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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

ACNE VULGARIS

What is the second line management of acne vulgaris?

A
  • Topical combination therapy = benzoyl peroxide and clindamycin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q
ATOPIC DERMATITIS (ECZEMA)
What are two key complications of atopic dermatitis?
A
  • Opportunistic bacterial infection

- Eczema herpeticum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q
ATOPIC DERMATITIS (ECZEMA)
What is the maintenance management for atopic dermatitis?
A
  • Avoid irritants
  • Simple emollients (E45)
  • Soap substitutes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PSORIASIS

What can trigger psoriasis?

A
  • Stress
  • Trauma
  • Steroid withdrawal
  • Alcohol
  • BALI drugs = Beta-blockers, Anti-malarials, Lithium, Indomethacin (NSAIDs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

PSORIASIS

What are the 5 types of psoriasis?

A
  • Chronic plaque #1
  • Flexural
  • Guttate
  • Pustular
  • Erythrodermic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

PSORIASIS

What are some complications of psoriasis?

A
  • Psoriatic arthritis
  • Metabolic syndrome
  • CVD
  • VTE
  • Psychological distress
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

PSORIASIS

What is the general management of psoriasis?

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

- Avoid triggers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

PSORIASIS

What is the secondary care management of psoriasis?

A
  • UVB phototherapy
  • Systemic = methotrexate > ciclosporin
  • Biologics like infliximab, adalimumab
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
CONTACT DERMATITIS | What are the two types of contact dermatitis and what classically causes them?
- Irritant (common) = non-allergic reaction typically detergents - Allergic = T4 hypersensitivity reaction typically head following hair dyes
26
CONTACT DERMATITIS How does irritant contact dermatitis present? How is it managed?
- Erythema, usually in the hands | - Emollients, topical corticosteroids
27
CONTACT DERMATITIS How does allergic contact dermatitis present? How is it managed?
- Acute weeping eczema affecting margin of hairline | - Topical potent corticosteroid
28
BASAL CELL CARCINOMA What is a basal cell carcinoma (BCC)? What is the epidemiology and most common type? What are some risk factors?
- 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
29
BASAL CELL CARCINOMA | What is the clinical presentation of BCC?
- Classically sun-exposed sites = head + neck - Pearly, flesh-coloured papule with surface telangiectasia - Rolled edges - Older lesions = centre necrotic/ulcerated (Rodent ulcer)
30
BASAL CELL CARCINOMA | What is the management of a BCC?
- Routine derm referral | - Surgical excision, curettage, cryotherapy, topical imiquimod, radiotherapy
31
SQUAMOUS CELL CARCINOMA What is a squamous cell carcinoma (SCC)? What is the spectrum of conditions that can result in SCC?
- Locally invasive malignant tumour of epidermal keratinocytes - Actinic keratosis > Bowen's disease (in situ SCC) > SCC
32
SQUAMOUS CELL CARCINOMA | What are some risk factors for SCC?
- Excessive UV light exposure + sun burn - Actinic keratoses + Bowen's disease - Immunosuppression (renal transplant, HIV) - Smoking - Long-standing leg ulcers
33
SQUAMOUS CELL CARCINOMA | What is the clinical presentation of SCC?
- Irregular, ill-defined red nodules (scaly, keratotic + ulcerated) - Sun-exposed areas = face, scalp, hands
34
SQUAMOUS CELL CARCINOMA | What is the management of SCC?
- <20mm diameter = surgical excision with 4mm margins - >20mm diameter = surgical excision with 6mm margins - Mohs micrographic surgery = high-risk patients + cosmetically important sites
35
MALIGNANT MELANOMA What is a malignant melanoma? Where do they commonly metastasise to?
- Neoplastic transformation of melanocytes | - Lungs + brain
36
MALIGNANT MELANOMA | What are the 4 types of malignant melanoma?
- Superficial spreading #1 - Nodular - Lentigo maligna - Acral lentiginous
37
MALIGNANT MELANOMA What are the unique features of... i) superficial spreading melanoma? ii) nodular melanoma? iii) lentigo maligna melanoma? iv) acral lentiginous melanoma?
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
38
MALIGNANT MELANOMA | What are some risk factors for malignant melanoma?
- UV light exposure + tanning beds - Fair skin + red hair - Large number of moles - FHx + increasing age
39
MALIGNANT MELANOMA | What is the clinical presentation of malignant melanoma?
