, exercise, stress.
25
Dermatographism is elicited by stroking the skin.
True – Most common inducible urticaria.
26
Urticaria pigmentosa is an inducible urticaria.
False – It's cutaneous mastocytosis.
27
Aquagenic urticaria is triggered by water temperature.
False – Independent of water temperature.
28
Sunlight can cause urticaria in solar urticaria.
True – UV exposure can trigger lesions.
29
Vibratory urticaria is associated with systemic symptoms.
False – Typically localized only.
30
Physical urticarias require challenge testing for diagnosis.
True – Provocation tests help confirm diagnosis.
31
Angioedema affects deeper dermis and subcutis.
True – Unlike urticaria which is superficial.
32
Angioedema is always itchy.
False – Itching is uncommon; more burning/pain.
33
ACE inhibitors can cause angioedema even after years of use.
True – Can appear even after years on ACEIs.
34
Hereditary angioedema is caused by C1-INH deficiency.
True – Type I (low levels) and Type II (dysfunction).
35
C1q is elevated in acquired angioedema.
False – C1q is low in acquired angioedema.
36
HAE attacks are histamine-mediated.
False – Bradykinin-mediated, not histamine.
37
Urticaria is commonly seen in hereditary angioedema.
False – Urticaria is typically absent in HAE.
38
Ecallantide is a treatment for HAE attacks.
True – Kallikrein inhibitor used acutely.
39
Danazol can be used for HAE prophylaxis.
True – Long-term prophylactic option.
40
Fresh frozen plasma can be used for acute HAE.
True – Provides C1-INH acutely.
41
Urticarial vasculitis lesions resolve in <24 hours.
False – Persist >24h and leave pigmentation.
42
Serum tryptase is always elevated in urticaria.
False – Usually normal unless systemic mastocytosis.
43
ANA can be checked in atypical chronic urticaria.
True – Useful to screen for autoimmunity.
44
Elevated ESR is typical in urticarial vasculitis.
True – Suggests systemic inflammation.
45
Skin prick testing is useful in CSU.
False – Allergy testing not useful in CSU.
46
Biologic therapy is reserved for mild CSU.
False – Used for moderate-severe refractory cases.
47
Acute urticaria is usually self-limited.
True – Usually resolves in days to weeks.
48
Thyroid dysfunction should be ruled out in CSU.
True – Check TSH and antibodies.
49
Montelukast is first-line for urticaria.
False – Add-on, not first-line.
50
CSU significantly impairs quality of life.
True – Major impact on QoL due to pruritus, sleep disruption.
51
What is aquagenic urticaria (AU)?
A rare form of chronic inducible urticaria triggered by contact with water, regardless of temperature or source.
52
What is the typical latency between water contact and symptom onset in AU?
Usually within 30 minutes.
53
What are the clinical features of aquagenic urticaria?
Pinpoint wheals or erythema, often on the trunk and upper limbs; associated with itching or burning.
54
What is the pathophysiology of aquagenic urticaria?
Unknown; hypotheses include water acting as a carrier for epidermal antigens or alteration in osmotic pressure activating mast cells.
55
What demographic is most commonly affected by aquagenic urticaria?
Young women; often onset during puberty.
56
What are key differentials for aquagenic urticaria?
Cholinergic urticaria, cold urticaria, heat urticaria.
57
How is aquagenic urticaria diagnosed?
Water challenge test: applying water (35–37°C) via compress for 30 min to upper body, observing for wheals.
58
What is the first-line treatment for aquagenic urticaria?
Non-sedating H1-antihistamines (second-generation).
59
What are additional treatment options for refractory aquagenic urticaria?
Higher-dose antihistamines, omalizumab, phototherapy (PUVA or NB-UVB), barrier creams (e.g., petrolatum).
60
Is aquagenic urticaria associated with systemic symptoms?
No, typically confined to skin. Rare systemic involvement.
61
What is exercise-induced urticaria (EIU)?
Urticaria or anaphylaxis triggered by physical exertion. May be isolated or food-dependent.
62
What is the latency between exercise and onset of symptoms in EIU?
5 to 30 minutes after starting exercise.
63
What are clinical features of EIU?
Generalised pruritus, flushing, urticaria, angioedema; may progress to anaphylaxis (hypotension, syncope, wheeze).
64
What is food-dependent EIU (FDEIA)?
Urticaria/anaphylaxis only occurs if specific food is consumed within ~4 hours of exercise.
65
What are common food triggers in FDEIA?
Wheat (ω-5 gliadin), shellfish, nuts, celery.
66
What is the proposed mechanism of EIU?
Physical exertion increases absorption of allergens or lowers threshold for mast cell degranulation.
67
How is EIU diagnosed?
