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Imperial Medicine Year 3 > Dermatology AS > Flashcards

Dermatology AS Flashcards

1
Q

What is the epidemiology of Malignant Melanoma?

A

F>M = 1.5:1

UK incidence = 10,000/yr and 2000 deaths a year. Increased 80% in 20yrs.

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2
Q

What are the features of malignant melanoma?

A 
Asymmetry 
Border: irregular
Colour: non-uniform
Diameter >6mm 
Evolving/Elevation
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3
Q

Risk factors for malignant melanoma?

A
  • Sunlight: esp intense exposure in early years.
  • Fair skinned (Low Fitzpatrick Skin Type)
  • Increased no. of common moles
  • +ve FH
  • Increased age
  • Immunosuppression
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4
Q

What is the classification of malignant melanoma?

A 
Superficial spreading 
Lentigo maligna melanoma - on the face normally
Acral lentiginous - most common in people with darker skin. On the palm
Nodular Melanoma
Amelanotic
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5
Q

What is superficial spreading malignant melanoma?

A
  • 70% of cases
  • Irregular border, colour variation
  • Commonest in Caucasian
  • Grow slowly, mets late = better prognosis
  • Common on legs in females. Grows slowly, often taking months or years to be recognised.
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6
Q

What is Lentigo Maligna malignant melanoma?

A

Melanoma in situ - slowly but may at some stage become invasive causing lentigo maligna melanoma.

Suspicious freckles on face or scalp of chronically sun-exposed patients. Location is face!

  • Often elderly patients
  • Face of scalp.
  • A growing mole
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7
Q

What is the acral lentiginous malignant melanoma?

A
  • Rare form
  • Asian/blacks
  • Palms, soles, subungual (with Hutchinson’s sign) (black line )
  • Can arise in the nail unit.
  • Enlarging discoloured skin patch on the palms.
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8
Q

What is nodular malignant melanoma?

A
  • All sites
  • Second most common.
  • Younger age, new lesions
  • Invade deeply and mets early = worst prognosis.
  • Presents with a red or black lump or lump which bleeds or oozes.

Tends to affect people over age of 50, with fairer skin, and occur in chronically sun exposed area.

Melanocytic naevi are risk factors

Congenital = typically appear at or soon after birth.

  • Usually greater than 1cm
  • Increased risk of malignant transformation

Junctional = melanocytic naevi = circular macules, may have heterogenous colour even within same lesion.
- Most naevi of the palms, soles.

Compound naevi = domed pigmented nodule up to 1cm in diameter
- Arise from junctional naevi .

Spitz naevi
= Children, red or pink in colour. Grow up to 1cm and growth can be rapid this usually results in excision.

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9
Q

What is amelanotic melanoma?

A

Atypical appearance –> delayed diagnosis.

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10
Q

What is the staging and prognosis of malignant melanoma?

A

Breslow Depth

  • Thickness of tumour to deepest point of dermal invasion
  • <1mm = 95-100% 5yrs
  • > 4mm = 50% 5yr survival.
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11
Q

Where do the mets go in malignant melanoma?

A

Liver

Eye

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12
Q

What is the management of Malignant melanoma?

A
  • Excision + secondary margin excision depending on Bres Depth.
    ± lymphadenopathy
    ± adjuvant chem
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13
Q

What are the margins of excision related to breslow thickness?

A

Lesions 0-1mm thick = 1cm
1-2mm thick = 1-2 cms
2-4mm = 2-3 cm
>4 = 3cm

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14
Q

What are the poor prognostic indicators of malignant melanoma?

A
  • Male sex
  • Increased mitoses
  • Satellite lesions
  • Ulceration
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15
Q

What is a squamous cell carcinoma?

A
  • Ulcerated lesions with hard, raised EVERTED edges
  • Telangiectasia scattered around periphery.
  • Sun exposed areas
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16
Q

Causes of squamous cell carcinoma?

A

Sun exposure: scalp, face, ears, lower leg

Arise due to immunosuppression eg HIV, renal transplant. this is because of the immunosuppressants (higher risk of SCC).

May arise in chronic ulcer: Marjolin’s Ulcer (long standing leg ulcer) due to chronic inflammation.

Xeroderma pigmentosa

Development from actinic keratoses and Bowen’s disease (isolated and well demarcated)

Actinic keratoses - sun-exposed area. = Crusty, small, scaly lesions. Sun-exposed areas and multiple lesions may be present.

May be pink, red, brown or same colour as the skin. Typically on sun-exposed areas. Multiple lesions may be present.

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17
Q

What are good prognostic factors for SCC?

A

Well differentiated tumours
<20mm diameter
<2mm deep
No associated disease

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18
Q

What are poor prognostic factors?

A

Poorly differentiated tumours
>20mm in diameter
>4mm deep
Immunosuppression for whatever reason.

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19
Q

What is the progression of SCC?

A

Solar/actinic keratosis –> Bowen’s –> SCC

Lymph node spread is rare.

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20
Q

What is the management of SCC?

A

Surgical excision:

  • 4mm margin if lesions <20mm in diameters.
  • 6mm margin if lesion >20mm.

Management of actinic keratoses

  • Sun avoidance, sun cream.
  • Fluorouracil cream - 2/3 week course. Red and inflamed skin
  • Topical diclofenac used for mild AKs.
  • topical imiquimod
  • Cryotherapy
  • Curettage and cautery.
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21
Q

What is actinic ketatoses?

A

Red, scaly lesion on his forehead. Initially small and flat but not erythematous and rough to touch.

Irregular, crust warty lesion
premalignant (1%/yr)

  • In a person with 7 actinic keratosis, risk of subsequent SCC is 10% at 10 yrs.
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22
Q

Management of AK?

A

Avoid sun, sun cream

  • Fluorouracil cream: 2-3 week course. Skin will become red and inflamed.
  • Topical diclofenac
  • Topical imiquimod
  • Cryotherapy
  • Curettage and cautery
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23
Q

What is Bowen’s Disease?

