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CP2 > DERM > Flashcards

DERM Flashcards

1
Q

Eruption

A

= rash

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2
Q

Lesion

A

= any small area of skin disease

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3
Q

Macule

A

= Flat (non-palpable) area of colour change <0.5cm

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4
Q

Patch

A

Flat (non-palpable) area of colour change >0.5cm

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5
Q

Papule

A

Raised (palpable) lesion <0.5cm (usually dome shaped)

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6
Q

Nodule

A

Raised (palpable) lesion >0.5cm (usually dome shaped)

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7
Q

Cyst

A

Fluctuant papule/nodule containing fluid/pus/keratin

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8
Q

Plaque

A

Palpable, flat-topped lesion

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9
Q

Vesicle

A

Fluid-filled lesion/papule <0.5cm

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10
Q

Bulla

A

Fluid-filled lesion/papule >0.5cm

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11
Q

Pustule

A

Pus-filled lesion

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12
Q

Wheal/weal

A

Smooth, skin-coloured superficial swelling lasting <24 hours

Often surrounded by erythema

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13
Q

Erosion

A

Partial break in skin: loss of epidermis only

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14
Q

Ulcer

A

Complete break in skin: dermis included

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15
Q

Fissure

A

Small, slit-like break in skin

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16
Q

Excoriation

A

Erosion or ulcer due to scratching

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17
Q

Lichenification

A

Thickening of skin and increased markings due to chronic scratching/rubbing

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18
Q

Scale

A

Visible white loosening of outermost layer of skin

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19
Q

Crust

A

Golden deposit on skin due to dried plasma

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20
Q

What is psoriasis?

A

= chronic, relapsing inflammatory skin disorder (involving increased skin turnover and epidermal thickening).

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21
Q

Who does psoriasis affect mostly?

A
  • Bi-peak onset – early 20s and 50s
  • Affects 2% of population
  • M = F
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22
Q

What other conditions is psoriasis linked with?

A
  • Inflammatory – IBD, uveitis, coeliac, arthritis
  • Obesity
  • CVD
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23
Q

Psoriasis - presentation

A

Red, scaly plaques on EXTENSOR surfaces and scalp

  • Causes pain, itching, bleeding
  • Significant psychological impact

Psoriatic Arthritis (in 10%)

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24
Q

Psoriasis - Risk Factors

A

Genetics – FHx or HLA-CW6 gene

Environmental

  • Strep throat infection
  • Medications – BBs, antimalarials, lithium
  • Stress, alcohol, smoking, trauma, sunlight
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25
Q

Psoriasis - principles of management

A

Depends on the severity and impact on the patient.
=> PASI
=> Dermatology Life Quality Index

Education – avoid lifestyle triggers (e.g. smoking, alcohol, stress)

Manage CV risk factors

1st line = topical
2nd line = phototherapy
3rd line = systemic Tx
Last line = biologics

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26
Q

Topical treatments for Psoriasis

A
  • Emollients (e.g. E45)
  • Corticosteroids +/- VitD analogues
  • Keratolytics (e.g. 5% salicylic acid) for thick plaques
  • Coal tar products for scalp
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27
Q

Phototherapy for Psoriasis

A

Requires 2o care referral

Exposure to UV light = immunosuppression to decrease symptoms from skin inflammation

2-3x per week for 15-30 episodes.
Base starting dose on skin type and gradually increase time of exposure.

UVB or PUVA

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28
Q

UVB vs PUVA phototherapy

A

Narrow band UVB = superficial (1st line, can be used if pregnant)

PUVA (UVA + Psoralen tablets) = deeper (not used if pregnant)

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29
Q

Side effects of phototherapy

A

Of UV – erythema/pruritis, cold sores, photoaging, SKIN CANCER

Of tablets – nausea, headaches

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30
Q

Dermatological indications for phototherapy

A
  • Acne
  • Psoriasis
  • Vitiligo
  • Lichen planus
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31
Q

Counselling for the patient before receiving phototherapy

A
  • Only very short exposure (seconds to minutes)
  • Dose carefully calculated for skin type
  • Goggles to protect eyes and genitalia covered
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32
Q

Systemic Treatments for Psoriasis (and their side effects / monitoring)

A

Methotrexate
=> Teratogenic, hepatotoxic, BM suppression, GI upset/nausea
=> Monitor LFTs, FBC

Acitretin
=> Teratogenic, hepatotoxic, increases lipids, dry skin/hair thinning
=> Monitor LFTs, lipids

Ciclosporin
=> Nephrotoxic, increases BP, tingling peripheries
=> Monitor BP and U&Es

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33
Q

Topical steroid choices

A

MILD 1% hydrocortisone
=> any age, anywhere

MODERATE	Eumovate (clobetasone)
=> any age, caution on face
POTENT	Betnovate (betamethasone)
=> adults only, not used on face/genitals

V. POTENT Dermovate (clobetasol)
=> adults only, not used on face/genitals

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34
Q

Side effects of topical steroids

A
  • Skin thinning
  • Can trigger acne/rosacea
  • Withdrawal can cause erythroderma
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35
Q

What is the most common type of leg ulcers?

A

Venous ulcers - Account for ~70% of ulcers

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36
Q

Pathophysiology of venous ulcers

A
  • Valve incompetence and reflux
  • Calf muscle dysfunction

Toxins accumulate => inflammation and necrosis of tissue.

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37
Q

Venous ulcers - risk factors

A 
DVT, 
varicose veins, 
age, 
pregnancy, 
surgery
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38
Q

Venous ulcers - location

A

Generally located in the gaiter area (= below the knee and above the ankle)

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39
Q

Venous ulcers - Features

A
  • Large and irregular
  • Shallow with sloping edges
  • Granulation tissue
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40
Q

Venous ulcers - Leg condition

A
  • Lipodermatosclerosis
  • Venous eczema
  • Haemosiderin (red/brown colour)
  • Atrophie Blanche (smooth, white sclerotic plaques)
  • Heavy, aching, pruritis, oedema
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41
Q

GENERAL treatment for all ulcers

A
  • Dressings +/- antibiotics +/- emollients

* Debridement – surgery/dressings/larvae

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42
Q

Specific treatment for venous ulcers

A

MUST exclude arterial insufficiency before starting compression therapy (ABPI)

Elevation and compression
=> 1st line = 4-layer bandaging
=> Other = stockings

Skin graft / superficial venous surgery

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43
Q

Arterial ulcer - pathophysiology

A

Atheromatous changes cause compromised blood flow

Results in hypoxia and accumulation of toxins => inflammation and necrosis of tissue.

