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Dermatology Flashcards

1
Q

ACNE VULGARIS

What is the pathophysiology of acne vulgaris?

A
  • Obstruction of the pilosebaceous follicles with keratin plugs with colonisation by anaerobic bacterium Propionibacterium acnes
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2
Q

ACNE VULGARIS

How is acne categorised based on clinical presentation?

A
  • Mild = open (blackheads) + closed (whiteheads) comedones ± sparse inflammatory lesions
  • Mod = widespread non-inflammatory lesions, numerous papules + pustules
  • Severe = extensive inflammatory lesions, may include nodules, pitting + scarring
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3
Q

ACNE VULGARIS

What is the first line management of acne vulgaris?

A
  • Single topical (non-Abx) therapy e.g., topical retinoid adapalene, benzoyl peroxide
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4
Q

ACNE VULGARIS

What is the second line management of acne vulgaris?

A
  • Topical combination therapy = benzoyl peroxide and clindamycin
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5
Q

ACNE VULGARIS
What is the third line management of acne vulgaris?
What are the exceptions to this?
How long can you do this treatment for?

A
  • PO tetracyclines (lyme/doxycycline) WITH topical combination therapy of retinoid + benzoyl peroxide to reduce Abx
  • Avoid tetracyclines in pregnancy (use erythromycin), breastfeeding + children <12m
  • Single PO Abx used for maximum of 3m
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6
Q

ACNE VULGARIS
Other than PO Abx, what else may be considered?
What is the secondary care management of acne vulgaris, an important contraindication and some side effects?

A
  • COCP with topical combination therapy
  • PO isotretinoin > C/I in pregnancy
  • SE = dry skin, depression, teratogenic, increased triglycerides.
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7
Q 
ATOPIC DERMATITIS (ECZEMA)
What is the pathophysiology of atopic dermatitis?
A
  • Defects in the skin barrier allows entrance to irritants, microbes + allergens which create an immune response + so inflammation
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8
Q 
ATOPIC DERMATITIS (ECZEMA)
What is the clinical presentation of atopic dermatitis?
A
  • Erythematous, dry, itchy patches over the flexor surfaces, face + neck
  • May be on extensor surfaces in younger children
  • May have PMHx/FHx of atophy (asthma, hayfever)
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9
Q 
ATOPIC DERMATITIS (ECZEMA)
What are two key complications of atopic dermatitis?
A
  • Opportunistic bacterial infection

- Eczema herpeticum

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10
Q 
ATOPIC DERMATITIS (ECZEMA)
How do opportunistic bacterial infections present?
What is the management?
A
  • Staph. aureus = increased erythema, yellow crust, pustules

- PO flucloxacillin or admit for IV if severe

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11
Q 
ATOPIC DERMATITIS (ECZEMA)
How does eczema herpeticum present?
What is the management?
A
  • Widespread vesicular lesions with pus + generally unwell secondary to HSV/VZV
  • Same day derm, PO or IV aciclovir
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12
Q 
ATOPIC DERMATITIS (ECZEMA)
What is the maintenance management for atopic dermatitis?
A
  • Avoid irritants
  • Simple emollients (E45)
  • Soap substitutes
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13
Q 
ATOPIC DERMATITIS (ECZEMA)
What is the flare management fo atopic dermatitis?
A
  • Thicket emollients
  • Topical steroids (weakest for shortest period) Help Every Budding Dermatologist = Hydrocortisone > Eumovate > Betnovate > Dermovate.
  • Wet wraps with thick emollient to keep moisture overnight
  • PO ciclosporin if very severe
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14
Q

ATOPIC DERMATITIS (ECZEMA)
What are some side effects of topical steroids?
What should you tell patients about applying emollients and topical steroids?

A
  • Thinning of skin, telangiectasia, bruising

- Apply emollients first, wait 30m, then topical steroids

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15
Q

PSORIASIS

What can trigger psoriasis?

A
  • Stress
  • Trauma
  • Steroid withdrawal
  • Alcohol
  • BALI drugs = Beta-blockers, Anti-malarials, Lithium, Indomethacin (NSAIDs)
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16
Q

PSORIASIS

What are the 5 types of psoriasis?

A
  • Chronic plaque #1
  • Flexural
  • Guttate
  • Pustular
  • Erythrodermic
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17
Q

PSORIASIS
Explain the presentation of…

i) chronic plaque psoriasis?
ii) flexural psoarisis?