A

SCC in situ
Red/brown scaly plaques.

Intraepidermal SCC

More common in elderly females.

Red scaly patch. Often occur in sun-exposred areas such as lower limbs.

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24
Q

Management of Bowen’s Disease?

A

As for AK

  • Cautery
  • Cryo
  • 5-FU
  • Imiquimod
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25
Q

Keratoacanthoma?

A

Benign epithelial tumour.

Fast-growing, dome-shaped with a keratin plug.
Looks like a volcano or crater filled with keratin.

Usually regress but may be excised.

Look like a volcano- crater.

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26
Q

What is a BCC - Basal Cell Carcinoma?

A
  • Commonest Cancer
  • Pearly nodule with rolled telangiectatic edge.
  • May ulcerate
  • Typically on face in sun-exposed area
    Above ling from tragus –> angle of mouth.

Can be called a rodent ulcer.

Morphoeic BCC usually is associated more extensive spread than nodular BCC.

Therefore need Mohs micrographic surgery to manage it. Important in cosmetically sensitive areas, where amount of skin removed should be minimised.

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27
Q

What is the behaviour of a BCC?

A
  • Low-grade malignancy - very rarely metastasis

- Locally invasive

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28
Q

Management of BCC?

A

Do a diagnostic punch biopsy taken if treatment other than standard surgical excision is planned.

Excision
- Mohs: complete circumferential margin assessment using frozen section histology.

  • Managed with surgical removal, curettage, cryotherapy, topical cream.
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29
Q

Epidemiology of psoriasis?

A 
Prevalence: 2% of Caucasians 
Age: peaks in 20s to 50s 
Sex: F=M
Genetics: 30% have FH
- Genetic predisposition
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30
Q

What is the pathology of Psoriasis?

A
  • Type 4 hypersensitivity reaction
  • Epidermal proliferation
    T-cell driven inflammatory infiltration
  • Histo
    Acanthosis: thickening of epidermis
    Parakeratosis: nuclei in stratum corneum
    Munro’s microabscesses: neutrophil
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31
Q

What are the triggers for psoriasis?

A
  • Stress
  • Infection: esp streps (triggers a guttate psoriasis)
  • Skin trauma: Kobner’s phenomenon
  • Drugs: Lithium, Antimalarials, ETOH and BETABLOCKERS, NSAIDS, ACEi, infliximab.
  • Smoking
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32
Q

What are the signs of psoriasis?

A

Plaques

  • Symmetrical well-defined red plaques with silvery scale
  • Extensor: elbow, knee
  • Flexures (no scales): axillae, groin, submammary
  • Scalp, behind ears, nael, sacrum.
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33
Q

What are the nail changes in psoriasis?

A

Nail pitting
Onycholysis
Subungual hyperkeratosis

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34
Q

How many people with psoriasis develop seronegative arthritis?

A
  • mono/oligo-arthritis: DIPs commonly involved
  • Rheumatoid-like
  • Asymmetrical polyarthritis
  • Psoriatic spondylitis
  • Arthritis mutilans
  • May –> Dactylitis
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35
Q

What are the variants of psoriasis?

A

Guttate: transient psoriatic rash frequently triggered by strep infection. Multiple red, teardrop lesions appear on the body. Mainly on the trunk.

Pustular: commonly occurs on the palms and soles

Plaque: Most common sub-type leading to well demarcated red, scaly patches affecting extensor surface, sacrum and scalp.

Flexural: in contrast to plaque psoriasis the skin is smooth.

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36
Q

What are the differentials for psoriasis?

A

Eczema
Tinea
Seborrhoeic dermatitis (includes the nasolabial folds)
Acne rosacea - spares this area

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37
Q

Management of psoriasis?

A

Education - avoid triggers (alcohol, trauma, B-Blockers, Lithium, antimalarials, NSAIDs, ACEi)

Soap substitute - aqueous cream, dermol, epaderm ointment.

Emollients - epaderm, dermal, diprobase.

Topical therapy

  • Vit D3 analogues: (works by reducing cell division) calcipotriol (1st line + steroids)
  • Steroids: betamethasone (Dovobet = calcipotriol + betamehasone)

Second line: no improvement after 8 weeks offer Vit D analogue twice daily.

Third line: offer potent corticosteroid 2x daily for 4 weeks or a coal tar prep applied once or twice daily.

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38
Q

Using topical steroids in psoriasis?

A

Can lead to skin atrophy, striae + rebound symptoms.

Systemic side-effect therfore aim for 4 week break before starting another topical steroid.

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39
Q

Management of scalp psoriasis?

A

Psoriasis as a circular, white, hyperkeratotic lesion on crown of his head.

Potent topical corticosteroids used once daily for 4 weeks.
If no improvement after 4 weeks either use a different steroid or topical agent to remove adherent scale.

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40
Q

Other management options for psoriasis?

A

Narrow band UVB light. - 3x a week. Photochemotherapy is also used - psoralen + UVA light (PUVA)
- Adverse effect: Skin ageing, SCC. (PUVA increases risk of Ca)

Systemic therapy

  • Oral methotrexate is 1st line.
  • Ciclosporin
  • Systemic retinoids
  • Bio agents: infliximab, etanercept + adalimumab.
  • Ustekinumab (IL-12+ IL-23)
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41
Q

What is the presentation of eczema?

A

Extremely itchy
Poorly demarcated rash
- Acute: oozing papules and vesicles
- Subacute: red and scaly.

Chronic eczema –> Lichenification with skin thickening with exaggeration of skin markings.

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42
Q

What is the pathology of eczema?

A

Epidermal spongiosis

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43
Q

What is the cause of eczema?

A

FH of atopy common
Specific allergens
- House dust mite
- Animal dander

Diet: e.g diary products

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44
Q

What is the presentation of eczema?

A 
Face: esp around eyes, cheeks
Flexures: Knees, elbows
May become 2ndry infection 
- Staph = fluclox 
- HSV --> Aciclovir
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45
Q

Associations of eczema?

