Derm Flashcards
Q: What is Acanthosis nigricans?
A: Acanthosis nigricans describes symmetrical, brown, velvety plaques often found on the neck, axilla, and groin.
Q: What is acne vulgaris?
A: Acne vulgaris is a disease of the pilosebaceous unit characterized by multiple types of acne lesions commonly seen in each patient.
Q: What are the common causes of Acanthosis nigricans?
Type 2 diabetes mellitus
Gastrointestinal cancer
Obesity
Polycystic ovarian syndrome
Acromegaly
Cushing’s disease
Hypothyroidism
Familial
Prader-Willi syndrome
Drugs (e.g., combined oral contraceptive pill, nicotinic acid)
Q: What is the pathophysiology of Acanthosis nigricans?
A: The pathophysiology involves insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1).
Q: What causes comedones in acne vulgaris?
A: Comedones are caused by a dilated sebaceous follicle. A whitehead forms if the top is closed, while a blackhead forms if the top opens.
Q: How do inflammatory lesions develop in acne vulgaris?
A: Inflammatory lesions form when the follicle bursts, releasing irritants, leading to the development of papules and pustules.
Q: What severe complications can result from excessive inflammation in acne vulgaris?
A: Excessive inflammation can lead to nodules, cysts, and ultimately scarring, such as ice-pick scars and hypertrophic scars.
Q: How does drug-induced acne differ from typical acne vulgaris?
A: Drug-induced acne is often monomorphic, with pustules being characteristic, especially in steroid use.
Q: What is acne fulminans, and how is it managed?
A: Acne fulminans is a very severe form of acne associated with systemic symptoms like fever, often requiring hospital admission and typically responding to oral steroids.
Q: What is the pathophysiology of acne vulgaris?
A: Acne vulgaris occurs due to obstruction of pilosebaceous follicles with keratin plugs, leading to comedones, inflammation, and pustules.
Q: How is acne vulgaris classified?
Mild: Open and closed comedones with or without sparse inflammatory lesions.
Moderate: Widespread non-inflammatory lesions and numerous papules and pustules.
Severe: Extensive inflammatory lesions, nodules, pitting, and scarring.
Q: What is the first-line treatment for mild to moderate acne?
A 12-week course of topical combination therapy:
Topical adapalene + benzoyl peroxide
Topical tretinoin + clindamycin
Topical benzoyl peroxide + clindamycin
Topical benzoyl peroxide alone can be used if retinoids or antibiotics are contraindicated.
Q: What is the first-line treatment for moderate to severe acne?
A 12-week course of:
Topical adapalene + benzoyl peroxide + oral lymecycline or doxycycline
Topical azelaic acid + oral lymecycline or doxycycline
Q: What important considerations apply to oral antibiotics in acne treatment?
Avoid tetracyclines in pregnancy, breastfeeding, and children under 12 years.
Minocycline is less preferred due to irreversible pigmentation risk.
Do not use oral antibiotics for more than 6 months except in exceptional cases.
Always co-prescribe a topical retinoid or benzoyl peroxide with oral antibiotics to reduce resistance.
Q: When are combined oral contraceptives (COCPs) used for acne management?
A: COCPs can be an alternative to oral antibiotics in women but should be combined with topical agents. Dianette (co-cyprindiol) may be used second-line due to increased VTE risk and should be limited to 3 months with proper counseling.
Q: When is oral isotretinoin used for acne?
A: Oral isotretinoin is only prescribed under specialist supervision, with pregnancy being a contraindication.
Q: What treatments should be avoided to reduce antibiotic resistance in acne?
Monotherapy with a topical antibiotic
Monotherapy with an oral antibiotic
Combination of a topical and an oral antibiotic
Q: What are the NICE referral criteria for acne?
Refer to a dermatologist if:
Acne conglobata (severe inflammatory nodules and cysts)
Nodulo-cystic acne
Consider referral if:
Mild to moderate acne unresponsive to two treatments
Moderate to severe acne unresponsive to oral antibiotics
Acne with scarring or persistent pigment changes
Acne causing psychological distress
Q: What is acne vulgaris?
A: Acne vulgaris is a common skin disorder affecting the face, neck, and upper trunk, characterized by obstruction of pilosebaceous follicles with keratin plugs, leading to comedones, inflammation, and pustules.
Q: What are the key components of acne vulgaris pathophysiology?