A

i) Well-demarcated, red scaly patches on extensor surfaces, sacrum + scalp
ii) Smooth, erythematous plaques without scale in flexures + skin folds

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18
Q

PSORIASIS
Explain the presentation of…

i) guttate psoriasis?
ii) pustular psoriasis?
ii) erythrodermic psoariasis?

A

i) Transient, multiple tear drop lesions 2w post-group A strep infection
ii) Multiple petechiae + pustules on palms + soles
iii) Extensive erythema + systemically unwell > emergency admit

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19
Q

PSORIASIS

What are some signs seen in psoriasis?

A
  • Nails = pitting, onycholysis, subungual hyperkeratosis
  • Koebner phenomenon = new plaques of psoriasis at sites of skin trauma
  • Auspitz sign = small points of bleeding when plaques scraped off
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20
Q

PSORIASIS

What are some complications of psoriasis?

A
  • Psoriatic arthritis
  • Metabolic syndrome
  • CVD
  • VTE
  • Psychological distress
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21
Q

PSORIASIS

What is the general management of psoriasis?

A
  • All patients use an emollient to reduce scale + itch

- Avoid triggers

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22
Q

PSORIASIS
What is the first line management of psoriasis?
What is the second line management of psoriasis?
What is the third line management of psoriasis?

A
  • Potent corticosteroid TOP OD plus vitamin D TOP OD (calcipotriol)
  • Vitamin D TOP BD
  • Potent corticosteroid BD or coal tar preparation BD
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23
Q

PSORIASIS

What is the secondary care management of psoriasis?

A
  • UVB phototherapy
  • Systemic = methotrexate > ciclosporin
  • Biologics like infliximab, adalimumab
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24
Q

PSORIASIS
What is the mechanism of action of vitamin D analogues?
What effect does this have?
What patient safety information is crucial?

A
  • Reduce cell division + differentiation > reduced epidermal proliferation
  • Reduce scale + thickness of plaques but NOT erythema
  • Can be used long-term unlike steroids but AVOID in pregnancy
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25
Q

CONTACT DERMATITIS

What are the two types of contact dermatitis and what classically causes them?

A
  • Irritant (common) = non-allergic reaction typically detergents
  • Allergic = T4 hypersensitivity reaction typically head following hair dyes
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26
Q

CONTACT DERMATITIS
How does irritant contact dermatitis present?
How is it managed?

A
  • Erythema, usually in the hands

- Emollients, topical corticosteroids

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27
Q

CONTACT DERMATITIS
How does allergic contact dermatitis present?
How is it managed?

A
  • Acute weeping eczema affecting margin of hairline

- Topical potent corticosteroid

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28
Q

BASAL CELL CARCINOMA
What is a basal cell carcinoma (BCC)?
What is the epidemiology and most common type?
What are some risk factors?

A
  • Locally invasive, slow growing tumour of epidermal keratinocytes (mets rare)
  • # 1 cancer in Western world, nodular BCC most common
  • Sun burn, increasing age, fair skin, immunosuppression, FHx
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29
Q

BASAL CELL CARCINOMA

What is the clinical presentation of BCC?

A
  • Classically sun-exposed sites = head + neck
  • Pearly, flesh-coloured papule with surface telangiectasia
  • Rolled edges
  • Older lesions = centre necrotic/ulcerated (Rodent ulcer)
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30
Q

BASAL CELL CARCINOMA

What is the management of a BCC?

A
  • Routine derm referral

- Surgical excision, curettage, cryotherapy, topical imiquimod, radiotherapy

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31
Q

SQUAMOUS CELL CARCINOMA
What is a squamous cell carcinoma (SCC)?
What is the spectrum of conditions that can result in SCC?

A
  • Locally invasive malignant tumour of epidermal keratinocytes
  • Actinic keratosis > Bowen’s disease (in situ SCC) > SCC
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32
Q

SQUAMOUS CELL CARCINOMA

What are some risk factors for SCC?

A
  • Excessive UV light exposure + sun burn
  • Actinic keratoses + Bowen’s disease
  • Immunosuppression (renal transplant, HIV)
  • Smoking
  • Long-standing leg ulcers
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33
Q

SQUAMOUS CELL CARCINOMA

What is the clinical presentation of SCC?

A
  • Irregular, ill-defined red nodules (scaly, keratotic + ulcerated)
  • Sun-exposed areas = face, scalp, hands
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34
Q

SQUAMOUS CELL CARCINOMA

What is the management of SCC?