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44
Q

Arterial ulcer - Risk Factors

A

Diabetes, HTN, arterial disease, high cholesterol, Raynaud’s disease

Smoking
Trauma

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45
Q

Arterial ulcer - Location

A

Located on bony prominences (usually lateral malleolus and toes)

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46
Q

Arterial ulcer - Features

A
  • Smaller and round
  • “Punched out” borders
  • Little granulation tissue and dry
  • Very painful
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47
Q

Arterial ulcer - Leg condition

A
  • 6Ps – pain, pulseless, pale, paraesthesia, paralysis, perishingly cold
  • Claudication/ischaemic rest pain symptoms
  • Cool, hairless, dry, shiny skin
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48
Q

Specific treatment for arterial ulcers

A
  • Manage vascular risk factors – e.g. antiplatelets, stop smoking
  • Surgical revascularisation
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49
Q

Neuropathic Ulcers - Pathophysiology

A
  • Peripheral neuropathy => loss of protective sensation and trauma goes unnoticed
  • Vascular disease => reduced wound healing
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50
Q

Neuropathic Ulcers - Risk factors

A

Diabetes,
Trauma,
Prolonged pressure

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51
Q

Neuropathic Ulcers - Location

A

Located on pressure areas

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52
Q

Neuropathic Ulcers - Features

A
  • Small, round, deep
  • “Punched out” borders
  • Thick rim
  • PAINLESS
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53
Q

Neuropathic Ulcers - Leg condition

A
  • Surrounding callous
  • Loss of sensation
  • Dry, cracked skin
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54
Q

Specific treatment for neuropathic ulcers

A
  • Optimise glycaemic control
  • Treat co-existing arterial disease
  • Good foot care
  • Offload pressure
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55
Q

What is eczema?

A

= itchy skin condition, characterised by erythema, dry skin and scaling.

\+/- vesicles and blisters (acute)
\+/- fissures and lichenification (chronic)
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56
Q

Atopic Eczema - features

A

red, dry, scaly skin affecting FLEXURES

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57
Q

How common is atopic eczema?

A

Affects 20-30% of schoolkids, 5-10% of adults

Onset usually <2 years

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58
Q

Atopic Eczema - causes / risk factors

A

Genetics – PMHx/FHx of atopies

Environmental – irritants, allergens, illness/infection/stress, cold weather

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59
Q

Atopic Eczema - complications

A

= susceptible to infection

S. aureus/Strep – weeping pustules/crusting; fever/malaise

HSV (Eczema Herpeticum) – pain, fever, lethargy; clustered blisters and punched-out erosions

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60
Q

Management of Eczema

A

Patient education - avoiding triggers, how to apply treatments, signs of infection

  1. First Line = TOPICAL emollients/steroids
  2. Second Line = TOPICAL Calcineurin Inhibitors
  3. Third Line = PHOTOTHERAPY / IMMUNOSUPPRESSANTS
  4. Additional Treatments
    => Systemic ABX / acyclovir (infection)
    => Antihistamines
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61
Q

First line management for eczema

A
  • Avoid irritants/allergens/triggers
  • Emollients for dry skin – liberally, as often as needed.
  • Topical steroids – for active areas; a “fingertip” portion 1-2x daily.
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62
Q

Second line management for eczema

A

Topical Calcineurin Inhibitors (e.g. Tacrolimus, Pimecrolimus)

=> Used if mod/severe eczema or if there are CIs to topical steroids

Usually initiated by specialists

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63
Q

Third line management for eczema

A

Phototherapy + emollients and topical steroids

Immunosuppressants (e.g. ciclosporin, methotrexate, azathioprine)

(Initiated by specialists)

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64
Q

Acne Vulgaris - Pathophysiology

A
  1. Hyperkeratinisation of follicle = pore blockage
  2. Increased sebum production (due to increased androgens at puberty)
  3. Overgrowth of P. Acnes (a gram +ve commensal)
    => Releases pro-inflammatory mediators
    => Follicles rupture and contents leak into surrounding dermis
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65
Q

Acne Vulgaris - Risk factors

A
  • Male
  • Cosmetic/hair products
  • Excess washing
  • Progesterone-only OCP/steroids
  • Hormonal changes / Endocrine disorders
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66
Q

Lesions of Acne

A
  1. Non-Inflammatory:
    - Closed comedones (whiteheads) – small papules that may burst
    - Open comedones (blackheads) – flat or raised with impacted keratin
  2. Inflammatory:
    - Papules – burst comedones cause inflammation
    - Pustules – papules containing pus
    - Nodules – painful swellings lasting weeks-months
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67
Q

Sequelae of acne

A
  1. Non-scarring:
    - Hyper/hypo-pigmentation
    - Eythematous macules
  2. Scarring:
    - “ICE-PICK” scars (atrophic) – collagen loss
    - “KELOID” scars (hypertrophic) – increased collagen
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68
Q

Management of Acne

A

Depends on severity, psychological impact, response to previous Tx.

  1. Topical retinoids/antibacterials/ABX = 1st line for mild/moderate
  2. Systemic ABX = 2nd line or 1st line for severe
  3. Oral Isotretinoin (Roaccutane) = severe or Tx resistant subtypes
  4. Hormonal Tx = Tx resistant females/ cyclical flares/hirsutism
  5. Tx for Scars
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69
Q

1st line for mild/moderate acne

A

= topical retinoids/antibacterials/ABX

Retinoids = unblock pores
Antibacterials – e.g. benzyl peroxide
Antibiotics – e.g. erythromycin/clindamycin

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70
Q

What is something to remember with all topical treatments for acne?

A

All may cause irritation/erythema and photosensitivity.

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71
Q

2nd line for mild/moderate acne

1st line for severe acne

A

Systemic ABX

=> Lymecycline/doxycycline

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72
Q

Treatment for severe or Tx-resistant acne

A

= Oral Isotretinoin (Roaccutane)

=> Retinoid, decreases sebum production

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73
Q

Side effects of Roaccutane

A
  • Teratogenic
  • Hepatitis – avoid alcohol (check LFTs)
  • Photosensitivity and dry skin
  • Muscle aches
  • Mood changes
  • Anaemia and thrombocytopaenia (check FBC)
  • Increased TGs and cholesterol (check lipids)
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74
Q

Contraindications for Roaccutane

A
  • Pregnancy
  • Liver/renal disease
  • Diabetes
  • Peanut allergy
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75
Q

When is hormonal Tx used in acne?

A

= Tx resistant females/ cyclical flares/hirsutism

=> COCP Dianette

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76
Q

What are contraindications for the COCP dianette?

A

Pregnancy/lactation,

PHx or FHx of VTE

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77
Q

Management of acne - Scar treatments

A

Microdermabrasion (removes dead skin) – superficial scars

Laser resurfacing – for atrophic scars

Punch biopsy/excision – for ice-pick scars

Intralesional steroids – for keloid scars

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78
Q

Severity of Psoriasis

A

=> PASI = Psoriasis Area and Severity Index.