Follicular epidermal hyperproliferation forming a keratin plug that obstructs the pilosebaceous follicle.
Sebaceous gland activity, possibly influenced by androgens (though levels are often normal).
Colonization by Propionibacterium acnes (anaerobic bacterium).
Inflammation.
Q: What are actinic keratoses (AK)?
A: Actinic keratoses (AK) are common premalignant skin lesions caused by chronic sun exposure.
Q: What are the clinical features of actinic keratoses?
Small, crusty or scaly lesions
May be pink, red, brown, or the same color as the skin
Typically found on sun-exposed areas, e.g., temples of the head
Multiple lesions may be present
Q: What are the management options for actinic keratoses?
Prevention: Sun avoidance, sun cream
Fluorouracil cream: 2-3 week course, causing redness and inflammation (topical hydrocortisone may be used after)
Topical diclofenac: For mild AK, moderate efficacy with fewer side effects
Topical imiquimod: Effective based on trials
Cryotherapy
Curettage and cautery
Q: What is alopecia areata?
A: Alopecia areata is a presumed autoimmune condition causing localized, well-demarcated patches of hair loss, often with small, broken ‘exclamation mark’ hairs at the edge of the lesion.
Q: What are the treatment options for alopecia areata?
Topical or intralesional corticosteroids
Topical minoxidil
Phototherapy
Dithranol
Contact immunotherapy
Wigs
Q: What are antihistamines used for?
A: Antihistamines (H1 inhibitors) are used in the treatment of allergic rhinitis and urticaria.
Q: Which non-sedating antihistamine may cause more drowsiness?
A: Cetirizine has some evidence suggesting it may cause more drowsiness than other drugs in its class.
Q: What is athlete’s foot?
A: Athlete’s foot, also known as tinea pedis, is a fungal infection usually caused by fungi in the genus Trichophyton.
Q: What are the clinical features of athlete’s foot?
A: Scaling, flaking, and itching between the toes.
Q: What is the first-line treatment for athlete’s foot according to NICE?
A: Topical imidazole, undecenoate, or terbinafine.
Q: What is basal cell carcinoma (BCC)?
A: Basal cell carcinoma (BCC) is a slow-growing skin cancer, also known as a rodent ulcer, characterized by local invasion with extremely rare metastases. It is the most common cancer in the Western world.
Q: What are the typical features of nodular basal cell carcinoma?
Commonly occurs on sun-exposed sites, especially the head and neck.
Initially presents as a pearly, flesh-colored papule with telangiectasia.
May later ulcerate, forming a central “crater.”
Q: What is the recommended referral pathway for suspected BCC?
A: A routine referral should be made if BCC is suspected.
Q: What are the management options for basal cell carcinoma?
Surgical removal
Curettage
Cryotherapy
Topical creams (imiquimod, fluorouracil)
Radiotherapy
Q: What is Bowen’s disease?
A: Bowen’s disease is a precancerous dermatosis and a precursor to squamous cell carcinoma, with a 5-10% chance of developing invasive skin cancer if left untreated. It is more common in elderly patients.
Q: What are the typical features of Bowen’s disease?
Red, scaly patches
Often 10-15 mm in size
Slow-growing
Commonly found on sun-exposed areas like the head (e.g., temples), neck, and lower limbs
Q: What are the management options for Bowen’s disease?
May sometimes be managed in primary care if the diagnosis is clear or in case of a repeat episode
Topical 5-fluorouracil: Applied twice daily for 4 weeks, often causing significant inflammation/erythema (topical steroids are used to control this)
Cryotherapy
Excision
Q: What is bullous pemphigoid?
A: Bullous pemphigoid is an autoimmune condition causing sub-epidermal blistering of the skin, triggered by antibodies against hemidesmosomal proteins BP180 and BP230.
Q: Who is more commonly affected by bullous pemphigoid?
A: Bullous pemphigoid is more common in elderly patients.
Q: What are the key features of bullous pemphigoid?
Itchy, tense blisters typically around flexures
Blisters usually heal without scarring
Typically no mucosal involvement (e.g., the mouth is spared), though 10-50% of patients may have some mucosal involvement
Q: What is the skin biopsy finding in bullous pemphigoid?
A: Immunofluorescence shows IgG and C3 at the dermoepidermal junction.
Q: What is the management for bullous pemphigoid?
