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Important Dermatology Topics Flashcards

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1
Q

What are the signs and symptoms of acne rosacea?

A
  • affects the nose, cheeks and forehead
  • flushing
  • telangiectasia
  • persistent erythema and pustules later on
  • rhinophyma (refer to dermatology)
  • blepharitis
  • may be exacerbated by sunlight
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2
Q

How do you manage rosacea?

A
  • topical brimonidine gel (if limited telangiectasia)
  • mild-moderate papules and pustules: topical ivermectin/topical metronidazole/topical azelaic acid
  • moderate to severe: combination topical ivermectin + oral doxycycline
  • laser therapy
  • referral for rhinopehyma
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3
Q

What is acne vulgaris caused by?

A

Obstruction of pilosebaceous follicles with keratin plugs causing comedones, inflammation and pustules

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4
Q

Mild, moderate and severe acne vulgaris:

A

Mild: open and closed comedones with sparse inflammatory lesions
Moderate: widespread non-inflammatory lesions with number of papules and pustules
Severe: extensive inflammatory lesions, may include nodules, pitting and scarring

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5
Q

What bacteria can contribute to acne vulgaris?

A

Propionibacterium Acnes

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6
Q

How can acne vulgaris be managed?

A
  • single topical: retinoids, benzoyl peroxide
  • topical combination therapy (add antibiotic)
  • oral antibiotic (max 3 months): tetracyclines, erythromycin (if pregnant)
  • COCP (in combination with topical agents)
  • oral isotretinoin (specialist supervision) - pregnancy contraindicated
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7
Q

In what cases should tetracyclines not be used to treat acne vulgaris?

A

pregnancy, breastfeeding or <12yo

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8
Q

What complication may occur as a result of acne vulgaris and how can you treat it?

A

Gram -ve folliculitis and treat with high dose trimethoprim

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9
Q

What are the 4 categories of burns?

A

Superficial epidermal
Partial thickness (superficial dermal)
Partial thickness (deep dermal)
Full thickness

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10
Q

What does a superficial epidermal burn look like?

A

Red and painful

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11
Q

What does a partial thickness (superficial dermal) burn look like?

A

Pale pink, painful, blistered

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12
Q

What does a partial thickness (deep dermal) burn look like?

A

White but may have patches of non-blanching erythema and reduced sensation

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13
Q

What does a full thickness burn look like?

A

White/brown/black in colour, no blisters, no pain

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14
Q

What is a Curling’s ulcer?

A

A stress ulcer that develops in the duodenum of burn patients

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15
Q

When should a burn be referred to secondary care?

A
  • deep dermal and full thickness
  • superficial dermal on >3% TBSA of adults and >2% in children
  • involving face, hands, feet, perineum, genitalia, flexure or circumferential limbs, torso or neck
  • inhalation injury
  • suspicion non-accidental
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16
Q

Management of burns:

A
  • superficial epidermal: symptomatic relief
  • superficial dermal: cleanse, leave blister, non-adherent dressing, avoid creams
  • severe burns: IV fluids if >10% TBSA in children and >15% in adults, escharotomies indicated in circumferential full thickness burns to torso or limbs (impaired ventilation otherwise)
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17
Q

How is the volume of IV fluids for burns calculated?

A

Parkland formula: TBSA x weight x 4

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18
Q

What is erythema nodosum?

A
  • inflammation of subcutaneous fat
  • cases tender, erythematous, nodular lesions
  • usually shins
  • resolves in 6 weeks
  • heal without scarring
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19
Q

What are the causes of erythema nodosum?

A
  • infection: streptococci, TB, brucellosis
  • systemic: sarcoidosis, IBD, Behcet’s
  • malignancy/infection
  • drugs: penicillins, sulphonamides, COCP
  • pregnancy
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20
Q

What is psoriasis exacerbated by?