Used to measure severity and extend of psoriasis

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79
Q

Non-cutaneous manifestations of Psoriasis

A

Psoriatic Arthritis (in 10%)

Cardiovascular risk factors and metabolic syndrome

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80
Q

Dermatology Life Quality Index

A

Used to identify the impact of a skin condition on the patient’s life

Guides treatment / monitor improvement

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81
Q

What is a problem with topical vit D analogues in management of psoriasis?

A

Skin irritation

Metabolic effects (limit use to 100 g per week)

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82
Q

How is methotrexate taken?

A

Taken once weekly

Folic acid on the OTHER days.

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83
Q

What is important to do before starting biologics?

A

screen for any sign of infection (esp. TB, HIV, Hep B&C)

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84
Q

What is erythroderma?

A

= a severe and potentially life-threatening inflammation of most of the body’s skin surface

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85
Q

Causes of erythroderma

A

Psoriasis - withdrawal from steroids
Eczema
Drugs
Cutaneous T cell Lymphoma

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86
Q

Management of erythroderma

A

Admission to hospital

IV fluid, thermoregulation
Regular emollients
Consider moderate potency topical steroids

Prevent/treat any complications (e.g. infection)

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87
Q

How long do systemic ABX take to show improvement in acne?

A

Around 3 months

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88
Q

What is required for females to take Roaccutane (oral retinoid) for acne?

A

requires 2x contraception and monthly urinary pregnancy test

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89
Q

What is rosacea?

Who does it affect?

A

= a chronic inflammatory skin condition affecting the centre of the face

Can affect ANYONE
=> Peak onset age 30-60
=> more common with fair skin and Celtic/North European descent.

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90
Q

Pathogenesis of rosacea

A

thought to be multifactorial

=> genetics and environmental factors

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91
Q

Cutaneous features of rosacea

A
  • Transient and persistent facial erythema
  • Inflammatory papules and pustules ( but no comedones)
  • Telangiectasia
  • Rhinophyma

(Occasionally) Facial lymphoedema, burning/pain

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92
Q

neurogenic rosacea

A

Features of rosacea and also facial tenderness/ burning pain

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93
Q

Morbihan Disease

A

= chronic and persistent erythematous lymphoedema on the face

Sometimes occurs in rosacea

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94
Q

Telangiectasia in rosacea

A

Telangiectasia = persistent dilated capillaries/small blood vessels in the skin

In rosacea - present on facial skin, apart from nasal alar region.

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95
Q

Rhinophyma

A

Nasal skin is thickened and the sebaceous (oil) glands are enlarged.

Due to hyperplasia/fibrosis of the sebaceous glands of the face

More common in M > F

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96
Q

Ophthalmic complications of rosacea

A

Dryness
Conjunctivitis
Blepharitis – ophthalmology referral
Keratitis – ophthalmology referral

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97
Q

Rosacea - diagnosis

A

One diagnostic and 2 major criteria are needed for a diagnosis.

DIAGNOSTIC

  1. Persistent centrofacial erythema, associated with periodic intensification by potential trigger factors
  2. Phymatous changes

MAJOR (must occur in centrofacial distribution):

  1. Flushing/transient centrofacial erythema
  2. Inflammatory papules and pustules
  3. Telangiectasia
  4. Ocular rosacea (lid margin telangiectasia, blepharitis, keratitis/conjunctivitis/sclerokeratitis/anterior uveitis).
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98
Q

General management of rosacea

A

Assess the patient’s psychosocial burden of disease and consider referral for psychological support where necessary.

Lifestyle advice:

  • Avoid triggers, oil-based products, exfoliants
  • Moisturise frequently
  • NEVER apply topical steroid
  • Sun protection
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99
Q

Tx for Papulopustular/Inflammatory Rosacea

A

Topical – metronidazole/ azelaic acid

Oral ABX – e.g. tetracyclines, metronidazole

Isotretinoin

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100
Q

Mx of Erythmatotelangiectatic Rosacea

A

Treat any inflammatory component first

Topical azelaic acid / metronidazole may also help erythema

Laser can be used for severe telangiectasia

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101
Q

When do drug eruptions usually occur?

A

Usually 8-21 days post-exposure

BUT can occur with drugs that have been used without issue for years.

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102
Q

Mechanism of Drug Eruptions

A
  1. Allergy – e.g. ABX
  2. Intrinsic Drug Action – e.g. tetracycline and photosensitivity
  3. Non-specific – e.g. vasculitis
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103
Q

What are some common drugs causing rashes?

A
  • Penicillins, sulphonamides
  • Thiazide diuretics
  • Gold, Penicillamine
  • NSAIDs
  • Allopurinol
  • Anticonvulsants
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104
Q

General Management of a drug eruption

A
  1. STOP DRUG
  2. Supportive care (burns etc.)
  3. Wound care
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105
Q

Features of Toxic Erythema

A

Drug reaction - ~7-10 days post-exposure

  • Measle-like Rash
  • Symmetrical erythematous macules & papules
  • May merge into larger plaques
  • +/- malaise, fever, pruritis
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106
Q

Complications of Toxic Erythema

A

can progress to erythroderma/TEN

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107
Q

Toxic erythema - management

A
  1. Stop drug (resolves in a week)

2. Consider emollients and antihistamines

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108
Q

Urticaria - features, causes, complications, Mx

A

Occurs ~24 hours post-exposure.

Features:
- Wheals = raised, pale red, itchy plaques.

Causes:

  • Drugs (salicylates, ACEIs)
  • Infection
  • Sun, exercise, stress

Complications = angioedema

Management = antihistamines

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109
Q

What is SJS/TEN?

A

= type 4 hypersensitivity reaction

Variants of severe skin reaction, with SJS being the less severe.

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110
Q

Who is affected by SJS/TEN?

A

Anyone on medication can develop SJS/TEN unpredictably.

It is more common in those with HIV

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111
Q

Features of SJS/TEN?

A

Usually a prodromal illness before the rash resembling an URTI or flu-like illness.

Abrupt onset of a tender/painful red skin rash
=> Starting on the trunk and extending rapidly over hours to days onto the face and limbs.
=> Symmetrical red macules and central blistering
=> 2+ mucosal sites involved (especially the mouth)
=> Severe eye involvement

Dermal necrolysis in TEN

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112
Q

How is severity/mortality measured in SJS/TEN?

