Dermatology

Question 1

Define atopic dermatitis e.g eczema

Answer 1

Eczema is a chronic inflammatory disorder of the skin characterised by dermal inflammation (dermatitis) with resultant spongiotic change in the epidermis histologically, with chronic features including epidermal acanthosis, hyperkeratosis, and parakeratosis.

Question 2

What is the epidemiology for eczema/atopic dermatitis?

Answer 2

Atopic dermatitis is one of the most common skin disorders globally, affecting people of all ages.
Childhood onset is common, with up to 20% of children affected.
Prevalence decreases with age, but adult-onset cases can occur.
A family history of atopy (e.g. asthma, allergic rhinitis) is a significant risk factor.
Urbanisation and industrialisation are associated with a higher prevalence

Question 3

What would a histology show in eczema/ atopic dermatitis?

Answer 3

Epidermal acanthosis: thickening of the epidermis due to hyperplasia.
Hyperkeratosis: thickening specifically of the stratum corneum.
Parakeratosis: retained nuclei in the stratum corneum indicating problems with the usual differentiation process.

Question 4

What type of immune mediated response is eczema?

Answer 4

In many cases, atopic dermatitis is associated with an IgE-mediated allergic response to environmental allergens. Sensitisation to allergens such as house dust mites, pet dander, pollen, and certain foods can lead to the production of specific IgE antibodies. Upon re-exposure to these allergens, IgE-mediated immune responses are triggered, resulting in skin inflammation and pruritus. This plays a significant role in exacerbations of atopic dermatitis.

Question 5

What is the pathophysiology of eczema?

Answer 5

Dermatitis triggers the disease process. The normal dermis has a small amount of lymphocytes and other immune cells but in skin with eczema there is a vast infiltrate visible.
Keratinocytes in the epidermis start detaching from one another, becoming rounder and the intercellular spaces widening between them. If the eczema has come on acutely, this separation may be so severe that vesicles form. Under the microscope, this makes the epidermis look like a sponge, hence ‘spongiotic’ change.

Question 6

Wha are the classifications of eczema?

Answer 6

Atopic eczema
Allergic contact dermatitis (see separate section on contact dermatitis)
Irritant contact dermatitis (see separate section on contact dermatitis)
Seborrheic dermatitis
Venous eczema (stasis dermatitis)
Asteatotic dermatitis (eczema craquele)
Erythrodermic eczema
Pompholyx eczema

Question 7

What is contact dermatitis:

Answer 7

Contact dermatitis is a skin condition marked by inflammation of the skin, resulting from direct contact with substances that irritate the skin (irritant contact dermatitis) or provoke an allergic response (allergic contact dermatitis). It is one of the most common dermatological conditions encountered in clinical practice.

Question 8

Define irritant contact dermatitis:

Answer 8

Occurs when the skin’s natural barrier is disrupted by exposure to irritating substances, such as harsh chemicals, detergents, or solvents. This results in direct damage to the skin’s cells and inflammation.

Question 9

Define allergic contact dermatitis:

Answer 9

This is a delayed type IV hypersensitivity reaction. Exposure to an allergen (often a low-molecular-weight chemical) sensitizes the immune system over time. Upon re-exposure (e.g. after repeated hair dyes), an immune response is triggered, leading to inflammation and the characteristic skin rash.

Question 10

Signs and symptoms of irritant contact dermatitis:

Answer 10

Eczema due to contact with an irritant. There may be burning, pain, and stinging. Eczematous rash appears localised to the direct area of contact
Anyone may develop this, but at higher risk of skin barrier is compromised from pre-existing skin disease (e.g. atopic eczema)
The response can be quick if the irritant is strong, or develop slowly over a much more prolonged time frame if the irritant is less potent/low level repeated exposure.
It is often associated with occupations that may be handling irritating materials, such as hairdressers, health care staff, builders, and cleaners.
Common irritants are detergents and bleach.
The hand is the site that is commonly affected.