A
  • trauma
  • alcohol
  • beta blockers
  • lithium
  • anti-malarials
  • NSAIDs
  • ACEi
  • infliximab
  • steroid withdrawal
  • strep infection and guttate psoriasis
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21
Q

Chronic plaque management in psoriasis:

A
  • regular emollients
  • 1st line: potent corticosteroids od with vitamin D analogue OD (one in morning and one in evening for up to 4 weeks)
  • 2nd line: after 8 weeks, vitamin D analogue BD
  • 3rd line: after 8-12 weeks, potent corticosteroids BD (e.g. betmethasone) or coal tar preparation
  • short-acting dithranol
  • phototherapy
  • systemic - oral methotrexate, ciclosporin, retinoids, biologics
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22
Q

What are the risks of phototherapy?

A
  • ageing

- squamous cell cancer

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23
Q

Scalp psoriasis management:

A
  • potent topical corticosteroids od for 4 weeks

- different corticosteroid formulations

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24
Q

What are some consequences of using topical corticosteroids?

A
  • skin atrophy
  • striae
  • rebound symptoms
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25
Q

What are vitamin D analogues and how are they used in psoriasis?

A

e. g. calcipotriol, calcitriol, tacalcitol
- reduced cell division and differentiation leading to reduced epidermal proliferation
- can be used long-term
- reduces scale and thickness but not erythema
- avoid in pregnancy

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26
Q

How does dithranol work and what are the ADRs?

A

inhibits DNA synthesis
wash off after 30 minutes
ADR: burning, staining

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27
Q

How does coal tar work in psoriasis?

A

inhibits DNA synthesis

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28
Q

What is acanthosis nigricans and how does it come about?

A
  • symmetrical, brown, velvet plaques often on neck, axilla and groin
  • insulin resistance leads to hyperinsulinaemia which causes keratinocyte and fibroblast proliferation via IGFR1
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29
Q

What is lichen planus, signs and symptoms and most common locations?

A
  • itchy papular rash
  • most common on palms, soles, genitalia and flexor surfaces
  • white lines on surface (Wickham’s striae)
  • Koebner phenomenon - lesion at site of trauma
  • oral involvement 50%
  • thinning nail plate and longitudinal ridging
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30
Q

Drug causes of lichen planus?

A
  • gold
  • quinine
  • thiazides
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31
Q

Management of lichen planus:

A
  • topical steroids
  • benzydamine mouthwash/spray
  • oral steroids or immunosuppression
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32
Q

What is seborrhoeic dermatitis, appearance and associations?

A
  • chronic dermatitis due to fungus Malassezia Furfur (pityrosporum ovale)
  • eczematous lesions on sebum-rich area: scalp, periorbital, auricular, nasolabial folds
  • associated with HIV and Parkinson’s
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33
Q

Scalp treatment for seborrhoeic dermatitis:

A
  • OTC zinc pyrithione (head and shoulders) and tar
  • second line: ketoconazole
  • selenium sulphide and topical corticosteroids
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34
Q

Face and body management for seborrhoeic dermatitis:

A
  • topical antifungals e.g. ketoconazole

- topical steroids (short periods)

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35
Q

Where are venous ulcers commonly found?

A

Above the medial malleolus

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36
Q

Investigations for venous ulceration:

A
  • ABPI normally 0.9-1.2
  • <0.9 indicates arterial disease
  • > 1.5 false negative due to calcification
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37
Q

Management of venous ulceration:

A
  • compression bandaging (4 layers)
  • oral pentoxyfylline (peripheral vasodilator)
  • (flavonoids)
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38
Q

What is pityriasis rosea and what are the typical features?

A
  • acute, self-limiting rash affecting young adults
  • HHV7 may have role
  • history of recent viral infection
  • herald patch usually on trunk
  • erythematous, oval, scaly patches with fir tree appearance
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39
Q

Differences between guttate psoriasis and pityriasis rosea?

A
  • guttate psoriasis preceded by streptococcal sore throat 2-4 weeks
  • guttate have tear drop appearance and scaly papules on trunk and limbs
  • pityriasis is a herald patch followed 1-2 weeks later by multiple erythematous, slightly raised oval lesions with a fine scale and fir tree appearance
  • guttate resolves spontaneously within 2-3 months
  • pityriasis is self-limiting and resolves after 6 weeks
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40
Q

What is pityriasis versicolor?