A

= SCORTEN

One point is scored for each of the seven criteria present at the time of admission

  1. > 40 years
  2. Urea >10 mmol/L
  3. HCO3- <20 mmol/L
  4. HR >120
  5. Glucose >14mmol/L
  6. > 10% surface area
  7. Presence of malignancy
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113
Q

SJS / TEN - complications

A

POTENTIALLY FATAL

  • Sepsis
  • Dehydration
  • Electrolyte imbalance
  • ARDS
  • Shock and multiple organ failure
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114
Q

SJS / TEN - Management

A
  1. STOP DRUG

2. ICU support (fluids, NG tube, analgesia)

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115
Q

Acanthrosis Nigricans

A

= Velvety, thickened, hyperpigmented skin

Affects skin folds (axilla, groin, neck)

Associations:

  • Obesity, T2DM, Cushing’s, Addison’s, PCOS
  • GI tract cancers
116
Q

Pyoderma Gangrenosum - features

A

= auto-inflammatory chronic, recurrent ulceration.

Sudden onset:

  • May start as a small pustule, red bump, or blood-blister, often misinterpreted as an insect bite.
  • Very painful, ulcerated nodules
  • Purple/blue border
  • +/- fever and systemic illness
117
Q

Pyoderma Gangrenosum - associations and differentials

A

ASSOCIATIONS
=> UC, Crohn’s, diverticulitis, vessel inflammation (Behcet’s)
=> Active hepatitis
=> Haematological malignancy

DIFFERENTIALS
Arterial/venous ulceration

118
Q

Pyoderma Gangrenosum - Mx

A

= topical/PO steroids

119
Q

What is dermatomyositis?

A

= rare, acquired muscle disease + RASH

120
Q

Features of dermatomyositis

A

Violaceous rash on photoexposed areas

Helitrope rash on eyelids

Gottron’s papules on knuckles

121
Q

Dermatomyositis - associations

A

MALIGNANCY (breast, cervix, ovaries, lungs, pancreas, GIT)

Autoimmune conditions

Drugs

122
Q

Acquired Ichthyosis

A

= Fish-scale skin (dry)

Associations:

  • Hodgkin’s Lymphoma (and other malignancies)
  • Drugs – e.g. allopurinol
123
Q

Erythema Multiforme

A

= inflammation of blood vessels

Red, “bulls-eye” lesions (usually on hands)

Associations:

  • HSV infection (may follow cold sores)
  • Drugs (penicillin, sulphonamides, allopurinol, phenytoin)
124
Q

Erythema Nodosum - features

A

= inflammation of s.c. fat.

Bilateral red, tender subcutaneous nodules (3-20cm in diameter)
=> Usually lower legs

+/- fever, malaise, arthralgia

125
Q

Erythema Nodosum - Associations

A

Associations:

  • Infection – strep, TB
  • Inflammatory disease – sarcoid, IBD, Behcet’s
  • Drugs – sulphonamides, OCP
126
Q

Dermatitis Herpetiformis

A

Chronic, recurrent pruritic rash.
=> Symmetrical
=> On extensor surfaces

Associations:
- Coeliac Disease

127
Q

Cutaneous Vasculitis - features

A

= inflammation of skin blood vessels.

On legs/ankles/feet

Non-blanching, erythematous, purpuric rash

\+/- pain, itching, burning
\+/- fever, arthralgia
128
Q

Cutaneous Vasculitis - investigations

A

Hx and examination

Skin biopsy

FBC and auto-Abs

U&E, BP, urine dip

129
Q

Cutaneous Vasculitis - Triggers

A
  • Infection – Meningococcus, strep, URTI, hep C
  • Autoimmune – RA, Lupus, IBD
  • Medications – ABX, NSAIDs, diuretics
  • Haematological disorders/malignancies
130
Q

Pre-tibial Myxoedema

A

= accumulation of excess glycosaminoglycans in the dermis and subcutis of the skin.

Most commonly seen on the shins (pretibial areas)

Characterised by swelling and waxy/ lumpiness of the lower legs.

Associations = Grave’s disease

131
Q

What skin changes can occur in SLE?

A 
Acute = malar (butterfly) rash
Subacute = discrete ring lesions => red & scaly
Chronic = discrete discoid lesions => thick & scarring

+/- photosensitivity, arthritis, Raynaud’s, renal disease

132
Q

Diagnostic criteria for SLE

A

Malar skin rash
Antiphospholipid / ANA / Anti-DNA antibodies
Persistent thromocytopaenia
Persistent proteinuria

133
Q

What skin changes can occur in diabetes?

A

Granuloma Annulare:
=> Small papules in annular configuration

Necrobiosis Lipodica:
=> Symmetrical plaques with telangiectasia +/- ulceration

Diabetic ulcer / gangrene / candidiasis

Acanthosis nigricans

Rubeosis & vitiligo

134
Q

Benign pigmented lesions

A
  1. Freckles
  2. Congenital Melanocytic Naevi (Moles)
  3. Acquired Melanocytic Naevi (Moles)
  4. Atypical Melanocytic Naevi (Moles)
135
Q

What is a mole?

A

A proliferation of melanocytes

Can be congenital or acquired (UV exposure, hormones, age)

136
Q

Atypical Melanocytic Naevi - features and risk factors

A

Mole, which looks similar to melanoma

RFs – FHx, UV exposure, <30 years.

Features:
•	5+ mm 
•	Irregular border
•	Variable pigmentation
•	Asymmetrical
•	Flat or raised
137
Q

Atypical Melanocytic Naevi - management

A
  1. Monitor for changes
  2. Sun protection advice
  3. Excision if suspicious
138
Q

Features of malignant melanoma

A
  • Asymmetrical
  • Border = IRREGULAR
  • Colour/pigmentation = VARIED
  • Diameter >6 mm
  • Evolution (ABCDE changes or bleeding/itching)
139
Q

Risk factors for Melanoma

A 
GENETIC
PHx or FHx melanoma
Pale skin / red hair
Many/large atypical naevi
Increasing age
ENVIRONMENTAL
Sun/UV exposure
Phototherapy
Tanning beds
Immunosuppression
140
Q

Differentials of melanoma

A

Pigmented BCC
Seborrheic Keratosis
Atypical Mole

141
Q

Melanoma - Ix

A

2WW referral to dermatology!!

  1. History & Examination
  2. Excision for biopsy – if suspected melanoma
  3. Histopathology – Breslow Thickness = best prognostic factor.
142
Q

Breslow Thickness

A

= the thickness of the tumour, measured from the granular layer of epidermis to the deepest point of invasion.

143
Q

Melanoma - Mx

A

Breslow Thickness <1mm = WIDE LOCAL EXCISION (1cm margins)

Breslow Thickeness 1-4 mm = WIDE LOCAL EXCISION (1-3cm margins) + SENTIAL LN BIOPSY
=> +ve biopsy = total LN dissection + chemo/radiotherapy
=> -ve biopsy = monitor

Breslow Thickness >4mm = WIDE LOCAL EXCISION (3cm margins)
+/- LN Biopsy

144
Q

What are signs of poor prognosis for melanoma?