ABCDE - Asymmetrical - Border irregular - Colour irregular - Diameter >6mm - Evolving in nature
40
MALIGNANT MELANOMA What would you do in suspected melanoma? What is the single most important prognostic marker?
- Urgent 2ww derm referral | - Breslow thickness > thicker = worse prognosis
41
MALIGNANT MELANOMA | What is the management of confirmed melanoma?
- Excision biopsy > stage 0 = 0.5cm, stage 1 = 1cm, stage 2 = 2cm - Stage III + IV metastatic = adjuvant immunotherapy, chemotherapy
42
BURNS | What are the various gradings of burns?
- 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
43
BURNS How can you assess the extend of the burn on the total body surface area? What is the most accurate method?
- Wallace's rule of nines | - Lung and broder chart
44
BURNS | What is Wallace's rule of nines?
- 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%
45
BURNS | What are some potential complications following burns?
- Hypovolaemic shock due to excess fluid loss in skin - Infection due to loss of skin barrier - Metabolic disturbance = high K+, high myoglobin (AKI)
46
BURNS | What are some indications to refer burns to secondary care?
- 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
47
BURNS What is your immediate management of burns? What are you particularly looking out for?
- ABCDE (soot + stridor) - IV fluids as per Parkland formula - Analgesia - Catheter
48
BURNS What is the Parkland formula? When is it indicated? How is it applied?
- 24h fluid requirement (ml) = TBSA % x kg x 4 - Adults >15% TBSA or paeds >10% TBSA - HALF given in FIRST 8H, remainder over 16h
49
BURNS | What is the management of burns post-ABCDE assessment?
- 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
50
ULCERS What is the cause of... i) venous ulcers? ii) arterial ulcers? iii) neuropathic ulcers?
i) Venous insufficiency ii) CVD risk factors (smoking, cholesterol, DM, HTN) iii) Peripheral neuropathy #1 diabetes, unable to feel pressure to skin > ulcer
51
ULCERS What is the location of... i) venous ulcers? ii) arterial ulcers? iii) neuropathic ulcers?
i) Medial malleolus ii) Forefoot + toes, incl. pressure sites iii) Pressure points (e.g., plantar surface)
52
ULCERS What are unique features of... i) venous ulcers? ii) arterial ulcers? iii) neuropathic ulcers?
i) Varicose veins, haemosiderin deposits (pigmentation), lipodermatosclerosis (hard, tight skin), venous eczema) ii) Punched out ulcers iii) Reduced sensation in foot
53
ULCERS Venous ulcers: comment on the following features... i) regularity ii) depth iii) temperature iv) pulses v) sensation
i) Irregular ii) Shallow iii) Normal iv) Present v) Painless
54
ULCERS Arterial ulcers: comment on the following features... i) regularity ii) depth iii) temperature iv) pulses v) sensation
i) Regular ii) Deep iii) Cold iv) Absent v) Painful
55
ULCERS Neuropathic ulcers: comment on the following features... i) regularity ii) depth iii) temperature iv) pulses v) sensation
i) Regular ii) Deep iii) Normal iv) Present v) Painless + reduced sensation overall
56
ULCERS What investigation would you do in the following, what would it show and what is the importance... i) venous ulcers? ii) arterial ulcers?
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
ULCERS What is the management of... i) venous ulcers? ii) arterial ulcers? iii) neuropathic ulcers?
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
CELLULITIS What is cellulitis? What is a similar condition and the differences? What are some risk factors for developing cellulitis?
- 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
CELLULITIS | What is the clinical presentation of cellulitis?
- Erythema, pain + swelling commonly at shins - Poorly demarcated, usually unilateral - May be systemically unwell with a fever
60
CELLULITIS | How is cellulitis diagnosed?
- 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
CELLULITIS | When would you consider admitting someone for IV Abx in cellulitis?
- Eron class III/IV - Rapidly deteriorating - <1y - Immunocompromised
62
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?
- Flucloxacillin - Clarithryomycin/doxycyline if pen allergic, erythromycin if pregnant - Co-amox, cefuroxime, clindamycin, ceftriaxone - Draw around lesion, analgesia, elevate leg
63
NECROTISING FASCIITIS What is necrotising fasciitis? What are the two types of necrotising fasciitis? What are some risk factors?
- 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
NECROTISING FASCIITIS What is the most affected site for necrotising fasciitis? What is the clinical presentation?