A

Asthma

Hay fever

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46
Q

Investigations of eczema?

A

increased IgE

RAST testing: identify specific ag.

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47
Q

What is irritant contact dermatitis?

A

Everyone is susceptible to irritants

Causes: detergents, soaps, oils, solvents, venous stasis

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48
Q

What is allergic contact dermatitis?

A 
Type IV hypersensitivity reaction 
- Common allergens 
Nickel: jewellery, watches coins 
Chromates: leather
Lanolin: creams, cosmetics
  • Location: correlated sharply with allergen exposure

Investigation with Patch testing - various allergens are applied to patient’s back, and skin assessed at 48hr.

Skin Patch = Delayed hypersensitivity.
Skin Prick = Type 1 immediate.

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49
Q

What is adult seborrhoeic dermatitis?

A

Itchy, red, scaly rash that affects the face and scalp.

Causes: overgrowth of skin yeasts (malasseiza)
Location: Scalp (dandruff), eyebrows, cheek, nasolabial folds

  • Associated with HIV and Parkinson’s

Management :

Scalp disease management:

  • hair shampoo containing zinc pyrithione.
  • Then use ketoconazole.
  • Then selenium

Face and body -
mild topical steroids/antifungal - ketoconazole
- topical corticosteroid.

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50
Q

What is the management of atopic eczema?

A
  • Avoid triggers e.g soap
  • Soap substitute: Aqueous cream, dermol cream, epaderm ointment
  • Emollients: Epaderm, Dermol, Diprobase, Oilatum (bath oil)
  • Topical therapy - if using steroid - do emollient first, then wait 30 mins before applying topical steroid.
    Steroid: 1% Hydrocortisone: fac, groin.
    Eumovate: can use briefly (<1 weeks) on face
    Betnovate
    Dermovate: very strong, brief use on thick skin - palms, soles.

2nd line

  • Topical tacrolimus
  • Phototherapy
  • Ciclosporin or azathioprine
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51
Q

Pruritus differentials?

A 
Generalised pruritus
- CRF
- Cholestasis 
- Haematological 
Polycythaemia
Hodgkin's 
Leukaemia
Iron deficiency

Endocrine

  • DM
  • Hyper/hypothyroidism
  • Pregnancy
  • ‘senile’ pruritus
  • urticaria
    -skin disorders: eczema, scabies, psoriasis,
    pityriasis rosea
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52
Q

Pruritus in dermatological disease?

A

Eczema
Urticaria
Scabies
Dermatitis herpetiformis

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53
Q

What is tinea infection

A

A superficial mycosis caused by dermatophytes

  • Microsporum
  • Epidermophyton
  • Trichophyton
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54
Q

What is the presentation of tinea?

A
  • Round scaly lesion
  • Itchy
  • Central clearing
  • Scalp, body, foot, groin, nails.
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55
Q

Types of tinea?

A

Tinea Capitis - scalp
Tinea Corporis - trunk, legs, arms
Tinea Pedis - feet

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56
Q

What is tinea capitis?

A

Scalp ringworm

  • Cause of scarring alopecia mainly seen in children. Causes a scarring alopecia.
  • If untreated a raised, pustular spongy/boggy mass called a kerion may form.
  • Most common cause is trichophyton tonsurans in the UK + USA.
  • May also be caused by microsporum canis from cats or dogs.
  • Diagnosis: lesions due to microsporum canis green fluorescence under Wood’s lamp. (Scalp scraping is most useful). Trichophyton lesion

Management - griseofulvin or terbinafine

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57
Q

What is tinea corporis? (ringworm)

A

Caused by trichophyton rubrum and verrucosum
- from contact with cattle.

  • Well-defined annular, erythematous lesions with pustules and papules. Raised.
  • Treat with Terbinafine or imidazole such as clotrimazole, miconazole, or econazole cream
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58
Q

What is tinea pedis?

A
  • Characterised by itchy, peeling skin between toes.
  • Common in adolescence.
  • Caused by fungi called Trichophyton.

Typically scaling, flaking and itching between the toes.

Topical imadazole/miconazole undecenoate. If this does not work,

Give oral terbinafine.

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59
Q

Presentation of candida infection?

A

Common
RFs: immunosuppression, abx, steroid inhaler.

Presentation

  • Pink + white patches
  • Moist
  • Satellite lesions
  • Mouth, vagina, skin fold, toe webs.
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60
Q

Management of tinea corporis, capitis?

A

Skin: terbinafine or topical ketoconazole

Scalp: griseofulvin or terbinafine

Nails: terbinafine

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61
Q

Management of candida infection?

A

Mouth: Nystatin

Vagina: Clotrimazole cream and pessary

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62
Q

What is pityriasis versicolour caused by?

A

Malassezia Furfur. A superficial cutaneous fungal infection caused. Dermatophyte fungal skin infection

  • Most commonly affects the trunk
  • Patches may be hypopigmented, pink or brown (versicolor).
  • More noticeable following a suntan.
  • Scale is common
  • Mild pruritus
  • Fine white scale.

Usually on the trunk or back and is scaly in appearance.

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63
Q

What is the investigation of pityriasis versicolor?

A

Spaghetti and meatballs appearance with KOH stain.

- Predisposing factors = 
occurs in healthy individuals 
immunosuppression
Malnurition 
Cushings
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64
Q

Management of Pityriasis Versicolour?

A

Selenium sulphate or

Ketoconazole shampoos.

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65
Q

What is impetigo ?

A

Contagious superficial skin rash caused by S.aureus.

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66
Q

Presentation of impetigo?

A
  • Age: peak @2-5 yrs.
  • Honey-coloured crust on erythematous base
  • Common on face.
  • Occur in the flexures and limbs not covered by clothing.
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67
Q

Management of impetigo?

A
  • Mild: Topical abx (fusidic acid, mupirocin).First line.
  • 2nd line = topical retapamulin
  • More severe: oral fluclox PO
  • Children should be excluded from school until the lesions are crusted and healed or 48hrs after commencing antibiotic treatment.