Question 11

Signs and symptoms of allergic contact dermatitis:

Answer 11

Presents as an itchy, eczematous rash (vesicles, fissures, erythema), typically 24-48 hours after exposure. The rash may extend beyond the boundaries of immediate contact.
This is unlike irritant contact dermatitis, where the skin changes are localised directly to the area of exposure.
The patient is sensitised to the allergen over time, so they may have never had a problem in the past with the material until their presentation.
Typical allergens are nickel (found in jewellery/watches/metal buttons on clothing), acrylates (in nail cosmetics), fragrance, rubber/plastics, hair dye, and henna (paraphenylenediamine)

Question 12

What is the investigation for contact dermatitis:

Answer 12

Contact dermatitis is a clinical diagnosis and investigations aren’t always needed. However, investigations may include:
Patch Testing: used to identify allergens responsible for allergic contact dermatitis.
Skin Biopsy: rarely necessary, but it can help confirm the diagnosis or rule out other conditions.

Question 13

What is the management for contact dermatitis?

Answer 13

If a causative agent has been identified, avoidance is the single most effective treatment, with 8-12 weeks of avoidancy required before improvements may be seen.
Aspects of management include:
Liberal emollient and soap substitutes use to maintain skin hydration and improve barrier repair
Topical steroids may be required to control symptoms — choice of topical corticosteroid depends on the severity, location and extent of dermatitis.
Oral antihistamines for pruiritus relief
In cases of occupational dermatitis, workplace modifications and protective measures may be necessary. For example, if it is impossible to avoid contact with the stimulus, use of gloves, and immediately rinsing with water or washing with soap/soap substitute as soon as possible after contact may help

Question 14

When do you consider referral to dermatology with contact dermatitis?

Answer 14

Dermatitis is severe, chronic, recurring or persistent
Previously stable dermatitis has become difficult or impossible to control with standard treatments
Allergy to prescribed or over-the-counter topical treatments is suspected
Suspected contact dermatitis does not respond to treatment in primary care, has atypical features or the diagnosis is unclear.
Contact dermatitis is thought to be associated with occupation

Question 15

What are the clinical features of atopic eczema?

Answer 15

Childhood predominance: symptoms tend to become less severe with age.
Typically manifests before two years of age
Associated with atopic phenotype: asthma, hayfever, raised eosinophils.
In infants, the face is a common site. In older children/adults, the antecubital fossa and posterior knee (flexor surfaces) are affected.
The skin is itchy, erythematous, and oozing. There may be vesicles, which may have crusted over.
Eventually, the skin becomes dry and flaky. Repeated scratching causes lichenification (thick, leathery skin, also called lichen simplex et chronicus.)

Question 16

Features of Erythrodermic eczema?

Answer 16

This is a dermatological emergency and may complicate atopic eczema.
It is syndrome characterised by widespread redness (>90%)
There is often skin exfoliation too, which leads to exfoliative dermatitis.

Question 17

Features of seborrhoeic dermatitis?

Answer 17

This common condition is thought to happen due to Malassezia Furfur, a commensal organism on the skin. A predisposed individual due to genetic and environmental factors may develop an inflammatory response to the organism.
The skin is flakey with a fine scale, oily, and erythematous. There is usually minimal pain or stinging or itch.
The scale may coalesce into thicker plaques.
It tends to affect the face (especially hairline, nasolabial fold, and brow area) in adults.
Risk factors for the development include:
Family history
Oily skin
Immunosuppression (such as HIV)
Neurological and psychiatric diseases (such as Parkinson’s Disease or Depression)
Stress
Dandruff is the common term used to describe a mild, non-inflamed form of seborrheic dermatitis
Managed with anti-fungal agents, such as ketoconazole shampoo.
Infantile seborrheic dermatitis (cradle cap) is asymptomatic. It appears as a diffuse, yellow, greasy scale, coalescing into plaaues on the scalp/groin/armpit. Emollients (such as olive oil) loosen the scales, which can then be brushed off. Antifungal shampoos may be used if the issue persists.

Question 18

Features of statis dermatitis:

Answer 18

Also known as venous eczema.
This is eczema associated with chronic venous insufficiency (venous hypertension), usually affecting the gaiter area.
There may be associated skin changes therefore, including: venous ulcers, lipodermatosclerosis, and hemasiderosis.

Question 19

What are the investigations for atopic dermatitis/ eczema?

