Dermatology Flashcards

Covers chronic skin conditions and common ones: Psoriasis Acne vulgaris Rosacea Eczema Seborrhoeic dermatitis contact dermatitis Skin cancers- BCC, SCC, Melanoma vs premalignant conditions (e.g. bowens, kerathoacanthoma etc, benign naevus) vitiligo

1
Q

Define psoriasis

A

Psoriasis is a chronic autoimmune & inflammatory skin condition characterised by well demarcated red scaly plaques.

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2
Q

Quick overview of the pathophysiology of psoriasis?

A

autoimmune and T cell mediated disease, inflammatory cells produce cytokines, this leads to infiltration of other inflammatory cells leading to redness, and keratinocyte proliferation - leading to scale as as stratum corenum is shed from the skin.

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3
Q

Risk factors for psoriasis?

A
  • genetics
  • caucasian
  • equal between M & F
  • infections - streptococcal & guttate psoriasis
  • hormonal changes (puberty and menopause) & post partum period (often improves during pregnancy)
  • change of medications - beta blockers, lithium, chloroquine and ACEi worsen, withdrawal of steroids
  • trauma/ sunburn - koebner phenomenon
  • smoking and alcohol
  • HIV
  • psychological stress
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4
Q

relieving factor for psoriasis?

A

sunlight improves symptoms (psoraisis better in summer vs winter)

In a small number of patients it can be an exacerbating factor

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5
Q

Types of psoriasis?

A

5 main types:

1) chronic plaque psoriasis –> commonest type, symmetrical plaques on extensor surfaces of the limbs - knees and elbows, scalp and lower back.
2) flexural psoriasis –> smooth red plaques without scale in flexures and skin folds
3) guttate psoriasis –> multiple small tear drop shaped red plaques on the trunk after streptococcal infection in young adults
4) pustular psoriasis –> multiple petechiae and pustules on the palms and soles
5) generalised erythrodermic psoriasis –> rare but serious form characterised by redness and systemic illness

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6
Q

Key features of a history of psoriasis?

symptoms

other key features on the history?

A

Symptoms of psoriasis:

  • pruritic lesion
  • typically erythematous, circumscribed scaly plaque

often elbows, knees, extensors, scalp, less commonly nails, ears, umbilical region

pain or burning sensation around lesion

joint pain and stiffness in psoriatic arthritis (affects 20%)

family history common

check medications - lithium, beta blockers, ACEi or steroid cessation

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7
Q

Type of psoriasis with this sign?

A

Nail pitting is common with psoriasis and psoriatic arthritis

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8
Q

What is the type of psoriasis?

A

Plaque psoriasis affecting the knee

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9
Q

Type of psoriasis?

A

Guttate psoriasis

widespread erythematous fine scaly papules with a water drop appearance often on trunk arms and legs. Often erupts after URTI

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10
Q

Type of psoriasis?

A

Pustular psoriasis - acute generalised pustular psoriasis, rare severe and urgent, affects palms and soles and is chronic

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11
Q

What type of psoriasis is this?

A

Eythrodermic psoriasis with generalised erythema and fine scaling, often associated with pain, irritation and sometimes severe itching

It is a rare but severe form of psoriasis which can occur acutely as first presentation or may evolve from chronic psoriasis. Widespread inflammation of the skin leads to significant fluid loss, resulting in dehydration, electrolyte loss, peripheral oedema and rarely hypothermia & HF. It requires hospital admission for inpatient mx.

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12
Q

Clinical examination features of psoriasis?

A

Psoriatic lesions are:

Well demarcated

erythematous

plaques

assocaited with overlying scale

auspitz’s sign - if you remove the scale the lesion bleeds

koebner phenomenon- new lesions at sites of damage

on extensor surfaces mostly, elbows, knees and scalp

if on flexural surfaces may be shiny and moist

usually discrete by may coalesce

nail changes - pitting, onycholysis, yellowing and ringing (associated with more severe disease if nail changes are present)

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13
Q

How do we diagnose psoriasis?

A

usually no investigations are necessary it is a clinical diagnosis.

Psoriasis area and severity index PASI is a clinical tool to assess the severity.

You can order a skin biopsy where there is doubt in diagnosis.

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14
Q

What are some of the associated conditions with psoriasis?

A
  • Psoriatic arthritis –> chronic seronegative inflammatory arthritis, estimated one third develop psoriatic arthritis
  • onset normally follows skin disease by 5-10 yrs but occasionally arthritis develops before skin changes
  • psoriatic nail changes occur in 90%
  • Other conditions associated include –> IBD, metabolic syndrome, CV disease, other autoimmuen conditions, eye pathologies including uveitis, blepharitis and conjunctivitis.
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15
Q

Management of chronic plaque psoriasis?