A
  • also known as tinea versicolor
  • superficial cutaneous fungal infection by malassezia furfur
  • most commonly affects trunk
  • patches of hypo pigmented pink or brown
  • scale
  • mild pruritus
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41
Q

Predisposing factors for pityriasis versicolor:

A
  • healthy individuals
  • immunosuppression
  • malnutrition
  • Cushing’s
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42
Q

Management of pityriasis versicolor:

A
  • topical anti fungal (ketoconazole shampoo)
  • if not, consider alternative diagnosis
  • oral itraconazole
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43
Q

What are actinic keratoses?

A
  • common premalignant skin lesion due to chronic sun exposure
  • small, crusty, scaly
  • pink, red, brown or skin colour
  • on sun-exposed areas
  • multiple lesions
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44
Q

Management of actinic keratoses:

A
  • prevent further exposure
  • fluorouracil cream (2-3 weeks), can cause inflammation (add topical hydrocortisone)
  • topical diclofenac
  • topical imiquimod
  • cryotherapy
  • curettage and cautery
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45
Q

What is eczema herpeticum and how do you treat it?

A
  • severe primary infection by HSV1 or 2
  • more in children with atopic eczema
  • rapidly progressing painful rash
  • monomorphic, punched out erosions 1-3mm
  • IV acyclovir and admit ASAP
46
Q

What is dermatitis herpetiformis and how do you manage it?

A
  • autoimmune blistering skin disorder associated with coeliac disease
  • caused by deposition of IgA in dermis
  • itchy, vesicular lesions on extensor surfaces
  • diagnosis with skin biopsy - direct immunofluorescence
  • manage with gluten free diet and dapsone
47
Q

What are fungal nail infections caused by?

A
  • onychomycosis
  • caused by dermatophytes, yeasts and moulds
  • RF: diabetes and age
  • thickened, rough, opaque
  • investigate with nail clippings (false negative in 30%
48
Q

Management of fungal nail infections:

A
  • dermatophytes - oral terbinafine, oral itraconazole
  • 6 weeks - 3 months for fingernails
  • 3-6 months for toenails
  • candida - mild topical antifungals - oral itraconazole
  • 6 months fingernails
  • 9-12 months toenails
49
Q

What is pyoderma gangrenosum?

A
  • affecting the lower limbs usually
  • starts as small red papule and develops into deep, red, necrotic ulcers with violaceous borders
  • may cause systemic symptoms e.g. fever, myalgia
50
Q

What are the causes of pyoderma gangrenosum?

A
  • idiopathic (50%)
  • IBD
  • RA
  • SLE
  • myeloproliferative
  • lymphoma
  • myeloid leukaemia
  • monoclonal gammopathy (IgA)
  • primary biliary cirrhosis
51
Q

Management of pyoderma gangrenosum:

A
  • oral steroids

- ciclosporin and infliximab

52
Q

What is scabies caused by and what are the symptoms?

A
  • mite - Sarcoptes Scabiei
  • spread by prolonged skin contact in children and young adults
  • lays eggs in stratum corneum
  • intense pruritus caused by delayed T4 hypersensitivity for 30 days
  • linear burrows on side of fingers, interdigital webs, flexor surfaces e.g. wrist
  • also affects face and scalp in infants
  • excoriation and infection
53
Q

Management of scabies:

A
  • permethrin 5%
  • malathion 0.5%
  • pruritus 4-6 weeks post-eradication common
  • avoid close contact until treatment complete
  • treat all contacts and laundry
54
Q

What is Norwegian scabies?