MRSA = Topical mupirocin (Bactroban)

Extensive

  • Oral flucloxacillin
  • Oral erythromycin if penicillin allergic
  • Children should be excluded from school until lesions are crusted and healed or 48hrs after antibiotic treatment.
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68
Q

What is erysipelas?

A
  • Sharply defined superficial infection of S.pyogenes. Superficial cellulitis affecting face.
  • Often affects the face
  • High fever + increased WCC

Management

  • Benpen IV
  • Pen V and fluclox PO.
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69
Q

What is Cellulitis?

A

Acute infection of skin and soft tissue - inflammation of skin + subcut tissues

Causes: B-haemolytic Strep + Staph A.

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70
Q

What is the primary cause of cellulitis?

A

B-Haemolytic Strep (Strep Pyogenes) + staph Aureus.

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71
Q

What is the presentation of cellulitis?

A
  • Deeper and less well defined than erysipelas
  • Pain, swelling, erythema and warm
  • Systemic upset
  • ± lymphadenopathy
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72
Q

Management of cellulitis?

A

Empiric: fluclox IV
Confirmed strep: Benpen or Pen V
Pen allergic: clindamycin

For more severe cellulitis = co-amoxiclav, cefuroxime, clindamycin, ceftriaxone.

73
Q

Cellulitis classification?

A

Eron classification
- I = no signs of systemic toxicity and the person has no uncontrolled co-morbidities

  • II = The person is either systemically unwell or systemically well but with a co-morbidity
  • III - person has significant systemic upset such as acute confusion, tachycardia, tachypnoea
  • IV - sepsis syndrome

IV antibiotics for III or IV

74
Q

What are warts caused by?

A

HPV Infection

75
Q

What is the management of warts?

A 
Expectant
Destructive 
- Topical salicylic acid
- Cryotherapy
- Podophyllin 
- Imiquimod
76
Q

What is Molluscum contagiosum caused by?

A

Pox virus

Majority occur in children - max incidence in preschool children aged 1-4.

Typically present with characteristic pinkish or pearly white papules with a central umbilication - 5mm in diameter.

77
Q

What is the self-care advice of molluscum?

A

reassure people that molluscum is self-limiting

Spontaneous resolution occurs within 18 months.

Explain that lesions are contagious - avoid sharing towels, clothing and bath with siblings.

Encourage people not to scratch lesions - if problematic - consider treatment to alleviate itch.

78
Q

Treatment of molluscum?

A
  • Not usually recommended - can use squeezing/piercing.

Cryotherapy
Eczema or inflammation
Itching is problematic/Skin looks infected (oedema) –> consider mild topical corticosteroid.

Referral for HIV + patients.

79
Q

Shingles?

A

Recurrent VZV infeciton
Dermatomal distribtuion of cropping vesicles and crust. Painful.
- Thoracic: 50%
- Ophthalmic: 20%
Cornea affected in 50% –> Keratitis, iritis
May –> post-herpetic neuralgia

Can occur in young people. Shingles vaccine in 70-79 yr olds. Live attenuated and given sub-cutaneously.

Management: aciclovir or famciclovir PO if severe.

80
Q

Herpes Simplex infection?

A
  • Gingivostomatitis or recurrent genital or oral infections
  • Triggered by infection (CAP), sunlight and immunosuppression
  • May complicate eczema: eczema herpeticum - Monomorphic punched out erosions usually 1-3 mm in diameter are typically seen. IV aciclovir.
  • Circular, depressed, ulcerated lesions.
  • Grouped painful vesicles on an erythematous base
  • Management: IV acyclovir or famciclovir indicated if immunosuppressed or recurrent genital herpes.
81
Q

What is pityriasis rosea?

A

HHV- 6/-7

Pityriasis rosea - viral infection.

Herald patch precedes rash, mainly on the trunk.
Acute self-limiting rash.
- Followed by erythematous, oval, scaly patches following a characteristic distribution with longitudinal diameters of the oval lesions running parallele to the line of Langer.

Fir-tree appearance.

Usually disappears after 6-12 weeks.

82
Q

Differentiating guttate psoriasis from pityriasis rosea

A

Guttate = prodrome (2-4 weeks strep sore throat)

  • Can occur after acute strep infection or viral infection.
  • Tear-drop scaly papule on the trunk and limbs.

Management = most resolve. No firm evidence to support the use of antibiotics to eradicate streptococcal infection. Use topical agents, UVB phototherapy.

Pityriasis

  • Herald patch - fir-tree.
  • Viral infection
83
Q

What is the skin presentation of Lichen Planus?

A
  • Flexors: wrist, forearms, ankles, legs.
  • Display Koebner phenomenon

Purple, pruritis, polygonal, planar, papules, lacy white marks: Wickman’s Striae

84
Q

What do the lesions of lichen planus elsewhere in the body (outside of skin/flexors) demonstrate?

A

Scalp: scarring alopecia
Nails: Longitudinal ridges
Mouth: Lacy white plaques on inner cheeks

Can be caused by gold, quinine, thiazide

Genitals

85
Q

Management of lichen planus?

A

Mild: topical steroids (benzydamine mouthwash for oral lichen planus)
Severe: Systemic steroids

86
Q

What is Bullous Pemphigoid?

A

Autoimmune blistering disease due to auto-abs against hemidesmosomes

87
Q

What does bullous pemphigoid present as?

A
  • Mainly affects the elderly
  • Tense bullae on erythematous base
  • Can be itchy
  • NO Mucosal involvement
88
Q

What is the investigation for bullous pemphigoid?

A

Biopsy shows linear IgG along the BM and subepidermal bullae.

89
Q

Management of bullous pemphigoid?

A
  • Referral to dermatologist for biopsy and confirmation if diagnosis
  • Oral corticosteroids are the mainstay of treatment
  • Topical corticosteroids, immunosuppressants and antibiotics - Clobetasol
90
Q

What are the investigations of Pemphigus Vulgaris?