Answer 19

Eczema is a clinical diagnosis and investigations aren’t always needed. However, investigations may include:
Tests prior to commencing systemic treatments with traditional DMARDs or biologics.
Bloods:
If concerns regarding superadded infection.
Total IgE and raised eosinophils may confirm atopic phenotype.
Patients with atopic eczema often have concerns about ‘allergies’ as triggers (i.e. Type 1 mediated immune reactions) The relationship between eczema and allergy is complicated, and it is not thought that eczema is a direct manifestation of a Type 1 allergic process. However, allergies are common amongst patients with eczema, especially atopic eczema. Therefore, it is often sensible to perform testing if it is a subject of genuine concern. This can be in the form of RAST IgE or skin-prick testing. These have a high sensitivity but low specificity, and as such if negative are useful, but if positive do not necessarily indicate allergy.
Patch test: The allergen is applied to the skin under occlusion for 48 hours to confirm a delayed (type IV) allergic process implicated in allergic contact dermatitis.
Swabs: bacterial and viral swabs if concerns regarding superadded infection.
Skin biopsy: if the diagnosis is uncertain, especially with erythrodermic presentations.

Question 20

What are the different severities of eczema?

Answer 20

Mild - areas of dry skin, and infrequent itching (with or without small areas of redness)

Moderate - areas of dry skin, frequent itching, and erythema (with or without excoriation and localized skin thickening)

Severe - widespread areas of dry skin, incessant itching, and erythema (with/without excoriation, extensive skin thickening, bleeding, oozing, cracking, and alteration of pigmentation)

Infected - if eczema is weeping, crusted, or there are pustules, with fever or malaise

Question 21

What are the conservative measurements for eczema?

Answer 21

Avoid triggers: soaps, perfumes, biological detergents, or synthetic fabrics. Replace these where possible (soap substitutes, non biological detergents, natural fabrics e.g. cotton.)
Avoid allergens.
Keep the area cool and dry.
Sedating antihistamine can reduce itching and aid sleep.
Liberal emollients should be applied frequently.
Psychological support may be needed.

Question 22

What is the topical treatment for mild eczema?

Answer 22

liberal emollient usage + mild topical corticosteroid (such as hydrocortisone 1%) for areas of red skin.

Question 23

What is the topical treatment for moderate eczema?

Answer 23

liberal emollient usage + moderate topical corticosteroid (such as clobetasone butyrate 0.5% - Eumovate) for 5 days. Hydrocortisone 1% should be used for the face and flexures. Consider prescribing maintenance topical corticosteroids to control areas of skin prone to frequent flares.

Question 24

What is the topical treatment for severe eczema?

Answer 24

liberal emollient usage + potent topical corticosteroid (for example betamethasone valerate 0.1% - Betnovate) to be used on inflamed areas. For the face and flexures, use a moderate potency corticosteroid (such as Eumovate).

If there is severe, extensive eczema causing psychological distress, consider prescribing a short course of an oral corticosteroid (refer children under 16 years of age).
Topical calcineurin inhibitors (e.g. tacrolimus) - can be considered as a steroid sparing agent. These are second-line and should be prescribed by a specialist.

Question 25

Name some systemic therapies for eczema?

Answer 25

Oral steroids: if widespread and severe, e.g. erythroderma.

Systemic retinoids: such as alitretinoin may be used for hand eczema recalcitrant to topical therapies.

Traditional DMARDs:
Methotrexate: a dihydrofolate reductase inhibitor.
Ciclosporin: a calcineurin inhibitor.
Azathioprine: inibits purine synthesis.

Biologics: as per the NICE guidelines, reserved for patients with moderate to severe eczema not responding to at least 1 traditional systemic therapy:
Dupilumab: IL-4Rα inhibitor
Baricitinib: JAK inhibitor

Question 26

When do you refer to dermatology in eczema?

Answer 26

Eczema is severe and has not responded to optimum topical treatment after 1 week (urgent referral; within 2 weeks)
The diagnosis is, or has become, uncertain.
Current management has not controlled eczema satisfactorily (for example the person is having one to two flares per month), or the person is reacting adversely to many emollients.
Facial eczema that is treatment-resistent.
Contact allergic dermatitis is suspected

Question 27

What are the complications of eczema?