- 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
NECROTISING FASCIITIS | What is the management of necrotising fasciitis?
- Urgent surgical debridement + IV Abx
66
GANGRENE What is gangrene? What are the two types and the differences?
- Necrosis of tissues due to poor vascular supply - Wet gangrene = infectious gangrene - Dry gangrene = ischaemic gangrene, non-infective
67
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?
- 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
GANGRENE What is the management of wet gangrene? What is the management of dry gangrene?
- Surgical debridement/amputation + broad-spectrum IV Abx | - Auto-amputation occurs in most cases
69
IMPETIGO What is impetigo? How does it present?
- Superficial skin infection 2º to staph aureus or strep pyogenes - Golden crusted lesions classically around mouth, pruritic, very contageous
70
IMPETIGO What are the conservative measures for impetigo? What is the first line management of impetigo?
- 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
IMPETIGO What is the second line management of impetigo? What is the management of systemically unwell impetigo?
- Topical fusidic acid (mupirocin if resistance suspected or MRSA) - PO flucloxacillin (erythromycin in pen allergy)
72
HEAD LICE What is head lice caused by? How does it present?
- Pediculus capitis = parasite that infest the hairs + feeds on blood from scalp - Itchy scalp, suboccipital lymphadenopathy
73
HEAD LICE How is head lice diagnosed? How is it managed? What are the conservative aspects to management?
- 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
SCABIES | What is scabies?
- Infestation of mites (Sarcoptes scabiei) that burrow under skin + lay eggs - Delayed T4 hypersensitivity reaction
75
SCABIES | How does scabies present?
- Widespread pruritus + linear burrows (finger webs, side of fingers) - Pruritus can be worse at night > excoriation + secondary bacterial infection - Often whole household itching
76
SCABIES What is a key complication of scabies? How does it present? How is it treated?
- Crusted scabies = serious infestation in immunocompromised (HIV) - Patches of red skin > scaly plaques - Rx = inpatient with PO ivermectin + isolation
77
SCABIES | What are the conservative aspects to scabies management?
- ALL close contacts treated even if asymptomatic > school exclusion until treated - Wash bed linen, towels, clothes + clean furniture etc. to destroy mites
78
SCABIES What is the first line treatment of scabies? What is the second line treatment of scabies?
- 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
BULLOUS PEMPHIGOID What is bullous pemphigoid? How does it present?
- 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
BULLOUS PEMPHIGOID | What is the management of bullous pemphigoid?
- Derm for skin biopsy + immunofluorescence (IgG on basement membrane) - PO corticosteroids, topical potent steroids (dermovate), Abx (doxy if mild)
81
PEMPHIGUS VULGARIS | What is pemphigus vulgaris?
- Autoimmune deposition of IgG autoantibodies within the epidermis (T2 hypersensitivity reaction)
82
PEMPHIGUS VULGARIS | What is the clinical presentation of pemphigus vulgaris?
- 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
PEMPHIGUS VULGARIS | What is the management of pemphigus vulgaris?
- Derm for skin biopsy + immunofluorescence (IgG within epidermis) - PO corticosteroids mainstay, immunosuppressants
84
PITYRIASIS ROSEA What is pityriasis rosea? How is it managed?
- Self-limiting rash in young adults 2º to herpes hominis virus 7 (HHV-7) - No treatment, resolves 6–12w
85
PITYRIASIS ROSEA | What is the clinical presentation of pityriasis rosea?
- 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
PITYRIASIS VERSICOLOR What is pityriasis versicolour? What are some predisposing factors?
- Superficial cutaneous fungal infection caused by Malassezia furfur - Healthy, immunosuppression, Cushing's
87
PITYRIASIS VERSICOLOR | What is the clinical presentation of pityriasis versicolor?
- Hypopigmented/pink/brown (versicolor) patches on trunk | - Mild pruritus + scale is common, noticed after suntan
88
PITYRIASIS VERSICOLOR | What is the management of pityriasis veriscolor?
- First line = topical antifungal ketoconazole shampoo, clotrimazole if small area
89
ROSACEA | What is rosacea? Who does it commonly affect? What are some triggers?
- Chronic skin condition - Females - Sun exposure, hot weather, stress
90
ROSACEA | What is the clinical presentation of rosacea?
- Flushing of nose, cheeks + forehead | - Erythema with papules, pustules + telangiectasia
91