A
  • <20mm diameter = surgical excision with 4mm margins
  • > 20mm diameter = surgical excision with 6mm margins
  • Mohs micrographic surgery = high-risk patients + cosmetically important sites
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35
Q

MALIGNANT MELANOMA
What is a malignant melanoma?
Where do they commonly metastasise to?

A
  • Neoplastic transformation of melanocytes

- Lungs + brain

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36
Q

MALIGNANT MELANOMA

What are the 4 types of malignant melanoma?

A
  • Superficial spreading #1
  • Nodular
  • Lentigo maligna
  • Acral lentiginous
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37
Q

MALIGNANT MELANOMA
What are the unique features of…

i) superficial spreading melanoma?
ii) nodular melanoma?
iii) lentigo maligna melanoma?
iv) acral lentiginous melanoma?

A

i) Pre-existing naevus which grows horizontal > vertical
ii) New lesion, aggressive, bleeds + ulcerates
iii) Sun damaged skin in elderly
iv) Subungual pigmentation (Hutchinson’s sign), non-whites

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38
Q

MALIGNANT MELANOMA

What are some risk factors for malignant melanoma?

A
  • UV light exposure + tanning beds
  • Fair skin + red hair
  • Large number of moles
  • FHx + increasing age
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39
Q

MALIGNANT MELANOMA

What is the clinical presentation of malignant melanoma?

A

ABCDE

  • Asymmetrical
  • Border irregular
  • Colour irregular
  • Diameter >6mm
  • Evolving in nature
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40
Q

MALIGNANT MELANOMA
What would you do in suspected melanoma?
What is the single most important prognostic marker?

A
  • Urgent 2ww derm referral

- Breslow thickness > thicker = worse prognosis

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41
Q

MALIGNANT MELANOMA

What is the management of confirmed melanoma?

A
  • Excision biopsy > stage 0 = 0.5cm, stage 1 = 1cm, stage 2 = 2cm
  • Stage III + IV metastatic = adjuvant immunotherapy, chemotherapy
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42
Q

BURNS

What are the various gradings of burns?

A
  • Superficial epidermal (1º) = red, painful
  • Superficial dermal (2º) = red, painful, blistered
  • Deep dermal (2º) = decreased sensation, white
  • Full thickness (3º) = white, no pain/blisters, may have muscle or bone involvement
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43
Q

BURNS
How can you assess the extend of the burn on the total body surface area?
What is the most accurate method?

A
  • Wallace’s rule of nines

- Lung and broder chart

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44
Q

BURNS

What is Wallace’s rule of nines?

A
  • Head + neck = 9%
  • Each arm = 9%
  • Anterior leg = 9% each
  • Posterior leg = 9% each
  • Anterior/posterior chest = 9% each
  • Anterior/posterior abdomen = 9% each
  • Groin = 1%
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45
Q

BURNS

What are some potential complications following burns?

A
  • Hypovolaemic shock due to excess fluid loss in skin
  • Infection due to loss of skin barrier
  • Metabolic disturbance = high K+, high myoglobin (AKI)
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46
Q

BURNS

What are some indications to refer burns to secondary care?

A
  • Any burn affecting face, neck, hands, feet or genitals
  • Deep dermal + full-thickness burns
  • Superficial dermal burns >3% TBSA adults, >2% paeds
  • Any smoking inhalation injury, chemical or electrical burns or NAI
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47
Q

BURNS
What is your immediate management of burns?
What are you particularly looking out for?

A
  • ABCDE (soot + stridor)
  • IV fluids as per Parkland formula
  • Analgesia
  • Catheter
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48
Q

BURNS
What is the Parkland formula?
When is it indicated?
How is it applied?

A
  • 24h fluid requirement (ml) = TBSA % x kg x 4
  • Adults >15% TBSA or paeds >10% TBSA
  • HALF given in FIRST 8H, remainder over 16h
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49
Q

BURNS

What is the management of burns post-ABCDE assessment?

A
  • Stop burning via irrigation with water (>10m)
  • Layered clingfilm NOT wrapped due to swelling + compartment syndrome
  • Cover in sterile, non-adherent dressing
  • Circumferential = escharotomy
  • Full thickness = skin grafting
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50
Q

ULCERS
What is the cause of…

i) venous ulcers?
ii) arterial ulcers?
iii) neuropathic ulcers?

A

i) Venous insufficiency
ii) CVD risk factors (smoking, cholesterol, DM, HTN)
iii) Peripheral neuropathy #1 diabetes, unable to feel pressure to skin > ulcer

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51
Q

ULCERS
What is the location of…

i) venous ulcers?
ii) arterial ulcers?
iii) neuropathic ulcers?

