Urticaria Flashcards
(38 cards)
1
Q
What is urticaria?
A
Urticaria is a disease characterised by the development of wheals (also known as hives), angioedema or both.
2
Q
What gender is more likely to get angioedema?
A
Women
3
Q
What % of the population get urticaria?
A
20%
4
Q
What are the 3 features of wheels?
A
- Pink or white raised areas of skin of variable size that resemble nettle stings
- They are usually itchy
- They have a fleeting nature with the skin returning to its normal appearance within 24 hours although the condition itself may last longer
5
Q
What takes longer to resolve: angioedema or urticaria?
A
Angiooedema - it can take up to 72 hours to resolve.
6
Q
What % of patients with urticaria will also get angioedema?
A
30%
7
Q
What is the pathophysiology of urticaria?
A
- Degranulation of mast cell -> histamine & platelet activating factor release. -> Pruritus and vasodilation and increased permeability (leakiness) of blood vessels causing swelling and redness of the skin.
- Cutaneous nerves stimulation may release neuropeptides, either directly onto the blood vessel or via the mast cell, which can generate the wheal and flare urticated response.
8
Q
Describe the Triple Response of Lewis.
A
- Red spot: due to capillary dilatation
- Flare: redness in the surrounding area due to arteriolar dilatation mediated by axon reflex
- Wheal: due to exudation of fluid from capillaries and venules
9
Q
What are the 3 types of Urticaria?
A
- Acute spontaneous urticaria (ASU) < 6 weeks.
- Chronic spontaneous urticaria (CSU) > 6 weeks.
- Physical Urticaria
10
Q
Aprt form length of time, what is the difference between ASU and CSU?
A
ASU usually has a trigger - Drugs, Antibiotics or Food.
CSU usually has no trigger.
11
Q
What physical reactions occur in ASU and CSU?
A
Spontaneous wheels +/- angioedema.
12
Q
In what age group does CSU occur in?
A
20-30 years.
13
Q
What test can you do in ASU (acute spontaneous urticaria)?
A
RAST test or a Skin Prick Test
14
Q
What are subtypes of physical urticaria?
A
- Dermographism
- Delayed Pressure urticaria
- Cholinergic urticaria
- Cold induced urticaria
- Solar urticaria
- Aquagenic urticaria
15
Q
What is the main management for physical urticaria?
A
Avoid the physical trigger
16
Q
Tell me about Dermographism
A
- 10% of population have it.
- Wheal lasts 30-60 mins.
- Symptomatic dermographism/factitious urticaria - severe cases of dermographism.
17
Q
Tell me about delayed pressure urticaria
A
- Due to prolonged pressure to the skin.
- Clapping - causes the hands to swell
- Prolonged kissing - lips can swell.
*
18
Q
Describe cholinergic urticaria.
A
- Micropapular urticaria that occursover the body after sweating.
- Not actually caused by acetylcholine but by neuropeptides released from nerve endings.
19
Q
Describe cold urticaria
A
- Urticarial response after cold response.
- To diagnose:
- Put ice cube on skin
- The urticarial response will occur on Re-Warming the skin.
20
Q
Describe solar urticaria
A
- Very rare
- Needs to be differentiated from polymorphic light eruption.
- Response is immediate.
- Light form the sun causes antigenic changes to proteins which mast cells then respond to by releasing histamine.
21
Q
Describe Contact Urticaria
A
- Very common
- Usually due to contact with a foreign agent.
22
Q
Describe the history taking
A
- Ask about the history of urticaria - where on the body, how long.
- Dietary history and correlation with food
- Medication history
- Allergy
- FH of atopy and urticaria
- Any concomitant medical history (e.g. bullous pemphigoid, SLE etc)
- Determine if angioedema+/- bronchospasm
- Recent infection or foreign travel.
23
Q
In urticaria, what investigations should be done?
A
- Often no further invetigation is needed.
- Allergy avoidance
- RAST test or prick test can be organised.
- If CSU - no investigations are needed.
24
Q
What conditions can mimic Chronic Spontaneous Urticaria (CSU)?
A
- SLE and other connective tissue diseases
- Bullous Pemphigoid and other immuno-bullous disorders
- Atopic eczema / pompholyx
- Thyroid dysfunction
- Contact dermatitis
- H.pylori gastritis
- Toxic erythema (especially drug reactions)
- Erythema multiforme
- Viral exanthema such as measles
25
**Describe the Urticaria Activity Score (UAS)**
26
What is the **treatment** for **Urticaria**?