Clinical history + exercise challenge (e.g., treadmill) ± food provocation; serum tryptase post-episode.
68
What is the key management strategy for EIU?
Avoid triggers (exercise or food/exercise combo), carry adrenaline autoinjector, pre-treatment with antihistamines.
69
Is EIU IgE-mediated?
Often yes, particularly in FDEIA (positive skin prick or specific IgE to food allergen).
70
What is the role of omalizumab in EIU?
May help in severe, refractory cases. Not first-line.
71
What is the most common form of inducible urticaria?
Dermographism.
72
What triggers dermographism?
Mechanical shearing or stroking of the skin.
73
What is the typical onset age for dermographism?
Late adolescence or early adulthood.
74
What is the pathophysiology of dermographism?
Mechanical stimulation → mast cell degranulation → histamine release.
75
How soon after stroking does dermographism occur and how long does it last?
Onset in 5–10 minutes, lasts <30 minutes.
76
What bedside test is used to diagnose dermographism?
FricTest or tongue blade (blunt object stroke).
77
What is first-line treatment for dermographism?
Non-sedating H1-antihistamines, up to 4× dose if needed.
78
What medications are used for refractory dermographism?
Omalizumab or montelukast.
79
What is the key trigger in cold urticaria?
Cold exposure.
80
What test is used to diagnose cold urticaria?
Ice cube test (wheal after rewarming).
81
What is the danger associated with cold immersion (e.g., swimming)?
Risk of systemic reactions including anaphylaxis.
82
What’s the pathophysiology of cold urticaria?
Cold triggers mast cell degranulation.
83
What are common systemic associations with cold urticaria?
Cryoglobulinemia, hepatitis, lupus, lymphoproliferative disorders.
84
First-line treatment for cold urticaria?
Avoidance of cold + H1-antihistamines.
85
What should be prescribed if systemic reactions are present?
Epinephrine auto-injector.
86
What triggers cholinergic urticaria?
Increase in core body temperature (sweating, exercise, hot showers, stress).
87
What type of wheals appear in cholinergic urticaria?
Pinpoint (1–3 mm) wheals with surrounding erythema.
88
What test is used to diagnose cholinergic urticaria?
Exercise challenge or passive heating.
89
Who is most commonly affected by cholinergic urticaria?
Young males (15–30 years).
90
What neurotransmitter is involved in cholinergic urticaria?
Acetylcholine.
91
What is the first-line treatment for cholinergic urticaria?
H1-antihistamines (regular + pre-exposure dosing).
92
What are adjunct treatments for refractory cholinergic urticaria?
Omalizumab, propranolol, anticholinergics.
93
What triggers heat urticaria?
Direct localized heat.
94
How quickly does heat urticaria appear and resolve?
Within minutes, resolves in <1 hour.
95
What is the bedside test for heat urticaria?
Apply warm stimulus (e.g., metal rod at 44°C for 5 min).
96
What is the underlying mechanism of heat urticaria?
Immediate hypersensitivity with mast cell degranulation.
97
First-line treatment for heat urticaria?
H1-antihistamines + heat avoidance.
98
What triggers delayed pressure urticaria?
Sustained pressure (e.g., belts, straps).
99
When do lesions appear in delayed pressure urticaria?
4–8 hours after pressure.
100
How long do lesions last in delayed pressure urticaria?
More than 24 hours.
101
What is the bedside test for delayed pressure urticaria?
Sandbag or pressure test for 10–15 minutes.
102
First-line therapy for delayed pressure urticaria?
H1-antihistamines (limited efficacy), montelukast, omalizumab.
103
What triggers solar urticaria?
Exposure to UV/visible light.
104
What test is used to confirm solar urticaria?
Phototesting (UVA, UVB, visible light).
105
When do lesions develop after light exposure?
Within minutes; resolve in <1 hour.
106
What is the pathophysiology of solar urticaria?
Light induces photoreactive compound → Type I hypersensitivity.
107
What are potential systemic signs of solar urticaria?
Hypotension in extensive cases.
108
First-line treatment for solar urticaria?
Sun protection + H1-antihistamines.
109
What can be used for severe solar urticaria?
Phototherapy, omalizumab, cyclosporine.
110
What triggers vibratory angioedema?
Vibration (e.g., towel drying, clapping).
111
How does vibratory angioedema present?
Localized angioedema within minutes, resolves in <1–2 hrs.
112
What is the bedside test for vibratory angioedema?
Lab shaker (vibratory challenge).
113
What is the inheritance pattern of familial vibratory angioedema?
Autosomal dominant.
114
What are treatment options for vibratory angioedema?
H1-antihistamines, montelukast, omalizumab in rare cases.
115
Causes of acute urticaria
116
causes of chronic urticaria