A

i) Medial malleolus
ii) Forefoot + toes, incl. pressure sites
iii) Pressure points (e.g., plantar surface)

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52
Q

ULCERS
What are unique features of…

i) venous ulcers?
ii) arterial ulcers?
iii) neuropathic ulcers?

A

i) Varicose veins, haemosiderin deposits (pigmentation), lipodermatosclerosis (hard, tight skin), venous eczema)
ii) Punched out ulcers
iii) Reduced sensation in foot

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53
Q

ULCERS
Venous ulcers: comment on the following features…

i) regularity
ii) depth
iii) temperature
iv) pulses
v) sensation

A

i) Irregular
ii) Shallow
iii) Normal
iv) Present
v) Painless

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54
Q

ULCERS
Arterial ulcers: comment on the following features…

i) regularity
ii) depth
iii) temperature
iv) pulses
v) sensation

A

i) Regular
ii) Deep
iii) Cold
iv) Absent
v) Painful

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55
Q

ULCERS
Neuropathic ulcers: comment on the following features…

i) regularity
ii) depth
iii) temperature
iv) pulses
v) sensation

A

i) Regular
ii) Deep
iii) Normal
iv) Present
v) Painless + reduced sensation overall

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56
Q

ULCERS
What investigation would you do in the following, what would it show and what is the importance…

i) venous ulcers?
ii) arterial ulcers?

A

i) ABPI normal 0.9–1.2
ii) ABPI abnormal <0.9 = do NOT use compression bandages as sign of arterial disease so could lead to critical limb ischaemia

57
Q

ULCERS
What is the management of…

i) venous ulcers?
ii) arterial ulcers?
iii) neuropathic ulcers?

A

i) First line = compression bandages, if not refer vascular
ii) Modify RFs, exercise, refer to vascular for bypass or angioplasty
iii) Education on diabetic foot health, orthotics

58
Q

CELLULITIS
What is cellulitis?
What is a similar condition and the differences?
What are some risk factors for developing cellulitis?

A
  • Inflammation of dermis + subcutaneous tissue usually due to streptococcus pyogenes or staphylococcus aureus
  • Erysipelas = infection of the dermis + upper s/c tissue
  • Venous insufficiency, obesity, immune deficiency (DM, HIV)
59
Q

CELLULITIS

What is the clinical presentation of cellulitis?

A
  • Erythema, pain + swelling commonly at shins
  • Poorly demarcated, usually unilateral
  • May be systemically unwell with a fever
60
Q

CELLULITIS

How is cellulitis diagnosed?

A
  • Clinical but Eron classification to guide management
  • I = systemically well
  • II = mildly systemically unwell or systemically well but co-morbidity which could slow healing (PVD)
  • III = significantly systemically unwell
  • IV = septic or life-threatening infection like necrotising fasciitis
61
Q

CELLULITIS

When would you consider admitting someone for IV Abx in cellulitis?

A
  • Eron class III/IV
  • Rapidly deteriorating
  • <1y
  • Immunocompromised
62
Q

CELLULITIS
What is the management of mild-moderate cellulitis?
What alternatives are there?
What is the management of severe cellulitis?
What conservative measures would you do?

A
  • Flucloxacillin
  • Clarithryomycin/doxycyline if pen allergic, erythromycin if pregnant
  • Co-amox, cefuroxime, clindamycin, ceftriaxone
  • Draw around lesion, analgesia, elevate leg
63
Q

NECROTISING FASCIITIS
What is necrotising fasciitis?
What are the two types of necrotising fasciitis?
What are some risk factors?

A
  • Infection of subcutaneous fascia + fat.
  • Type 1 (#1) = mixed anaerobes + aerobes often post-surgery in patients with DM
  • Type 2 = streptococcus pyogenes
  • DM (esp. if on SGLT-2i), IVDU, immunosuppression, skin trauma
64
Q

NECROTISING FASCIITIS
What is the most affected site for necrotising fasciitis?
What is the clinical presentation?

A
  • Perineum/external genitalia (Fournier’s gangrene)
  • Rapidly worsening cellulitis with pain out of keeping with physical features
  • Swelling, erythema, sepsis
  • Skin necrosis + crepitus are LATE signs
65
Q

NECROTISING FASCIITIS

What is the management of necrotising fasciitis?

A
  • Urgent surgical debridement + IV Abx
66
Q

GANGRENE
What is gangrene?
What are the two types and the differences?