A
  • Conservatively –> avoid exacerbating factors, smoking cessation, reduce alcohol consumption and maintain optimal weight
  • Medical:
  • topical therapy first line - they reduce itch and clear plaques
    • regular emollient to reduce scale and itch
    • potent corticosteroid applied OD plus vitamin D analogue applied OD (calcipotriol)
    • applied separately one in the morning and one in the evening
    • up to 4 weeks as initial tx
  • 2nd line if there is no improvement
    • vitamin D analogue twice daily
  • 3rd line if no improvement
    • potent corticosteroid twice daily or coal tar prep

Secondary care:

  • phototherapy UVB 3x/ wk
  • adverse effects include ageing and SCC

Systemic therapy

  • oral methotrexate used 1st line especially if assocaited joint disease
  • other immunosuppressants e.g ciclosporin, retinoids, biologics
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16
Q

Complications of psoriasis?

A

chronic plaque psoriasis is a lifelong condition and is frequently resistant to treatment.

Therefore it is associated with significant psychosocial burden, screen regularly for anxiety and depression.

Systemic upset e.g. erythrodermic psoriasis and generalised pustular psoriasis are lifethreatening and severe.

medication used to tx psoriasis often has troubling or severe side effects:

E.g. steroids with skin atrophy, striae and rebound symtoms, aim for 4 week break before starting another course of topical corticosteroid

Vitamin D analogues e.g. calcipotriol can be used long term, reduce scale and plaques not erythema but avoid in pregnancy

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17
Q

what are the differentials for a scaly rash?

A
  • Pityriasis rosea
  • Tinea
  • Seborrhoeic dermatitis
  • discoid eczema
  • bowen’s disease
  • discoid lupus
  • scabies
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18
Q

What are the potencies of topical steroids?

What are important points to communicate to patients with steroids?

A

Topical corticosteroids are available in 4 different potencies - “Help Every Budding Dermatologist”

Hydrocortisone (mild)

Eumovate (moderate)

Betnovate (potent)

Dermovate (very potent)

  • Potent topical corticosteroids should not be used on the face or genitals
  • very potent topical steroids should not be used in primary care only by dermatologists
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19
Q

Define acne vulgaris

A

common condition in adolescence resulting from inflammation of the pilosebaceous unit, leads to the development of comedones, pustules and papules.

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20
Q

cause of acne vulgaris

A
  • Due to increased sebum production
  • & increased androgenic hormones at adolescence that cause hyperplasia of the sebaceous glands
  • bacterial colonisation ( P acnes) leading to inflammation of the pilosebaceous unit.
  • hyperactive immune response
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21
Q

risk factors of acne vulgaris

A
  • Typically related to natural hormonal shifts that occur during puberty or excess androgens - PCOS, congenital adrenal hyperplasia, exogenous steroid
  • exacerbated by steroids & antiepileptics
  • worsened by topical skin products e.g. cosemetics and shaving products
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22
Q

Clinical features of acne

A

non inflammatory comedones - closed and open comedones. Closed comedones (whiteheads) are plugged follicles, open comedones (black heads)

inflammatory papules, pustules, nodules and cysts.

Papules and pustules are small raised lesions < 5mm

Nodules and cysts are deeper larger lesions > 5mm

often located in face chest and back with many pilosebaceous units.

Chronic disease may lead to scarring due to healing of lesions.

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23
Q

Definitions of derm terminology with acne:

Comedone

Papule

Pustule

A

Comedone = dilated sebaceous follicle in the skin (pore) which can be open (blackhead) or closed (whitehead) due to accumulation of bacterial and cellular debris

Papule = solid raised lesion less than 0.5cm in diameter

Pustule = a lesion less than 0.5cm in diameter that contains pus

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24
Q

Definitions of derm terminology in acne:

Nodule

Cyst

A

Nodule = solid raised lesion less than 0.5cm in diameter but with a deeper component

Cyst = thin walled closed capsule or sac containing fluid

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25
Q

What are some of the classifications of acne vulgaris?

A
  • Mild –> prescence of non inflammatory lesions, sparse inflammatory lesions
  • Moderate –> widespread non inflammatory lesions, numerous papules and pustules
  • Severe –> extensive inflammatory lesions including nodules, pitting and scarring
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26
Q

what is the difference between inflammatory lesions vs non inflammatory lesions in acne?

A
  • Non inflammatory lesions are the comedones- either open (blackhead) or closed (white head).
  • Inflammatory lesions include the papules, pustules, nodules and cysts. Papules and pustules are less than 5mm whereas the nodules and cysts are deeper larger lesions > 5mm
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27
Q

typical features on the history of acne?

A
  • onset usually around adolescence 12-17yrs
  • females may notice worsening and improvement around the menstrual cycle
  • open and closed comedones, papules, pustules, nodules and cysts may be described
  • post inflammatory hyperpigmentation and scarring may occur
  • skin tenderness
  • thorough history of lifestyle factors e.g. skincare, makeup, shaving, diet, medications needed
  • family history
  • ascertain what the patient has tried before
  • depression and social isolation are common, screen for anxiety and depression
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28
Q

Features on examination of acne vulgaris

A
  • non inflammatory lesions include white heads (closed comedones) and blackheads (open comedones)
  • inflammatory lesiosn include papules, pustules, nodules and cysts
  • often fount face, chest, back, upper arms
  • post inflammatory hyperpigmentation and atrophic scars
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29
Q

What is a commonly associated condition with acne?

