Dermatology Flashcards

1
Q

State some basic functions of the skin

A
  • Protective barrier
  • Temperature regulation
  • Sensation
  • Vit D synthesis
  • Immunosurveillance
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2
Q

State 3 layers of skin

A
  • Epidermis
  • Dermis
  • Hypodermis/subcutaneous tissue
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3
Q

State the 5 layers of the epidermis

A
  • Stratum corneum
  • Statum lucidum
  • Stratum granulosum
  • Stratum spinosum
  • Stratum basale

*Remember, Stratum Lucidum isn’t always present (not present in thin skin)

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4
Q

Which layer of epidermis are melanocytes most commonly found in

A

Stratum basale

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5
Q

Compare thick and thin skin

A
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6
Q

State the thinnest areas of skin on body

A
  • Eyelids
  • Scrotum
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7
Q

What is the dermis made of?

What 4 structures are found in the dermis?

A
  • Collagen, elastin, fibrillin
  • Contains nerve endings, glands, hair follicles and blood vessels
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8
Q

State 2 functions of subcutaneous tissue/hypodermis

A
  • Insulation
  • Protective padding
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9
Q

Remind yourself of the Fitzpatrick skin types

A

*Ignore bottom bit- referring to laser hari

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10
Q

What is the pH of normal skin?

A

5.5

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11
Q

State some key questions you should ask when taking a dermatology history

A

Presenting Complaint

  • Site of onset
  • Evolution
  • Duration
  • Distribution- asymmetrical/symmetrical, flexors/extensors, mucous membranes, sun exposed sites
  • Describe appearance (if can’t see in practice)
  • Symptoms e.g. itchy, sore
  • Exacerbating & relieving factors
  • Tried any treatments: where, how much used, how long for

PMH

  • History of skin diseases or atopy
  • History of systemic diseases
  • History of sunburn, sunbathing, sunbed use
  • FH of skin diseases including atopy
  • FH of autoimmune diseases
  • Drug history (including timeline)

Social History

  • Social
  • Occupation (sun exposure, contactants), does it improve when awary from work
  • Travel history
  • Sexual history

ICE

  • Pyschosocial impact
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12
Q

Discuss some key components of a good dermatological examination

A

KEY IDEAS: inspect, palpate, describe, systemic check

  • Ensure have adequete exposure & lighting (pt should remove makeup if wearing)
  • Examination of affected areas and other areas such as hair/scalp, nails, mucous membranes
  • Palpate
  • Examine other systems if appropriate e.g. joints (e.g. is psorasis), lymph nodes (e.g.infection, malignancy)
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13
Q

Define the following terms:

  • Papule
  • Nodule
  • Erythema
  • Vesicle
  • Bulla
  • Pustule
  • Telangiecta
  • Alopecia
  • Hirsutism
  • Excoriations
  • Striae
A
  • Papule: small lump <5mm
  • Nodule: larger lump 5-10mm
  • Erythema: redness
  • Vesicle: small water blister
  • Bulla: large water blister
  • Pustule: pus-filled vesicle
  • Telangiecta: thread vein
  • Alopecia: hair loss/thinning
  • Hirsutism: hairness
  • Excoriations: scratch marks
  • Striae: stretch marks
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14
Q

Define the following terms:

  • Pruritus
  • Atrophy
  • Macule
  • Patch
  • Plaque
  • Erosion
  • Ulcer
  • Lichenification
A
  • Pruritus: ithcing
  • Atrophy: thinning
  • Macule: non palpable area of discolouration
  • Patch: macule >3cm
  • Plaque: palpable flat topped area >1-2cm
  • Erosion: loss of epidermis (superifcial)
  • Ulcer: loss of epidermis & dermis (deep)
  • Lichenification: thickening of skin with exagerated skin markings
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15
Q

Remind yourself of the SCAM mneumonic to help you describe skin lesions

A
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16
Q

Remind yourself of the framework for describing pigmented lesions

A
  • Asymmetry
  • Border (regular or irregular)
  • Colour
  • Diameter
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17
Q

Remember to see Sem 4: Integration for clinical application for further dermatology revision

A
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18
Q

Discuss the potential psychological, social and emotional impact of skin disorders

A
  • Decreased confidence
  • Self-conscious
  • Decreased involvement in activities
  • Impact on education
  • Pressure to try and resolve condition
  • Feeling like no-one understands
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19
Q

What is eczema?

At what ages is it prevelant?

A

Atopic eczema is a chronic, ithcy, inflammatory skin condition that can affect people of all ages although 70-90% present under 5 yrs with a high incidence in 1st year

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20
Q

What are signs & symptoms of eczema?