Answer 27

Scratching:
Poor sleep - sedating antihistamines (e.g. chlorphenamine) can be prescribed to aid sleep
Poor mood
Skin breakdown: bacterial infection (take a swab - usually Staphylococcal or Streptococcal), scarring, and post inflammatory hyper/hypopigmentation. -Skin thickening (lichenification) with chronic scratching.
Psycho-social:
Insecurities surrounding skin appearance, especially if there are scars/pigment changes/lichenified skin, or changes from long term steroid use.
Normal daily activities may be disrupted due to skin condition e.g. avoiding swimming.
Poor mood and poor sleep from itch.

Question 28

Explain eczema herpeticum? Diagnosis and management

Answer 28

A dermatological emergency.
This is a disseminated herpes simplex virus in a patient with eczema, usually atopic eczema, and normally occurs when the patient is first infected with HSV.
Vesicles and punched out erosions where the vesicles have deroofed will appear, and may affect large areas of skin, including sites that are apparently not currently eczematous.
There may be multi organ involvement, and the patient is unwell.
Admission is required for intravenous antiviral therapy (aciclovir.) Often given concomitantly with antibiotics as concomitant bacterial infection is common and difficult to exclude clinically.
Diagnosis can be confirmed with a swab & Tzanck test.

Question 29

Define cellulitis:

Answer 29

Cellulitis is a bacterial soft tissue infection of the dermis and subcutaneous tissue.

Question 30

What is the pathophysiology of cellulitis:

Answer 30

The pathophysiology of cellulitis involves bacterial entry through breaks in the skin’s barrier, leading to infection and inflammation. The bacteria multiply in the subcutaneous tissue, triggering an immune response, which results in the characteristic signs and symptoms of cellulitis.

The most common offending organisms are Streptococcus pyogenes or Group A beta-haemolytic streptococci (i.e. Streptococci, these strains are also associated with more severe infection), followed by Staphylococcus aureus.

Question 31

What are the risk factors for cellulitis:

Answer 31

Breaks in the skin, such as cuts, abrasions, insect bites, or surgical wounds
Chronic conditions that compromise skin integrity - venous insufficiency or lymphedema, pressure sores, ulcers, recent trauma
Obesity
Diabetes
Immunosuppression
Intravenous drug use
Recent history of cellulitis

Question 32

What are the clinical features of cellulitis:

Answer 32

Erythema
Calor (heat)
Swelling
Pain
Poorly demarcated margins
Systemic upset: fever, malaise
Lymphadenopathy
Rarely blisters and pustules (severe disease)
Often evidence of breach of skin barrier e.g. trauma, ulcer etc.

Question 33

What is classification system is used to categorise cellulitis severity and guide treatment decisions:

Answer 33

Eron classification system

Question 34

What are the different classifications under the Eron system?

Answer 34

Class I — there are no signs of systemic toxicity and the person has no uncontrolled comorbidities.
Class II — the person is either systemically unwell or systemically well but with a comorbidity (for example peripheral arterial disease, chronic venous insufficiency, or morbid obesity) which may complicate or delay resolution of infection.
Class III — the person has significant systemic upset, such as acute confusion, tachycardia, tachypnoea, hypotension, or unstable comorbidities that may interfere with a response to treatment, or a limb-threatening infection due to vascular compromize.
Class IV — the person has sepsis or a severe life-threatening infection, such as necrotizing fasciitis.

Question 35

What are the investigations for cellulitis:

Answer 35

Cellulitis can usually be diagnosed and treated clinically, however investigations when patients are systemical unwell include:
Blood tests - FBC (high WCC), CRP, U+E (may be AKI if severe infection), blood cultures
Wound swab if there is an open wound, penetrating injury, drainage, or an obvious portal for microbial entry, exposure to water borne-organisms, an infection acquired outside the UK or in severe cellulitis
Ultrasound scan - for distinguishing nonpurulent cellulitis from cellulitis with underlying abscess and for identifying drainable fluid collection

Question 36

What are the indications for admission with cellulitis?