A
  • Necrosis of tissues due to poor vascular supply
  • Wet gangrene = infectious gangrene
  • Dry gangrene = ischaemic gangrene, non-infective
67
Q

GANGRENE
What are some causes of wet gangrene and how does it present?
What are some causes of dry gangrene and how does it present?

A
  • Nec fasc, gas gangrene + gangrenous cellulitis
  • Necrotic area, poorly demarcated from surrounding tissue, septic
  • Atherosclerosis (PVD), thrombosis (vasculitis, thrombophilia), vasospasm (cocaine, Raynaud’s)
  • Necrotic area, well demarcated from surrounding tissue, systemically well
68
Q

GANGRENE
What is the management of wet gangrene?
What is the management of dry gangrene?

A
  • Surgical debridement/amputation + broad-spectrum IV Abx

- Auto-amputation occurs in most cases

69
Q

IMPETIGO
What is impetigo?
How does it present?

A
  • Superficial skin infection 2º to staph aureus or strep pyogenes
  • Golden crusted lesions classically around mouth, pruritic, very contageous
70
Q

IMPETIGO
What are the conservative measures for impetigo?
What is the first line management of impetigo?

A
  • School exclusion until lesions crusted/healed or 48h after Abx, no sharing towels
  • Hydrogen peroxide 1% cream (if not systemically unwell or high risk)
71
Q

IMPETIGO
What is the second line management of impetigo?
What is the management of systemically unwell impetigo?

A
  • Topical fusidic acid (mupirocin if resistance suspected or MRSA)
  • PO flucloxacillin (erythromycin in pen allergy)
72
Q

HEAD LICE
What is head lice caused by?
How does it present?

A
  • Pediculus capitis = parasite that infest the hairs + feeds on blood from scalp
  • Itchy scalp, suboccipital lymphadenopathy
73
Q

HEAD LICE
How is head lice diagnosed?
How is it managed?
What are the conservative aspects to management?

A
  • Fine-toothed combing of hair (nits/eggs + lice visible)
  • Dimeticone 4% or malathion 0.5% lotions (apply twice, 7d apart)
  • No school exclusion, only treat household contacts if symptomatic
74
Q

SCABIES

What is scabies?

A
  • Infestation of mites (Sarcoptes scabiei) that burrow under skin + lay eggs
  • Delayed T4 hypersensitivity reaction
75
Q

SCABIES

How does scabies present?

A
  • Widespread pruritus + linear burrows (finger webs, side of fingers)
  • Pruritus can be worse at night > excoriation + secondary bacterial infection
  • Often whole household itching
76
Q

SCABIES
What is a key complication of scabies?
How does it present?
How is it treated?

A
  • Crusted scabies = serious infestation in immunocompromised (HIV)
  • Patches of red skin > scaly plaques
  • Rx = inpatient with PO ivermectin + isolation
77
Q

SCABIES

What are the conservative aspects to scabies management?

A
  • ALL close contacts treated even if asymptomatic > school exclusion until treated
  • Wash bed linen, towels, clothes + clean furniture etc. to destroy mites
78
Q

SCABIES
What is the first line treatment of scabies?
What is the second line treatment of scabies?

A
  • Permethrin 5% (cover whole body 8–12h > wash off > repeat in 1w)
  • Malathion 0.5% (cover whole body 24h > wash off > repeat in 1w)
79
Q

BULLOUS PEMPHIGOID
What is bullous pemphigoid?
How does it present?

A
  • Autoimmune condition causing sub-epidermal blistering of the skin (T2 hypersensitivity reaction)
  • Deep tense blisters (often around flexures) which heal without scarring, NO mucosal involvement, common in elderly
80
Q

BULLOUS PEMPHIGOID

What is the management of bullous pemphigoid?

A
  • Derm for skin biopsy + immunofluorescence (IgG on basement membrane)
  • PO corticosteroids, topical potent steroids (dermovate), Abx (doxy if mild)
81
Q

PEMPHIGUS VULGARIS

What is pemphigus vulgaris?

A
  • Autoimmune deposition of IgG autoantibodies within the epidermis (T2 hypersensitivity reaction)
82
Q

PEMPHIGUS VULGARIS

What is the clinical presentation of pemphigus vulgaris?

A
  • Fragile, superficial blisters that rupture easily
  • Nikolsky sign = slight rubbing of skin causes outermost layer to peel away
  • More common in the Ashkenazi Jewish population
83
Q

PEMPHIGUS VULGARIS

What is the management of pemphigus vulgaris?