Referral to a dermatologist for biopsy and confirmation of diagnosis
Oral corticosteroids are the mainstay of treatment
Topical corticosteroids, immunosuppressants, and antibiotics may also be used
Q: What is the immediate first aid for burns caused by heat?
A: Remove the person from the source. Irrigate the burn with cool (not iced) water for 10-30 minutes within 20 minutes of injury. Cover the burn with layered cling film (not wrapped around a limb).
Q: What should be done for electrical burns?
A: Switch off the power supply and remove the person from the source.
Q: What is the first aid for chemical burns?
A: Brush off any powder and irrigate with water. Attempts to neutralize the chemical are not recommended.
Q: What are the methods for assessing the extent of a burn?
Wallace’s Rule of Nines: Head + neck = 9%, each arm = 9%, each anterior leg = 9%, etc.
Lund and Browder chart: Most accurate method.
Palmar surface: Roughly 1% of total body surface area (TBSA).
Q: How is the depth of a burn assessed?
Superficial epidermal (First degree): Red, painful, dry, no blisters
Partial thickness (superficial dermal, Second degree): Pale pink, painful, blistered
Partial thickness (deep dermal, Second degree): White with patches of erythema, reduced sensation
Full thickness (Third degree): White, brown, or black, no blisters, no pain
Q: What are the referral criteria for burns to secondary care?
Deep dermal and full-thickness burns
Superficial dermal burns >3% TBSA in adults or >2% in children
Burns involving the face, hands, feet, perineum, genitalia, or flexures
Any inhalation injury, electrical, or chemical burn
Suspected non-accidental injury
Q: What is the initial management for severe burns?
Assess the airway first, considering early intubation if necessary
IV fluids for children >10% TBSA and adults >15% TBSA (using the Parkland formula)
Urinary catheter insertion
Provide analgesia
Transfer to a burns unit if necessary
Q: What is the management of more severe burns?
Resuscitate and stop the burning process
Manage airway, including intubation if necessary
Administer IV fluids based on TBSA
Transfer to a burns unit for complex cases
Conservative management for superficial burns, excision, and grafting for more complex burns
Q: What is the pathology behind extensive burns?
Hemolysis due to heat damage and microangiopathy
Loss of capillary membrane integrity, causing plasma leakage into the interstitial space
Extravasation of fluids, leading to hypovolemic shock (up to 48 hours after injury)
Protein loss
Secondary infection (e.g., Staphylococcus aureus)
ARDS (Acute Respiratory Distress Syndrome)
Risk of Curling’s ulcer (acute peptic stress ulcers)
Danger of compartment syndrome in full-thickness circumferential burns
Q: How do superficial burns heal?
A: Keratinocytes migrate to form a new layer over the burn site.
Q: How do full-thickness burns heal?
A: Full-thickness burns result in dermal scarring and typically require skin grafts to provide optimal coverage.
Q: What are cherry haemangiomas (Campbell de Morgan spots)?
A: Benign skin lesions with an abnormal proliferation of capillaries, more common with advancing age, and equally affect men and women.
Q: What are the features of cherry haemangiomas?
Erythematous, papular lesions
Typically 1-3 mm in size
Non-blanching
Not found on mucous membranes
Q: Is treatment required for cherry haemangiomas?
A: No, as they are benign, treatment is usually not required.
Q: What is chronic plaque psoriasis?
A: The most common form of psoriasis, accounting for around 80% of presentations.
Q: What are the features of chronic plaque psoriasis?
Erythematous plaques covered with a silvery-white scale
Typically on extensor surfaces such as elbows and knees
Common on the scalp, trunk, buttocks, and periumbilical area
Clear delineation between normal and affected skin
Plaques range from 1 to 10 cm in size
Auspitz’s sign: red membrane with pinpoint bleeding points when the scale is removed
Q: What are the two main types of contact dermatitis?
A: 1. Irritant contact dermatitis: A non-allergic reaction caused by weak acids or alkalis (e.g., detergents). Commonly seen on the hands with erythema, but crusting and vesicles are rare.
2. Allergic contact dermatitis: A type IV hypersensitivity reaction, often seen on the head following hair dyes. Presents as acute weeping eczema affecting the margins of the hairline.
Q: What is a common cause of irritant contact dermatitis?
A: Cement, due to its alkaline nature.
Q: What can cause allergic contact dermatitis in cement workers?
A: The dichromates present in cement.
Q: What is dermatitis herpetiformis?