Answer 36

Class III - Class IV cellulitis
Rapidly deteriorating cellulitis
Under 1 year of age or frail
Immunosuppression
Significant lymphoedema
Facial cellulitis (unless very mild)
Suspected orbital or periorbital cellulitis (admit to ophthalmology)
Class II cellulitis (systemically unwell or systemically well but with a comorbidity)

Question 37

What are the general requirements for treatment of cellulitis?

Answer 37

Mark the area of erythema to aid in detection of rapidly spreading cellulitis, and to monitor treatment response
Elevate if possible
Review if wound debridement is required

Question 38

What is the treatment of cellulitis according to eron classification?

Answer 38

Class I - high-dose oral flucloxacillin (clarithromycin/doxycyline if penicillin allergic and erythomycin if pregnant)
Class II - admit systemically unwell patients or those systemically well but with a comorbidity. May be able to ambulate with IV antibiotics.
Class III-IV - admit for IV antibiotics

Question 39

What are the complications of cellulitis?

Answer 39

Abscess formation
Lymphangitis (infection of lymphatic vessels)
Systemic spread of infection (sepsis)
Recurrence of cellulitis
Chronic or recurrent lymphedema
Scarring and changes in skin texture

Question 40

Define pressure sores?

Answer 40

Pressure sores are localised areas of tissue damage caused by prolonged pressure or friction, typically occurring over bony prominences. They can range from superficial skin damage to deep tissue injury and are often associated with immobility and prolonged pressure on specific body areas.

Question 41

Name risk factors for pressure sores?

Answer 41

Immobility and reduced ability to change positions
Prolonged pressure on specific body areas (e.g., bedridden or wheelchair-bound individuals)
Poor nutrition and hydration
Advanced age
Chronic illnesses and those which impair healing (e.g. diabetes, peripheral vascular disease)
Incontinence
Reduced sensory perception

Question 42

What is the pathophysiology of pressure sores?

Answer 42

Pressure and Tissue Ischemia: Continuous pressure or friction reduces blood flow to affected areas, leading to tissue ischemia (lack of oxygen and nutrients).
Cellular Damage: Lack of oxygen and nutrients causes cellular damage, primarily affecting skin and underlying tissues.
Inflammation: Injured tissues trigger an inflammatory response, which can further exacerbate tissue damage.
Necrosis and Ulceration: Severe tissue damage may lead to tissue necrosis, ultimately resulting in an open wound or ulcer.

Question 43

What are the signs and symptoms of pressure sores?

Answer 43

Skin changes, ranging from redness to skin breakdown and ulceration.
Pain or discomfort at the affected site.
Warmth or coolness over the affected area.
Swelling or induration (hardening) of the surrounding tissue.
Open sores or wounds with varying degrees of tissue involvement (stages I to IV - see below)
Stage 1 - non-blanching
Stage 2 - partial thickness
Stage 3 - full thickness skin loss
Stage 4 - full thickness tissue loss
Unstageable: full thickness skin or tissue loss

Question 44

What are the investigations for pressure sores?

Answer 44

Pressure sores are diagnosed clinically in correlation to their appearance, however additional investigations which may form part of their management include:
Imaging studies (e.g. X-rays, MRI) to assess underlying tissue involvement
Blood tests (e.g. full blood count, serum albumin) to assess overall health and nutritional status
Wounds should only be swabbed if infection is suspected

Question 45

What is the management for pressure sores?

Answer 45

Pressure Relief: Minimising pressure on affected areas through repositioning, specialised mattresses, and cushions.

Wound Care: Appropriate wound cleaning, debridement, and dressing changes. Regular review of wounds to monitor any changes in size and appearance.

Nutritional Support: Ensuring adequate nutrition and hydration, addressing deficiencies.

Pain Management: Managing pain associated with pressure sores.
Infection Control: Preventing and treating wound infections.

Surgical Interventions: In some cases, surgical procedures (e.g. flap reconstruction) may be necessary.

MRI is the imaging modality of choice to assess for complications such as osteomyelitis or abscesses in the context of a stage 4 pressure ulcer with systemic symptoms.

Question 46

What are the potential complications of pressure sores?