A
  • Derm for skin biopsy + immunofluorescence (IgG within epidermis)
  • PO corticosteroids mainstay, immunosuppressants
84
Q

PITYRIASIS ROSEA
What is pityriasis rosea?
How is it managed?

A
  • Self-limiting rash in young adults 2º to herpes hominis virus 7 (HHV-7)
  • No treatment, resolves 6–12w
85
Q

PITYRIASIS ROSEA

What is the clinical presentation of pityriasis rosea?

A
  • May have viral prodrome
  • Initial = herald patch on trunk (single, large, discoid erythematous patch)
  • Later = erythematous, oval, scaly patches on trunk (fir-tree appearance)
86
Q

PITYRIASIS VERSICOLOR
What is pityriasis versicolour?
What are some predisposing factors?

A
  • Superficial cutaneous fungal infection caused by Malassezia furfur
  • Healthy, immunosuppression, Cushing’s
87
Q

PITYRIASIS VERSICOLOR

What is the clinical presentation of pityriasis versicolor?

A
  • Hypopigmented/pink/brown (versicolor) patches on trunk

- Mild pruritus + scale is common, noticed after suntan

88
Q

PITYRIASIS VERSICOLOR

What is the management of pityriasis veriscolor?

A
  • First line = topical antifungal ketoconazole shampoo, clotrimazole if small area
89
Q

ROSACEA

What is rosacea? Who does it commonly affect? What are some triggers?

A
  • Chronic skin condition
  • Females
  • Sun exposure, hot weather, stress
90
Q

ROSACEA

What is the clinical presentation of rosacea?

A
  • Flushing of nose, cheeks + forehead

- Erythema with papules, pustules + telangiectasia

91
Q

ROSACEA

What are two potential complications of rosacea?

A
  • Ocular involvement = blepharitis, conjunctivitis or keratitis
  • Rhinophyma = skin thickening + disfiguration of nose > dermatology
92
Q

ROSACEA

What general measures may be used in rosacea?

A
  • Camouflage creams, sun protection

- Laser therapy if prominent telangiectasia

93
Q

ROSACEA
What is the management of mild-moderate rosacea?
What is the management of severe/unresponsive rosacea?

A
  • Topical metronidazole, topical ivermectin

- PO Abx (oxytetracycline)

94
Q

SEBORRHOEIC KERATOSES

What is the clinical presentation of seborrhoeic keratoses?

A
  • Flesh/light brown/black benign epidermal skin lesions in older people
  • ‘Stuck-on’ appearance
  • Keratotic plugs may be seen on surface
95
Q

SEBORRHOEIC KERATOSES

What is the management of seborrhoeic keratoses?

A
  • Reassurance

- Removal via curettage, cryosurgery + shave biopsy

96
Q

ACTINIC KERATOSES
What are actinic keratoses?
How do they present?

A
  • Common pre-malignant skin lesion (cutaneous SCC) due to chronic sun exposure (temples of head, nose)
  • Small, thickened lesions with surrounding erythema + keratotic, rough surface
97
Q

ACTINIC KERATOSES
What is the general management of actinic keratoses?
What is the management for localised?
What is the management for large lesions?

A
  • Prevent further risk = avoid sun, SPF50+ all year round
  • Cryotherapy, curettage, or surgical excision
  • Topical 5-fluorouracil, NSAID or imiquimod
98
Q

KERATOACANTHOMA
What is a keratoacanthoma?
How does it present?

A
  • Benign epithelial tumour common with increased age

- Initially smooth dome-shaped papule > rapidly grows to become crater centrally filled with keratin

99
Q

KERATOACANTHOMA

What is the management of keratoacanthoma?

A
  • Spontaneous regression <3m but urgently excised as clinically difficult to say if SCC = leaves a scar
100
Q

MOLLUSCUM CONTAGIOSUM
What is molluscum contagiosum caused by?
How is it transmitted?

A
  • Molluscum contagiosum virus (pox virus)

- Direct skin contact, also sharing towels

101
Q

MOLLUSCUM CONTAGIOSUM
What is the clinical presentation of molluscum contagiosum?
How does this differ in immunocompromised?

A
  • Small, smooth, pearly coloured papules in clusters with central umbilication
  • Immunocompromised = face, extensive lesions
102
Q

MOLLUSCUM CONTAGIOSUM

What is the management of molluscum contagiosum?