A: An autoimmune blistering skin disorder associated with coeliac disease, caused by deposition of IgA in the dermis.
Q: What percentage of patients with dermatitis herpetiformis exhibit findings of gluten-sensitive enteropathy?
A: More than 90% of patients.
Q: What are the typical features of dermatitis herpetiformis?
A: Itchy, vesicular skin lesions on extensor surfaces such as elbows, knees, and buttocks.
Q: How is dermatitis herpetiformis diagnosed?
A: Skin biopsy with direct immunofluorescence showing deposition of IgA in a granular pattern in the upper dermis.
Q: What is the management for dermatitis herpetiformis?
A: A gluten-free diet and dapsone.
Q: What are dermatofibromas?
A: Common benign fibrous skin lesions caused by the abnormal growth of dermal dendritic histiocyte cells, often following a precipitating injury.
Q: Where are dermatofibromas commonly located?
A: On the arms and legs.
Q: What are the typical features of dermatofibromas?
A: Solitary firm papule or nodule, typically 5-10mm in size, located on a limb. The overlying skin dimples when pinched.
Q: What is eczema herpeticum?
A: A severe primary skin infection caused by herpes simplex virus 1 or 2, often seen in children with atopic eczema.
Q: How does eczema herpeticum typically present?
A: As a rapidly progressing, painful rash with monomorphic punched-out erosions, usually 1-3 mm in diameter.
Q: What is the management for eczema herpeticum?
A: Children should be admitted for IV aciclovir as it is potentially life-threatening.
Q: What is erysipelas?
A: A localized skin infection caused by Streptococcus pyogenes, which is a more superficial and limited version of cellulitis.
Q: What is the treatment of choice for erysipelas?
A: Flucloxacillin.
Q: What causes erythema ab igne?
A: Erythema ab igne is caused by overexposure to infrared radiation, often from sitting next to an open fire.
Q: What are the characteristic features of erythema ab igne?
A: Reticulated, erythematous patches with hyperpigmentation and telangiectasia.
Q: What risk is associated with untreated erythema ab igne?
A: It can lead to the development of squamous cell skin cancer.
Q: What is erythema multiforme?
A: Erythema multiforme is a hypersensitivity reaction, commonly triggered by infections, that can be classified into minor and major forms.
Q: What are the key features of erythema multiforme?
A: Target lesions, initially appearing on the back of the hands/feet before spreading to the torso, with the upper limbs more commonly affected than the lower limbs. Mild pruritus may also be present.
Q: What are some common causes of erythema multiforme?
A: Viral infections (e.g., herpes simplex), Mycoplasma and Streptococcus bacteria, drugs (e.g., penicillin, sulphonamides), connective tissue diseases (e.g., systemic lupus erythematosus), sarcoidosis, and malignancy.
Q: What distinguishes erythema multiforme major from minor?
A: Erythema multiforme major is a more severe form that involves mucosal involvement.
Q: What is Orf?
A: Orf is a skin disease of sheep and goats caused by a parapox virus, which can trigger erythema multiforme.
Q: What is erythema nodosum?
A: Erythema nodosum is inflammation of subcutaneous fat, typically causing tender, erythematous, nodular lesions, usually on the shins, but can also occur on the forearms or thighs.
Q: How long do lesions in erythema nodosum take to resolve?
A: Lesions typically resolve within 6 weeks and heal without scarring.
Q: What are some common causes of erythema nodosum?
A: Infections (e.g., streptococci, tuberculosis, brucellosis), systemic diseases (e.g., sarcoidosis, inflammatory bowel disease, Behcet’s), malignancy/lymphoma, certain drugs (e.g., penicillins, sulphonamides, combined oral contraceptive pill), and pregnancy.
Q: What is erythrasma?
A: Erythrasma is an asymptomatic, flat, slightly scaly, pink or brown rash, typically found in the groin or axillae, caused by an overgrowth of Corynebacterium minutissimum.
Q: How can erythrasma be diagnosed?
A: Erythrasma can be diagnosed with Wood’s light examination, which reveals a coral-red fluorescence.
Q: What is the treatment for erythrasma?
A: Topical miconazole or antibacterial treatments are usually effective, and oral erythromycin may be used for more extensive infections.
Q: What is erythroderma?
A: Erythroderma is a condition in which more than 95% of the skin is involved in a rash of any kind.
Q: What are the causes of erythroderma?