A 
Breslow Thickness (most important prognostic factor)
Ulceration
145
Q

Sun protection advice

A

Sunscreen – at least SPF 30 (UVB protection) and high star rating (UVA protection), applied as per manufacturers advice.

Wear protective clothing in sunny weather

Direct sunlight:
=> Spend time in the shade between 11am and 3pm when it is sunny
=> Keep babies and young children out of direct sunlight

Avoid sunbeds

146
Q

What risk factors are there for both BCC and SCC?

A

UV Exposure
Fair skin
Immunosuppression
Sites of inflammation/infection/wounds

147
Q

What risk factors are there for SCC only (i.e. not necessarily BCC)?

A

Smoking

Actinic keratosis / Bowen’s disease

148
Q

What is the most common skin cancer?

A

Basal Cell Carcinoma

149
Q

Where does BCC originate?

A

From basal cells of epidermis.

150
Q

BCC - features

A
  • Slow Growth (months/years)
  • Locally invasive but decreased mets
  • Generally asymptomatic
  • Shiny or pearly nodule with a smooth surface (may have central depression or ulceration)
  • Blood vessels cross the surface
151
Q

BCC - Management

A

If elderly, may not treat.

  • Simple Surgical Excision – margins 4mm
  • Moh’s Micrographic Excision
  • Curettage & Cautery – scrape & cauterise to stop bleed
  • Cryotherapy – only if low-risk tumour
  • Photodynamic Therapy (PDT) – only superficial BCC
152
Q

What is Moh’s Micrographic excision

A

Remove a layer of the lesion at a time & re-examine

153
Q

Photodynamic therapy for skin lesions

A

photosensitiser + UV => phototoxic reaction destroys lesion

154
Q

Where does SCC originate?

A

From keratinocytes.

155
Q

SCC - features

A
  • Rapid Growth (weeks/months)
  • Highly metastatic
  • Present as enlarging scaly or crusted lumps
  • May ulcerate
  • Often tender/painful
  • Present on sun-exposed areas
156
Q

Risk factors for metastasis of SCC

A
  • > 2cm or deep
  • Poorly differentiated
  • Lip/ear lesions
  • Previous Tx failure
  • Immunocompromised
157
Q

SCC - management options

A
  1. Simple surgical excision – margins 5mm
  2. Moh’s Micrographic Excision
  3. Radiotherapy – if extensive surgery not an option
158
Q

SCC - 5-year survival

A

Non-metastatic – 75-90%

Metastatic – 25%

159
Q

Malignant non-pigmented skin lesions

A

BCC

SCC

160
Q

What is Bowen’s Disease?

A

SCC in situ = epidermal dysplasia (considered SCC if penetrate basement membrane)

161
Q

Bowen’s Disease - features

A

Erythematous, scaly plaque/patch

162
Q

Bowen’s Disease - differentials

A
  • Psoriasis
  • Eczema
  • Actinic Keratosis
  • Superficial BCC
163
Q

Bowen’s Disease - Mx

A
  • 5-flurouracil cream
  • Cryotherapy
  • Curette & cautery
  • Photodynamic Therapy
164
Q

Actinic Keratosis - features

A

Also “solar keratosis”
=> Results from long-term exposure to UV radiation

  • Often appear as small dry, scaly or crusty patches of skin
  • May be red, light or dark tan, white, pink, flesh-toned or a combination of colours and are sometimes raised
  • Often easier to feel than see
  • Common on sites often exposed to the sun
165
Q

What are the risks/complications of actinic keratosis?

A

Can develop into SCC (~10% of AK)

166
Q

Actinic Keratosis - Mx

A

excision / curettage / cryotherapy

167
Q

When and where does Seborrhoeic Keratosis occur?

A

A common sign of skin aging (~90% of adults aged >60 years)

Can arise on any area of skin, with the exception of palms and soles and mucous membranes

168
Q

Why is the name of seborrhoeic keratosis misleading?

A

not limited to a seborrhoeic distribution;
not produced by sebaceous glands;
not associated with sebum.

169
Q

Seborrhoeic Keratosis - features

A
  • Flat or raised papule or plaque
  • 1 mm to several cm in diameter
  • Skin coloured/ yellow/ grey/ light brown/ dark brown/ black or mixed colours
  • Smooth, waxy or warty surface
  • Solitary or grouped in certain areas, such as within the scalp, under the breasts, over the spine or in the groin
170
Q

Is seborrhoeic keratosis malignant?

A

Not malignant or pre-malignant, but are sometimes hard to tell apart from malignant tumours.

(Very rarely, eruptive seborrhoeic keratoses may denote an underlying internal malignancy, most often gastric adenocarcinoma)

171
Q

Seborrhoeic Keratosis - Mx

A

Can be left alone or removed – reasons for removal may be that it is unsightly, itchy, or catches on clothing.

  • Cryotherapy for thinner lesions (repeated if necessary)
  • Curettage and/or electrocautery
  • Ablative laser surgery
  • Shave biopsy
  • Focal chemical peel with trichloracetic acid
172
Q

What are the normal bacterial skin commensals?

A
  • Staph. epidermidis
  • Corynebacteria
  • Micrococci
  • Propriobacteria
173
Q

What bacteria tend to cause skin infections?

A

Staphylococci
(Staph. Aureus = ALWAYS pathogenic)

Streptococci
(Strep. pyogenes (group A strep) = ALWAYS pathogenic.)

174
Q

What skin infections do staphylococci cause?

A

Primary Infections:

  • Folliculitis
  • Cellulitis
  • Impetigo

Secondary Infections:

  • Cellulitis
  • Wound/ulcer/eczema infection

Infections due to bacterial toxins:

  • Bullous impetigo
  • Staphylococcal Scalded Skin Syndrome
  • Toxic Shock Syndrome
175
Q

What skin infections do streptococci cause?