A

Autoimmune blistering disease due to auto-ab against desmosomes.

  • may be ppted by drugs
    NSAIDS
    ACEi
    L-dopa
91
Q

Presentation of Pemphigus Vulgaris?

A

Younger patients
Large flaccid bullae which rupture easily
Nikolsky’s sign +ve
Mucosa is often affected - oral ulceration is common in 50-70%.

More common in Ashkenazi Jewish.

92
Q

Investigations of pemphigus vulgaris?

A

Intraepidermal bullae

93
Q

Management of pemphigus vulgaris?

A

Prednisolone
Rituximab
IVIg

94
Q

What is Acne vulgaris caused by?

A

Affects 80-90% of teenagers. May persist beyond adolescence. 10-15% of females and 5% of males over 25yrs old.

Increased sebum production: androgens and CRH

P. acnes is a skin commensal that flourishes in the anaerobic environment of the blocked follicle.

Propionibacterium acnes - anaerobic rod therefore need tetracyclines, macrolides or trimethoprim.

Leads to inflammation.

95
Q

Presentation of acne vulgaris?

A

Inflammation of pilosebaceous follicle

Mild = Comedones - white and blackheads (dilated sebaceous follicle)

Moderate papules, pustules are inflammatory lesions formed when the follicle bursts releasing irritants.

Severe nodules, cysts (excessive inflammatory response)
= ice-pick scars, hypertrophic scars.

Face, neck, upper chest and back.

96
Q

Management of acne?

A

Pt education

Mild: topical therapy
- Benzoyl peroxide

Then topical benzoyl +

  • Erythromycin, Clindamycin
  • Tretinoin, Isotretinoin (retiniods)

Then oral antibiotics

  • Tetracycline: lymecycline, oxytetracycline (avoid in pregnancy)
  • Use for max 3 months.
  • Minocycline is less appropriate due to irreversible pigmentation.
  • Always co-prescribe oral antibiotics to reduce risk of antibiotics.

Topical retinoid or benzoyl peroxide should be co-prescribed with oral antibiotics.

  • Then COCP as alternative to oral antibiotics.
  • Oral isotretinoin - only under specialist supervision (vitamine A analogue). SE: teratogenic, hepatitis, increased lipids, depression, dry skin, myalgia. Hair thinning, nose bleeds, ICH. Photosensitivity.

Most common is dry skin!
Avoid in pregnancy.

Monitor: LFTs, lipids, FBC.

97
Q

Acne rosacea - what is it?

A

Chronic relapsing remitting disorder affecting the face.

98
Q

Presentation of acne rosacea?

A

Erythematous pustular rash appearing in 30-50 yr old woman which can also affect the eyes. Sunlight is a key feature which can exacerbate symptoms.

Chronic flushing ppted by alcohol or foods. (nose, cheeks and forehead).

Fixed erythema: chin, nose, cheeks, forehead.

Telangiectasia, papules, pustules (No comedones).

99
Q

Associations of acne rosacea?

A

Rhinophyma: Swelling and soft tissue overgrowth of the nose in males

Blepharitis: scaling and irritation at the eyelashes.

100
Q

Management of acne rosacea ?

A
  • Avoid sun exposure
  • Topical metronidazole
  • Topical brimonidine gel for predominant flushing but limited telangiectasia
  • More severe disease is treated with systemic antibiotics - oxytetracycline.

For prominent telangiectasia - give laser therapy or use topical tacrolimus.

101
Q

Maculopapular drug eruptions?

A
  • Commonest type
  • Generalised erythematous macules and papules
  • ± fever and increased eosinophils
  • Develops within two weeks of onset of drug

Due to
- Penicillin, cephalosporins, AEDs.

102
Q

Urticaria drug eruption?

A 
Wheals ± angioedema and anaphylaxis 
- Rapid onset after taking drug 
- Immune (IgE) 
Penicillin
Cephalosporin

Non-immune (direct mast cell degranulation)

  • Morphine
  • Codeine
  • NSAIDs
  • Contrast
103
Q

Erythema Multiforme?

A
  • Symmetrical target lesions on palms, soles and limbs,
  • pruritis usually mild
  • Occurs 1-2 weeks after insult
  • Infections are commoner cause of EM
104
Q

What causes erythema multiforme?

A
  • Idiopathic
  • Infections: HSV (most common cause) - parapox, mycoplasma

Drugs: Sulphonamides, NSAIDs, allopurinol, penicillin, phenytoin

  • SLE
  • Sarcoidosis
  • Malignancy
105
Q

What is Stevens-Johnson syndrome?

A

More severe variant of EM

Blistering mucosa: conjunctiva, oral, genital.

106
Q

What is Toxic epidermal necrolysis?

A 
Extreme form of SJS
Nearly always a drug reaction 
Features 
- Severe mucosal ulceration 
- Widespread erythema followed by epidermal necrosis 
- Loss of large sheets of epidermis
- Leads to dehydration.

Caused by

  • Phenytoin
  • Sulphonamides
  • Allopurinol
  • Penicillin
  • Carbamazapine
  • NSAIDs.

Increased risk in HIV+
- Management: dexamethasone, IVIg (first line)

Mortality: 30%.

107
Q

Infestations in dermatology - Scabies?

A

Sarcopetes scabei

  • Highly contagious: spread by direct contact
  • Female mite digs burrows and lays eggs.

Presentation

  • Burrows: short, serpiginous grey line, block dot.
  • Hypersensitivity rash: eczematous, vesicles
  • Extremely itchy –> Excoriation
  • Delayed Type IV
  • Pruritis may persist up to 4-6 weeks.
  • Particularly affects the finger web spaces (esp 1st)
  • Also: axillae, groin, umbilicus.
108
Q

Management of scabies?

A

Permethrin cream: applied from neck down for 24hrs
2nd line: Malathion
3rd line: oral ivernectin

Treat all members of the household.
Apply insecticide everywhere. Allow to dry and leave on skin for 8-12 hrs. Malathion = 24hrs.
Reapply if insecticide is removed during treatment.