A
  • crusted scabies
  • suppressed immunity e.g. HIV
  • ivermectin and isolation
55
Q

What is shingles and the risk factors + symptoms:

A
  • acute, unilateral, painful blistering rash caused by reactivation of VZV
  • RF: increasing age, HIV, immunosuppressed
  • most commonly T1-L2
  • burning pain for 2-3 days, severe fever, headache, lethargy
  • rash initially erythematous, macular rash becoming vesicular
  • does not cross mid-line of dermatome but some bleeding into adjacent areas
56
Q

Diagnosis and management of shingles:

A
  • clinical diagnosis
  • paracetamol and NSAIDs
  • amitriptyline (or other neuropathic agents)
  • oral corticosteroids if immunocompetent
  • antivirals within 72 hours (unless <50yo and mild truncal rash with mild pain and no underlying risk factors) - reduced incidence post hepatic neuralgia
  • aciclovir, famciclovir, valaciclovir
57
Q

Complications of shingles:

A
  • post-herpetic neuralgia
  • herpes zoster ophthalmic (ocular division of trigeminal nerve)
  • herpes zoster oticus (Ramsay Hunt Syndrome)
  • may result in ear lesions and facial paralysis
58
Q

What are the possible rashes occurring in pregnancy:

A
  • atopic eruption of pregnancy
  • polymorphic eruption of pregnancy
  • pemphigoid gestationis
59
Q

What is atopic eruption of pregnancy?

A
  • most common skin disorder in pregnancy
  • eczematous, itchy red rash
  • no treatment needed
60
Q

What is polymorphic eruption of pregnancy and how do you treat it?

A
  • pruritic condition in last trimester
  • lesions first in abdominal striae
  • use emollients, mild potency topical steroids and oral steroids
61
Q

What is pemphigoid gestationis and how do you treat it?

A
  • pruritic blistering lesions
  • often peri-umbilical region to trunk, back, buttocks and arms
  • second and third trimester
  • treat with oral corticosteroids
62
Q

What are the risk factors for squamous cell carcinoma of the skin?

A
  • excessive sun exposure
  • actinic keratoses and Bowen’s disease
  • immunosuppression e.g. following renal transplant, HIV
  • smoking
  • Marjolin’s ulcer
  • genetic: xeroderma pigmentosum, oculocutaneous albinism
63
Q

Management of squamous cell carcinoma:

A
  • surgical excision with 4mm margins if <20mm diameter

- 6mm if >20mm diameter

64
Q

What are signs of good prognosis with squamous cell cancer?

A
  • well differentiated tumours
  • <20mm diameter
  • <2mm deep
  • no associated diseases
65
Q

What are signs of poor prognosis with squamous cell carcinoma?

A
  • poorly differentiated
  • > 20mm diameter
  • > 4mm deep
  • immunosuppression
66
Q

What is erythema multiforme?

A
  • hypersensitivity reaction mostly triggered by infections
  • causes target lesions initially on back of hands/feet and moving to torso, upper limbs (more than lower) and sometimes mild pruritus
67
Q

What are the causes of erythema multiforme?

A
  • viruses (herpes)
  • idiopathic
  • mycoplasma
  • strep
  • drugs: penicillin, sulphonamides, carbamazepine, allopurinol, NSAIDs, COCP
  • CTD: SLE, sarcoidosis, malignancy
68
Q

What is erythema multiforme major?

A
  • most severe form

- mucosal involvement

69
Q

What is hereditary haemorrhagic telangiectasia and the 4 diagnostic criteria?

A
  • Osler-Weber-Rendu syndrome
  • autosomal dominant

4 diagnostic criteria:

  • epistaxis - spontaneous, recurrent
  • telangiectasia
  • visceral lesions: e.g. GI, pulmonary AV malformations, hepatic AVM, cerebral, spinal
  • FHx: 1st degree relative
70
Q

Types of malignant melanoma:

A
  • superficial spreading
  • nodular
  • lentigo maligna
  • acral lentiginous
71
Q

What is superficial spreading malignant melanoma?

A
  • 70% cases
  • arms, legs, back and chest
  • young people
  • growing moles
72
Q

What is nodular malignant melanoma?