A
  • Prurutic rash
  • Erythematous rash
  • Dry skin
  • Excoriations
  • History of atopy
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21
Q

Disucss how you diagnose eczema

A
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22
Q

What might make you suspect that someone’s eczema is infected?

A

Yellow crusting, signs of systemic infection e.g. pyrexia

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23
Q

State the7 different types of eczema and discuss how you can distinguish between them

A
  • Atopic dermatitis:typical widespread itchy, erythematous, dry eczema
  • Contact dermatitis: eczema in response to contact with iritant or allergen
  • Neurodermatitis: usually confined to one or two patches of skin​- continued scratching can irritate nerve endings in skin, intensifying both itching and scratching
  • Dyshidrotic eczema: small, intensely itchy blisters on the palms of hands, soles of feet and edges of the fingers and toes
  • Nummular eczema: scattered circular, often itchy and sometimes oozing patches
  • Seborrheic dermatitis: appears on the body where there are a lot of oil-producing (sebaceous) glands like the upper back, nose and scalp​
  • Stasis dermatitis: gravitational dermatitis, venous eczema, and venous stasis dermatitis, happens when there is venous insufficiency, or poor circulation in the lower legs​

It is possible to have more than one type of eczema on your body at the same time. Each form of eczema has its own set of triggers and treatment requirements, which is why it’s so important to consult with a healthcare provider who specializes in treating eczema. Dermatologists in particular can help identify which type or types of eczema you may have and how to treat and prevent flare-ups.

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24
Q

Discuss the management of eczema

A
  • Education regarding triggers & management
  • First line= emollients
  • Second line= topcial corticosteroids
    • Mild= Hydrocortisone 0.1-2.5%
    • Moderate= Eumovate (active ingredient= clobetasone butyrate)
    • Strong= Betnovate (betamethasone 17-valerate)
    • Very strong= Dermovate (clobetasol propionate)
  • Third line= non-sedating antihistamine
  • Fourth line= oral corticosteroids (would be with specialist at this point)
  • Antibiotics e.g. flucloxacillin if infected
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25
Q

State 3 examples of emollients that may be used in eczema

A
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26
Q

What advice would you give patients about the use of topical steroids?

A
  • Work by reducing inflammation: decreased redness & itching
  • Steroid ointments= more oily therefore better for treating dry skin
  • Wash hands
  • Apply fingertip amount (last crease of finger to tip) this is enough to treat an area of skin the size of two hands with fingers together
  • Avoid applying steroids with emollients as this will dilute steroids
  • Wash hands afterwards
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27
Q

What concerns do patients commonly have about topical steroids?

A
  • Skin thinning (if use correctly risk is very low)
  • Weight gain (risk low as topical not systemic)
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28
Q

What advice would you give to patients in regards to emollient use?

A
  • Explain how emollients work: form layer on top of skin that prevents water loss and helps to keep skin moist
  • Diff types: (least water) ointments, creams and lotions (most water)
  • Always was or dry hands thoroughly
  • If emollient in tub, use spatula or clean spoon to decant emollient to prevent introduction of bacteria into tub
  • Apply in stroking motion in direction of hairs
  • How much: depends- if dry skin more the better. OFten advised 4/5 times a day if very dry.
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29
Q

What are acneirorm eruptions?

A

Acneiform eruptions refer to the presence of one or more of the classical features of acne vulgaris. Those are comedones, papules, pustules and nodular cysts.

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30
Q

What is acne vulgaris?

Who is it common in?

A
  • Chronic, inflammatory skin condition affecting mainly face, back and chest; charcterised by blockage and inflammation of pilosebaceous unit. Presents wtih lesions that can be non-inflammatory (comedones), inflammatory (papules, pustules, nodules) or both.
  • Common in adolescents
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31
Q

Briefly discuss the pathophysiology of acne vulgaris

A
  • Follicylar hyperkeratinisation
  • Propionibacterium acne colonisation
  • Increased skin sebum production
  • Complex inflammatory response involving both innate and acquired immunity
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32
Q

State some potential differential diagnoses for acne vulgaris

A
  • Rosacea
  • Perioral dermatitis
  • Folliculitis and boils
  • Drug induced acne
  • Keratosis pilaris
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33
Q

State some signs & symptoms of acne vulgaris

A
  • Comedones
    • Open= black heads
    • Closed= white heads
  • Papules
  • Pustules
  • Nodules or cysts which are often deeper palpable lesiosn which are painful and fluctuant
  • Scarring
  • Pigmentation (depigmentation post inflam or hyperpigmentation)
  • Seborrhoea
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34
Q

There is no universally agreed scoring system for acne however we can categorise into mild, moderate and severe; discuss these categories

A
  • Mild= predominatly non-inflammed lesions
  • Moderate= more widespread with increased number of inflammatory lesions
  • Severe= widespread inflammatory lesions. Scarring may be present
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35
Q