A

PCOS is the most common endocrinopathy in women. It leads to increased thecal ovarian androgen production which exacerbates acne.

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30
Q

differential diagnoses for acne vulgaris?

A

Acne rosacea - presents with papules and sometimes pustules, affecting central face. presents with more generalised erythema & telangiectasia.

Tends to affect older women 30-50s

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31
Q

Investigations for acne vulgaris?

A

Acne is diagnosed clinically and does not require any further investigation

If patients have persisten or unusual acne you can swab for M& Culture

In women with persistent acne then testing for underlying hormonal disorder may be required

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32
Q

Management of acne vulgaris?

A

Management for acne involves skincare advice, topical or oral therapies and support for any mental health disorder.

  • Conservative:
    • advise to use non alkaline, skin neutral cleansers twice daily
    • advise to avoid oil based moisturisers and suncreams
    • advise those using makeup to avoid oil based and remove it at the end of the day
    • advise to avoid picking or scratching as this increases risk of scarring
  • Medical:
    • Need to adhere to treatment for at least 6-8 weeks before full effect will be seen
    • Step up management:
      • Single topical therapy - topical retinoids, benzoyl peroxide
      • topical combination therapy - topical antibiotic plus retinoid or benzoyl peroxide
      • oral antibiotics: tetracycline, oxytetracycline or doxycyline
      • Avoid tetracyclines in pregnant / breastfeeding women (erythromycin may be used in pregnancy)
      • Single oral antibiotic used for max of 3 months
      • topical retinoid or benzoyl peroxide always co prescribed with oral abx to reduce abx resistance developing.
      • COCP alternative to Abx
      • Dianette (cocyrindiol) used as it has anti androgen properties (only given 3m as increased risk VTE)
    • Oral isoretinoin only under specialist (pregnancy is CI to both topical and oral retinoid)
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33
Q

Specialist points for retinoid treatment?

A
  • Oral retinoids are reserved for severe resistant cases of acne vulgaris and are only prescribed under a specialist
  • they are thought to work by reducing sebum production and inhibiting bacterial growth
  • highly teratogenic therefore CI in pregnancy
  • common practice to prescribe two forms of contraception for women
  • other SE:
    • Dry mucus membranse
    • headaches
    • hairthinning or loss
  • Avoid in hepatic impairment and liver function eeds ot be monitored due to risk of hepatitis
  • increased risk of suicide and depression when taking retinoids, change in mood needs to be closely monitored.
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34
Q

explaining acne to a patient:

Key points

A

” Acne is a really common skin condition that often arises during your teenage years. It is characterised by the spots you have been describing that can affect your face, chest and upper back. It can range from being mild to severe and is not a serious condition from a medical point of view but can cause a lot of distress.

It is caused by the clogging of your pores by a substance called sebum, which your body produces naturally. It can cause a build up of a bacteria on the skin called P Acnes. It is improtant to know this is not because of being dirty or eating greasy foods, and is usually made worse by hormones called androgens that naturally increase during puberty. It can also run in your family.

To treat it:

  • No change in diet will cyre acne
  • important to only wash your face twice a day, do not overwash
  • avoid picking which causes scarring
  • cosmetics can worsen spots look for the word - noncomedogenic
  • there are lots of treatments, if one does not work we can try another. But we need to try a treatment for at least 6-8 weeks to see if it has an effect.
  • Treatments include topical creams that include antibiotics, benzoyl peroxide or retinoids (Differin).
  • Next in line are oral antibiotics or the oral contraceptive pill known as diannette. (cannot use if migraines or history of VTE)
  • Important to know these treatments will treat the spots but not scars, scars need time to heal.
  • If the above treatments do not work we can refer to dermatology.
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35
Q

Define rosacea

A

Rosacea is a chronic disorder of the skin characterised by redness, flushing, roughened skin, telangiectasia and general inflammation that can resemble acne.

It primarily affects the central face but may extend to upper trunk

36
Q

Common features on the history of a patient with rosacea?

A
  • Facial flushing is often the first symptom
  • flushing may be transient, recurrent or persistent
  • usually presents age 30-60
  • affects women more than men, most common in pale skin
  • red rash affecting the central face including the nose, cheeks and forehead
  • rash consists of papules and pustules on a red background often with telangiectasia (dilated superifial small blood vessels).
  • rosacea is exacerbated by sun exposure, hot weather, warm baths, stress and spicy foods (all generally cause facial flushing)
  • develop prominent sebaceous glands on the nose leading to rhinophyma
37
Q

examination features of rosacea?

A
  • papules and pustules in central face
  • flushing - frequent or persistent flushing
  • telangiectasia
  • ocular manifestations - lid margin telangiectasia, conjunctival injection, scleritis, blepharitis
38
Q

Investigations for rosacea?