A: Causes of erythroderma include eczema, psoriasis, drugs (e.g. gold), lymphomas, leukaemias, and idiopathic origins.
Q: What is erythrodermic psoriasis?
A: Erythrodermic psoriasis may result from chronic psoriasis progressing to an exfoliative phase with plaques covering most of the body. It can be triggered by factors such as the withdrawal of systemic steroids, requiring hospitalization for management.
Q: What is fungal nail infection (onychomycosis)?
A: Fungal nail infection (onychomycosis) involves any part of the nail or the entire nail unit, with toenails being more commonly affected than fingernails.
Q: What are the causative organisms of fungal nail infections?
A: The causative organisms of fungal nail infections include dermatophytes (mainly Trichophyton rubrum), yeasts (e.g. Candida), and non-dermatophyte moulds.
Q: What are the risk factors for fungal nail infections?
A: Risk factors include increasing age, diabetes mellitus, psoriasis, and repeated nail trauma.
Q: What are the common features of fungal nail infections?
A: Common features include thickened, rough, opaque nails, and patients may present due to unsightly nails.
Q: How is fungal nail infection diagnosed?
A: Diagnosis is done via nail clippings and/or scrapings of the affected nail, followed by microscopy and culture. Cultures have a false-negative rate of about 30%, so repeat samples may be necessary if clinical suspicion is high.
Q: How is fungal nail infection treated?
For limited involvement (≤50% nail affected, ≤ 2 nails affected, more superficial white onychomycosis), topical amorolfine 5% nail lacquer is used.
For more extensive dermatophyte infection, oral terbinafine is the first-line treatment (6 weeks for fingernails, 3-6 months for toenails).
For extensive Candida infection, oral itraconazole is used with pulsed weekly therapy.
Q: What is guttate psoriasis?
A: Guttate psoriasis is a type of psoriasis more common in children and adolescents, often precipitated by a streptococcal infection 2-4 weeks prior to the appearance of lesions.
Q: What are the features of guttate psoriasis?
A: Features of guttate psoriasis include tear drop-shaped, pink, scaly papules or plaques, typically on the trunk and limbs, with an acute onset over days.
Q: How is guttate psoriasis managed?
Spontaneous resolution in most cases within 2-3 months.
No firm evidence for the use of antibiotics to eradicate streptococcal infection.
Topical treatments as per general psoriasis care.
UVB phototherapy.
Tonsillectomy may be needed for recurrent episodes.
Q: How can guttate psoriasis be differentiated from pityriasis rosea?
Q: What is hereditary haemorrhagic telangiectasia (HHT)?
A: HHT, also known as Osler-Weber-Rendu syndrome, is an autosomal dominant condition characterized by multiple telangiectasias on the skin and mucous membranes. It can occur spontaneously in 20% of cases without a prior family history.
Q: What are the diagnostic criteria for hereditary haemorrhagic telangiectasia?
There are four main diagnostic criteria for HHT. If a patient meets two of them, they are considered to have a possible diagnosis. If three or more are met, they have a definite diagnosis. The criteria are:
Epistaxis: Spontaneous, recurrent nosebleeds.
Telangiectases: Multiple at characteristic sites such as the lips, oral cavity, fingers, and nose.
Visceral lesions: E.g., gastrointestinal telangiectasia (with or without bleeding), pulmonary, hepatic, cerebral, or spinal arteriovenous malformations (AVMs).
Family history: A first-degree relative with HHT.
Q: What are the typical findings in imaging for hereditary haemorrhagic telangiectasia?
Chest x-ray: Multiple pulmonary nodules representing arteriovenous malformations (AVMs).
CT scan: Multiple hepatic arteriovenous malformations.
Q: What is hidradenitis suppurativa (HS)?
A: Hidradenitis suppurativa is a chronic, painful, inflammatory skin disorder characterized by the development of inflammatory nodules, pustules, sinus tracts, and scars, primarily in intertriginous areas.
Q: What are the risk factors for developing hidradenitis suppurativa?
Family history
Smoking
Obesity
Diabetes
Polycystic ovarian syndrome
Mechanical stretching of the skin
Q: What are the clinical features of hidradenitis suppurativa?
Recurrent, painful, and inflamed nodules, often with rupture and purulent discharge.
Common sites: axillae, inguinal area, inner thighs, perineum, perianal region, and inframammary skin.
Coalescence of nodules may lead to plaques, sinus tracts, and ‘rope-like’ scarring.