State soem drugs and underlying conditions which can exacerbate acneform rashes

A

Drugs:

  • Corticosteroids
  • Isoniazid
  • Ciclosporin
  • Lithium
  • Androgens

Underlying conditions:

  • PCOS
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36
Q

State some potential causes of an allergic rash/urticaria

A
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37
Q

Discuss the management of acne vulgaris

A
  • Advice:
    • Don’t overclean face
    • Gentle cleansers
    • Avoid picking & squeezing spots
    • Healthy diet
  • Pharmacological:
    • Comedonal acne: topical retinoid e.g. adapalene
    • Mild inflammatory lesions: topical antibiotics (e.g. clindamycin or erythromycin), topcial retinoids & topical benzoyl peroxide. Topical antibiotic ALWAYS presribed with benzyole peroxide. Azelaic acid may also be used as an adjunct/
    • Moderate inflammatory lesions: add oral antibiotic e.g. tetracycline & consider anti-androgens or COCP
    • Severe, scarrring or treatment resistance: dermatology review & additional treatment e.g. oral isotretinoin)
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38
Q

How do topical retinoids work?

State some examples

What advice should be given to someone using topical retinoids?

A
  • Comedolytic and anti-inflammatory. They normalize follicular hyperproliferation and hyperkeratinization. Topical retinoids reduce the numbers of microcomedones, comedones, and inflammatory lesions.
  • Examples include: adapalene, tazarotene, and tretinoin
  • Think stratum corneum & have been associated with photosensitivity therefore advise on sun protection
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39
Q

State some ADRs of isotretion

What monitoring is required when pt is on isotretion?

A
  • Alopecia
  • Dry eyes
  • Headache
  • Arthralgia
  • Anaemia

Need monitoring of LFTs and lipids

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40
Q

What is conglobate acne?

What is acne fulminans?

A
  • Conglobate acne= extensive papules and nodules which coalesce to form sinuses & cysts on trunk & upper limbs
  • Acne fulminans= sudden severe inflammatory reactin with deep ulcerations and sometimes systemic effects e.g. pyrexia and athralgia
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41
Q

What regions of face does rosacea commonly affect?

State signs & symptoms of rosacea

A

Chronic, inflammatory, relapsing skin condition predominantly affecting the convexities of the centrofacial region

Signs & symptoms:

  • Phymatous changes
  • Persistent erythema
  • Telangiectasia
  • Erythema acoss nose, cheeks, forehead and chin that comes and goes (facial flushing)
  • Burning or stinging sensation when using water or other products on face
  • Occular roseacea: eye discomfort, dryness, itching, photophobia, blurred vision, chalazion
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42
Q

At what age does rosacea commonly present?

A

Aged 30-50yrs, more common in those with fair skin

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43
Q

State some common triggers for rosacea

A
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44
Q

Discuss the diagnosis of acne rosacea

A

Rosacea should be diagnosed and managed using a ‘phenotype approach’, based on the presenting features in each person if there is at least one ‘diagnostic’ or two ‘major’ clinical features present:

  • Diagnostic featuresphymatous changes, persistent erythema
  • Major featuresflushing/transient erythema, papules and pustules, telangiectasia, eye symptoms (ocular rosacea)
  • Minor featuresskin burning and/or stinging sensation, skin dryness, oedema
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45
Q

Discuss the management of rosacea

A
  • Education & lifestyle:
    • Identify & avoid triggers
    • Sun protection
    • Signpost to sources of information
    • Eyelid hygiene information & lubricating drops
    • Camouflage creams
  • Papulopustular lesions:
    • Topical ivermectin
    • Plus oral antibiotics if severe (e.g. tetracycline or erythromycin)
  • For erythema:
    • Topical brimonidine
  • Referral to dermatologist, plastic surgeon or opthalmologist (if suspsect keratitis) for specialist treatment e.g. CO2 laser ablation for rhinophyma
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46
Q

State, and briefly describe, the 2 types of contact dermatitis- highlighting main difference in pathophysiology

A
  • Allergic contact dermatitis: type IV hypersensitivity reaction to contact with allergens. Prior sensitisation needed.
  • Irritant contatct dermatitis: non-immunological localised skin reaction due to direct contact with irritant. No prior sensitisation needed.
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47
Q

Which is the more common cause of contact dermatitis, allergic contact dermatitis or irritant contact dermatitis?

A

Irritatnt contact dermatitis (80%)

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48
Q

What is the most common cause of allergic contact dermatitis?