A

Rosacea is a clinical disorder characterised by stages:

stage 1 - flushing with erythema lasting hours to days

stage 2 - persistent erythema - unremitting redness of the skin

stage 3- papules and pustules, comedones

stage 4 - telangiectasias

Investigations:

  • To exclude other conditions - e.g. ANA for SLE, skin biopsy if sarcoidosis is suspected
39
Q

DDx for rosacea?

A
  • Seborrhoeic dermatitis - yellow greasy scales on red base
  • contact dermatitis - vesicles and patch testing positive for allergen
  • SLE - butterfly rash with photosensitvity, ANA +ve
  • Dermatomyositis - heliotrope rash, gottrons papules photosensitivity, muscle weakness, +Ve ANA
  • sarcoidosis - yellow red papules
  • polycythaemia vera - other symptoms including headache, weakenss, splenomegaly, burning and redness of fingers or toes
  • acne vulgaris - usually younger, comedones more present than erythema and flushing
  • allergic conjunctivitis
40
Q

Management of rosacea?

A
  • Conservative:
    • camouflage creams for redness
    • sun protection
    • avoiding exacerbating factors
  • Medical:
    • topical treatments e.g. azeliac acid, brimonidine (for predominant flushing but limited telangiectasia)
    • Topical antibiotics - e.g. metronidazole for mild
    • more severe oral antibiotics e.g. oxytetracycline
    • adjunct - emmolient used as soap substitute for dry skin
    • adjunct - laser therapy for persistent telangiectasia
    • patients with rhinophyma need referral to dermatology
41
Q

Define seborrhoeic dermatitis

What is the cause?

A

Seborrhoeic dermatitis (also known as seborrhoeic eczema) is a common dermatitis affecting areas of skin rich in sebaceous glands. It manifests as erythema & scaling of the scalp, nasolabial folds, glabella & central face or anterior chest. Tends to worsen with stress. In infants SD manifests as cradle cap.

it can be chronic or relapsing and is most common in young adults or the elderly.

It appears as ill defined, greasy, flaky scales on an erythematous background

affects sebum rich areas such as nasolabial folds, posterior auricular skin and scalp.

thought to be caused by inflammatory reaction to proliferation of malassezia furfur, a yeast normally found on the skin

42
Q

Key features of seborrhoeic dermatitis

A
  • scalp itching
  • scalp scaling
  • glabella scaling
  • nasolabial fold scaling
  • post auricular scaling
  • white flakes
  • erythema
43
Q

associated conditions with seborrhoeic dermatitis?

A
  • HIV
  • Parkinsons disease
  • otitis externa and blepharitis may develop
44
Q

Investigations in seborrhoeic dermatitis?

A

Usually none required, clinical diagnosis

45
Q

Management of seborrhoeic dermatitis?

A

For the scalp:

  • OTC preparations containing zinc pyrithione (head and shoulders) and tar are first line
  • Second line agent is ketoconazole
  • selenium sulphide and topical corticosteroid

For the body:

  • Topical antifungals - ketoconazole
  • topical steroids - for short periods

In children: cradle cap is very common, seborrhoeic dermatitis often affects scalp, flexural surfaces, nappy area and face

Mild to moderate cradle cap use baby shampoo and oils to remove scale

Severe - use mild topical steroid e.g. 1% hydrocortisone

tends to resolve spontaneously in children around 8 months

46
Q

Define Eczema

A

Eczema is an inflammatory skin condition characterised by dry pruritic skin with a chronic relapsing course.

affects all age groups but most commonly diagnosed before 5 yrs and affects up to 20% of children

Acute eczema describes a flare of symptoms whereas chronic eczema describes the condition when the patient has chronic signs of inflammation

47
Q

What are the risk factors for eczema?

A

risk factors:

  • allergic rhinitis or asthma
  • < 5 yrs
  • family history
  • smoke exposure
48
Q

What is atopy?

what is the mechanism?

What triad of conditions are involved?

what other conditions are involved?

what is atopic march?

A

Atopy invovled the sensitisation of the body via TH2 helper lymphocytes to allergens

Causes an exaggerated IgE response, leading to hypersensitivity reactions

atopic individuals are at risk of developing a triad of conditions - atopic eczema, allergic rhinitis, and asthma.

Other related conditions include food allergies and allergic conjunctivitis.

Atopic march refers to the progressive development of atopic disease often with atopic eczema presenting in infancy followed by asthma or allergic rhinitis in childhood.

49
Q

What are the typical features of atopic eczema on a history?

A
  • scaly itchy erythematous patches commonly affecting the flexural surfaces (elbows, knees, wrists)
  • infants often have a rash on their cheeks
  • those of black ethnicity may demonstrate the rash on their extensor surfaces, affected skin can develop patches of hypo and hyperpigmentation
  • itchiness leads to scratching and excoriations with time thickening known is lichenification develops.
  • often presents before 5 yrs
  • Often family history present or PMHx of allergic rhinitis or asthma
50
Q

NICE criteria for atopic eczema?

A

Need to have itching of the skin with 3/5 of the following:

  • Visibile flexural eczema
  • history of flexural eczema
  • history of dry skin
  • history of astham or allergic rhinitis
  • onset < 2 yrs old
  • or on the cheeks or extensors in children < 18 months
51
Q

Examination features for eczema?