109
Q

Headlices management?

A

Pediculus humanus capitis

  • spread by head to head contact
  • Nits = empty eggs.

Presentation

  • itch
  • papular rash @ the nape of the neck

Management

  • Malathion
  • Combing.
110
Q

Erythema nodusum (skin manifestation of systemic disease? )

A

Inflammation of subcut fat

Sarcoid, 
TB, 
Brucellosis
IBD, 
Behcet's. 
Malignancy/lymphoma. 
Strep infection
Sulphonamides, COCP

NOT CAUSED BY HIV FUCK SAKE.

Painful blue-red lesions on anterior shins. Resolves in 6 weeks. Lesions heal without scarring.

Generally leave to follow up.

111
Q

Erythema multiforme?

A

Symmetrical target lesions on palms, soles, limbs.

Possibly mediated by IgM deposition.
Usually 2ndry to infection

Infection: HSV, mycoplasma.

Drugs: Sulphonamides, NSAIDs, Allopurinol, phenytoin, penicillin.

112
Q

SJS and TEN?

A

Nearly always drug induced

113
Q

Pyoderma gangrenosum

A
  • Wide (10cm) deep ulceration with violaceous border
  • Purulent surface
  • Undermined edge
  • Commonly occurs on legs

Looks like a pizza.

  • Heal with cribiform (pitted) scars
  • Associated with: IBD, AIH, Wegener’s RA, leukaemia.

High dose systemic steroids.

Given oral first due to the high risk that this could develop rapidly.

114
Q

What is vitiligo?

A

AI condition resulting in loss of melanocytes and consequent depigmentation of skin.

  • Chalky white patches with
  • hyperpigmented borders
    Itch in sunlight
  • Associated with autoimmune disorders (T1DM, Addision, AI thyroid, pernicious anaemia, alopecia areata)

Management

  • Sunblock, camouflage make-up, topical steroids.
  • Maybe phototherapy
115
Q

Livedo reticularis

A

Persistent mottled red/blue lesions that don’t blank
Commonly found on the legs
Triggered by cold

Caused

  • Idiopathic
  • Vasculitis: RA, SLE, PAN
  • Obstruction: anti-phos, cryoglobulinaemia
  • Sneddon’s syndrome: LR + CVAs
116
Q

Skin rash in rheumatic fever?

A

Erythema marginatum

117
Q

Skin rash in lyme disease /

A

Erythema chronicum migrans

118
Q

Skin rash in Crohn’s

A

Perianal ulcers and fistulas
EN
Pyoderma gangrenosum

119
Q

Dermatomyositis skin rash

A 
Heliotrope rash on eyelids
Shawl sign (macular rash) 
Gottron's Papules
Mechanic's hands
Nailfold erythema
120
Q

Diabetes mellitus skin rash?

A

Ulcers
Candida
Acanthosis nigrans (velvety, plaques that are often found on the neck, axilla, groin). Caused by DM, obesity, PCOS, Acromegaly, Cushing’s, hypothyroidism, familial, PWS.

Necrobiosis lipoidica (shins) 
Granuloma annulare (hands, feet)
121
Q

Sarcoidosis skin rash

A 
Erythema nodusum
Erythema multiforme 
Lupus pernio
Hypopigmented areas
Red/violet plaques
122
Q

Coeliac’s disease skin rash

A

Dermatitis herpetiformis (elbows)

Itchy, vesicular skin lesions on the extensor surface (elbows, knees, buttocks).

Skin biopsy = deposition of IgA in the granular pattern in the upper dermis.

Can use Dapsone.

123
Q

Grave’s Disease skin rash

A

Pre-tibial myxoedema

124
Q

RA skin rash?

A

Rheumatoid nodules

Vasculitis (palpable purpura)

125
Q

SLE skin rash

A

Facial butterfly rash

126
Q

Systemic sclerosis skin rash

A 
Calcinosis
Raynaud/s
Sclerodactyly
Telangiectasia
Generalised skin thickening
127
Q

Liver disease skin rash

A 
Palmar erythema
Spider naevi
Gynacomastia
Decreased 2ndry hair 
Jaundice
Bruising 
Excoriations
128
Q

ESRD skin rash

A

Associated with cause?
- DM, vasculitis, sclero, RA, SLE

Associated with ESRD?
- Pruritus, xerosis, pigment change, bullous disease

Associated with transplant
- Cushingoid, gingival hyperplasia, infections, BCC, SCC, melanoma, Kaposi’s

129
Q

Neoplasia skin rash?

A

Acanthosis nigricans
Dermatomyositis
Thrombophlebitis migrans
Acquired ichthyosis

130
Q

What is first line treatment of hyperhidrosis?

A

Topical aluminium chloride

2nd line = iontophoresis - those with palmar, plantar and axillary hyperhidrosis

3rd lien :botulinum toxin

Surgery - endoscopy transthoracic sympathectomy

131
Q

Cherry haemangioma on torso?

A

Benign skin lesions which contain an abnormal proliferation of capillaries. They are more common with advancing age and affect men and women equally.

Erythematous, papular lesions
typically 1-3 mm in size
Non-blanching
Not found on mucous membranes.

132
Q

Venous ulceration

A

Typically above the medial malleolus

ABPI is important in non-healing ulcers to assess poor arterial flow.
Normal ABPI = 0.9-1.2. <0.9 indicate arterial disease.

133
Q

Management of venous ulcers?

A
  • Compression bandaging, usually four layer
  • Oral pentoxifylline - peripheral vasodilator.
  • Small evidence base supporting use of flavinoids
  • Little evidence to suggest benefit from hydrocolloid dressing, topical growth factors, US therapy and intermittent pneumatic compression.
134
Q

Fungal Nail infection

A

Onychomycosis

  • dermatophytes - trichophyton rubrum (90%).
  • Yeast
  • Non-dermatophyte mould

Thickened unsightly nails are a common reason.