A

Allergy to nickel (e.g. in jewellery)

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49
Q

Discuss the typical presentation of allergic contact dermatitis

State some common causes

A
  • Pruritic erythemmatous scaly rash
  • Usually develops hours-days after contact with irritatnt
  • Location of rash helps identify irritant e.g. cosmetics & eyelids, jewellery and fingers, wrists etc…

Common causes: cosmetics, topical medications, rubber additives, epoxy resin adhesives, plants

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50
Q

How is allergic contact dermatitis diagnosed?

A
  • Skin patch testing (patch tests with suspected allergens applied to skin and observe for reaction)
  • *NOTE: latex allergy is diagnosed with skin prick testing as it causes a type I hypersensitivity reaction (contact uritcaria) which presents within minutes of contact*
51
Q

Discuss the management of allergic contact dermatitis

A
  1. Identify & avoid stimulus
  2. If acute contact dermatitis, use emollients liberally and topical corticosteroids (increase potency if response is poor) and consider short term systemic steroids in severe cases
  3. Identify & treat any secondary infection
  4. Phototherapy & immunosupressants e.g. ciclosporin, methotrexate
  5. Advice to speak to health & safety/occupational health if it is occupational contact dermatitis
52
Q

What is:

  • Skin prick testing
  • Skin patch testing

… used for

A
  • Skin prick testing: detects type I hypersensitivity
  • Skin patch testing: detetecs type IV hypersensitivity
53
Q

Discuss the typical presentation of irritant contact dermatitis

State some common causes

A
  • Usually presents within 48hrs of exposure (to either strong irritants or repeated exposure to weak irritants)
  • Erythematous scaly rash on site of exposure
  • Rash usually burns & stings

Common causes: water, detergents, soaps, solvents, machining oils, reducing agents, acids, soil, dust

54
Q

Discuss the management of irritant contact dermatitis

A

***SIMILAR TO ALLERGIC CONTACT DERMATITIS

  1. Identify & avoid stimulus
  2. If acute contact dermatitis, use emollients liberally and topical corticosteroids (increase potency if response is poor) and consider short term systemic steroids in severe cases
  3. Identify & treat any secondary infection
  4. Advice to speak to health & safety/occupational health if it is occupational contact dermatitis
  5. Consider skin patch testing if think allergic contact dermatitis
55
Q

For seborrhoeic dermatitis, discuss:

  • What it is
  • Who it commonly affects
  • Typical presentation- think about how this differs in infants and in adults
A
  • Chronic, inflammatory relapsing skin disorder with a predilection for regions that are rich in sebaceous glands e.g scalp, chest, nasolabila folds, eyebrows…
  • Common in children <3 months (cradle cap) and adults 30-60, more commonly in those with HIV and Parkinson’s disease. More prevelant in winter
  • Presentation:
    • Scaly erythemaouts patches/plaques associated with mild dandruff or dense adhesive scale in seborrhoeic regions
    • In infants (cradle cap) look like large, greasy yellow brown scales-crusts
    • Infantile disease usually clears in few weeks whereas in adults it is chronic relapasing
56
Q

Discuss the management of seborrhoeic dermatitis of scalp (cradle cap) in infants

A
  • Wash scalp regularly with baby shampoo
  • Brush scalp gently with soft brush
  • Scales can be soaked in olive oil, baby oil or petroleum jelly
  • Topical imidazole (e.g. clotrimazole) if above doesn’ work
57
Q

Discuss the management of seborrhoeic dermatits of scalp in adults

Discuss the management of seborrhoeic dermatitis of face and body in adults

A

Scalp

  1. First line= ketoconazole 2% shampoo (can also use selenium sulphide shampoo or shampoo containing salicyclic acid or coal tar)
  2. Second line= add in topical corticosteroid if severe itching for max of 4 weeks e.g.betamethasone valerate 0.1%​

Face & Body

  1. Topical imidazole e.g. ketoconazole
  2. Add in mild corticosteroid e.g. hydrocortisone 0.5% for short duration
58
Q

For venous eczema, discuss:

  • What it is
  • Pathophysiology
  • Risk factors
  • Typical presentation
  • Management
A
  • Eczema associated with chronic venous insufficiency
  • Exact mechanism unknown but thought that venous hypertension results in blood constituents leaking into surroudning tissues resulting in activation of inflammatory cells and fibroblasts
  • Risk factors: obesity, physical inactivity, hypertension, diabetes, older age, PMH DVT
  • Presents as erythematous scaly rash involving gaiter regions
  • Investigations:
    • Peripheral cardiovascular examination; palpate for pedal pulses to assess for arterial insufficiency
    • Ankle-brachial index
    • Venous duplex ultrasound to confirm venous insufficiency
    • Swabs if think secondary bacterial infection present
  • Management:
    • General advice e.g. elevate legs, lifestyle changes
    • Emollients
    • Topical steroids for acute flares
    • Venous compression stockings (once ruled out arterial insufficiency)
    • Treat any secondary bacterial infections with antibiotics
59
Q

What is psoriasis?