Q: How is hidradenitis suppurativa diagnosed and managed?
Clinical diagnosis
Good hygiene and loose-fitting clothing
Smoking cessation
Weight loss in obese patients
Acute flares treated with steroids or flucloxacillin
Long-term treatment with topical (clindamycin) or oral antibiotics (lymecycline, clindamycin and rifampicin)
Surgical excision of persistent lumps
Q: What are some complications of hidradenitis suppurativa?
Sinus tracts and fistulas
Comedones
Severe scarring, which can lead to dense, rope-like bands, strictures, and lymphedema
Contractures
Lymphatic obstruction
Q: How does hidradenitis suppurativa differ from acne vulgaris?
A: Acne vulgaris primarily affects the face, upper chest, and back, whereas HS primarily involves intertriginous areas such as the axilla and inguinal regions.
Q: How does hidradenitis suppurativa differ from follicular pyodermas?
A: Follicular pyodermas (e.g., folliculitis, furuncles, carbuncles) are transient and respond rapidly to antibiotics, while HS is a chronic condition that involves recurrent and persistent lesions.
Q: How does hidradenitis suppurativa differ from granuloma inguinale (donovanosis)?
A: Granuloma inguinale is a sexually transmitted infection caused by Klebsiella granulomatis, often presenting with enlarging, bleeding ulcers in the inguinal area, whereas HS involves recurrent nodules and abscesses without ulceration.
Q: What is the difference between hirsutism and hypertrichosis?
A: Hirsutism refers to androgen-dependent hair growth in women, while hypertrichosis refers to androgen-independent hair growth.
Q: What are some common causes of hirsutism?
Polycystic ovarian syndrome (PCOS)
Cushing’s syndrome
Congenital adrenal hyperplasia
Androgen therapy
Obesity (due to insulin resistance)
Adrenal tumor
Androgen-secreting ovarian tumor
Drugs (e.g., phenytoin, corticosteroids)
Q: How is hirsutism assessed?
A: The Ferriman-Gallwey scoring system is used to assess hirsutism. Nine body areas are scored from 0 to 4, and a score greater than 15 is considered moderate or severe hirsutism.
Q: What is the management for hirsutism?
Weight loss if overweight
Cosmetic techniques like waxing or bleaching (not available on the NHS)
Combined oral contraceptive pills (e.g., co-cyprindiol or ethinylestradiol with drospirenone)
Topical eflornithine for facial hirsutism (contraindicated in pregnancy and breastfeeding)
Q: What are some causes of hypertrichosis?
Drugs (e.g., minoxidil, ciclosporin, diazoxide)
Congenital conditions (e.g., congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis)
Porphyria cutanea tarda
Anorexia nervosa
Q: What is hyperhidrosis?
A: Hyperhidrosis is the excessive production of sweat.
Q: What are the first-line management options for hyperhidrosis?
First-line management options include:
Topical aluminium chloride preparations (with skin irritation as a main side effect)
Iontophoresis (especially useful for palmar, plantar, and axillary hyperhidrosis)
Q: What is another management option for axillary hyperhidrosis?
A: Botulinum toxin is licensed for the treatment of axillary hyperhidrosis.
Q: What surgical option is available for hyperhidrosis?
A: Endoscopic transthoracic sympathectomy is a surgical option for hyperhidrosis. Patients should be informed about the risk of compensatory sweating.
Q: What is impetigo?
A: Impetigo is a superficial bacterial skin infection usually caused by Staphylococcus aureus or Streptococcus pyogenes. It can be a primary infection or a complication of existing skin conditions such as eczema, scabies, or insect bites.
Q: Where do impetigo lesions typically occur?
A: Lesions tend to occur on the face, flexures, and limbs not covered by clothing.
Q: How is impetigo spread?
A: Impetigo spreads through direct contact with discharges from infected scabs, or indirectly via toys, clothing, and equipment. It can also spread through scratching.
Q: What are the features of impetigo?
A: Impetigo typically presents with ‘golden’, crusted skin lesions, often found around the mouth. It is very contagious.
Q: What is the management for limited, localized impetigo?
A: For limited, localized disease, NICE recommends hydrogen peroxide 1% cream. Topical antibiotics like fusidic acid or mupirocin may also be used if fusidic acid resistance is suspected.
Q: What is the management for extensive impetigo?
A: For extensive disease, oral flucloxacillin is recommended, or oral erythromycin for those allergic to penicillin.
