Derm Flashcards
1
Q
Q: What is Acanthosis nigricans?
A
A: Acanthosis nigricans describes symmetrical, brown, velvety plaques often found on the neck, axilla, and groin.
2
Q
Q: What is acne vulgaris?
A
A: Acne vulgaris is a disease of the pilosebaceous unit characterized by multiple types of acne lesions commonly seen in each patient.
2
Q
Q: What are the common causes of Acanthosis nigricans?
A
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)
2
Q
Q: What is the pathophysiology of Acanthosis nigricans?
A
A: The pathophysiology involves insulin resistance → hyperinsulinemia → stimulation of keratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1).
3
Q
Q: What causes comedones in acne vulgaris?
A
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.
4
Q
Q: How do inflammatory lesions develop in acne vulgaris?
A
A: Inflammatory lesions form when the follicle bursts, releasing irritants, leading to the development of papules and pustules.
5
Q
Q: What severe complications can result from excessive inflammation in acne vulgaris?
A
A: Excessive inflammation can lead to nodules, cysts, and ultimately scarring, such as ice-pick scars and hypertrophic scars.
6
Q
Q: How does drug-induced acne differ from typical acne vulgaris?
A
A: Drug-induced acne is often monomorphic, with pustules being characteristic, especially in steroid use.
7
Q
Q: What is acne fulminans, and how is it managed?
A
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.
8
Q
Q: What is the pathophysiology of acne vulgaris?
A
A: Acne vulgaris occurs due to obstruction of pilosebaceous follicles with keratin plugs, leading to comedones, inflammation, and pustules.
9
Q
Q: How is acne vulgaris classified?
A
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.
10
Q
Q: What is the first-line treatment for mild to moderate acne?
A
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.
11
Q
Q: What is the first-line treatment for moderate to severe acne?
A
A 12-week course of:
Topical adapalene + benzoyl peroxide + oral lymecycline or doxycycline
Topical azelaic acid + oral lymecycline or doxycycline
12
Q
Q: What important considerations apply to oral antibiotics in acne treatment?
A
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.
13
Q
Q: When are combined oral contraceptives (COCPs) used for acne management?
A
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.
14
Q
Q: When is oral isotretinoin used for acne?
A
A: Oral isotretinoin is only prescribed under specialist supervision, with pregnancy being a contraindication.
15
Q
Q: What treatments should be avoided to reduce antibiotic resistance in acne?
A
Monotherapy with a topical antibiotic
Monotherapy with an oral antibiotic
Combination of a topical and an oral antibiotic
16
Q
Q: What are the NICE referral criteria for acne?
A
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
17
Q
Q: What is acne vulgaris?
A
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.
18
Q
Q: What are the key components of acne vulgaris pathophysiology?
A
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.
19
Q
Q: What are actinic keratoses (AK)?
A
A: Actinic keratoses (AK) are common premalignant skin lesions caused by chronic sun exposure.
20
Q
Q: What are the clinical features of actinic keratoses?
A
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
21
Q
Q: What are the management options for actinic keratoses?
A
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
22
Q
Q: What is alopecia areata?
A
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.
23
Q: What are the treatment options for alopecia areata?
Topical or intralesional corticosteroids
Topical minoxidil
Phototherapy
Dithranol
Contact immunotherapy
Wigs
24
Q: What are antihistamines used for?
A: Antihistamines (H1 inhibitors) are used in the treatment of allergic rhinitis and urticaria.
25
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.
26
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.
27
Q: What are the clinical features of athlete's foot?
A: Scaling, flaking, and itching between the toes.
28
Q: What is the first-line treatment for athlete's foot according to NICE?
A: Topical imidazole, undecenoate, or terbinafine.
29
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.
30
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."
31
Q: What is the recommended referral pathway for suspected BCC?
A: A routine referral should be made if BCC is suspected.
32
Q: What are the management options for basal cell carcinoma?
Surgical removal
Curettage
Cryotherapy
Topical creams (imiquimod, fluorouracil)
Radiotherapy
33
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.
34
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
35
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
36
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.
37
Q: Who is more commonly affected by bullous pemphigoid?
A: Bullous pemphigoid is more common in elderly patients.
38
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
39
Q: What is the skin biopsy finding in bullous pemphigoid?
A: Immunofluorescence shows IgG and C3 at the dermoepidermal junction.
40
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
41
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).
42
Q: What should be done for electrical burns?
A: Switch off the power supply and remove the person from the source.
43
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.
44
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).
45
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
46
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
47
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
48
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
49
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
50
Q: How do superficial burns heal?
A: Keratinocytes migrate to form a new layer over the burn site.
51
Q: How do full-thickness burns heal?
A: Full-thickness burns result in dermal scarring and typically require skin grafts to provide optimal coverage.
52
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.
53
Q: What are the features of cherry haemangiomas?
Erythematous, papular lesions
Typically 1-3 mm in size
Non-blanching
Not found on mucous membranes
54
Q: Is treatment required for cherry haemangiomas?
A: No, as they are benign, treatment is usually not required.
55
Q: What is chronic plaque psoriasis?
A: The most common form of psoriasis, accounting for around 80% of presentations.
56
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
57
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.
58
Q: What is a common cause of irritant contact dermatitis?
A: Cement, due to its alkaline nature.
59
Q: What can cause allergic contact dermatitis in cement workers?
A: The dichromates present in cement.
60
Q: What is dermatitis herpetiformis?
A: An autoimmune blistering skin disorder associated with coeliac disease, caused by deposition of IgA in the dermis.
61
Q: What percentage of patients with dermatitis herpetiformis exhibit findings of gluten-sensitive enteropathy?
A: More than 90% of patients.
62
Q: What are the typical features of dermatitis herpetiformis?
A: Itchy, vesicular skin lesions on extensor surfaces such as elbows, knees, and buttocks.
63
Q: How is dermatitis herpetiformis diagnosed?
A: Skin biopsy with direct immunofluorescence showing deposition of IgA in a granular pattern in the upper dermis.
64
Q: What is the management for dermatitis herpetiformis?
A: A gluten-free diet and dapsone.
65
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.
66
Q: Where are dermatofibromas commonly located?
A: On the arms and legs.
67
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.
68
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.
69
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.
70
Q: What is the management for eczema herpeticum?
A: Children should be admitted for IV aciclovir as it is potentially life-threatening.
71
Q: What is erysipelas?
A: A localized skin infection caused by Streptococcus pyogenes, which is a more superficial and limited version of cellulitis.
72
Q: What is the treatment of choice for erysipelas?
A: Flucloxacillin.
73
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.
74
Q: What are the characteristic features of erythema ab igne?
A: Reticulated, erythematous patches with hyperpigmentation and telangiectasia.
75
Q: What risk is associated with untreated erythema ab igne?
A: It can lead to the development of squamous cell skin cancer.
76
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.
77
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.
78
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.
79
Q: What distinguishes erythema multiforme major from minor?