Discuss pathphysiology

A
  • Psoriasis is an immune mediated, inflammatory genetic disorder mainfesting in the skin, or joints or both; typically has a relapsing & remitting course
  • Epithelial hyperproliferation resulting in improper maturation of epithelial cells of skin which is mediated by macrophages, dendritic cells, T cells, cytokines etc…
60
Q

State some triggers/exacerbating factors for psoriasis

A
  • Stress
  • UV light
  • Smoking
  • Alcohol
  • Drugs e.g. corticosteroid withdrawal, beta blockers, lithium
  • Hormonal changes
  • Trauma (Koebner phenomenon is when psoriatic lesions occur at injury site- including sunburn)
61
Q

State some conditions associated with psoriasis

A
  • Psoriatic arthritis
  • Metabolic syndrome
  • Inflammatory bowel disease (particularly Crohn’s disease)
  • Anxiety and depression.
62
Q

What is a common trigger for guttate psoriasis?

A

Streptococcal URTI

63
Q

State, and briefly describe, the 6 types of psoriasis

A
  • Chronic plaque psoriasis: well demarcated erythematous plaques covered by silvery white scales often found on extensor surfaces, scalp, retroauricular, perianal and periumbilical regions. Lesions are usually asymptomatic.
  • Inverse/flexural psoriasis: affects flexural regions. Usually less scaley due to moisture at these sites.
  • Guttate psoriasis: scaly, raindrop-shaped plaques on the trunk commonly following a streptococcal URTI
  • Pustular psoriasis: white coalescing pustules which can be localised e.g. hands & feet or generalised
  • Erythrodermic psoriasis: when psoriasis affects >90% of body- potentially life threatening
  • Nail psoriasis: thickening of nail plate, pitting, ridging, oncholysis, subungal hyperkeratosis
64
Q

Discuss how you should assess a pt with suspected psoriasis

A
  • Examine full body (including scalp, nails, retroauricular, periumbilical & perianal regions)
  • Assess for psoriatic arthritis
  • Consider assessing for features of metabolic syndrome (e.g. check bp, diabestes screen etc…) as often associated with psoriasis
  • Use PASI (psoriasis area & severity index score) to assess severity
  • Use DLQI (dermatology life quality index) questionnaire may be done to assess impact of psorasis on this patient
65
Q

Discuss the management of psoriasis (focusing on managemetn of CPP as this accounts for 90% of cases)

A
  • General lifestyle advice:
    • Weight reduction
    • Smoking cessation
    • Avoiding triggers
  • Management of associated conditions e.g. stress & anxiety

Pharmacological

  • Emollient use
  • First line: Potent topcial steroid & topical calcipotriol (vit D analogue)
  • Second line: if above doesn’t work, stop topcial steroid and continue calcipotriol cream
  • Third line: other topical treatments e.g. coal tar, dithranol cream
  • Fourth line: refer to specialist for specialist treatments e.g. phototherapy (narrow band UVB), ciclosporin, methotrexate. They may also try biologics e.g. adalimumab
    *
66
Q

Discuss the management of generalised pusutular psoriasis and erythrodermic psoriasis

A

Urgent referral to dermatology

67
Q

State 2 important side effects of ciclosporin

State 2 important side effects of methotrexate

A
  • Ciclosporin: hypertension & renal toxicity
  • Methotrexate: hepatotoxicity & bone marrow supression
68
Q

For pityriasis rosea, discuss:

  • What it is
  • Epidemiology
  • Typical presentation
A
  • Self-limiting skin condition characterised by erythematous oval scaley eruption predominantly affecting the trunk
  • Young adults (10-35yrs), females > males
  • Typical presentation:
    • Usually, but not always begins as a herald patch (salmon coloured plaque/patch with peripheral collarette scaling
    • Within days to 3 weeks multiple smaller lesions of similar appearance develop over turnk & proximal limbs symmetrically. Lesions follow Langer lines giving christmas tree appearnce on back and V shape on upper chest
    • Some pts may have mild pro-dromal period with flu like symptoms
    • May be pruritic
69
Q

Discuss the management of pityriasis rosea

Discuss the managament of pityriasis rosea in pregnant women

A

For most people with pityriasis rosea, no treatment is required. The rash may worsen before it resolves, with new crops of lesions continuing to appear for up to 6 weeks. It will usually settle without treatment within 2–3 months, but may take up to 5 months to disappear. If itchy, can offer an emollient, sedating antihistamine or mild topical corticosteroid (if severe itch). Canr refer to dermatology and they may do phototherapy but htis only shortens course of disease by a few weeks.

Pregnant women must be urgently referred to secondary care as in the first 15 weeks of pregnancy it has been associated with adverse outcomes including miscarriage and premature delivery.