A

Primary Infections:

  • Erysipelas
  • Necrotising Fasciitis
  • Impetigo

Secondary Infections:

  • Cellulitis
  • Wound/ulcer/eczema infections:

Infections due to bacterial toxins:
- Scarlet Fever

Hypersensitivity Reactions (group A strep):

  • Erythema Nodosum
  • Vasculitis
176
Q

Impetigo - cause and features

A

Stalphyococci/streptococci

Primary infection, affects young children

=> Golden crust +/- oozing blisters

CONTAGIOUS

177
Q

Impetigo - Mx

A
  • Soak crust with soap and water
  • Topical antiseptic / ABX
  • Systemic ABX if widespread

CONTAGIOUS – no school for 48 hours after starting oral ABX or until wounds are crusted (topical ABX)

178
Q

Bullous Impetigo - features

A

Toxin reaction – specifically from Staph. aureus

2-3cm blisters (bullae)
Usually in areas with skin folds

179
Q

Bullous Impetigo - Mx

A

Oral flucloxacillin

180
Q

Bullous Impetigo - Complications

A

Can develop into a more severe and generalized form called staphylococcal scalded skin syndrome (SSSS)

RFs – Newborns/children (<5), immunocompromise, kidney failure

181
Q

Folliculitis - features

A

Primary infection

Erythematous pustules around hair follicles

182
Q

Folliculitis - Mx:

A

Screen and treat nasal carriage (mupirocin cream)

Topical or systemic ABX

183
Q

Staphylococcal Scalded Skin Syndrome

A

Toxin reaction

Presentation:

  • Erythema & sheets of peeling skin
  • Malaise and fever
184
Q

Why is Staphylococcal Scalded Skin Syndrome mostly seen in neonates and children <5 ?

A

Protective antibodies against staphylococcal exotoxins are usually acquired during childhood which makes SSSS much less common in older children and adults

185
Q

Staphylococcal Scalded Skin Syndrome - Mx

A

ADMIT (emergency)

Supportive management (fluids & analgesia)

IV flucloxacillin/erythromycin

186
Q

Toxic Shock Syndrome - features and associations

A

Toxin reaction

Presentation:

  • Septic shock
  • Days 1-3: widespread macular erythema
  • Days 10-21 – desquamation, mucosal oedema & ulceration

Associations:

  • Tampon use
  • GI tract infection
187
Q

Toxic Shock Syndrome - management

A

Supportive (fluids & analgesia)

IV flucloxacillin/erythromycin

188
Q

What ABX are typically used for staphylococcal skin infections?

A

Topical ABX – fusidic acid, mupirocin

Oral ABX – flucloxacillin, clindamycin

189
Q

What ABX are typically used for streptococcal skin infections?

A

Topical ABX – clindamycin

Oral ABX – penicillin V (Phenoxymethylpenicillin)

190
Q

Erysipelas - features

A

Primary infection
= a specific form of cellulitis caused by strep

Affects the upper layers of the skin

Presentation:

  • Unilateral “beefy” red plaque
  • PAINFUL
191
Q

Erysipelas - Mx

A

Oral ABX – Penicillin V

192
Q

Necrotising Fasciitis - cause

A

group A strep

+/- S. aureus
+/- others

193
Q

Necrotising Fasciitis - presentation

A

Rapidly spreading erythema & necrosis

Systemic sepsis – high fever, intense pain, vomiting

194
Q

Necrotising Fasciitis - Mx

A 
Surgical debridement
IV ABX (vancomycin +/- gentamicin)
195
Q

What is Cellulitis?

A

= infection of the deeper layers of skin and the underlying tissue

196
Q

Erisypelas vs Cellulitis

A

Erysipelas affects the upper layers of skin and is specifically caused by streptococci

Cellulitis is an infection of the deeper layers of skin and the underlying tissue and can be strep or staph infection

197
Q

Cellulitis - presentation

A

Gross oedema, erythema, heat

PLUS pain

198
Q

Cellulitis - Mx

A

Elevate affected limb

UNCOMPLICATED cellulitis (no signs of systemic illness or extensive infection)
=> oral ABX, analgesia, fluids
COMPLICATED cellulitis (severe / systemic upset / limb threatened)
=> admission, fluids, IV penicillin-based ABX
199
Q

Scarlet Fever - cause and features

A

Toxin-mediated, follows strep throat infection.

Presentation:

  • Widespread pink/read papules
  • Preceding sore throat, fever, lymphadenopathy
  • Strawberry tongue
200
Q

When can a child with scarlet fever go back to school?

A

Can go back to school 24 hours after starting ABX

201
Q

Scarlet fever - Mx

A

Oral penicillin

202
Q

How do viral warts spread?

A

Via direct contact or indirect contact (e.g. swimming)

203
Q

Management options for viral warts

A
  1. Topical Paints – salicylic acid + lactic acid
    => 5 mins soak in warm water, apply Tx, nail file away dead skin
  2. Cryotherapy – painful & may cause blisters
  3. Curettage & cautery – need local anaesthetic
  4. Formalin soaks / podophyllin – for RESISTANT warts
204
Q

Types of viral wart

A

Common Warts (HPV 2):

  • Elevated papules
  • Dorsum of hands
  • Common in children

Plane Warts (HPV 3):

  • Flat-topped
  • Face and back of hands

Plantar Warts (HPV 1, 2, 4, 57):

  • May be uncomfortable to put pressure on
  • Tend to be quite Tx resistant

Anogenital Warts (HPV 6 & 11):

  • RF for cervical neoplasia in women
  • Refer for STI screen
205
Q

Chicken Pox - cause

A

= infection caused by varicella zoster virus

Usually an uncomplicated, self-limiting disease
=> More severe in adults

206
Q

Chicken pox - presentation

A

Widespread rash

Itchy red papules progressing to vesicles on the stomach, back and face, and then spreading to other parts of the body.

Fever, headache, malaise

207
Q

Chicken pox - complications

A

Pneumonia
Hepatitis
Encephalitis
Secondary bacterial infection of skin lesions caused by scratching

208
Q

Chicken pox - Mx

A

Calamine lotion and oral antihistamines may relieve itching.

Only if immunocompromised – Oral/IV acyclovir

209
Q

Shingles - cause

A

= herpes zoster

=> reactivation of dormant VZV (anyone who has had chickenpox may subsequently develop shingles)

210
Q

Shingles - presentation

A

Dermatomal distribution of vesicles
DOES NOT CROSS MIDLINE

Preceding pain/tingling

211
Q

Shingles - complications

A

Persisting pain, Scarring

Ramsay Hunt Syndrome
Ophthalmic Shingles

Deafness/dizziness
Encephalitis

212
Q

Shingles - Mx

A

Oral acyclovir if:

  • within 72 hours of onset
  • mod/severe pain or mod/severe rash
  • Immunocompromise
  • Non-truncal involvement

Analgesia

If severely immunocompromised, consider admission.

213
Q

What can HSV infection cause?

What is the presentation and management of these?