A
  • All patients offered full STI test, especially if anogenital lesions
  • Supportive (avoid sharing towels)
  • If cosmetic distress = cryotherapy (risk of scarring)
103
Q

MOLLUSCUM CONTAGIOSUM

When would you consider referral in molluscum contagiosum?

A
  • HIV +ve with extensive lesions = HIV specialist

- Eyelid margin/ocular lesions with red eye = ophthalmology

104
Q

SEBORRHOEIC DERMATITIS
What is the pathophysiology of seborrhoeic dermatitis?
What is it particularly associated with?

A
  • Chronic dermatitis caused by inflammatory reaction to proliferation of a normal skin fungus Malassezia furfur
  • HIV, Parkinson’s, stress, oily skin
105
Q

SEBORRHOEIC DERMATITIS

What is the clinical presentation of seborrhoeic dermatitis in paeds?

A
  • ‘Cradle cap’ = erythematous rash with coarse yellow scales
106
Q

SEBORRHOEIC DERMATITIS

What is the clinical presentation of seborrhoeic dermatitis in adults?

A
  • Eczematous, flaky lesions in sebum rich areas (scalp = dandruff, periorbital, auricular + nasolabial folds)
  • Otitis externa + blepharitis may occur
107
Q

SEBORRHOEIC DERMATITIS

What is the management of cradle cap?

A
  • Mild-mod = baby shampoo + baby oils

- Severe = mild topical 1% hydrocortisone

108
Q

SEBORRHOEIC DERMATITIS
What is the management of scalp seborrhoeic dermatitis?
What is the management of face/body seborrhoeic dermatitis?

A
  • First line = OTC shampoo with zinc pyrithione (Head & Shoulders), second line = ketoconazole shampoo
  • First line = topical anti fungals (ketoconazole), topical steroids (short periods)
109
Q

TINEA
What is tinea?
What causes it?

A
  • Dermatophyte fungal infections, usually trichophyton

- If Microsporum canis = fluoresce under Wood’s lamp

110
Q

TINEA

What are the 4 main types of tinea?

A
  • Tinea capitis (scalp ringworm)
  • Tinea corporis (ringworm)
  • Tinea pedis (athlete’s foot)
  • Onychomycosis
111
Q

TINEA
What is the clinical presentation of…

i) tinea capitis?
ii) tinea corporis?

A

i) Scaly + patchy alopecia, can lead to spongy mass (kerion) if untreated
ii) Well-defined, annular, erythematous lesions with pustules + papules

112
Q

TINEA
What is the clinical presentation of…

i) tinea pedis?
ii) onychomycosis?

A

i) Itchy, peeling skin between the toes

ii) Thickened, rough + opaque nails (can be secondary to Candida too)

113
Q

TINEA
How do you investigate tinea?
What is the management?

A
  • Culture of skin scrapings/nail clippings for fungal hyphae
  • Topical antifungals = clotrimazole, ketoconazole
  • Systemic antifungals = terbinafine, itraconazole for tinea capitis or onychomycosis
114
Q

ERYTHEMA NODOSUM
What is erythema nodosum?
How does it present?

A
  • Inflammation of subcutaneous fat

- Tender, erythematous, nodules often on shins

115
Q

ERYTHEMA NODOSUM

What are the causes of erythema nodosum?

A

NODOSUM –

  • NO cause = idiopathic
  • Drugs = penicillins, sulfonamides
  • OCP
  • Sarcoidosis
  • Ulcerative colitis/Crohn’s
  • Micro = streptococci, TB
116
Q

ERYTHEMA MULTIFORME
What is erythema multiforme?
What is the most common cause?

A
  • Hypersensitivity reaction usually triggered by infections

- Herpes simplex virus

117
Q

ERYTHEMA MULTIFORME

What are some other causes of erythema multiforme?

A
  • Bacteria = mycoplasma, streptococcus
  • Drugs = penicillin, sulfonamides, NSAIDs, OCP
  • SLE, sarcoidosis + malignancy
118
Q

ERYTHEMA MULTIFORME

What is the clinical presentation of the two types of erythema multiforme?

A
  • Minor = well-defined circular papules which form target-shaped lesions, usually start on palms/soles then spread up limbs to trunk
  • Major = similar but also mucous membrane involvement e.g., oral mucosa
119
Q

ERYTHRODERMA
What is erythroderma?
What are some causes?

A
  • > 95% of skin involved in a rash of any kind
  • Derm = eczema, psoriasis (esp. after steroid withdrawal)
  • Drugs = gold
  • Haem = lymphomas, leukaemias
  • Idiopathic
120
Q

ERYTHRODERMA

What is the management of erythroderma?