A: Erythema multiforme major is a more severe form that involves mucosal involvement.
80
Q: What is Orf?
A: Orf is a skin disease of sheep and goats caused by a parapox virus, which can trigger erythema multiforme.
81
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.
82
Q: How long do lesions in erythema nodosum take to resolve?
A: Lesions typically resolve within 6 weeks and heal without scarring.
83
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.
84
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.
85
Q: How can erythrasma be diagnosed?
A: Erythrasma can be diagnosed with Wood's light examination, which reveals a coral-red fluorescence.
86
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.
87
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.
88
Q: What are the causes of erythroderma?
A: Causes of erythroderma include eczema, psoriasis, drugs (e.g. gold), lymphomas, leukaemias, and idiopathic origins.
89
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.
90
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.
91
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.
92
Q: What are the risk factors for fungal nail infections?
A: Risk factors include increasing age, diabetes mellitus, psoriasis, and repeated nail trauma.
93
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.
94
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.
95
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.
96
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.
97
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.
98
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.
99
Q: How can guttate psoriasis be differentiated from pityriasis rosea?
100
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.
101
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.
102
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.
103
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.
104
Q: What are the risk factors for developing hidradenitis suppurativa?
Family history
Smoking
Obesity
Diabetes
Polycystic ovarian syndrome
Mechanical stretching of the skin
105
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.
106
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
107
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
108
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.
109
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.
110
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.
111
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.
112
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)
113
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.
114
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)
115
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
116
Q: What is hyperhidrosis?
A: Hyperhidrosis is the excessive production of sweat.
117
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)
118
Q: What is another management option for axillary hyperhidrosis?
A: Botulinum toxin is licensed for the treatment of axillary hyperhidrosis.
119
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.
120
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.
121
Q: Where do impetigo lesions typically occur?
A: Lesions tend to occur on the face, flexures, and limbs not covered by clothing.
122
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.
123
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.
124
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.
125
Q: What is the management for extensive impetigo?
A: For extensive disease, oral flucloxacillin is recommended, or oral erythromycin for those allergic to penicillin.
126
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.
127
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.
128
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.
129
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.
130
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.
131
Q: How are early keloids treated?
A: Early keloids may be treated with intra-lesional steroids, such as triamcinolone.
132
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.
133
Q: What is keratoacanthoma?
A: Keratoacanthoma is a benign epithelial tumor more common with advancing age and rare in young people.
134
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.
135
Q: What is the typical course of keratoacanthoma?
A: Spontaneous regression of keratoacanthoma within 3 months is common, often leading to scarring.
136
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.
137
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%).
138
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.
139
Q: What causes lichenoid drug eruptions?
A: Lichenoid drug eruptions can be caused by medications such as gold, quinine, and thiazides.
140
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.
141
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.
142
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.
143
Q: What is the management for lichen sclerosus?
A: The mainstay of treatment for lichen sclerosus is topical steroids and emollients.
144
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.
145
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.
146
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.
147
Q: How is a lipoma diagnosed?
A: Diagnosis is primarily clinical, based on typical examination findings.
148
Q: What is the management for a lipoma?
A: Lipomas may be observed if they are asymptomatic. If the diagnosis is uncertain or the lipoma is compressing surrounding structures, it may be surgically removed.
149
Q: What are the features suggestive of liposarcoma?
A: Features suggesting sarcomatous change include a size greater than 5 cm, increasing size, pain, and a deep anatomical location. The presence of all four features is associated with a higher likelihood of liposarcoma, with up to 85% of cases being sarcomatous.
150
Q: What is livedo reticularis?
A: Livedo reticularis is a purplish, non-blanching, reticulated rash caused by the obstruction of capillaries, leading to swollen venules.
151
Q: What are the common causes of livedo reticularis?
idiopathic
Polyarteritis nodosa
Systemic lupus erythematosus
Cryoglobulinaemia
Antiphospholipid syndrome
Ehlers-Danlos Syndrome
Homocystinuria
152
Q: What are the four main subtypes of melanoma?
Superficial spreading melanoma
Nodular melanoma (most aggressive)
Lentigo maligna melanoma
Acral lentiginous melanoma (rare form)
153
Q: What are the diagnostic features of melanoma?
Change in size
Change in shape
Change in colour
Minor diagnostic criteria include:
Diameter ≥7mm
Inflammation
Oozing or bleeding
Altered sensation
154
Q: What is the treatment for malignant melanoma?
A: Suspicious lesions should undergo excision biopsy. The lesion should be removed completely. The pathology report will determine if further re-excision of margins is required, depending on Breslow thickness. Additional treatments like sentinel lymph node mapping, isolated limb perfusion, and block dissection of regional lymph nodes may be selectively applied.
155
Q: What is the most important prognostic factor for malignant melanoma?
A: The most important prognostic factor for malignant melanoma is the invasion depth of the tumour, known as Breslow depth.
156
Q: What are milia?
A: Milia are small, benign, keratin-filled cysts that typically appear around the face.
157
Q: At what age are milia most commonly seen?
A: Milia are more common in newborns but can appear at any age.
158
Q: What is molluscum contagiosum?
A: Molluscum contagiosum is a common skin infection caused by the molluscum contagiosum virus (MCV), a member of the Poxviridae family. It is transmitted through close personal contact or indirectly via contaminated surfaces.
159
Q: Who is most commonly affected by molluscum contagiosum?
A: The majority of cases occur in children, especially those with atopic eczema, with the highest incidence in preschool children aged 1-4 years.
160
Q: What does molluscum contagiosum look like?
A: It typically presents with pinkish or pearly white papules with a central umbilication, up to 5 mm in diameter. Lesions often appear in clusters, commonly on the trunk and flexures in children, and on the genitalia, pubis, thighs, and lower abdomen in adults.
161
Q: How is molluscum contagiosum transmitted?
A: It is transmitted through direct contact or indirectly via fomites like shared towels or clothing.
162
Q: Is treatment always necessary for molluscum contagiosum?
A: Treatment is usually not necessary as the condition is self-limiting and resolves within 18 months. However, treatment like cryotherapy or simple trauma may be used for troublesome or unsightly lesions.
163
Q: When should someone be referred for molluscum contagiosum?
A: Referral is needed for people who are HIV-positive with extensive lesions, those with eyelid-margin or ocular lesions, or adults with anogenital lesions, who should be screened for other sexually transmitted infections.
164
Q: What is mycosis fungoides?
A: Mycosis fungoides is a rare form of T-cell lymphoma that primarily affects the skin.
165
Q: What are the initial features of mycosis fungoides?
A: It typically presents with itchy, red patches that are often mistaken for eczema or psoriasis initially.
166
Q: How do the lesions of mycosis fungoides differ from those of eczema or psoriasis?
A: Lesions in mycosis fungoides tend to be of different colors, whereas eczema and psoriasis typically show more homogeneity in lesion color.