A
  • Dry skin with erythema scaling, papules or vesicles in acute flares
  • infancts- extensors and cheeks predominatly affected
  • in older children and adults , usually fle_xural surfaces_
  • affect areas may have hyper or hypo pigmentation
  • excoriations
  • chronic eczema - skin is thick and lichenified
52
Q

Diagnosis of eczema?

A
  • Diagnosis may be made using the NICE criteria.
  • other investigations may be needed if there are concerns for allergy such as hives and urticaria
  • Allergy testing only recommended where this is history of allergy
  • peripheral IgE often elevated but not diagnostic or specific
  • skin prick testing if there seems to be an allergy e.g. to food/ pets etc
  • patch testing for cases where there is a suspicion of allergic contact dermatitis
  • in cases where there really is diagnostic uncertainty use skin biopsy to differentiate allergic contact dermatitis from atopic eczema.
53
Q

Differentials for atopic eczema?

A

Psoriasis

seborrheic dermaitits

fungal infection

contact dermatitis

scabies

54
Q

Management of atopic eczema?

A
  • Conservatively
    • stepped approach with emollients forming the base of treatment
    • identify triggers - detergents, soaps, clothes, foods
    • diaries to identify temporal relationships between triggers and flares
  • Medical
    • emollients are moisturising agents that help soothe smooth and hydrate skin, strengthen the barrier between your skin cells to prevent allergens and irritants and bacteria entering
    • effects are short lived therefore they need to be used regularly and liberally even between flares of the disease
    • used first if a corticosteroid is also to be used, in a ratio of 10:1
    • come in multiple forms e.g. lotions, creams, gels, sprays and ointments
      • emollients can be used as soap substitures
      • Topical steroids are used and categorised based on potency (help every budding dermatologist - hydrocortisone, eumovate, betnovate, dermovate)
      • more potent steroids are used only be specialists
  • specialist:
    • if topical steroids have failed then topical calcineurin inhibitors (tacrolimus and pimecrolimus) may be used
    • Phototherapy for moderate to severe eczema (not in children)
    • last line is systemic immunosuppression
55
Q

OSCE station: explaining eczema to a patient

A
  • First check the patients understanding “:What do you think is causing your symptoms?” “have you heard of eczema?” “what do you know about eczema so far/ what have you been told so far?”
  • ICE
  • Then explain the condition clearly:
    • eczema is a long term condition that can affect all ages. It can flare up and improve over time, causing the areas of redness, itchiness, dry skin.
    • It usually affects your flexural surfaces on your elbows, back of you kness, wrists etc. Infants often have eczema on their face or extensor surfaces. Adults often present with affected hands.
    • The cause isnt exactly known but we know it often runs in families and is associated with conditions such as hayfever or asthma. You are also more likely to have allergic reactions to food or clothing however eczema itself is not an allergy.
    • In eczema the skin cells are like bricks with cement between them that prevents water leaving the skin and also things like bacteria and allergens from getting in. In eczema the bricks become dry and cracked and the cement doesnt work properly which allows water to leave causing the skin to become dry and cracked. This allows irritants to get into the skin which causes the itchiness and can lead to scratching and sore red skin.
    • eczema can get times where it suddenly gets worse known as “flares” and with repeated epsisodes of scratching the skin can thicken
    • It can also mean you are more at risk of a skin infection as the barrier of the skin isnt working well
    • signs to look out for are oozing, crusting or blisters in your skin or any fever. If at any point you feel your eczema is suddenly worse or infected come to see us that day or attend A&E.
56
Q

OSCE station:

Explaining treatment of eczema to a patient

A
  • Try to avoid any triggers that make your eczema worse
  • to find out what makes it worse it may be useful to keep a diary of foods and soaps used and how your symptoms are
  • the management of eczema is step wise, starting at the bottom with emollients, then steroids, then immunosuppresant therapy, phototherapy and then systemic therapy
  • emollients are the most important treatment to prevent your flares of eczema
  • they help fill the cracks between the skin, which stops irritants getting in and water leaving, preventing the skin getting dry and irritated
  • They need to be used regularly regardless of your symptoms at the time, up to 8 times a day
  • apply a thin film and in the direction of hair growth
  • they come in many forms we can find the one that suits you, ointments are more oil based and work well but some patients find them too greasy. Creams lotions and gels are more water based. We can give you samples of them today to see which works best for you.
  • Emollients can be used as a replacement for soaps and shampoos to avoid using detergents that are too harsh on the skin

Steroids:

  • they are used to manage flares not prevent them. They work by reducing the inflammation.
  • they should be applied 30 mins after the emollient has been applied
  • use the fingertip rule, applying one finger tip which can cover a skin area twice the size of the flat of the hand
  • they should be used during your flares and up to 48 hours after it has resolved
  • they should not be used long term as they can cause the skin to become thin and weak
  • avoid using steroids on your face and always wash your hands after applying the creams.