A
  • Med emergency = admit for IV fluids, analgesia, emollients

- Monitor for complications = dehydration, infection, high-output heart failure, hypothermia

121
Q

LICHEN PLANUS

What drugs can cause a lichenoid eruption?

A
  • Gold
  • Antimalarials
  • Beta-blockers, ACEi + thiazides
122
Q

LICHEN PLANUS

What is the clinical presentation of lichen planus?

A
  • Ps = Purple, Pruritic, Papular, Polygonal rash on flexor surfaces
  • “White-lines” pattern on surface = Wickham’s striae
  • Nails = longitudinal ridging
  • White lace pattern on buccal mucosa + Koebner’s phenomenon may be seen
123
Q

LICHEN PLANUS

What is the management of lichen planus?

A
  • Potent topical steroids, ?PO immunosuppression if extensive
  • Benzydamine mouthwash/spray if oral lichen planus
124
Q

VITILIGO
What is vitiligo?
What conditions is it associated with?

A
  • Autoimmune condition leading to loss of melanocytes + skin depigmentation
  • T1DM, Addison’s, thyroid, pernicious anaemia, alopecia areata
125
Q

VITILIGO

What is the clinical presentation of vitiligo?

A
  • Well-demarcated patches of depigmented skin + white hair in those areas
  • Peripheries are MOST affected
  • Koebner phenomenon = new lesions at site of trauma
126
Q

VITILIGO

What is the management of vitiligo?

A
  • Sunblock for affected areas, camouflage make-up
  • Topical corticosteroids may reverse changes if early
  • ?Role for topical tacrolimus + phototherapy
127
Q

ALOPECIA AREATA

What is alopecia areata and how does it present?

A
  • Autoimmune condition causing localised, well demarcated patches of hair loss
  • At edge of hair loss, may be small, broken ‘exclamation mark’ hairs
128
Q

ALOPECIA AREATA

What is the management of alopecia areata?

A
  • Hair will regrow in 50% in 1y and 80–90% eventually

- Options = topical corticosteroids or minoxidil, phototherapy, wigs

129
Q

URTICARIA
What is urticaria?
What are some drug causes?
How does it present?

A
  • Local/generalised superficial swelling of skin often secondary to allergy (T1HR)
  • NSAIDs/aspirin, penicillins, opiates
  • Pale, pink, pruritic, raised lesion “hives/wheals”
130
Q

URTICARIA

What is the management of urticaria?

A
  • First line = non-sedating antihistamines like cetirizine, loratadine
  • Severe/resistant = PO prednisolone
131
Q

FOLLICULITIS
What is folliculitis?
What causes it?

A
  • Inflammation of hair follicle > papules or pustules (pimples) + can occur anywhere except palms + soles
  • Mostly staph aureus, can be gram -ve after prolonged acne Abx treatment
132
Q

FOLLICULITIS
What is eosinophilic folliculitis?
How is it diagnosed?
How is it managed?

A
  • Sterile folliculitis caused by immunosuppression (HIV)
  • Skin biopsy = eosinophils in skin surface
  • HAART + topical corticosteroids
133
Q

LYME DISEASE

What causes Lyme disease?

A
  • Spirochaete Borrelia burgdoferi + is spread via ticks
134
Q

LYME DISEASE

What are the early features of Lyme disease?

A

Within 30d –

  • Erythema migrans = ‘bulls-eye’ rash at site of tick bite, painless, >5cm + slowly increases
  • Systemic = headache, lethargy, fever, arthralgia
135
Q

LYME DISEASE

What are the late features of Lyme disease?

A

After 30d –

  • Cardio = heart block + peri/myocarditis
  • Neuro = facial nerve palsy, meningitis
136
Q

LYME DISEASE

How is Lyme disease diagnosed?

A
  • Erythema migrans present = clinical Dx
  • ELISA for Borrelia burgdorferi = first line test
    – If test within 4w from symptoms and negative, repeat test after 4–6w
137
Q

LYME DISEASE
What is the management of asymptomatic ticks in general?
What is the management of Lyme disease?

A
  • Fine-tipped tweezers, grasp as close to skin + pull upwards firmly
  • Doxycycline if early disease, amoxicillin if C/I (pregnancy)
  • Ceftriaxone if disseminated disease
138
Q

LYME DISEASE

What potential complication may be seen after treating Lyme disease?

A
  • Jarisch-Herxheimer reaction = fever, rash, tachycardia after 1st dose Abx

FINALS (20 decks)

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