167
Q: What is the plaque stage of mycosis fungoides?
A: The plaque stage is characterized by raised, thicker lesions that may develop as the disease progresses.
168
Q: What is pellagra?
A: Pellagra is a condition caused by a deficiency of nicotinic acid (niacin), characterized by the 3 D's: dermatitis, diarrhoea, and dementia.
169
Q: What can cause pellagra?
A: Pellagra can occur due to isoniazid therapy (which inhibits the conversion of tryptophan to niacin) and is more common in alcoholics.
170
Q: What are the features of pellagra?
Dermatitis (brown scaly rash on sun-exposed areas, termed Casal's necklace when around the neck)
Diarrhoea
Dementia, depression
Death if untreated.
171
Q: What is pemphigus vulgaris?
A: Pemphigus vulgaris is an autoimmune disease caused by antibodies against desmoglein 3, an epithelial cell adhesion molecule. It is more common in the Ashkenazi Jewish population.
172
Q: What are the features of pemphigus vulgaris?
Mucosal ulceration (common and often the presenting symptom, seen in 50-70% of patients)
Skin blistering: flaccid, easily ruptured vesicles and bullae, painful but not itchy, typically developing months after mucosal symptoms
Nikolsky's sign: bullae spread with tangential pressure on the skin
Acantholysis seen on biopsy
173
Q: How is pemphigus vulgaris managed?
A: Management involves first-line steroids and immunosuppressants.
174
Q: What is periorificial dermatitis?
A: Periorificial dermatitis is a condition typically seen in women aged 20-45 years, often caused by the use of topical corticosteroids, and to a lesser extent, inhaled corticosteroids.
175
Q: What are the features of periorificial dermatitis?
Clustered erythematous papules, papulovesicles, and papulopustules
Most commonly found in the perioral region, but also in the perinasal and periocular regions
Skin adjacent to the vermilion border of the lip is typically spared
176
Q: How is periorificial dermatitis managed?
A: Management involves avoiding steroids, as they may worsen symptoms, and treating with topical or oral antibiotics.
177
Q: What is pityriasis rosea?
A: Pityriasis rosea is an acute, self-limiting rash typically affecting young adults, with its aetiology not fully understood but believed to involve herpes hominis virus 7 (HHV-7).
178
Q: What are the features of pityriasis rosea?
A herald patch (usually on the trunk)
Followed by erythematous, oval, scaly patches
Lesions follow a characteristic distribution with the longitudinal diameters running parallel to the line of Langer, producing a 'fir-tree' appearance
In most cases, there is no prodrome, but some patients report a recent viral infection
179
Q: How is pityriasis rosea managed?
A: Management is typically self-limiting, with the rash resolving after 6-12 weeks.
180
Q: How can pityriasis rosea be differentiated from guttate psoriasis?
Guttate Psoriasis:
Often preceded by a streptococcal sore throat
Appears as tear-drop, scaly papules on the trunk and limbs
Treats with topical agents and UVB phototherapy
Most cases resolve in 2-3 months
Pityriasis Rosea:
Herald patch followed by multiple erythematous, oval lesions with a fine scale
May produce a 'fir-tree' appearance
Self-limiting, resolves within 6 weeks
181
Q: What is pityriasis versicolor?
A: Pityriasis versicolor, also called tinea versicolor, is a superficial fungal infection caused by Malassezia furfur.
182
Q: What are the features of pityriasis versicolor?
Most commonly affects the trunk
Patches may be hypopigmented, pink, or brown (versicolor)
The rash may be more noticeable after sun exposure
Scaling is common
Mild pruritus (itching)
183
Q: What are the predisposing factors for pityriasis versicolor?
Occurs in healthy individuals
Immunosuppression
Malnutrition
Cushing's disease
184
Q: How is pityriasis versicolor managed?
Topical antifungal treatment; NICE recommends ketoconazole shampoo as it is more cost-effective for large areas
If the condition fails to respond to topical treatment, alternative diagnoses should be considered, and scrapings can be sent for confirmation. Oral itraconazole may be used if necessary.
185
Q: What is polymorphic eruption of pregnancy?
A: Polymorphic eruption of pregnancy is a pruritic condition that occurs during the last trimester of pregnancy.
186
Q: Where do lesions in polymorphic eruption of pregnancy often first appear?
A: Lesions often first appear in abdominal striae, with the periumbilical area usually spared.
187
Q: How is polymorphic eruption of pregnancy managed?
Emollients
Mild potency topical steroids
Oral steroids if necessary
188
Q: What is pompholyx?
A: Pompholyx, also known as dyshidrotic eczema, is a type of eczema that affects the hands (cheiropompholyx) and feet (pedopompholyx).
189
Q: What can precipitate pompholyx eczema?
A: Pompholyx eczema may be precipitated by humidity (e.g., sweating) and high temperatures.
190
Q: What are the features of pompholyx?
Small blisters on the palms and soles
Pruritus (intensely itchy)
Sometimes a burning sensation
Skin may become dry and crack once blisters burst.
191
Q: How is pompholyx managed?
Cool compresses
Emollients
Topical steroids
192
Q: What is porphyria cutanea tarda?
A: Porphyria cutanea tarda is the most common hepatic porphyria, caused by an inherited defect in uroporphyrinogen decarboxylase or by hepatocyte damage due to factors like alcohol, hepatitis C, or oestrogen.
193
Q: What are the features of porphyria cutanea tarda?
Photosensitive rash with blistering and skin fragility on the face and dorsal aspect of hands (most common)
Hypertrichosis
Hyperpigmentation
194
Q: How is porphyria cutanea tarda investigated?
Urine: Elevated uroporphyrinogen and pink fluorescence under Wood's lamp
Serum iron ferritin level is used to guide therapy
195
Q: What is the management for porphyria cutanea tarda?
Chloroquine
Venesection (preferred if iron ferritin level is above 600 ng/ml)
196
Q: What are port wine stains?
A: Port wine stains are vascular birthmarks that are typically unilateral. They are deep red or purple in color.
197
Q: How do port wine stains differ from other vascular birthmarks?
A: Unlike other vascular birthmarks, such as salmon patches and strawberry haemangiomas, port wine stains do not spontaneously resolve. They often darken and become raised over time.
198
Q: What is the treatment for port wine stains?
A: Treatment options include cosmetic camouflage or laser therapy, which may require multiple sessions.
199
Q: What is the most common subtype of psoriasis?
A: The most common subtype of psoriasis is plaque psoriasis, which results in well-demarcated red, scaly patches.
200
Q: What are the common areas affected by plaque psoriasis?
A: Plaque psoriasis commonly affects the extensor surfaces, sacrum, and scalp.
201
Q: What is flexural psoriasis?
A: Flexural psoriasis is a subtype of psoriasis where the skin lesions are smooth, typically found in skin folds.
202
Q: What triggers guttate psoriasis?
A: Guttate psoriasis is frequently triggered by a streptococcal infection, resulting in red, teardrop-shaped lesions.