* **Antihistamines**
* **1st line** - Cetirizine, Loratidine and Fexofenadine
* **2nd line** - Increase up to **4 times** the recommended dose.
* Use **antihistamines continously** at a **low dose** rather than PRN.
* Can take 4 weeks to work.
* Reduce doses every 3-6 months.
* **Steroids**
* Short courses of 20-50mg/day for 7-10 days.
* **Monteleukast** - **3rd line**.
* Further therapy:
* Ciclosporin - moderate direct effect on mast cells. Effective when used in combination with 2nd generation antihistamines.
* **Omalizumab** - 400mg every 4 weeks - useful if antihistamines aren't working.
* **Dapsone** and **H2**-**recetpor antagonists** (e.g. ranitidine) - low evidence - consider as **3rd line**.
27
Describe the **_hereditary_ causes** of **angioedema without urticaria**
* **C1-Esterase Inhibitor** **Deficiency** - **_C1-INH-HAE_**.
* **Normal** **C1**-**Esterase Inhibitor**
* **FXII mutation** = Hereditary angioedema w FXII mutations - **_FXII-HAE._**
* **Uknown cause** - Hereditary Angioedema of unknown origin - **_U-HAE_.**
28
Describe the causes of **Acquired Angioedema** without wheals.
* **No cause** identified
* **Idiopathic histaminergic - _IH-AAE._-** Response to antihistamines -
* **Idiopathic non-histaminergic - _InH-AAE_ -** No response to antihistamines -
* **Acquired angioedema related to ACE-I - _ACEI-AAE_**. - Caused by ACE-I Treatment.
* **Acquired angioedema with C1-INH deficiency** - **_C1-INH-AAE_**. - C1-INH Deficiency with no family history.
29
What is the most common cause of Hereditary angioedema?
**Defect** with the enzyme **C1 esterase** inhibitor (C1-INH)
* Usually a family history.
* Can also develop stomach cramps - due to angioedema of the guts
30
What is the invetigation for hereditary angioedema (HAE)?
* Measure C1-INH levels and function.
* C4 levels are also usually low.
31
What is the difference between **Type 1 and Type 2 Hereditary angioedema** (**HAE**)?
* **Type** 1 **disease** - low levels of C1-INH.
* **Type 2** **disease** - poorly functioning.
(Note: Some patients will have a defect in the Factor XII gene)
32
What is the treatment for **Hereditary Angioedema** (**HAE**)?
* **Emergency setting**
* **Adrenaline** and resuscitation.
* **Fresh frozen plasma** or **C1 esterase inhibitor concrete**.
* Many patients will have their own **concrete** in their fridge for emergency situations.
* **Long term management**
* Need a **Medic** Alert **Bracelet**.
* Close access to C1 Esterase Inhibitor **Concrete**.
* **Anabolic** steroids - Danazol or **Stanozol**.
33
What is urticarial vasculitis?
* Urticated **rash** with **wheals**, **flare** and **itching**.
* Lesions last **\>24 hours**.
* They may resolve with **purpura** or **bruising**.
* **Systemic** **symptoms**: joint pain, fever, abdominal pain and photosensitivity.
* **Associated** with **Connective Tissue Disease**.
34
How is urticarial vasculitis classified?
* **Normocomplementaemic**
* **Hypocomplementaemic** - Connective Tissue Disease and Systemic Symptolms are most common in this.
35
How is the diagnosis of urticarial vasculitis made?
With a skin biopsy.
36
What is the treatment for urticarial vasculitis?
* **Anti-histamines**
* **NSAIDs**
* **Recalcitrant disease** - Dapsone, Colchicine, Hydroxychloroquine or a course of oral steroids.
37
What is a mastocytoma?
* A congregation of small individual lesions of **mastocytes**.
* They **urticate** on **rubbing** (**Darier's sign**)
* Usually occur in **children**.
* **No** pathological **significance**.
38
What is Urticaria pigmentosa?
* **Widespread** reddish **brown macules**
* Urticate on **rubbing** (**Darier’s sign**).
* **Gradually resolve** with time but will leave areas of **hyperpigmentation**
* Treatment: **antihistamines** and sometimes **PUVA**. **Ketotifen** is **sometimes** used.