70
Q

What are Langer lines?

A

Show diretion of the lowest naturally occuring skin tension. Incision along langer lines results in better wound healing.

71
Q

For lichen planus, discuss:

  • What it is
  • Who it i scommon in
  • Pathophysiology
A
  • Chronic inflammtory disease that involves skin, scalp, mucous membranes & nails
  • Predilection for african americans
  • Considred to be T cell mediated; these attack altered self antigens which are expressed on babsal keratinocytes. Associated with hep C vrius and some drugs e..g antihypertensives, antibiotics
72
Q

Describe the typical presentation of lichen planus

A

Cutaneous lesions are described the 6 P’s; pruritic, planar (flat topped), purple, polygonal, papules or plaques:

  • Pruritic, flat topped papules & plaques covered by Wicham striae (white reticular lines) involving extremeties e.g. ventral wrists, forearms, ankles, legs, oral cavity, genitalia
  • Displays Koebner phenomenon
  • Nail changes: longitudinal riding, scaring, splitting
  • Scalp involvement may lead to scarring alopecia
73
Q

For urticaria, discuss:

  • What it is
  • Aetiology/pathophysiology
A
  • Superficial swelling of skin (epidermis & mucous membranes) that results in red, raised, itchy rash
  • May be idiopathic, immune mediated (IgE, autoimmune or immune complex mediated) or non-immune mediated. Can be triggered by foods, stiings/bites, drugs, physical stimuli, chemicals etc..
74
Q

Discuss classification of urticaria

A

Urticaria can be classified according ot its duration:

  • Acute: < 6 weeks
  • Chronic: >6 weeks

Chronic urticaria can then be further classified:

  • Chronic spontaneous urticaria (chronic idiopathic urticaria): no identifiable external cause but may be aggravated by heat, stress, drugs and infections
  • Autoimmune urticaria: IgG autoantibodies to the high affinity receptor for IgE FceR1.
  • Chronic inducible urticaria (physical urticaria): occurs in response to physical stimuli and can be further classified according to it’s cause e.g. solar, cold, heat,, delayed pressure, contact, aquagenic etc…
75
Q

What are some key aspects of urticaria history?

A
  • Time of onset
  • Frequency, duration and pattern on recurrence of weals
  • Triggers: exlpore occurence in relatio to menstrual cycle, foreign travel, work, hobbies etc..
  • Treatments tried and response
  • If the weals are itchy or painful
  • Family history of urticaria or atopy
  • Co-exisiting conditions
  • Any GI symptoms
76
Q

Discuss the typical presentation of urticaria

A
  • Transient (resolves 24hr)
  • Non-scaley, smooth plaques with surrounding erythema
  • May be associated with angioedema & anaphylaxis
77
Q

Discuss the use of investigations in urticaria

A
  • Skin prick testing reserved for pts with a history that suggests IgE mediated
  • For spontaneous urtiaria (idiopathic chronic) consider tests such as FBC, ESR, TFTs, LFTs to help identify underlying cause e.g. autoimmun thyroiditis, lupus
  • Urticarial vasculitis require biopsy and vasculitic screen
78
Q

Discuss the management of urticaria

A
  • Identify & avoid triggers
  • Non-sedating antihistamine (can double standard of the licensed dose i.e. give off-label- this is widely practiced)
  • Try an alternative non-sedating antihistamine
  • Adding topical antipruritic agent e.g. calamine lotion
  • Add sedating antihistamine at night if interfering with sleep
  • If severe give short course of oral corticosteroids
  • Refer to dermatologist if vasculitic urticaria is suspected (if urticaria is painful & persistent) or if food or latex allergy or form of CINDU that may be difficult to manage in primary care e.g. solar or cold uritcaria
  • If have food allergies or anaphylaxis refer to immunologist
79
Q

For basal cell carcinoma (BCC), discuss:

  • What it is
  • How common it is
  • Risk factors
A
  • BCC is slow growing, locally invasive epidermal skin tumour arising from the basal cell
  • Accounts for 80% of all skin cancer
  • Risk factors:
    • Fitzpatrick skin types I & II
    • UV exposure
    • Increasing age
    • Male
    • Smoking
    • Immunosuppresion
80
Q

If someone has multiple BCCs presenting at a young age- what autosomal dominant condition may this be?

A

Basal cell naevus (Gorlin) syndrome

81
Q

State the 4 subtypes of BCC and state which are low and which are high risk

A

Low risk

  • Nodular
  • Superficial

High risk

  • Morpheic/sclerosing
  • Basosquamous
82
Q

Discuss the typcial presentation of each of the following subtypes of BCC:

  • Nodular
  • Superficial
  • Morpheic/sclerosing & basosquamous
A

Nodular BCC

  • Pearly, shiny nodule with telangiectasia- usually on head & neck region. Tend to ulcerate with time resulting in a rolled edge.