A
  • most aggressive
  • second most common
  • sun exposed skin
  • middle aged people
  • red/black lump or easily bleeds/oozes
73
Q

What is lentigo maligna malignant melanoma?

A
  • less common
  • chronically sun-exposed skin
  • older people
  • growing mole
74
Q

What is acral lentiginous malignant melanoma?

A
  • rare form
  • nails, palms or soles
  • African Americans or Asians
  • subungual pigmentation (Hutchinson’s sign) or on palms or feet
75
Q

Main diagnostic features (major criteria) for malignant melanoma:

A
  • change in size
  • change in shape
  • change in colour
76
Q

Secondary features (minor criteria) for malignant melanoma:

A
  • diameter >=7mm
  • inflammation
  • oozing or bleeding
  • altered sensation
77
Q

Margins of excision related to Breslow thickness for malignant melanoma:

A
  • 0-1mm thick: 1cm
  • 1-2mm thick: 1-2cm
  • 2-4mm thick: 2-3cm
  • > 4mm thick: 3cm
78
Q

What is toxic epidermal necrolysis?

A
  • potentially life-threatening secondary to drug reaction
  • scalded appearance
  • systemically unwell - pyrexia and tachycardia
  • positive Nikolsky’s signs - epidermis separates with mild lateral pressure
79
Q

Drugs causing toxic epidermal necrolysis:

A
  • phenytoin
  • sulphonamides
  • allopurinol
  • penicillins
  • carbamazepine
  • NSAIDs
80
Q

Management of toxic epidermal necrolysis:

A
  • supportive care (electrolyte derangement and volume loss)

- ciclosporin, cyclophosphamide, plasmapheresis

81
Q

What is vitiligo?

A
  • autoimmune loss of melanocytes - depigmentation of skin
  • 20-30yo
  • well-demarcated patches of depigmentation, mostly peripheral
  • Koebner phenomenon
82
Q

What conditions are associated with vitiligo?

A
  • T1DM
  • Addison’s
  • autoimmune thyroid
  • pernicious anaemia
  • alopecia areata
83
Q

Management of vitiligo:

A
  • sunblock
  • topical corticosteroids
  • topical tacrolimus
  • phototherapy
84
Q

Basal cell carcinomas and management:

A
  • rodent ulcers - slow growth and local invasion
  • metastases rare
  • sun-exposed areas
  • pearly, flesh-coloured papules and telangiectasia with central craters
  • surgical removal, curettage, cryotherapy, imiquimod, fluorouracil, radiotherapy
85
Q

What is hirsutism?

A

androgen-dependent hair growth in women

86
Q

What are the causes of hirsutism?

A
  • PCOS (most common)
  • Cushing’s
  • congenital adrenal hyperplasia
  • androgen therapy
  • obesity
  • adrenal tumour
  • androgen secreting ovarian tumour
  • phenytoin
  • corticosteroids
87
Q

What assessment is used for hirsutism?

A

Ferriman-Gallway

88
Q

What is the management for hirsutism?

A
  • weight loss
  • COCP
  • facial - topical eflornithine
89
Q

What are the causes of androgen-independent hypertrichosis?

A
  • minoxidil, ciclosporin, diazoxide
  • congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
  • porphyria cutanea tarda
  • anorexia nervosa
90
Q

What is impetigo?

A
  • superficial bacterial skin condition caused by staph aureus or strep pyogenes
  • primary infection or complication of eczema, scabies or insect bites
  • common in children and warm weather
  • spread by direct contact
  • very contagious
91
Q

What is the incubation of impetigo?

A

4-10 days

92
Q

What is the management of impetigo and exclusion rules?

A
  • limited/localised: hydrogen peroxide cream, topical fusidic acid, mupicorin
  • extensive: oral flucloxacillin, erythromycin
  • exclude until lesions crusted and healed or 48 hours after starting Abx
93
Q

What is lichen sclerosus?

A
  • inflammatory condition affecting genitalia and common in elderly females
  • atrophy of epidermis
  • white plaques
  • prominent itch
  • diagnosis clinical or biopsy
94
Q

What are you at increased risk of with lichen sclerosus and the management?