Q: When should children with impetigo return to school?
A: Children should be excluded from school until the lesions are crusted and healed or 48 hours after starting antibiotic treatment.
Q: What are keloid scars?
A: Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound.
Q: What are the predisposing factors for keloid scars?
A: Keloid scars are more common in individuals with dark skin, young adults (rare in the elderly), and are frequently seen on the sternum, shoulder, neck, face, extensor surfaces of limbs, and trunk.
Q: Where are keloid scars most commonly found?
A: The most common sites for keloid scars (in order of frequency) are the sternum, shoulder, neck, face, extensor surface of limbs, and trunk.
Q: How can the risk of keloid formation be reduced?
A: Keloid scars are less likely to form if incisions are made along relaxed skin tension lines.
Q: How are early keloids treated?
A: Early keloids may be treated with intra-lesional steroids, such as triamcinolone.
Q: When is excision considered for keloid scars?
A: Excision may be required for keloid scars, but careful consideration is needed due to the potential for creating further keloid scarring.
Q: What is keratoacanthoma?
A: Keratoacanthoma is a benign epithelial tumor more common with advancing age and rare in young people.
Q: How does keratoacanthoma present?
A: Keratoacanthoma initially appears as a smooth dome-shaped papule that rapidly grows into a crater, centrally filled with keratin, resembling a volcano or crater.
Q: What is the typical course of keratoacanthoma?
A: Spontaneous regression of keratoacanthoma within 3 months is common, often leading to scarring.
Q: How should keratoacanthoma be managed?
A: Keratoacanthomas should be urgently excised, as it is difficult to clinically distinguish them from squamous cell carcinoma, and removal may prevent scarring.
Q: What is leukoplakia?
A: Leukoplakia is a premalignant condition characterized by white, hard spots on the mucous membranes of the mouth. It is more common in smokers and is considered a diagnosis of exclusion. It is important to rule out candidiasis, lichen planus, and squamous cell carcinoma, and regular follow-up is required due to the small risk of malignant transformation (around 1%).
Q: What is lichen planus?
A: Lichen planus is an immune-mediated skin disorder of unknown origin. It presents as an itchy, papular rash that is often polygonal in shape and typically appears on the palms, soles, genitalia, and flexor surfaces of the arms. Wickham’s striae (a white-line pattern on the surface) may be seen, and the Koebner phenomenon can occur. Oral involvement occurs in around 50% of cases, presenting as a white-lace pattern on the buccal mucosa. Nail changes, such as thinning and longitudinal ridging, can also occur.
Q: What causes lichenoid drug eruptions?
A: Lichenoid drug eruptions can be caused by medications such as gold, quinine, and thiazides.
Q: How is lichen planus managed?
A: Potent topical steroids are the primary treatment for lichen planus. For oral involvement, benzydamine mouthwash or spray is recommended. In extensive cases, oral steroids or immunosuppression may be required.
Q: What is lichen sclerosus?
A: Lichen sclerosus is an inflammatory condition, primarily affecting the genitalia, and is more common in elderly females. It leads to epidermal atrophy and the formation of white plaques. Symptoms include significant itching, and it may cause pain during intercourse or urination.
Q: How is lichen sclerosus diagnosed?
A: The diagnosis is generally made clinically, but a biopsy may be performed if atypical features are present, particularly if there is suspicion of vulvar intraepithelial neoplasia (VIN) or cancer.
Q: What is the management for lichen sclerosus?
A: The mainstay of treatment for lichen sclerosus is topical steroids and emollients.
Q: What follow-up is required for patients with lichen sclerosus?
A: Patients with lichen sclerosus should be followed up regularly due to an increased risk of vulvar cancer. A biopsy is required if there is suspicion of neoplastic change or if the disease fails to respond to treatment, especially in cases with extragenital involvement, pigmented areas, or atypical features.
Q: What is a lipoma?
A: A lipoma is a common, benign tumour of adipocytes (fat cells), typically found in subcutaneous tissues. It is smooth, mobile, and painless. Malignant transformation to liposarcoma is rare.
Q: What are the features of a lipoma?
A: Lipomas are usually smooth, mobile, and painless lumps. They are generally found in subcutaneous tissues, though they can occasionally occur in deeper adipose tissues.
Q: How is a lipoma diagnosed?
A: Diagnosis is primarily clinical, based on typical examination findings.