In most people the emollient and steroid will treat the eczzema well, but we have other options if these do not work. We can discuss this if after a trial of treatment your symptoms are still not well controlled, but hopefully your symptoms will be better within 4 weeks. It would be a good idea to arrange a follow up appointment in 4 weeks to see how you are getting on. If in the meantime you have any concerns please do not hesitate to call us. Some good informatin is also available on the NHS website and patient. info on eczema.

Do you have any further questions or anything youd like me to go over again?

57
Q

What is contact dermatitis?

A

Contact dermatitis is a type of eczema that occurs after exposure to a causative agent. It is an allergic reaction or irritant skin reaction caused by an external agent. It is a delayed hypersensitivity reaction.

It presents with a dry painful and itchy skin rash. It will be localised with burning, stinging, itching, blistering, redness and swelling in the area of contact with the allergen.

On examination the skin may be dry, red, with blistering and fissuring seen. The rash is commonly located on the hands in assymetrical distribution.

58
Q

History of contact dermatitis

A

Patients generally report pruritus, buring, erythema, swelling and blistering with acute contact dermatitis

There may be fissuring and scaling with chronic contact dermatitis.

eruption often has sharp borders confined to areas of contact with the allergen.

secondary infection can occur leading to appearance of crusting.

History should explore: 1) recent exposures 2) occupation 3) recreational activities (gardening) 4) change in cosemetics or detergents 5) jewellery

59
Q

What are the types of contact dermatitis?

A
  • Irritant contact dermatitis –> follows repeated exposure to irritants such as metals, solvents or detergents. More common in those with an already weakened skin barrier e.g. those with atopic eczema. The rash is painful, burning and red
  • Allergic contact dermatitis –> occurs in a minority that have become sensitised to an allergen such as metal rubber or plastic. Allergic contact dermatitis is an example of a delayed type 4 cell mediated reaction
  • patch testing can be used to identify the allergen causing the reaction
60
Q

Management of contact dermatitis

A
  • Emollient creams
  • topical corticosteroids
  • idetification and avoidance of the allergen
61
Q

What is skin cancer divided into?

What is the most lifethreatening?

What is the most common?

What is the single most important risk factor?

A
  • Skin cancer is divided into melanoma and non melanomas. Non melanomas include basal cell carcinoma and squamous cell carcinoma.
  • Malignant melanoma is the most life threatening and affects the younger population.
  • Basal cell carcinoma is the most common.
  • sun exposure is the sinlge most preventable risk factor for skin cancer.
62
Q

Define basal cell carcinoma

Key features

A

Basal cell carcinoma is a slow growing locally invasive malignant epidermal (basal layer) skin tumour.

  • Typically slow growing over months to years
  • occurs on sun exposed sites of the body
  • commonest form of skin cancer
  • generally affects middle aged to elderly
  • locally destructive and rarely metastasise, the centre can become necrotic or ulcerated therefore sometimes referred to as the “Rodent ulcer”
  • Typically TURP features –> telangiectasia, ulcerated, rolled edges, pearly or pink coloured.
63
Q

Key risk factors for BCC

A
  • UV radiation and sunburn history
  • outdoor occupation or hobbies
  • xray exposure, arsenic exposure
  • male
  • increasing age
  • immunosuppression - transplants and HIV
  • Fitzpatrick skin types 1 and 2 (always burn, never tan)
  • Genetics - xeroderma pigmentosum, gorlin goltz syndrome
  • family history or personal history of skin cancer
64
Q

features on the history for BCC

A
  • Clinical features of BCC : TURP
    • Telangiectasia - contains small blood vessels on the surface, when compressed and released they refill with blood.
    • Ulcer (central ulceration occurs later hence known as rodent ulcer)
    • Rolled edges
    • Pearly or pink (shiny)
  • Slow growing over months to years
  • appear on sun exposed sites e.g. scalp, face, lower legs
  • two main types: nodule BCC (most common) and superficial plaque like
  • Ask about UV and sun exposure
  • Xrays or arsenic
  • Family history or personal history of cancer
  • Skin type and how they react in the sun
65
Q

examination features BCC

A
  • Pearly papule or plaque
  • non healing scab
  • small crust non healing wound
  • plaque or nodule with rolled borders
  • papules with telangiectasia
66
Q

Sub types of BCC?

A
  • 5 common variants of BCC
  • The most common type is nodular BCC
  • Next most common is superficial BCC
  • Others include basosquamous BCC, pigmented BCC and morphoeic BCC.
  • Nodular BCC are red or flesh coloured, have well defined borders with overlying telangiectasia and as they grow develop central ulceration. Commonly arise on the face, can develop on mucosal surfaces
  • Superficial BCCs are slow growing erythematous plaques that can be dry/crusted/ blue tinged. Hard to distinguish between dermatitis or SCC
  • Morphoeic BCC - scar like lesions or indentations, deeply invasive
  • Pigemented BCC - hard to distinguish from a melanoma, pigmentation from melanin production, often excised with 2mm margin as any pigmented lesion suspicious of melanoma
  • basosquamous - rare but aggresive form of BCC with increased risk recurrence and metastasis
67
Q

High risk features of BCC?