A
  1. Cold Sores (HSV 1):
    - 30-50% recur
    - Pain, tingling, vesicular eruption
    - Mx = topical acyclovir
  2. Genital Herpes (HSV 2):
    - 95% recur
    - Pain, tingling, dysuria
    - Mx = oral acyclovir
214
Q

Molluscum Contagiosum - cause and features

A

Caused by Molluscipox virus (MCV)

Presentation:

  • Small, umbilicated papules (mainly trunk)
  • Erythema, pus, crusting

Common in infants/children = contagious

215
Q

Molluscum Contagiosum - Mx

A

Mx = self-limiting (if not, cryotherapy/topical podophyllin)

216
Q

Hand, foot & mouth disease - cause and presentation

A

Caused by Coxsackie Virus

Presentation:
=> Erythematous vesicles on hands, soles of feet, mouth

Common in infants/young children

217
Q

Hand, foot & mouth disease - Mx

A

self-limiting (5-7 days)

218
Q

Pityriasis Rosea - cause

A

Unknown cause

?herpes virus

219
Q

Pityriasis Rosea - presentation

A

Initially – herald patch (oval erythematous plaque + scaling)

5-15 days later – generalised, smaller, well-defined erythematous macules (CHRISTMAS TREE DISTRIBUTION)

220
Q

Pityriasis Rosea - Mx

A

if symptomatic/itchy => topical steroids or UVB

221
Q

What are dermatophytes?

A

fungi that require keratin for growth.

Cause tinea / ringworm (most common fungal infections).

222
Q

Wood’s UV lamp

A

= a light that uses long wave ultraviolet light

When an area of scalp that is infected with tinea is viewed under a Wood’s light, the fungus may glow.

223
Q

What are the genera of fungi in the dermatophyte group?

A

Microsporum,
Trichophyton,
Epidermophyton

224
Q

Dermatophyte infection - Ix

A

Skin scrapings, Hair pluckings, Nail clippings => microscopy & culture

Or view under wood’s lamp

225
Q

Dermatophyte infection - Tx

A

Topical Anti-fungals for LOCALISED INFECTION
=> Miconazole, ketonazole, terbinafine, nystatin

Systemic anti-fungals for WIDESPREAD INFECTION or HAIR/SCALP/NAILS or IMMUNOCOMPROMISED
=> Terbinafine, itraconazole, griseofulvin (for <12 years)

226
Q

Candida

A

A yeast that causes the fungal infection thrush (can affect genitalia, periungual, oral).

227
Q

Candidiasis - features

A

Erythema extending from body folds (unclear border)

Small satellite lesions +/- pustules at edges of eruption.

228
Q

Candidiasis - risk factors

A

Extremes of age

Immunocompromise

229
Q

Candidiasis - Mx

A
  1. Topical Azoles – clotrimazole
  2. Systemic Azoles – fluconazole
  3. Nystatin / amphotericin B
230
Q

What are the fungal skin commensals?

A

Malassezia (formerly known as Pityrosporum)

231
Q

What infections can be caused by Malassezia/Pityrosporum?

A
  1. Pityriasis Versicolor

2. Seborrhoeic Dermatitis

232
Q

Pityriasis Versicolor - features and treatment

A

Features:

  • Finely scaled, yellow/brown macules on trunk
  • Hypo/hyperpigmented

Treatment:

  • Topical antifungal – miconazole
  • Selenium sulphide shampoo
  • Systemic itraconazole if immunocompromised.
233
Q

Seborrhoeic Dermatitis - features and Tx

A

Affects scalp, eyebrows, paranasal/periorbital areas.

Features:

  • Yellow/white flaking
  • +/- erythematous, itchy, GREASY/WET-looking skin
  • +/- patchy hair loss.

Treatment:

  • Topical azoles
  • Low potency steroids (rapid, short-term Tx)
234
Q

Tinea Corporis

A

Affects body

Erythematous ANNULAR SCALY PLAQUE
Central clearing
Very itchy

235
Q

Tinea Cruris

A

Affect genitals

Well-demarcated, erythematous plaque
Very itchy

236
Q

Tinea Manum

A

Affects hands

Scaling that spreads proximally
Asymmetrical involvement

237
Q

Tinea Unguium (onchomycosis)

A

Very common => often with atheletes foot

Hyperkeratosis of nail
White discolouration
Loss of nail plate and lifting from bed (oncholysis)

238
Q

Athlete’s foot

A

= Tinea Pedis

White maceration between toes

RFs – communal floors, occlusive shoes, wet feet.

239
Q

Moccasin foot

A

= severe form of Tinea Pedis / Athlete’s foot

Erythema, scaling, pustules, widespread

240
Q

Tinea Capitis

A

Affects scalp

More common in afro-Caribbean’s & children

Patchy hair loss
Scales, erythema, pustules

241
Q

Kerion

A

= complication of tinea capitis

Boggy, painful swelling (honey-coloured)
+ alopecia/lymphadenopathy

(Occurs due to epidermal invasion & inflammatory response)

242
Q

Skin infestations

A

= parasites living on the host’s skin

Scabies
Head lice

243
Q

Scabies - cause and features

A

Caused by the sarcoptes scabies mite.

Features:

  • Itchy papules (worse at night)
  • Burrows/small tracts
  • Usually symmetrical

Common sites – Finger webs, Axillae, Breasts, Scalp, Ankles, Feet

244
Q

Scabies - RFs

A
  1. Close contact – dorms, wards, care homes
  2. Extremes of age or immunocompromise
    => risk of “crusted scabies” = severe form
245
Q

Scabies - management

A
  1. Permethrin / Malathion creams (insecticides)
    - Apply to whole body for 12 hours
    - Repeat in 1 week
    - TREAT ALL CLOSE CONTACTS AT SAME TIME
  2. Wash all bedding/clothing.
246
Q

Head lice - features

A

Live on hair, feed on blood, spread via close contact.

Features:

  • Persistent itching of scalp
  • Redness & excoriated papules
247
Q

Head lice - Mx

A
  1. Fine comb & conditioner REGULARLY = most important

2. (Malathion/ Permethrin) = not very effective

248
Q

What is important to remember in a dermatology history?

A

Identify site, onset, character, exacerbating/relieving factors, associated Sx, time course.

Any treatments tried already?

Any previous episodes similar to this?

Contact Hx with infectious diseases (e.g. chickenpox)

PMHx (especially skin cancer)

DHx, Allergies

FHx of skin conditions or cancers

Travel Hx
Sun exposure (including sunbed use)
Occupation
Recent changes (in diet, washing powder, etc.)