203
Q: What is pustular psoriasis, and where does it commonly occur?
A: Pustular psoriasis is a subtype of psoriasis that commonly occurs on the palms and soles.
204
Q: What genetic markers are associated with psoriasis?
A: Psoriasis is associated with HLA-B13, HLA-B17, and HLA-Cw6.
205
Q: What environmental factors can trigger or worsen psoriasis?
A: Skin trauma, stress, and streptococcal infection can trigger or worsen psoriasis, while sunlight can improve it.
206
Q: What immunological abnormality is involved in psoriasis?
A: Psoriasis involves abnormal T-cell activity, leading to keratinocyte proliferation, potentially mediated by Th17 cells.
207
Q: What are the common nail signs in psoriasis?
A: Common nail signs in psoriasis include pitting and onycholysis.
208
Q: What are the cardiovascular risks associated with psoriasis?
A: Psoriasis increases the incidence of metabolic syndrome, cardiovascular disease, and venous thromboembolism.
209
Q: What are some characteristics of pruritus caused by liver disease?
A: Liver disease may present with a history of alcohol excess, stigmata of chronic liver disease (e.g., spider naevi, bruising, palmar erythema, gynaecomastia), and evidence of decompensation (e.g., ascites, jaundice, encephalopathy).
210
Q: What signs are associated with iron deficiency anemia?
A: In iron deficiency anemia, the patient may present with pallor, koilonychia, atrophic glossitis, post-cricoid webs, and angular stomatitis.
211
Q: How does polycythaemia cause pruritus?
A: Polycythaemia causes pruritus, particularly after a warm bath, and is associated with a ruddy complexion.
212
Q: What are the symptoms of chronic kidney disease?
A: Chronic kidney disease can cause lethargy, pallor, oedema, weight gain, and hypertension.
213
Q: What are the key features of lymphoma associated with pruritus?
A: Lymphoma may present with night sweats, lymphadenopathy, splenomegaly, hepatomegaly, and fatigue.
214
Q: What are other causes of pruritus?
A: Other causes of pruritus include hyperthyroidism, hypothyroidism, diabetes, pregnancy, senile pruritus, urticaria, and skin disorders such as eczema, scabies, psoriasis, and pityriasis rosea.
215
Q: What are common nail changes seen in psoriasis?
Pitting
Onycholysis (separation of the nail from the nail bed)
Subungual hyperkeratosis
Loss of the nail.
216
Q: What factors may exacerbate psoriasis?
Trauma
Alcohol
Drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs, ACE inhibitors, infliximab
Withdrawal of systemic steroids
217
Q: What infection may trigger guttate psoriasis?
A: Streptococcal infection may trigger guttate psoriasis.
218
Q: What is the step-wise approach for managing chronic plaque psoriasis according to NICE guidelines?
First-line treatment:
A potent corticosteroid applied once daily
Plus a vitamin D analogue applied once daily
Both applied separately (one in the morning, one in the evening) for up to 4 weeks.
Second-line treatment:
If no improvement after 8 weeks, offer a vitamin D analogue twice daily.
Third-line treatment:
If no improvement after 8-12 weeks, offer either:
A potent corticosteroid applied twice daily for up to 4 weeks, or
A coal tar preparation applied once or twice daily.
Short-acting dithranol can also be used.
219
Q: What is first-line treatment for scalp psoriasis?
A potent topical corticosteroid applied once daily for 4 weeks.
If no improvement after 4 weeks, consider:
Using a different formulation (e.g. shampoo or mousse), and/or
Topical agents (e.g. salicylic acid) to remove adherent scale before applying the corticosteroid.
220
Q: What is the recommended treatment for face, flexural, and genital psoriasis?
A mild or moderate potency corticosteroid applied once or twice daily for a maximum of 2 weeks.
221
Q: What is the first-line systemic therapy for psoriasis with joint disease?
A: The first-line systemic therapy for psoriasis with joint disease is oral methotrexate.
222
Q: What are the adverse effects of phototherapy for psoriasis treatment?
Skin ageing
Squamous cell carcinoma (not melanoma).
223
Q: How should topical steroids be used in psoriasis treatment?
Avoid prolonged use on the scalp, face, and flexures due to risk of skin atrophy.
Potent steroids should not be used for more than 1-2 weeks/month in these areas.
Systemic side effects may occur if used on large areas (>10% body surface area).
Aim for a 4-week break before starting another course of topical corticosteroids.
Use potent steroids for no longer than 8 weeks at a time, and very potent steroids for no longer than 4 weeks at a time.
224
Q: What is the mechanism of action of vitamin D analogues in treating psoriasis?
Decreasing cell division and differentiation, which reduces epidermal proliferation.
They are effective at reducing scale and thickness of plaques but not erythema.
225
Q: What are the precautions when using vitamin D analogues in psoriasis treatment?
They should be avoided in pregnancy.
The maximum weekly amount for adults is 100g.
226
Q: What is purpura?
A: Purpura describes bleeding into the skin from small blood vessels, resulting in a non-blanching rash. It can be caused by low platelets or bleeding disorders like von Willebrand disease. Smaller petechiae (1-2 mm in diameter) may also be seen.
227
Q: What is the importance of recognizing purpura in children?
A: In children, purpura can indicate serious underlying conditions like meningococcal septicaemia or acute lymphoblastic leukaemia. Immediate investigation and admission are required, and parenteral antibiotics should be administered if meningococcal septicaemia is suspected.
228
Q: What are the causes of purpura in children and adults?
A: Causes in children:
Meningococcal septicaemia
Acute lymphoblastic leukaemia
Congenital bleeding disorders
Immune thrombocytopenic purpura
Henoch-Schonlein purpura
Non-accidental injury
A: Causes in adults:
Immune thrombocytopenic purpura
Bone marrow failure (secondary to leukaemias, myelodysplasia, or bone metastases)
Senile purpura
Drugs (quinine, antiepileptics, antithrombotics)
Nutritional deficiencies (vitamins B12, C, and folate)
229
Q: What condition may cause petechiae in the upper body, but not purpura?
A: Raised superior vena cava pressure (e.g., secondary to a bad cough) may cause petechiae in the upper body but would not cause purpura.
230
Q: What is pyoderma gangrenosum?
A: Pyoderma gangrenosum is a rare, non-infectious inflammatory disorder that causes painful skin ulceration. It typically affects the lower legs but can occur anywhere on the skin.
231
Q: What are the causes of pyoderma gangrenosum?
Idiopathic (50% of cases)
Inflammatory bowel disease (10-15%), e.g., ulcerative colitis and Crohn's disease
Rheumatological conditions, e.g., rheumatoid arthritis, SLE
Haematological disorders, e.g., myeloproliferative disorders, lymphoma, myeloid leukaemias, monoclonal gammopathy (IgA)
Granulomatosis with polyangiitis
Primary biliary cirrhosis
232
Q: What are the features of pyoderma gangrenosum?