A

High risk BCC:

1) size > 2cm
2) site - around eyes nose lips or ears
2) poorly defined margins
4) histology - morphoeic infiltrative or basosquamous
5) previous treatment failure
6) immunosuppression

68
Q

Management options for BCC?

A
  • Management can be surgical or non surgical, based on clinical suspicion of what the lesion looks like and histology results.
  • surgery is the most effective treatment for reducing recurrence
  • non surgical options are less effective but recurrence rates are acceptable
  • topical treatment only for superficial BCC nodular and morphoeic need surgery
  • BCC can be referred routinely due to slow growing nature (Not 2WW)
  • Surgical options:
    • excisional with wide local excision
    • mohs micrographic surgery for high risk or cosmetically challenging
    • destructive with curettage, cautery, cryotherapy or laser (low risk lesions only as not histological sample can be provided)
  • Surgical excision margins:
    • low risk lesion i.e under 2cm and well defined –> 4-5 mm margin
    • high risk lesion (i.e > 2cm poorly defined) –> 5 mm margin, consider Moh’s surgery
  • Non surgical treatment:
    • radiotherapy as adjuvant, prevention, or for recurrent bCCs
    • Topical immunotherapy - e.g. imiquimod, fluorouracil
69
Q

Define Squamous cell carcinoma

A

SCC = malignant tumour that arises from keratinocytes of epidermis

typically fast growing - weeks to months

locally invasive with greater potential to metastasise than BCCs

Ranges from in situ tumours (bowens disease), precursor lesions for SCC are called actinic keratosis.

70
Q

Risk factors for SCC?

A
  • UV exposure
  • Older age
  • Male
  • ionising radiation e.g. xray
  • Carcinogen exposure e.g. arsenic
  • actinic keratosis or previous skin cancer
  • fitzpatrick skin type 1 and 2
  • immunosuppression or organ transplant recipient.
  • albinism, xeroderma pigmentosum
71
Q

Important features in the history of SCC?

A
  • Change in shape or size of a skin lesion, new or enlarging skin lesion
  • increased redness
  • inflammation or induration
  • bleeding
  • tender and itchy
  • non healing wound (may orignally be caused by trauma)
  • AKs tend to be multiple whereas SCC tends to be solitary
  • skin type
  • uv radiation exposure - occupation, hobbies, tanning beds, holidays, sunburns, light therapy
  • exposure to radiation e.g. xrays
  • immunosuppresion or previous skin cancer?
  • family history of skin cancer?
72
Q

examination features of SCC?

A
  • Examination via dermoscopy
  • Type of SCC:
    • Bowens disease
    • invasive scc
    • metastatic scc
  • Presents as:
    • usually head, neck or upper limbs
    • bowens disease –> presents as thin flesh coloured or red plaque with scale or crust
    • SCC:
      • Keratotic with scaly, crusty surface arising from keratinocytes
      • ill defined borders
      • non healing
      • nodular
      • may be friable and bleed easily
      • may be ulcerated
      • fast growing over weeks to months
      • on sun exposed sites e.g. scalp, face, ears, lower legs
73
Q

Investigations of SCC

A
  • To confirm the diagnosis a biopsy must be performed, followed by histological analysis
  • suspected SCCs require 2WW referral to dermatology
  • patients undergo surgical excision biopsy or punch biopsy (usually done in aras that do not have a lot of excess skin or aesthetically challenging areas).
  • If there is a high risk SCC identified & suspicion of metastases/ lymphadenopathy then CT/MRI or PET scan may be ordered.
74
Q

Management of SCC?

A
  • All suspected SCC need a 2WW referral to dermatology
  • Patients undergo either excisional biopsy or punch biopsy
  • Punch biopsy usually in areas without excess skin/ aesthetically challenging

Surgical:

  • surgical excision biopsy with 4 mm border for those < 2cm or 6mm if > 2cm
  • excisional biopsy is done with histological examination of the tumour and margins to ensure adequate removal
  • adjuvant radiotherapy if there are affected LNs
  • Mohs surgery in cosmetically challening locations, tumour removed layer by layer
  • curettage and cautery

non surgical options include radiotherapy and cryotherapy

75
Q

What are two forms of premalignant conditions for SCC?

A
  • Actinic keratoses
  • Bowens disease
76
Q

What is actinic keratosis?

What are the features?

Management?

A
  • AK = common premalignant skin lesion develops after chronic sun exposure
  • features:
    • small crusty or scaly lesions
    • often multiple lesions may be present
    • can be pink, red brown or skin coloured
    • typically sun exposed sites e.g. temples
  • Management:
    • Malignant transformation is common therefore treatment is required
    • prevent further risk - sun avoidance and sun cream
    • fluoroacil cream 2- 3 week course
    • topical diclofenac - for milk AKs
    • topical imiquimod
    • crytherapy
    • curettage and cautery
77
Q

what is bowens disease?

What are the features

Management?

A

Bowens disease also known as SCC in situ is where the SCC has yet to breach the basement membrane

More common in elderly females

Can arise de novo or from preexisting actinic keratoses.