Investigation
- Nail clippings

Management
- If dermatophyte
oral terbinafine is first line with oral itraconazole as alternative
- itraconazole, 6 weeks to 3 months.

Must give oral as topical won’t have necessary penetration.

Candida - mild disease should be treated with topical antifungals

135
Q

Measles or rubella rash?

A

Must wait 4 days following the onset of the rash to return to work or school.

136
Q

Clobetasone and skin?

A

Topical steroids may cause patchy depigmentation in patients with darker skin.

137
Q

Melasma

A

Hyperpigmentated brown or grey macules. More common with people with darker skin and associated with sun exposure, NSAIDs, drugs and oral contraceptives.

138
Q

Milia

A

Common and normal finding on examination of the newborn seen in up to half of babies typically on the face. Will resolve spontaneously over the course of a few weeks.

139
Q

Port-wine stain

A

Capillary malformation seen at birth which usually requires no treatment.

Typically flat and dark red/purple in colour.

Morphea is not typically found in neonates.

Angiosarcoma is a cancer of the blood vessel lining.

140
Q

Strawberry naevi

A

Soft raised vascular swellings on the skin surface.

Usually bright red in colour.

Reassure the mother that most lesions spontaneously regress and suggest review in 3 months.

Capillary haemangiomas are present in 10% of white infants. Female infants premature infants and those of mothers who have undergone chorionic villous sampling.

Potential complication

  • Mechanical
  • Bleeding
  • Ulceration
  • Thomobocytopaenia
141
Q

Salmon patch

A

Flat, dull red areas usually found on the face or neck.

142
Q

Erythrasma

A

Erythrasma is a generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae. It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum

Examination with Wood’s light reveals a coral-red fluorescence.

Erythrasma is an infection caused by Corynebacterium minutissimum which is treated with oral erythromycin. There are no other antibiotics which are licensed to treat this so this is the only possible answer.

143
Q

Solar lentigo

A

Well circumscribed and in clusters in sun-exposed areas.

144
Q

Hypopigmented lesions

A

Pityriasis versicolor = fungal infection on back, itchy and more prominent in suntan. Comes out in warm moist climates and why holiday brings it out.

Melasma - dark skin discolouration in pregnant women and those who are taking oral or patch contraceptives.

Pityriasis alba - hypopigmentation is skin in adults + young children. Pink scaly patches which later leave pale areas on the skin. Nore noticeable on darker skin NOT ITCHY.

145
Q

Alopecia Areata

A

Autoimmune condition causing localised, well demarcated patches of hair loss.

No scarring.

Looking for broken, exclamation mark hairs.

Hair regrows in 50% in 1 yrs, and 80-90% eventually.

  • Topical or intralesional corticosteroids, topical minoxidil, phototherapy, dithranol.

Screening for other AI conditions = TFTs, FBC, HbA1c, B12.

146
Q

Pyogenic granuloma?

A

Mimic a amelanotic melanoma.

Differentiated based on the history of trauma eg a splinter.

Amelanotic melanoma occur on the sole of foot or under a nail. More slowly with no history of trauma.

Eruptive haemangioma is the most useful name to describe it.

  • Linked to trauma, pregnancy, more common in women and young adults.
  • Most common sites are head, neck, upper trunk and hands. Lesions in the oral mucosa are common in pregnancy.
  • Initially small red/brown spot.
  • Rapidly progress within days to weeks forming raised red/brown lesions.
  • Bleed on contact.

Can resolve post partum. May need curettage, cauterisation, cryotherapy and excision.

147
Q

Ketoconazole

A

Side effect is gynaecomastia

S: Spironolactone
A: Alcohol
C: Cimetidine
K: Ketocanazole
E: Estrogen
D: Digitalis
148
Q

Sebaceous cyst

A

Epidermoid and pilar cyst.

Proliferation of epidermal cells within the dermis.

most common on scalp, ears, back, face, upper arms.

Typically contain a punctum.

149
Q

Hereditary haemorrhagic telangiectasia

A

Osler Weber Rendu syndrome.

AD characterised by multiple telangiectasia over skin and mucous membranes.

4 main diagnostic criteria.

  • epistaxis : spontaneous, recurrent nosebleeds
  • telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
  • visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
  • family history: a first-degree relative with HHT

Peutz Jegher has macular melanin deposition rather than telangiectasia.

150
Q

Hirsuitism and Hypertrichosis

A 
Polycystic ovarian syndrome is the most common causes of hirsutism. Other causes include:
Cushing's syndrome
congenital adrenal hyperplasia
androgen therapy
obesity: thought to be due to insulin resistance
adrenal tumour
androgen secreting ovarian tumour
drugs: phenytoin, corticosteroids

Ferriman-Gallwey scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism

Management of hirsutism
advise weight loss if overweight
cosmetic techniques such as waxing/bleaching - not available on the NHS
consider using combined oral contraceptive pills such as co-cyprindiol (Dianette) or ethinylestradiol and drospirenone (Yasmin). Co-cyprindiol should not be used long-term due to the increased risk of venous thromboembolism
facial hirsutism: topical eflornithine - contraindicated in pregnancy and breast-feeding

151
Q

Hypertichosis?

A

Excessive hair growing rather than hair in a female following a male distributions.

drugs: minoxidil, ciclosporin, diazoxide
congenital hypertrichosis lanuginosa, congenital hypertrichosis terminalis
porphyria cutanea tarda
anorexia nervosa

152
Q

Polymorphic eruption of pregnancy?

A

Pruritic condition associated with last trimester
Lesions often first appear in abdo striae
Management depends on severity: emollients, mild potency, topical steroids and oral steroids.

153
Q

Pemphigoid gestationis

A

Pruritic blistering lesions
Often develop in peri-umbilical region, later spreading to trunk, back, buttocks and arms.
Usually presents 2nd or 3rd trimester.
Oral corticosteroids are usually required.

154
Q

Purpura in children?

A

New onset purpura should be referred immediately for investigations to exclude ALL and meningococcal disease.