Superficial BCC

  • Slow growing erythematous patch or plaque that is usually found on trunk

Morpheic/sclerosing & basosquamous

  • Can only distinguish between these two histologically
  • Shiny, scar-like plaque with ill defined border
83
Q

BCC rarely metastasises; true or false

A

True

84
Q

Discuss how BCC is diagnosed

A
  • Diagnosis usually made clinically
  • Do biopsy when there is clinical doubt or when histological subtype may influence treatment & prognosis
85
Q

Discuss the management of BCCs

A

Refer via routine pathway (not 2 week cancer referral) unless concerns that delay may have significant impact e.g. due to size, position… Treatment then involves:

  • MOST BCCs: surgical excision with histological assessment of magins (target excision depends on subtype e.g. 3mm for nodular BCC)
  • SOME LOW RISK BCCs: destructive surgical techniques e.g. curettage & cautery, cryosurgery. Destructive non-surgical techniques include topcial imiquimod (more for sBCC) & photodynamic therapy
  • Others: radiotherapy, Mohs microsurgery
    *
86
Q

For squamous cell carcinoma (SCC), discuss:

  • What it is
  • How common it is
  • Pathophysiology
A
  • Cutaneous carcionma arsing from the keratinocytes of the epidermis or its appendages
  • Second most common skin cancer. Men > women
  • May arise de novo or from precursors e.g. actinic keratosis, Bowen disease
  • Risk factors:
    • Chronic UV radiation
    • Skin phototype
    • Immuonosupression
    • Co-carcinogens e.g. smoking for lower lip SCC, HPV for genital or anal SCC
87
Q

Discuss the typical presentation of SCC

A
  • Indurating (hardened) keratinising (scaley) or crusted plaques or nodules at sun exposed sights
  • Lesion often symptomatic: pain, discomfort, bleeding, ulcerating, sensory changes
88
Q

Discuss the management of squamous cell carcinoma

A
  • Refer via 2 week cancer referal
  • Treatment involves surgical excision with wide borders. May also use radiosurgery, curettage & cautery, cyrotherapy
  • Advise on sun protection
89
Q

Acinitic keratosis and Bowen’s disease are common precursors of squamous cell carcinoma; discuss difference between the two

A
  • AK= mutiple asymptomatic erythematous scaley macules and papules; these may be very hyperkeratotic sclaes some with cutaenous horn
  • Bowen’s disease= asymptomatic well defined erythematous patches/plaques with a finer scale
90
Q

For melanomas discuss:

  • What they are
  • Risk factors
A
91
Q

We can classify melanomas based on whether they are predominantly radial growing or predominantly vertical growing; what ‘rules’ do predominantly radially growing melanomas follow

A

ABCDE rules:

  • Asymmetry
  • Border irregular
  • Colour- multicoloured
  • Diamter >0.6cm
  • Evolution (changed)

NOTE: radially growing have potential to progress into vertical growth phase which carries higher metastatic risk

92
Q

We can classify melanomas based on whether they are predominantly radial growing or predominantly vertical growing; what ‘rules’ do predominantly vertically growing melanomas follow

A

May not exhibit ABCDE features and may instead follow EFT rule:

  • Elevation
  • Firm
  • Growing

*Prognosis is poorer as vertical growth phase starts earlier

93
Q

We have already discussed that melanomas can be predominantly radially or predominantly vertically growing; state the types of melanoma in each

A

Predominantly radially growing

  • Supeficial spreading melanoma (SSM)
  • Acral lentiginous melanoma (ALM)
  • Lentigo maligna melanoma (LMM)

Predominalty vertically growing

  • Nodular melanoma
94
Q

Describe the typical presentation of each of the following types of melanoma:

  • Superficial spreading melanoma (SSM)
  • Acral lentiginous melanoma (ALM)
  • Lentigo maligna melanoma (LMM)
  • Nodular melanoma (NM)
A

Remember the ABCDE and EFG rules for melanomas. Symptoms of skin malignancy may include: bleeding, ulceration, pain, itching, oozing & crusting). Remember some melanomas may be amelanotic (therefore be pink in colour). For all melaonas, be aware of the ugly duckling sign (lesion that stands out from others):

  • Superficial spreading melanoma (SSM): begins as hyperpigmented patch growing radially, which may be asymmetric and have numerous colours
  • Acral lentiginous melanoma (ALM): occurs on palms, soles or nails. May have Hutchinson sign.
  • Lentigo maligna melanoma (LMM): occurs most frequenlty on face & sun exposed lesions. Typically starts as irregularly shaped, may become raised or change colour.
  • Nodular melanoma (NM): hyperpigmented blue-black/amelanotic firm papule, nodule or plaque
95
Q

What is Hutchinson sign in melanoma?