A
  • vulval cancer

- topical steroids and emollients

95
Q

What is molluscum contagiosum?

A
  • poxviridae
  • transmission by direct personal contact or via contaminated surfaces
  • mostly children
  • characteristic pink or pearly white papules with central umbilication up to 5mm
  • self-limiting (spontaneous resolution in 18 months)
96
Q

Where does molluscum contagiosum appear?

A
  • children: trunk, flexures, anogenital

- adults: genitalia, pubis, thighs, abdo

97
Q

Management of molluscum contagiosum:

A
  • not recommended
  • squeezing, cryotherapy
  • emollients or mild topical corticosteroids for itching
  • appears infected - topical antibiotics
  • HIV or ocular lesions - refer to specialist
98
Q

What are seborrhoeic keratoses and how do you treat?

A
  • benign epidermal lesions in older people
  • may have keratitis plugs
  • curettage, cryosurgery and shave biopsy
99
Q

What is alopecia areata?

A
  • autoimmune condition
  • localised, well-demarcated patches of hair loss
  • broken exclamation mark hairs at edge
  • regrows in 1 year for 50% and 80-90% eventually
100
Q

Management of alopecia areata:

A
  • topical/intralesional corticosteroids
  • topical minoxidil
  • phototherapy
  • dithranol
  • contact immunotherapy
  • wigs
101
Q

What is bullous pemphigoid, how do you investigate?

A
  • autoimmune sub-epidermal blistering condition
  • secondary to development of antibodies against hemidesmosomal proteins BP180 and BP230
  • itchy, tense blisters around flexures which heal without scarring
  • usually no mucosal involvement
  • skin biopsy with immunofluorescence showing IgG and C3 at dermoepidermal junction
102
Q

In whom is bullous pemphigoid more common?

A

elderly

103
Q

Management of bullous pemphigoid?

A
  • refer to dermatology
  • oral corticosteroids
  • topical corticosteroids
  • immunosuppressants and antibiotics
104
Q

What is erysipelas and management?

A
  • localised skin infection caused by streptococcus pyogenes
  • more superficial, limited version of cellulitis
  • flucloxacillin
105
Q

What is guttate psoriasis?

A
  • more common in children and adolescents
  • precipitated by streptococcal infection 2-4 weeks before lesions
  • teardrop papules on trunk and limbs
  • resolves spontaneously in 2-3 months
  • no antibiotics needed
  • topical agents as per psoriasis
  • tonsillectomy to prevent recurrence
106
Q

What are keloid scars?

A

tumour-like lesions from connective tissue of scar which extend beyond original margins

107
Q

Predisposing factors for keloid scar:

A
  • ethnicity
  • young adults
  • sternum
  • shoulder
  • neck
  • face
  • extensor surfaces
  • trunk
108
Q

Management of keloid scars:

A
  • less likely if incisions made along relaxed skin tension lines
  • early treated with intra-lesional steroids e.g. triamcinolone
  • sometimes excision
109
Q

What is Koebner phenomenon?

A
  • lesions appearing at site of injury

- psoriasis, vitiligo, warts, lichen planus, lichen sclerosus, molluscum contagiosum

110
Q

Causes of pruritus:

A
  • liver disease
  • iron deficiency
  • polycythaemia
  • CKD
  • lymphoma
  • hypo/hyperthyroidism
  • diabetes
  • pregnancy
  • senile pruritus
  • urticaria
  • skin disorders: eczema, scabies, psoriasis, pityriasis rosacea
111
Q

What are salmon patches?

A
  • vascular birthmark
  • pink and blotchy
  • forehead, eyelids, nape of neck
  • fade over few months
112
Q

What is Kaposi sarcoma?

A
  • tumour of vascular and lymphatic endothelium
  • purple cutaneous nodules
  • associated with immunosuppression - aggressive
  • affects elderly females
  • growing

Dermatology (2 decks)

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