ROSACEA | What are two potential complications of rosacea?
- Ocular involvement = blepharitis, conjunctivitis or keratitis - Rhinophyma = skin thickening + disfiguration of nose > dermatology
92
ROSACEA | What general measures may be used in rosacea?
- Camouflage creams, sun protection | - Laser therapy if prominent telangiectasia
93
ROSACEA What is the management of mild-moderate rosacea? What is the management of severe/unresponsive rosacea?
- Topical metronidazole, topical ivermectin | - PO Abx (oxytetracycline)
94
SEBORRHOEIC KERATOSES | What is the clinical presentation of seborrhoeic keratoses?
- Flesh/light brown/black benign epidermal skin lesions in older people - 'Stuck-on' appearance - Keratotic plugs may be seen on surface
95
SEBORRHOEIC KERATOSES | What is the management of seborrhoeic keratoses?
- Reassurance | - Removal via curettage, cryosurgery + shave biopsy
96
ACTINIC KERATOSES What are actinic keratoses? How do they present?
- 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
ACTINIC KERATOSES What is the general management of actinic keratoses? What is the management for localised? What is the management for large lesions?
- Prevent further risk = avoid sun, SPF50+ all year round - Cryotherapy, curettage, or surgical excision - Topical 5-fluorouracil, NSAID or imiquimod
98
KERATOACANTHOMA What is a keratoacanthoma? How does it present?
- Benign epithelial tumour common with increased age | - Initially smooth dome-shaped papule > rapidly grows to become crater centrally filled with keratin
99
KERATOACANTHOMA | What is the management of keratoacanthoma?
- Spontaneous regression <3m but urgently excised as clinically difficult to say if SCC = leaves a scar
100
MOLLUSCUM CONTAGIOSUM What is molluscum contagiosum caused by? How is it transmitted?
- Molluscum contagiosum virus (pox virus) | - Direct skin contact, also sharing towels
101
MOLLUSCUM CONTAGIOSUM What is the clinical presentation of molluscum contagiosum? How does this differ in immunocompromised?
- Small, smooth, pearly coloured papules in clusters with central umbilication - Immunocompromised = face, extensive lesions
102
MOLLUSCUM CONTAGIOSUM | What is the management of molluscum contagiosum?
- All patients offered full STI test, especially if anogenital lesions - Supportive (avoid sharing towels) - If cosmetic distress = cryotherapy (risk of scarring)
103
MOLLUSCUM CONTAGIOSUM | When would you consider referral in molluscum contagiosum?
- HIV +ve with extensive lesions = HIV specialist | - Eyelid margin/ocular lesions with red eye = ophthalmology
104
SEBORRHOEIC DERMATITIS What is the pathophysiology of seborrhoeic dermatitis? What is it particularly associated with?
- Chronic dermatitis caused by inflammatory reaction to proliferation of a normal skin fungus Malassezia furfur - HIV, Parkinson's, stress, oily skin
105
SEBORRHOEIC DERMATITIS | What is the clinical presentation of seborrhoeic dermatitis in paeds?
- 'Cradle cap' = erythematous rash with coarse yellow scales
106
SEBORRHOEIC DERMATITIS | What is the clinical presentation of seborrhoeic dermatitis in adults?
- Eczematous, flaky lesions in sebum rich areas (scalp = dandruff, periorbital, auricular + nasolabial folds) - Otitis externa + blepharitis may occur
107
SEBORRHOEIC DERMATITIS | What is the management of cradle cap?
- Mild-mod = baby shampoo + baby oils | - Severe = mild topical 1% hydrocortisone
108
SEBORRHOEIC DERMATITIS What is the management of scalp seborrhoeic dermatitis? What is the management of face/body seborrhoeic dermatitis?
- First line = OTC shampoo with zinc pyrithione (Head & Shoulders), second line = ketoconazole shampoo - First line = topical anti fungals (ketoconazole), topical steroids (short periods)
109
TINEA What is tinea? What causes it?
- Dermatophyte fungal infections, usually trichophyton | - If Microsporum canis = fluoresce under Wood's lamp
110
TINEA | What are the 4 main types of tinea?
- Tinea capitis (scalp ringworm) - Tinea corporis (ringworm) - Tinea pedis (athlete's foot) - Onychomycosis
111
TINEA What is the clinical presentation of... i) tinea capitis? ii) tinea corporis?
i) Scaly + patchy alopecia, can lead to spongy mass (kerion) if untreated ii) Well-defined, annular, erythematous lesions with pustules + papules
112
TINEA What is the clinical presentation of... i) tinea pedis? ii) onychomycosis?
i) Itchy, peeling skin between the toes | ii) Thickened, rough + opaque nails (can be secondary to Candida too)
113
TINEA How do you investigate tinea? What is the management?