Features:

  • Erythematous scaly plaque with sharp borders
  • sun exposed sites e.g. LL

Management: 10% undergo malignant transformation therefore tx required

  • surgical excision
  • cryotherapy
  • topical treatment - fluoroacil cream & topical hydrocortisone
78
Q

What is the diagnosis?

What is the lesion and its features?

Management?

A

Keratoacanthoma

Benign epithelial tumour that occurs in sun damaged skin.

More common with increasing age

Appears similar to SCC therefore usually referred and treated surgicallyh

Features –> dome shaped papule, rapidly grows to become centrally filled with keratin

Management –> often spontaenously resolve within 3 months leaving a scar. As they look similar to SCC, 2WW often occurs with surgical removal.

79
Q

Define malignant melanoma

A

An invasive malignant tumour of epidermal melanocytes.

80
Q

Where do melanomas arise from?

What is the pathophysiology?

A

Melanomas arise from melanocytes that sit in the stratum basale in the lowest level of the epidermis. They proliferate uncontrollably.

They are melanin producing cells derived from neural crest cells.

Pathophysiology:

Benign naevus –> dysplastic naevus (atypical mole) . Then Melanomas have two different growth phases 1) the radial growth phase, expansion within the epidermis 2) vertical growth phase with invasion into the dermis and they acquire the ability to metastasise. (the exception is nodular melanomas that skip the radial growth phase).

81
Q

What are the types of melanomas?

A
  • Superficial spreading melanoma most common. Typically begins as asymmetrical dark spot with irregular borders or colour change. Related to intermittent high intensity UV exposure
  • Nodular melanoma - starts as a raised spot the grows rapidly vertically, high rate metastasis
  • acral lentiginous melanoma - found on palms soles or nailbeds. Hutchinsons sign on the nail bed - dark line is characteristic.
  • Lentigo maligna- an in situ melanoma confined to the epidermis
82
Q

Risk factors for melanoma?

A
  • UV exposure
  • fitzpatrick skin types 1&2
  • multiple moles or atypical moles
  • family history of skin cancer
  • personal history skin cancer
  • immunosuppression
  • xeroderma pigmentosum
83
Q

history of melanoma?

Examination features

A
  • Altered pigmented lesion with ABCDE signs:
    • Asymmetry
    • irregular border
    • colour alterations
    • diameter > 6mm
    • evolving lesion
    • symptomatic - itching, bleeding or pain
  • Melanomas mostly arise de novo but can arise from a congenital naevus
  • if melanocytic naevi do not resemble other naevi, regardless of ABCDE criteria then also treat this as suspicious “ugly duckling sign”.
  • spontaenous bleeding or ulceration
  • nail signs - hutchinsons sign with subungal melanoma
  • lymphadeopathy
  • weight loss, fatigue, night sweats, headache or cough in metastatic
  • in transit metastases - subcutaenous masses between the primary site and draining LNs
84
Q

Investigations melanoma

A

2WW referral to dermatologist that inspects the lesion with dermatoscope.

If it is suspected to be a melanoma then excision biopsy occurs.

Or in cases of a large melanoma or close to vital structures e.g. eyes ears nose then incisional or punch biopsy

All patients need careful skin and lymph node examination

in cases of suspicous LN then FNA and cytology should be done

For high risk lesions total body CT or PET CT should be done

LDH - useful marker of cell turnover can risk stratify

85
Q

Management of melanoma?

What is breslow thickness

Relevance of ulceration?

Mitotic index meaning?

A
  • For suspicious lesions excisional biopsy occurs where lesion is completely excised with 2mm margin (usually LA as a day case)
  • occassionally punch biopsy or incisional biopsy where lesion is large or close to ears eyes nose then small sample taken.
  • Breslow thickness:
    • based on vertical thickness of tumour in mm, correlates strongly with mortality
  • ulceration also correlates with poorer prognosis
  • mitotic index - is how invasive the melanoma is
86
Q

If asked to explain management Melanoma in OSLER

A
  • Complex and guided by the MDT
  • Divided into surgical and medical
  • Initially you need to confirm histologically that it is a melanoma therefore 1st line an ellipsoidal excisional biopsy is done, taking the entirety of the skin down to subcutaenous fat with a 2mm border. Punch or incision only in difficult areas.
  • Plus sentinel lymph node biopsy - injection of radiolabelled dye into the lesion prior to surgery to identify any affected nodules with a gamma probe. These are also excised and sent for histological analysis.
  • This is then histologically analysed giving three things:
    • 1) breslow thickness - vertical depth of the tumour
    • 2) ulceration - break in epidermis correlates with poorer prognosis
    • 3) mitotic index - indicator of cell turnover
  • Wide local excision is the standard treatment for primary melanoma which involves removal of biopsy scar with a surrounding margin of healthy skin which is determined by the breslow thickness.
    • If in situ 0.5 cm thickness
    • If less than 2mm then 1cm thickness
    • If more than 2mm then 2cm thickness
  • Additional medical therapy includes chemotherapy, radiotherapy and immunotherapy