Location: Often affects the lower limb, usually starting at the site of a minor injury (pathergy).
Initial features: Small pustule, red bump, or blood-blister.
Later features: Ulcer formation, often painful with purple, violaceous, and undermined edges. The ulcer may be deep and necrotic.
Systemic symptoms: May include fever and myalgia.
233
Q: How is pyoderma gangrenosum diagnosed?
Characteristic appearance
Associations with other diseases
Presence of pathergy
Histology (though not specific, can help rule out other causes of ulcers)
Ruling out other diseases
234
Q: What is the first-line treatment for pyoderma gangrenosum?
A: Oral steroids are usually the first-line treatment. For difficult cases, other immunosuppressive therapies like ciclosporin and infliximab may be used. Surgery should be postponed until the disease is controlled to avoid worsening due to pathergy.
235
Q: What is isotretinoin used for?
A: Isotretinoin is an oral retinoid used in the treatment of severe acne. Two-thirds of patients experience long-term remission or cure after a course of oral isotretinoin.
236
Q: What are the adverse effects of isotretinoin?
Teratogenicity: Females should use two forms of contraception (e.g., combined oral contraceptive and condoms).
Dry skin, eyes, and lips/mouth: The most common side effect.
Low mood: There is a controversial association with depression and psychiatric problems.
Raised triglycerides.
Hair thinning.
Nose bleeds due to dryness of the nasal mucosa.
Intracranial hypertension: Should not be combined with tetracyclines due to this risk.
Photosensitivity.
237
Q: What is rosacea?
A: Rosacea (sometimes called acne rosacea) is a chronic skin disease of unknown aetiology, often affecting the nose, cheeks, and forehead.
238
Q: What are the features of rosacea?
Flushing (often the first symptom).
Telangiectasia.
Persistent erythema with papules and pustules.
Rhinophyma (thickening of the skin on the nose).
Ocular involvement such as blepharitis.
Symptoms may worsen with sunlight exposure.
239
Q: What is the management for rosacea?
Simple measures: Daily high-factor sunscreen and camouflage creams for redness.
Predominant erythema/flushing: Topical brimonidine gel (alpha-adrenergic agonist) can be used to temporarily reduce redness.
Mild-to-moderate papules/pustules: First-line is topical ivermectin, with alternatives being topical metronidazole or topical azelaic acid.
Moderate-to-severe papules/pustules: Combination of topical ivermectin and oral doxycycline.
240
Q: When should a patient with rosacea be referred to a specialist?
Symptoms do not improve with primary care management.
Laser therapy may be appropriate for prominent telangiectasia.
Rhinophyma is present.
241
Q: What are salmon patches?
A: Salmon patches, also known as stork marks or stork bites, are vascular birthmarks that appear as pink and blotchy marks on the skin.
242
Q: Where are salmon patches most commonly found?
A: Salmon patches are commonly found on the forehead, eyelids, and nape of the neck.
243
Q: Do salmon patches resolve over time?
A: Yes, salmon patches usually fade over a few months, though marks on the neck may persist longer.
244
Q: What is scabies caused by?
A: Scabies is caused by the mite Sarcoptes scabiei, which is spread by prolonged skin contact.
245
Q: What is the primary cause of the pruritus in scabies?
A: The pruritus is due to a delayed-type IV hypersensitivity reaction to the mites and their eggs, which occurs about 30 days after initial infection.
246
Q: What are some common features of scabies?
widespread pruritus
linear burrows on the side of fingers, interdigital webs, and flexor aspects of the wrist
In infants, the face and scalp may be affected.
Secondary features include excoriation and infection due to scratching.
247
Q: What is the first-line treatment for scabies?
A: Permethrin 5% is the first-line treatment for scabies.
248
Q: What is the second-line treatment for scabies?
A: Malathion 0.5% is the second-line treatment for scabies.
249
Q: How should patients be guided on scabies treatment?
Avoid close physical contact until treatment is complete.
Treat all household and close contacts simultaneously, even if asymptomatic.
Launder, iron, or tumble dry clothing, bedding, towels, etc., on the first day of treatment.
Apply the insecticide cream to cool, dry skin and leave it on for 8-12 hours for permethrin or 24 hours for malathion before washing it off.
Repeat treatment 7 days later.
250
Q: What is crusted (Norwegian) scabies?
A: Crusted scabies is a severe form of scabies seen in patients with suppressed immunity, such as those with HIV. It is characterized by thick, crusted skin teeming with large numbers of mites.
251
Q: What is the treatment for crusted scabies?
A: The treatment of choice for crusted scabies is Ivermectin, and isolation is essential.
252
Q: What are sebaceous cysts?
A: Sebaceous cysts is a general term that includes both epidermoid and pilar cysts. It's a misnomer and is best avoided in medical terminology.
253
Q: What is the difference between epidermoid cysts and pilar cysts?
Epidermoid cysts are due to the proliferation of epidermal cells within the dermis.
Pilar cysts (also known as trichilemmal cysts or wen) originate from the outer root sheath of the hair follicle.
254
Q: Where are sebaceous cysts most commonly found?
A: Sebaceous cysts are most commonly found on the scalp, ears, back, face, and upper arm. They are not typically seen on the palms of the hands or soles of the feet.
255
Q: What is a common characteristic of sebaceous cysts?
A: Sebaceous cysts often contain a punctum (a small opening).
256
Q: What is important in the management of sebaceous cysts?
A: Excision of the cyst wall needs to be complete to prevent recurrence.
257
Q: What is seborrhoeic dermatitis in adults?
A: Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of Malassezia furfur, a normal skin fungus. It affects about 2% of the general population.
258
Q: What are the common features of seborrhoeic dermatitis in adults?
Eczematous lesions occur on sebum-rich areas, including:
Scalp (which may cause dandruff)
Periorbital, auricular, and nasolabial folds
Additionally, otitis externa and blepharitis may develop.
259
Q: What conditions are associated with seborrhoeic dermatitis in adults?
HIV
Parkinson's disease
260
Q: What is the management for scalp disease in seborrhoeic dermatitis?
The first-line treatment for scalp disease is ketoconazole 2% shampoo.
Over-the-counter preparations such as zinc pyrithione ("Head & Shoulders") or tar ("Neutrogena T/Gel") may also be used if ketoconazole is not appropriate.
Selenium sulphide and topical corticosteroids may also be useful.
261
Q: How is seborrhoeic dermatitis on the face and body managed?
Topical antifungals like ketoconazole
Topical steroids, but they should be used for short periods
Recurrences are common, making the condition difficult to treat.
262
What are seborrhoeic keratoses?
A: Seborrhoeic keratoses are benign epidermal skin lesions seen in older people.
263
What are the key features of seborrhoeic keratoses?
Large variation in color from flesh to light-brown to black
"Stuck-on" appearance
Keratotic plugs may be seen on the surface
264
How is seborrhoeic keratosis managed?