- Culture of skin scrapings/nail clippings for fungal hyphae - Topical antifungals = clotrimazole, ketoconazole - Systemic antifungals = terbinafine, itraconazole for tinea capitis or onychomycosis
114
ERYTHEMA NODOSUM What is erythema nodosum? How does it present?
- Inflammation of subcutaneous fat | - Tender, erythematous, nodules often on shins
115
ERYTHEMA NODOSUM | What are the causes of erythema nodosum?
NODOSUM – - NO cause = idiopathic - Drugs = penicillins, sulfonamides - OCP - Sarcoidosis - Ulcerative colitis/Crohn's - Micro = streptococci, TB
116
ERYTHEMA MULTIFORME What is erythema multiforme? What is the most common cause?
- Hypersensitivity reaction usually triggered by infections | - Herpes simplex virus
117
ERYTHEMA MULTIFORME | What are some other causes of erythema multiforme?
- Bacteria = mycoplasma, streptococcus - Drugs = penicillin, sulfonamides, NSAIDs, OCP - SLE, sarcoidosis + malignancy
118
ERYTHEMA MULTIFORME | What is the clinical presentation of the two types of erythema multiforme?
- 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
ERYTHRODERMA What is erythroderma? What are some causes?
- >95% of skin involved in a rash of any kind - Derm = eczema, psoriasis (esp. after steroid withdrawal) - Drugs = gold - Haem = lymphomas, leukaemias - Idiopathic
120
ERYTHRODERMA | What is the management of erythroderma?
- Med emergency = admit for IV fluids, analgesia, emollients | - Monitor for complications = dehydration, infection, high-output heart failure, hypothermia
121
LICHEN PLANUS | What drugs can cause a lichenoid eruption?
- Gold - Antimalarials - Beta-blockers, ACEi + thiazides
122
LICHEN PLANUS | What is the clinical presentation of lichen planus?
- 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
LICHEN PLANUS | What is the management of lichen planus?
- Potent topical steroids, ?PO immunosuppression if extensive - Benzydamine mouthwash/spray if oral lichen planus
124
VITILIGO What is vitiligo? What conditions is it associated with?
- Autoimmune condition leading to loss of melanocytes + skin depigmentation - T1DM, Addison's, thyroid, pernicious anaemia, alopecia areata
125
VITILIGO | What is the clinical presentation of vitiligo?
- Well-demarcated patches of depigmented skin + white hair in those areas - Peripheries are MOST affected - Koebner phenomenon = new lesions at site of trauma
126
VITILIGO | What is the management of vitiligo?
- Sunblock for affected areas, camouflage make-up - Topical corticosteroids may reverse changes if early - ?Role for topical tacrolimus + phototherapy
127
ALOPECIA AREATA | What is alopecia areata and how does it present?
- Autoimmune condition causing localised, well demarcated patches of hair loss - At edge of hair loss, may be small, broken 'exclamation mark' hairs
128
ALOPECIA AREATA | What is the management of alopecia areata?
- Hair will regrow in 50% in 1y and 80–90% eventually | - Options = topical corticosteroids or minoxidil, phototherapy, wigs
129
URTICARIA What is urticaria? What are some drug causes? How does it present?
- Local/generalised superficial swelling of skin often secondary to allergy (T1HR) - NSAIDs/aspirin, penicillins, opiates - Pale, pink, pruritic, raised lesion "hives/wheals"
130
URTICARIA | What is the management of urticaria?
- First line = non-sedating antihistamines like cetirizine, loratadine - Severe/resistant = PO prednisolone
131
FOLLICULITIS What is folliculitis? What causes it?
- 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
FOLLICULITIS What is eosinophilic folliculitis? How is it diagnosed? How is it managed?
- Sterile folliculitis caused by immunosuppression (HIV) - Skin biopsy = eosinophils in skin surface - HAART + topical corticosteroids
133
LYME DISEASE | What causes Lyme disease?
- Spirochaete Borrelia burgdoferi + is spread via ticks
134
LYME DISEASE | What are the early features of Lyme disease?
Within 30d – - Erythema migrans = 'bulls-eye' rash at site of tick bite, painless, >5cm + slowly increases - Systemic = headache, lethargy, fever, arthralgia
135
LYME DISEASE | What are the late features of Lyme disease?
After 30d – - Cardio = heart block + peri/myocarditis - Neuro = facial nerve palsy, meningitis
136
LYME DISEASE | How is Lyme disease diagnosed?
- 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
LYME DISEASE What is the management of asymptomatic ticks in general? What is the management of Lyme disease?
- 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
LYME DISEASE | What potential complication may be seen after treating Lyme disease?
- Jarisch-Herxheimer reaction = fever, rash, tachycardia after 1st dose Abx