155
Q

Emollient application

A

Should be actually applied immediately after washing.

Bathing and showering remove oils and skin which cause it to dry out.

  • Initially applying emollients 2-3 times a day.
  • When skin worsens emollient can be applied hourly
  • Wash hands before applying emollient to prevent infection of damaged skin
  • Either dispense emollient using a pump or spoon from a tub to avoid contamination of the tub.
  • Apply emollient generously to all areas of the body onto the skin in a downward motion.
  • Do not rub emollients, but rather leave them to soak in.
156
Q

Fitzpatrick Classification

A

I = Never tans, always burns (red hair, freckles, blue eyes)
II: Usually tans, always burns
III: always tans, sometimes burns
IV: always tans rarely burns
V: Sunburn and tanning after extreme UV exposure (brown
VI: black skin. Never tans, never burns.

157
Q

Lymphoma

A

Mostly in 24-34 yr old with asymptomatic enlarged lymph node in the neck.

Cause of leuconychia.

158
Q

Other causes of leuconychia?

A

Hypoalbuminaemia

Less common: fungal disease, lymphoma.

159
Q

Yellow nail syndrome?

A

Lymphoedema
Pleural effusions
Bronchiectasis
Chronic sinus infections

160
Q

Blue nails?

A

Wilson’s disease

161
Q

Seborrhoeic keratoses?

A

Epidermal skin lesions seen in older people

Features

  • Large variation in colour from flesh to light-brown to black.
  • Have a stuck-on appearance
  • Keratotic plugs may be seen.

Management

  • Benign nature of lesions
  • Options for removal include curettage, cryosurgery, shave biopsy.
162
Q

Spider naevi vs telangiectasia?

A

When you press down, spider naevi fill form the centre.

Telangiectasia from the edge.

Spider naevi described a central red papule with surrounding capillaries. Lesions blanch upon pressure.

Caused by liver, pregnancy and COC (high presence of oestrogen dilatation).

163
Q

Erythema ab igne

A

Skin disorder caused by over exposure to infrared radiation.

Reticulated erythematous patches with hyperpigmentation and telangiectasia.

Can go on to develop squamous cell skin cancer.

164
Q

Dermatofibroma?

A

Benign lesion.
Firm elevated nodules.
Usually history of trauma.
Lesion consists of histiocytes, blood vessels and fibrotic changes.

165
Q

Oral leukoplakia?

A

Premalignant condition - white, hard spots on the mucous membranes.
asymptomatic and prolonged nature goes against candidiasis.

More common in smokers.

Candidiasis and lichen planus should be considered especially if lesion can be rubbed off.

166
Q

Pruritus?

A

Liver disease - history of alcohol, chronic liver disease.

Iron deficiency anaemia - pallor, koilonychia, atrophic glossitis.

Polycythaemia - Pruritus particularly after warm bath. ruddy complexion, Gout, peptic ulcer disease.

Chronic kidney disease - lethargy and pallor, oedema and weight gain, HTN.

Lymphoma - Night sweats, lymphadenopathy, splenomegaly, hepatomegaly.

167
Q

Lanugo hair

A 
Newborn babies 
Chronic malnutrition (anorexia nervosa).
168
Q

Necrobiosis lipoidica diabeticorum?

A

Shiny painless area of yellow/red skin typically on the shin of diabetics.

Often associated with telangiectasia.

169
Q

Shin lesions

A

Erythema nodosum
Pretibial myxoedema
Pyoderma gangrenosum
Nefcrobiosis lipoidica diabeticorum

170
Q

Chondrodermatitis nodularis helicis?

A

Painful crusty lesion back of ear.

Common and benign condition development of a painful nodule on the ear.

Management

  • Reducing pressure on the ear: form ‘ear protectors’ ay be used during sleep
  • Other treatment options include cryotherapy, steroid injection, collagen injection
  • Surgical treatment may be used but there is a high recurrence rate.
171
Q

Lichen sclerosis

A

Inflammatory condition
- Atrophy of epidermis with white plaques forming.

Itch is prominent.

Skin biopsy is not necessary when a diagnosis can be made.

Management with steroids and emollients.

172
Q

Zoon’s balanitis

A

Affecting uncircumcised men.

Secondary to lichen sclerosis or erythroplasia of Queyrat. Orange-red lesions with pinpoint redder spots on the glands and adjacent areas of the foreskin in uncircumcised men.

Circinate balanitis - chronic balanitis in men with Reiter’s syndrome. Can occur in isolation.

Well-demarcated erythematous plaque with a ragged white border.

Erythroplasia of Queteat is in-situ SCC. Multiple plaques with a red, velvety appearance.

SCC - may be papillary or flat.

173
Q

Keratoderma blenorrhagica?

A

Waxy yellow papules on the palms and soles. Seen in Reiter’s syndrome

174
Q

Skin disorders associated with SLE?

A

Photosensitive butterfly rash
Discoid lupus
alopecia
Livedo reticularis: net-like rash

175
Q

Keloid scar

A

Keloid scar are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound.

Common sites - sterum, shoulder, neck, face, extensor limbs.

Can be treated with intralesional steroids.
Excision is sometimes required.

176
Q

Lipoma?

A

Pathophysiology

  • They are generally found in subcut tissues.
  • rately they occur in deeper adipose tissues.
  • Smooth, mobile and painless.

If >5cm, ultrasound is required to rule out a liposarcoma.

177
Q

Liposarcoma?

A

Size >5cm
Increasing size
Pain
Deep anatomical location

178
Q

Granuloma annulare

A

Papular lesions that are often slightly hyperpigmented and depressed centrally

Typically occur on the dorsal surface of the hands and feet, and on the extensor aspects of the arms and legs.

179
Q

Erythroderma?

A

Inpatient treatment of erythroderma must be monitored for complications like dehydration, infection, high-output heart failure.

95% of skin is involved in a rash of any kind

Eczema, psoriasis, drugs, lymphoma.

Erythrodermic psoriasis

Imperial Medicine Year 3 (35 decks)

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