Reassurance about the benign nature of the lesion
Removal options include curettage, cryosurgery, and shave biopsy
265
What are the differential diagnoses of shin lesions?
Erythema nodosum
Pretibial myxoedema
Pyoderma gangrenosum
Necrobiosis lipoidica diabeticorum
266
What are the features of erythema nodosum?
Symmetrical, erythematous, tender nodules
Heal without scarring
Common causes: streptococcal infections, sarcoidosis, inflammatory bowel disease, and drugs (penicillins, sulphonamides, oral contraceptive pill)
267
What are the features of pretibial myxoedema?
Symmetrical, erythematous lesions seen in Graves' disease
Shiny, orange peel-like skin
268
What are the features of pyoderma gangrenosum?
Initially a small red papule
Progresses to deep, red, necrotic ulcers with a violaceous border
Idiopathic in 50%, also seen in inflammatory bowel disease, connective tissue disorders, and myeloproliferative disorders
269
What are the features of necrobiosis lipoidica diabeticorum?
Shiny, painless areas of yellow/red skin, typically on the shins of diabetics
Often associated with telangiectasia
270
What is shingles, and what causes it?
A: Shingles (herpes zoster infection) is an acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV). The virus lies dormant in the dorsal root or cranial nerve ganglia after primary infection with chickenpox.
271
What are the risk factors for shingles?
Increasing age
HIV (15 times more common)
Other immunosuppressive conditions (e.g., steroids, chemotherapy)
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What dermatomes are most commonly affected by shingles?
A: The most commonly affected dermatomes are T1-L2.
273
What are the prodromal features of shingles?
Burning pain over the affected dermatome for 2-3 days
Pain may be severe and interfere with sleep
Around 20% of patients experience fever, headache, and lethargy
274
What are the features of the shingles rash?
Initially erythematous and macular over the affected dermatome
Quickly becomes vesicular
Well demarcated by the dermatome and does not cross the midline (though minor 'bleeding' into adjacent areas may occur)
275
How is shingles diagnosed?
A: The diagnosis is usually clinical.
276
What are the management steps for shingles?
Infectious precautions:
Avoid contact with pregnant women and immunosuppressed individuals until vesicles crust over (5-7 days)
Cover lesions to reduce transmission
Pain management:
Paracetamol and NSAIDs are first-line
Neuropathic agents (e.g., amitriptyline) if pain persists
Oral corticosteroids may be considered in severe cases within the first 2 weeks
Antivirals:
Recommended within 72 hours for most patients
Aciclovir, famciclovir, or valaciclovir reduce post-herpetic neuralgia, especially in older people
277
When are antivirals typically not recommended for shingles?
A: Antivirals may not be needed if the patient is under 50 years old, has a mild truncal rash, mild pain, and no underlying risk factors.
278
What are the complications of shingles?
Post-herpetic neuralgia:
Most common complication (affects 5%-30% depending on age)
Often resolves within 6 months but may persist longer
Herpes zoster ophthalmicus:
Shingles affecting the ocular division of the trigeminal nerve, associated with various ocular complications
Herpes zoster oticus (Ramsay Hunt syndrome):
May result in ear lesions and facial paralysis
279
What are the main types of skin malignancies?
Basal cell carcinoma
Squamous cell carcinoma
Malignant melanoma
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What are the key features of basal cell carcinoma (BCC)?
Most common form of skin cancer
Commonly occurs on sun-exposed sites (excluding the ear)
Subtypes: nodular, morphoeic, superficial, and pigmented
Slow-growing with low metastatic potential
Treatment includes standard surgical excision, topical chemotherapy, and radiotherapy
Diagnostic punch biopsy is recommended if treatments other than excision are planned
281
What are the key features of squamous cell carcinoma (SCC)?
Linked to sun exposure
May arise from pre-existing solar keratoses
Can metastasize if left untreated
Immunosuppression increases risk
Treatment: wide local excision; repeat surgery may be required to ensure adequate margins if SCC is confirmed by biopsy
282
What are the major and minor diagnostic criteria for malignant melanoma?
Major criteria:
Change in size
Change in shape
Change in colour
Minor criteria:
Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation
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How are malignant melanomas excised, and what are the recommended margins based on Breslow thickness?
Suspicious lesions should undergo excision biopsy with complete removal to allow proper histopathological assessment.
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What are the further treatments for malignant melanoma if necessary?
Sentinel lymph node mapping
Isolated limb perfusion
Block dissection of regional lymph node groups (selectively applied)
285
What are the key features of Kaposi sarcoma?
Tumor of vascular and lymphatic endothelium
Purple cutaneous nodules
Associated with immunosuppression
Classical form: affects elderly males, slow-growing
Immunosuppression-associated form: more aggressive, often seen in HIV-related disease
286
What are the features of dermatitis herpetiformis?
Chronic itchy clusters of blisters
Linked to underlying gluten enteropathy (coeliac disease)
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What are the features of dermatofibroma?
Benign lesion
Firm, elevated nodules
Often has a history of trauma
Composed of histiocytes, blood vessels, and fibrotic changes
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What are the features of pyogenic granuloma?
Overgrowth of blood vessels
Red nodules
Usually follows trauma
May mimic amelanotic melanoma
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What are the features of acanthosis nigricans?
Brown to black, poorly defined, velvety hyperpigmentation of the skin
Common in body folds (neck, axilla, groin, etc.)
Most commonly caused by insulin resistance (increased circulating insulin)
In the context of malignancy, called acanthosis nigricans maligna
Mucous membrane involvement suggests a coexisting malignant condition
290
What is the most common skin disorder found in pregnancy?
A: Atopic eruption of pregnancy.
291
What are the key features of atopic eruption of pregnancy?
Eczematous, itchy, red rash
No specific treatment is needed
292
What is polymorphic eruption of pregnancy, and when does it typically occur?
Pruritic condition associated with the last trimester of pregnancy
Lesions often first appear in abdominal striae
293
How is polymorphic eruption of pregnancy managed?
Management depends on severity
Treatments may include emollients, mild potency topical steroids, and oral steroids
294
What are the key features of pemphigoid gestationis?
Pruritic blistering lesions
Often start in the peri-umbilical region, later spreading to the trunk, back, buttocks, and arms
Typically presents in the 2nd or 3rd trimester
Rarely seen in first pregnancies
295
What is the treatment for pemphigoid gestationis?
A: Oral corticosteroids are usually required.
296
What are the key skin manifestations of systemic lupus erythematosus (SLE)?
Photosensitive 'butterfly' rash
Discoid lupus
Alopecia
Livedo reticularis (net-like rash)
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What is characteristic about the butterfly rash in SLE?
It is photosensitive.
Typically spares the nasolabial folds.
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What is livedo reticularis, and how does it present in SLE?
A: Livedo reticularis is a net-like rash that can be seen in patients with SLE.