Answer 46

Potential complications of pressure sores include:
Infection of the wound
Cellulitis or abscess formation
Osteomyelitis (bone infection)
Sepsis
Delayed wound healing
Scarring or tissue contractures
Effective management and prevention strategies are crucial to reducing complications associated with pressure sores

Question 47

Which scoring system is used to screen patients at risk of developing a pressure ulcer?

Answer 47

Waterlow Score

Question 48

Define psoriasis:

Answer 48

Psoriasis is a chronic autoimmune disease characterised by well-demarcated, erythematous, scaly plaques.

Question 49

What are the 5 types of psoriasis?

Answer 49

Chronic plaque psoriasis- this is the commonest type and causes symmetrical plaques on the extensor surfaces of the limbs (knees + elbows), scalp and lower back.
Flexural (inverse) psoriasis- smooth, erythematous plaques without scale in flexures and skin folds.
Guttate psoriasis- multiple small, tear-drop shaped, erythematous plaques occur on the trunk after a Streptococcal infection in young adults.
Pustular psoriasis- multiple petechiae and pustules on the palms and soles.
Generalised/erythrodermic psoriasis- this is rare but serious form characterised by erythroderma and systemic illness.

Question 50

What are the risk factors for psoriasis?

Answer 50

Skin trauma (Koebner phenomenon)
Infection: Streptococcus, HIV
Drugs: B-blockers, Anti-malarials, Lithium, Indomethacin/NSAIDs (BALI)
Withdrawal of steroids
Stress
Alcohol + smoking
Cold/dry weather
Risk factors for developing psoriasis include family history, HIV infection, obesity and smoking.

Question 51

What are the clinical features of chronic plaque psoriasis?

Answer 51

Itchy, well-demarcated circular-to-oval bright red/pink elevated lesions (plaques) with overlying white or silvery scale, distributed symmetrically over extensor body surfaces and the scalp.
Nail changes
In many patients with psoriasis, nail changes are seen:
Nailbed pitting: superficial depressions in the nailbed
Onycholysis: separation of nail plate from nailbed
Subungual hyperkeratosis: thickening of the nailbed
Auspitz sign: the appearance of punctate bleeding spots when psoriasis scales are scraped off

Question 52

What is the underlying management for psoriasis?

Answer 52

Chronic plaque psoriasis is characterised by inflammation (resulting in redness) and hyperproliferation of keratinocytes (resulting in scale). The treatment of plaque psoriasis targets this pathology- corticosteroids reduce inflammation and vitamin D reduces keratinocyte proliferation. Flexural psoriasis is less scaly and so is treated solely with a topical corticosteroid.

Question 53

What is the topical treatment for psoriasis?

Answer 53

All patients should use an emollient to reduce scale and itch
1st: potent topical corticosteroid OD (eg Betnovate) + topical vitamin D OD (eg Dovonex) applied at different times
2nd: stop the topical corticosteroid, apply topical vitamin D twice daily
3rd: stop the topical vitamin D, apply potent topical corticosteroid twice daily
Dithranol + tar are alternatives

Question 54

What phototherapy is used for psoriasis?

Answer 54

Narrowband UVB phototherapy
Psoralen + UVA (PUVA)

Question 55

What is the systematic treatment for psoriasis?

Answer 55

1st line: Methotrexate
2nd line: Ciclosporin (1st line if rapid disease control needed/palmoplantar pustulosis/are considering conception)
3rd line: Acitretin

Question 56

What are the biologics for psoriasis?

Answer 56

Infliximab
Etanercept
Adalimumab

Question 57

What are the complications of treatment in psoriasis?

Answer 57

Methotrexate can cause pneumonitis and hepatotoxicity (monitor LFTs). Additionally methotrexate may cause myelosuppression leading to pancytopenia (monitor FBCs)
Acitretin is teratogenic and can cause hepatotoxicity and elevated lipids
Anti-TNF biological drugs (such as adalimumab) are associated with reactivation of latent tuberculosis (always do CXR before initiation of treatment)

The side effects of ciclosporin can be remembered by the 5 H’s:
Hypertrophy of the gums, Hypertrichosis, Hypertension, Hyperkalaemia and Hyperglycaemia (diabetes)
As such U&Es, BP and fasting glucose should be monitored routinely

Question 58

Define urticaria/hives

Answer 58

Urticaria, commonly referred to as hives, is characterised by the rapid development of pruritic (itchy), erythematous (red), raised wheals that may vary in size and shape. These wheals typically resolve within hours to days and can occur anywhere on the body. Angio-oedema is a deeper form of urticaria with swelling in the dermis and submucosal or subcutaneous tissues.