249
Q

Inspection of an eruption

A

=> DCM

D – Distribution
• Where is it?
• E.g. flexures/extensors, sun exposed/covered

C – Configuration
• Shape or outline of rash
• Symmetrical/asymmetrical
• Any articular patter? e.g. diffuse, linear, grouped or scattered

M – Morphology
•	The form and structure of the rash
•	E.g. papules, plaques, etc.
•	Weeping, crusting, bleeding, excoriations 
•	Odour
250
Q

Inspection of a pigmented lesion

A

=> ABCDE

A – Asymmetry
B – Border
C – Colour
D – Diameter
E – Elevation / evolution
251
Q

Inspection of a non-pigmented lesion

A 
Site and Side
Shape (macule, papule, plaque, nodule, cyst, etc.)
Size 
Symmetry
Surface
Surrounding Skin 
Colour
252
Q

What is important to palpate for in examination of a skin eruption/lesion?

A

Tenderness

Surface texture

Scaling

Elevation

Skin thickness
=> Any atrophy (tissue loss)?
=> Wrinkling or dimpling (loss of fat)?

Firmness
=> Solid or fluctuant?

Tethering

Blanching (if necessary)

Temperature

253
Q

How can you differentiate between erythema and purpura?

A

Erythema - blanches with light pressure

Purpura - non-blanching

254
Q

Flat vs palpable purpura

A

Flat purpura suggests leakage without inflammation

Palpable purpura suggests associated inflammation (likely to be caused by a small-vessel cutaneous vasculitis)

255
Q

Why is it important to compare temperature of skin abnormality to normal skin?

A

Inflamed skin is hot

Poorly perfused skin is cold

256
Q

Where are flexures?

A

Inside of elbows
Front of neck
Back of knees
Under buttocks

257
Q

How would you counsel a patient about emollients?

A

Moisturiser - creates a barrier on the skin to prevent water loss

Apply liberally to the skin, following direction of hair growth

Use MINIMUM twice a day - no limit to how much you can use them

Use even when you have no flare-ups

Re-apply after bathing/showering

Most contain paraffin which is EXTREMELY FLAMMABLE => avoid contact with open flames/cigarettes

258
Q

Important things to remember about use of ointments as a topical formulation

A

Best option for dry skin

BUT - more greasy and less cosmetically acceptable for the patient

259
Q

How much topical steroid should be applied?

A

Finger-tip units are a useful way to explain to a patient how much topical steroid should be applied.

260
Q

How would you counsel a patient for applying topical steroid?

A

Used more sparingly (not liberally like the emollient).

Try to leave 30-60 minutes between applying any emollients and the steroid

Side effects are usually with prolonged/ regular/ inappropriate use and are rare with topical use.
=> skin thinning
=> with potent/very potent steroids, sometimes adrenal suppression and Cushing’s

261
Q

How long are topical steroids used for?

A

Once or Twice daily for maximum 14 days

5 days on the face

262
Q

Maintenance topical steroids

A

Initiated by specialist

use of topical steroids twice weekly as a preventative measure for patients who suffer frequently from flare ups

263
Q

Methotrexate - important drug interactions

A

Trimethoprim / co-trimoxazole - FATAL IMMUNIOSUPPRESSION

NSAIDs - increases risk of toxicity

Penicillins / ABX - increased risk of toxicity

Can increase the risk of nephrotoxicity if given alongside nephrotoxic drugs

264
Q

Nikolsky’s sign

A

Positive when slight rubbing / mild lateral pressure of the skin results in separation of the epidermis

almost always present in SJS/ TEN and SSSS

265
Q

How would you differentiate Spider naevi from telangiectasia?

A

When pressure is applied to blanch the area, spider naevi refill from the centre and telangiectasia refills from the edges.

266
Q

Erythema Nodosum - Mx

A

Treat underlying cause
Analgesia and follow-up

Usually resolves within 6 weeks and lesions heal without scarring

267
Q

How long do children with Molluscum contagiosum need to stay off school for?

A

Not required to stay off school

Contagious but the chances of passing it on during normal school activities are low.

Advice should be given to limit spread amongst family members e.g. no sharing towels.

268
Q

What can trigger/exacerbate rosacea?

A

Sunlight,
Pregnancy,
Certain drugs and food

269
Q

Koebner phenomenon

A

= the appearance of new skin lesions of a pre-existing dermatosis on areas of cutaneous injury in otherwise healthy skin.

270
Q

Hutchinson’s Sign

A

a rash on the tip, side, or root of the nose in a patient with shingles

Representing the dermatome of the nasociliary nerve

=> prognostic factor for subsequent eye inflammation and permanent corneal denervation.

271
Q

Guttate psoriasis

A

= a form of acute psoriasis described as a shower of small, pink-red, scaly ‘raindrops’ that has fallen over the body.

Typically develops 1–2 weeks after a streptococcal URTI, and some viral URTIs

272
Q

Lichen Planus - presentation

A

planus = Ps
=> purple, pruritic, papular, polygonal rash on flexor surfaces.

Oral involvement common

273
Q

Cutaneous manifestations of SLE

A

Photosensitive ‘butterfly’ rash
Discoid lupus (coin-shaped lesions)
Alopecia
Livedo reticularis (net-like rash)

274
Q

What is Vitiligo?

A

Autoimmune condition which results in the loss of melanocytes and consequent depigmentation of the skin

Features:
- well-demarcated patches of depigmented skin

  • peripheries tend to be most affected
  • trauma may precipitate new lesions (Koebner phenomenon)
275
Q

Types of BCC

A
  1. Nodular BCC
  2. Superficial BCC – shallow plaques, pink to almost skin coloured, that slowly expand over many years.
  3. Sclerosing BCC – can look like a small white scar on the skin (can expand to a very large size before it is clinically obvious as a skin cancer)
  4. Pigmented BCC – occurs in darker skinned individuals.
276
Q

Skin Type I

A

Pale white skin, blue/green eyes, blond/red hair

Always burns, does not tan

277
Q

Skin Type II

A

Fair skin, blue eyes

Burns easily, tans poorly

278
Q

Skin Type III

A

Darker white skin

Tans after initial burn

279
Q

Skin Type IV

A

Light brown skin

Burns minimally, tans easily

280
Q

Skin Type V

A

Brown skin

Rarely burns, tans darkly easily

281
Q

Skin Type VI

A

Dark brown or black skin

Never burns, always tans darkly

282
Q

Alopecia Atreata

A

Presumed to be an autoimmune condition

Features:

    • Localised, well demarcated patches of hair loss.
    • At the edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs

Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually.

283
Q

Pompholyx eczema

A

Characterised as an itchy vesicular rash over the palms and soles of feet and is associated with sweating.

Heat often exacerbates the rash.

284
Q

Dermatofibroma

A

A solitary firm papule/nodule that dimples when pinched.

Tend to occur following injury

285
Q

Lichen Planus - Mx

A

POTENT topical steroids are the mainstay of treatment

Benzydamine mouthwash or spray is recommended for oral lichen planus

Extensive lichen planus may require oral steroids or immunosuppression

CP2 (8 decks)

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