299
Q: What are the most common types of non-melanoma skin cancer (NMSC)?
A: Basal cell carcinoma (BCC) and squamous cell carcinoma (SCC).
300
Q: What is the relationship between UV light exposure and NMSC?
SCC: Linked to chronic long-term UV exposure.
BCC: Linked to sporadic exposure with episodes of burning.
301
Q: What are the risk factors for squamous cell carcinoma (SCC) in organ transplant recipients?
Length of immunosuppression
Ethnic origin
Sunlight exposure
HPV DNA found in many cases of transplant recipient SCC
302
Q: What is actinic keratosis, and why is it significant?
Premalignant lesion with atypical keratinocytes.
Risk of developing SCC is about 10% in 10 years for those with 7 or more lesions.
Appears as a rough erythematous papule with white to yellow scale, often in sun-exposed areas.
303
Q: What is Bowen's disease (SCC in situ)?
Erythematous scaling patch or elevated plaque on sun-exposed skin.
Full-thickness atypia of dermal keratinocytes, nuclear pleomorphism, and abnormal mitoses.
304
Q: What is invasive SCC and how does it present?
Erythematous keratotic papule or nodule with possible ulceration.
May show exophytic or endophytic growth and regional lymphadenopathy.
Pathologically involves downward proliferation of malignant cells and basement membrane invasion.
305
Q: What is the most common type of basal cell carcinoma (BCC)?
A: Nodular BCC: Raised translucent papule, usually on the face.
306
Q: What are the characteristics of superficial BCC?
Superficial erythematous macule, typically on the trunk.
Younger age of presentation (mean age 57).
High recurrence rate due to subclinical lateral spread.
307
Q: What is morpheaform BCC?
Flat, slightly atrophic lesion with ill-defined borders.
Subclinical lateral spread increases recurrence rates.
308
Q: What is cystic BCC?
Appears with a clear or blue-grey color.
Cystic degeneration may not be obvious, resembling nodular BCC.
309
Q: What is basosquamous carcinoma?
Atypical BCC with features of both BCC and SCC.
More biologically aggressive and locally destructive.
Can metastasize in 9-10% of cases.
310
Q: What is keratoacanthoma, and how does it present?
Dome-shaped erythematous lesion with central keratin pit.
Grows rapidly, necroses, and sloughs off.
Generally benign but may be treated with curettage and cautery or excision if diagnostic doubt exists.
311
Q: What is pyogenic granuloma?
Friable overgrowth of granulation tissue at sites of minor trauma.
May ulcerate and bleed on contact.
Treated with curettage and cautery, or excision if diagnostic doubt exists.
312
Q: What are spider naevi (spider angiomas)?
A: Central red papule with surrounding capillaries that blanch upon pressure, usually found on the upper part of the body.
313
Q: How can spider naevi be differentiated from telangiectasia?
Spider naevi fill from the center when pressed.
Telangiectasia fills from the edges.
314
Q: What are some associations with spider naevi?
Liver disease
Pregnancy
Combined oral contraceptive pill
315
Q: What are the main risk factors for squamous cell carcinoma (SCC) of the skin?
Excessive sunlight/psoralen UVA therapy
Actinic keratoses and Bowen's disease
Immunosuppression (e.g. renal transplant, HIV)
Smoking
Long-standing leg ulcers (Marjolin's ulcer)
Genetic conditions (e.g. xeroderma pigmentosum, oculocutaneous albinism)
316
Q: Where do squamous cell carcinomas (SCC) typically occur on the body?
A: Sun-exposed sites such as the head, neck, dorsum of the hands, and arms.
317
Q: What are the clinical features of squamous cell carcinoma (SCC) of the skin?
Rapidly expanding, painless, ulcerating nodules
May have a cauliflower-like appearance
Possible areas of bleeding
318
Q: What is the treatment for squamous cell carcinoma (SCC) of the skin?
Surgical excision with 4mm margins for lesions <20mm in diameter
For lesions >20mm, 6mm margins are recommended
Mohs micrographic surgery for high-risk patients or cosmetically important sites
319
Q: What factors contribute to a good prognosis for squamous cell carcinoma (SCC) of the skin?
Well-differentiated tumors
Lesions <20mm in diameter
Lesions <2mm deep
No associated diseases
320
Q: What factors contribute to a poor prognosis for squamous cell carcinoma (SCC) of the skin?
Poorly differentiated tumors
Lesions >20mm in diameter
Lesions >4mm deep
Immunosuppression
321
Q: What is Stevens-Johnson syndrome (SJS)?
A: A severe systemic reaction affecting the skin and mucosa, almost always caused by a drug reaction. It is now considered separate from erythema multiforme.
322
Q: What are some common causes of Stevens-Johnson syndrome (SJS)?
Penicillin
Sulphonamides
Lamotrigine, carbamazepine, phenytoin
Allopurinol
NSAIDs
Oral contraceptive pill
323
Q: What are the characteristic features of Stevens-Johnson syndrome (SJS)?
Maculopapular rash with target lesions
May develop into vesicles or bullae
Positive Nikolsky sign in erythematous areas (blisters and erosions appear when skin is gently rubbed)
Mucosal involvement
Systemic symptoms: fever, arthralgia
324
Q: What is the management for Stevens-Johnson syndrome (SJS)?
A: Hospital admission for supportive treatment.
325
Q: What is a strawberry naevus (capillary haemangioma)?
A: A raised, erythematous, multilobed tumour that usually develops in the first month of life and increases in size until 6-9 months before regressing by around age 10.
326
Q: Where are strawberry naevi (capillary haemangiomas) commonly found?
A: Common sites include the face, scalp, and back. Rarely, they can be present in the upper respiratory tract, potentially leading to airway obstruction.
327
Q: What factors increase the likelihood of an infant developing a strawberry naevus (capillary haemangioma)?
Female infants
Premature infants
Infants whose mothers had chorionic villous sampling
328
Q: What are the potential complications of strawberry naevi (capillary haemangiomas)?
Mechanical issues like obstructing visual fields or airway
Bleeding
Ulceration
Thrombocytopaenia
329
Q: What is the first-line treatment for strawberry naevi (capillary haemangiomas) if treatment is required?
A: Propranolol is increasingly replacing systemic steroids as the treatment of choice. Topical beta-blockers like timolol may also be used.
330
Q: What is a cavernous haemangioma?
A: A deep capillary haemangioma.
331
Q: What is tinea?
Tinea refers to dermatophyte fungal infections. It is categorized based on the body area affected:
Tinea capitis (scalp)
Tinea corporis (trunk, legs, or arms)
Tinea pedis (feet)
332
Q: What is a kerion in tinea capitis and why is it significant?
A: A kerion is a raised, pustular, spongy/boggy mass that may form if tinea capitis is untreated. It is a severe inflammatory reaction to the infection.
333
Q: How can tinea capitis caused by Microsporum canis be diagnosed?