Question 59

What are the risk factors for urticaria?

Answer 59

Allergens (e.g. foods, medications, insect stings)
Physical stimuli (e.g. pressure, cold, heat)
Infections (e.g. viral or bacterial)
Autoimmune processes
Stress and emotional factors
Genetics may play a role in predisposition

Question 60

Define urticaria?

Answer 60

The pathophysiology of urticaria involves the release of histamine and other mediators from mast cells and basophils, leading to increased vascular permeability and the formation of wheals. Both immune-mediated and non-immune mechanisms contribute to the development of urticaria.

Question 61

What are the common signs and symptoms for urticaria?

Answer 61

Pruritus (itching), often intense
Erythematous wheals with well-defined borders
Wheals that vary in size and shape
Rapid onset and resolution (usually within 24 hours)
Occasionally, angioedema (swelling of deeper tissues), which can involve the lips, eyelids, or extremities

Question 62

What are the investigations for urticaria?

Answer 62

Urticaria is a clinical diagnosis and a thorough history and examination should be done to identify any potential triggers, however, investigations which may aid this include:
Allergy testing (skin or patch testing) for suspected allergens
Blood tests to assess inflammatory markers and rule out underlying systemic diseases (FBC, LFTs, TFTs, ESR and CRP)
Urinalysis if suspected vasculitic cause
Skin biopsy in certain cases to confirm the diagnosis
Symptom diaries can also be helpful to establish the timing, potential triggers and duration of episodes. The severity of urticaria can be assessed using the Urticaria Activity Score (UAS7), where the patient records the severity of itching and the number of weals daily for 7 days (<7 indicates good disease control; >28 suggests severe disease).

Question 63

What are the complications of urticaria?

Answer 63

Complications of urticaria are generally related to angioedema and may include:
Respiratory compromise in severe cases of angioedema involving the upper airway.
Psychological distress and decreased quality of life due to chronic or recurrent symptoms.
Side effects from long-term medication use if required for chronic urticaria.

Question 64

What is the treatment for urticaria?

Answer 64

dentification and removal of triggers: If possible, identify and avoid triggers, such as allergens or physical stimuli. Mild urticaria that has a clear trigger is self-limiting and does not require any further treatment.
If the patient is taking a medication associated with chronic urticaria e.g. NSAIDs, they should try avoiding this for at least several weeks.
Pharmacological treatment:
First-line: Non-sedating antihistamines (e.g., cetirizine, loratadine; H2-receptor antagonists) are the primary treatment for urticaria, and can be given for up to 6 weeks for an acute episode, or longer (3-6 months before review) if it is anticipated symptoms will be recurrent or persistent
Second-line: If symptoms persist, higher doses of antihistamines or other medications like leukotriene receptor antagonists or omalizumab may be considered. If symptoms are severe, a short course of oral corticosteroid can be given e.g. 40mg prednisolone for 7 days, in addition to the above.
Symptomatic management includes antipruritic creams such as calamine lotion or topical menthol 1% in aqueous cream. If there is sleep disturbance, sedating antihistamines such as chlorphenamine can be given.

Question 65

When does NICE recommend referral to a dermatologist/immunologist if you have wheals

Answer 65

People with urticaria that is painful and persistent (suspect vasculitic urticaria)
People whose symptoms are not well controlled on antihistamine treatment. Secondary care treatment options include cyclosporine, omalizumab, mycophenolate mofetil, or tacrolimus
People with angio-oedema and no wheals that do not respond to first-line treatment
People with acute severe urticaria which is thought to be due to a food or latex allergy
People with forms of chronic inducible urticaria that may be difficult to manage in primary care, for example, solar or cold urticaria