A: Lesions due to Microsporum canis will show green fluorescence under a Wood's lamp. However, the most useful investigation is scalp scrapings.
334
Q: What is the recommended management for tinea capitis?
Oral antifungals: terbinafine for Trichophyton tonsurans infections and griseofulvin for Microsporum infections
Topical ketoconazole shampoo for the first two weeks to reduce transmission
335
Q: What is tinea corporis and what are its common causes?
A: Tinea corporis, also known as ringworm, causes well-defined annular erythematous lesions with pustules and papules. It is commonly caused by Trichophyton rubrum and Trichophyton verrucosum (e.g. from contact with cattle).
336
Q: How is tinea corporis typically treated?
A: Tinea corporis may be treated with oral fluconazole.
337
Q: What are the typical features of tinea pedis (athlete's foot)?
A: Tinea pedis is characterized by itchy, peeling skin between the toes. It is more common in adolescence.
338
Q: What is toxic epidermal necrolysis (TEN)?
A: TEN is a potentially life-threatening skin disorder, often caused by a drug reaction, where the skin develops a scalded appearance over an extensive area. It is considered the severe end of a spectrum of skin disorders, which also includes erythema multiforme and Stevens-Johnson syndrome.
339
Q: What are common features of toxic epidermal necrolysis (TEN)?
Systemically unwell: pyrexia (fever), tachycardia (increased heart rate)
Positive Nikolsky's sign: the epidermis separates with mild lateral pressure, causing blister formation.
340
Q: What drugs are known to induce toxic epidermal necrolysis (TEN)?
Phenytoin
Sulphonamides
Allopurinol
Penicillins
Carbamazepine
NSAIDs
341
Q: How is toxic epidermal necrolysis (TEN) managed?
Stop the precipitating drug or factor
Supportive care, often in an intensive care unit
Manage complications like volume loss and electrolyte derangement
Intravenous immunoglobulin is commonly used first-line
Other treatment options: immunosuppressive agents (ciclosporin, cyclophosphamide), plasmapheresis
342
Q: What is urticaria?
A: Urticaria is a condition characterized by local or generalized superficial swelling of the skin. It is commonly caused by allergies, although non-allergic causes are also seen.
343
Q: What are the typical features of urticaria?
Pale, pink raised skin
Described as "hives," "wheals," or "nettle rash"
Pruritic (itchy)
344
Q: How is urticaria managed?
First-line treatment: Non-sedating antihistamines (e.g., loratadine, cetirizine)
Continue antihistamines for up to 6 weeks following an acute episode
For troublesome sleep symptoms: Add sedating antihistamine (e.g., chlorphenamine) at night
For severe or resistant episodes: Prednisolone may be used
345
Q: What is the varicella-zoster virus?
A: Varicella-zoster is the herpes virus that causes chickenpox and, upon reactivation, causes shingles (herpes zoster).
346
Q: What are the two types of varicella-zoster vaccines?
Vaccine to prevent primary varicella infection (chickenpox).
Vaccine to reduce the incidence of herpes zoster (shingles) caused by reactivation of varicella-zoster virus (VZV).
347
Q: What are large vessel vasculitides?
Temporal arteritis
Takayasu's arteritis
348
Q: What are medium vessel vasculitides?
Polyarteritis nodosa
Kawasaki disease
349
Q: What are small vessel vasculitides?
ANCA-associated vasculitides
Granulomatosis with polyangiitis (Wegener's granulomatosis)
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
Microscopic polyangiitis
Immune complex small-vessel vasculitis
Henoch-Schonlein purpura
Goodpasture's syndrome (anti-glomerular basement membrane disease)
Cryoglobulinaemic vasculitis
Hypocomplementemic urticarial vasculitis (anti-C1q vasculitis)
350
Q: Where are venous ulcers typically seen?
Above the medial malleolus (inner side of the ankle).
351
Q: What investigation is important in non-healing venous ulcers to assess for arterial flow?
Ankle-brachial pressure index (ABPI).
352
Q: What are the ABPI values indicating normal and abnormal arterial flow?
Normal ABPI: 0.9 - 1.2
Below 0.9: Indicates arterial disease.
Above 1.3: May also indicate arterial disease due to false-negative results from arterial calcification (e.g., in diabetics).
353
Q: What is the main treatment for venous ulcers?
Compression bandaging, usually four-layer, is the only treatment with significant benefit.
354
Q: What medications may improve the healing of venous ulcers?
Oral pentoxifylline (a peripheral vasodilator) improves healing rate.
355
Q: What is Vitiligo?
Vitiligo is an autoimmune condition that causes the loss of melanocytes, leading to depigmentation of the skin.
356
Q: What are some associated conditions with Vitiligo?
Type 1 diabetes mellitus
Addison's disease
Autoimmune thyroid disorders
Pernicious anaemia
Alopecia areata
357
Q: What are the typical features of Vitiligo?
Well-demarcated patches of depigmented skin.
The peripheries tend to be most affected.
Koebner phenomenon: Trauma may precipitate new lesions.
358
Q: What is the management of Vitiligo?
Sunblock for affected skin areas.
Camouflage make-up.
Topical corticosteroids may reverse changes if applied early.
Topical tacrolimus and phototherapy may help, but caution is needed with light-skinned patients.
359
Q: What are the features of Zinc deficiency?
Acrodermatitis: Red, crusted lesions.
Acral distribution: Lesions commonly appear on extremities.
Peri-orificial: Affected areas include around the mouth, nose, and eyes.
Perianal: Affected area around the anus.
Alopecia: Hair loss.
Short stature: Growth retardation.
Hypogonadism: Reduced function of the gonads.
Hepatosplenomegaly: Enlargement of the liver and spleen.
Geophagia: Ingestion of clay or soil.
Cognitive impairment: Reduced cognitive function.
360
Q: What is Acrodermatitis enteropathica?
It is a recessively inherited condition caused by a partial defect in intestinal zinc absorption.
361
If a Lipoma is >5cm what do you do
US
362
What are features of toxic epidermal necrolysis
most serious skin hypersensitivity reaction; it has a high mortality rate and usually affects 30–100% of the body’s surface area. Nikolsky’s sign is usually present and the skin sloughs off easily. It is a drug-induced condition, most commonly caused by NSAIDs, steroids, methotrexate, allopurinol and penicillins.
363
What is the characteristic lesion in scabies
burrows
364
what causes erythema ab igne
Erythema ab igne - Over exposure to infrared radiation
365
what causes erythema nodosum
Erythema Nodosum - Sarcoidosis, IBD, TB
366
what causes erythema chronicum migrans
Erythema chronicum migrans - Lyme Disease
367
what causes erythema marginatum
Erythema Marginatum - Rheumatic Fever
368
what causes erythema multiforme
Erythema Multiforme - HSV
369
what is gold standard for diagnosing contact dermatitis
skin patch testing
370
what are examples of non sedating antihistamines
loratadine or cetirizine
371