A

Extension of pigment under the nail gold; raises supsicion of subungal melanoma. It is not associated with sun exposure and is more common in Afro-Carribean & Asian ethnicities.

96
Q

Discuss how you would manage the investigations of suspected melanoma in primary care

A

Two week referral via dermatology cancer pathway where they will:

  • Excisional biopsy to produce pathology report; report will include variuos prognostic factors e.g. Breslow thickness, Clark level, lymphatic/vascualr invasion etc…
  • Consider sentinel lymph node biopsy
  • TNM staging
  • Consider CT head, chest, abdomen & pelvis in those with stage IIIb or IIIc
  • Consider PET scan in those with stage IV
97
Q

Once a pt has been referred via 2 week cancer referral pathway, how will their melanoma be managed?

A
  • Gold standard= surgial excision with varying surgical margins dependnt on type of melanoma and Breslow thickness
  • Radical lymph node resection
  • Chemo & radio for selected pts
  • Review regularly if invasive melanoma
  • Advise on sun protection

*Breslow thickness= vertical thickness of melanoma in mm. Clark level= refers to level of invasion of melanoma into anatomical layers of skin.

98
Q

What is meant by dermatophytosis?

A

Superficial fungal infection of keratinised tissues caused by dermatophytes. Dermatophytes are a specific group of fungi known as ring worms or tineas. Various names dependent on location of fungal infection:

99
Q

Discuss the typical presentation of the folowing dermatophytosis (superficial infection caused by ringworms/tineas):

  • Tinea capitis
  • Tinea corporis
  • Tinea pedis
  • Tinea unguium/onychomycosis
A

ALL dermatophytosis has similar presentation- name is lesion dependent. Asymmetrical erythematous scaley annular plaque with central clearing and advancing scaley edge.

  • Tinea capitis: scaling & itching of scalp, pathes of hair loss, scalp erythema, associated fungal infections at other sites
  • Tinea corporis: asymmetrical erythematous scaley annular plaque with central clearing and advancing scaley edge- found on body (no specific region)
  • Tinea pedis: often found interdigitally, itching, scaling, white/cracked areas, areas of maceration, malodorous. Various subtypes.
  • Tinea unguium/onychomycosis: thickened & yellow nail
100
Q

State and describe 3 types of tinea pedis

A
  • Interdigital — most common; affects the lateral toe web spaces first; usually caused by Trichophyton rubrum.
  • Moccasin or dry — diffuse chronic scaling and hyperkeratosis affecting the sole and lateral foot; usually caused by Trichophyton rubrum.
  • Vesicobullous — least common; multiple small vesicles and blisters mainly on the arches and soles of the feet; usually caused by Trichophyton interdigitale.
101
Q

State some risk factors tinea pedis

A
  • Hot/humid climate
  • Occlusive footwear
  • Hyperhidrosis
  • Walking on contaminated surfaces
  • Immunocompromised
102
Q

Who is tinea capitis more common in?

A
  • Children aged 6 months - 12yrs
  • Immunocompromised
103
Q

Discuss how dermatophytosis is investigated

A
  • Diagnosis largely clinical
  • Skin scrapings or nail clipping for microscopy & culture useful if uncertain of diagnosis
104
Q

Discuss the management of the following dermatophytosis:

  • Tinea capitis
  • Tinea corporis
  • Tinea pedis
  • Onychomycosis
A

Tinea Capitis

  • Advise to soften & remove crust
  • Educate on transmission/infectivity e.g. don’t share towels
  • Ketoconazole shampoo in combination with oral antifungal e.g. terbinafine

Tinea corporis

  • Advice on self-care strategies
  • First line= topical antifungal e.g. terbinafine or imidazole e.g. clotrimazole
  • If associated inflammation, can prescribe mild topical corticosteroid e.g. hydrocortisone
  • If severe or extensive disease, consider oral antifungal e.g. terbinafine as first line

Tinea pedis

  • Self care (non-occlusive footwear, good foot hygiene, cotton absorbent socks, dry thoroughly, wear protective footwear to reduce transmission in e.g. swimming pools)
  • First line mild, non-extensive disease= topical antifungal e.g. terbinafine or imidazole e.g. clotrimazole
  • If associated inflammation, can consider prescribing mild topical corticosteroid e.g. hydrocortisone
  • If severe or extensive disease, consider oral antifungal e.g. terbinafine as first line

Onychomycosis

  • Self care management e.g. keep nails short, non-occlusive footwear
  • If superficial/early infection can try amorolfine nail lacquer (antifungal)
  • If initial management not successful/more advanced need oral antifungals- may require these for weeks to months:
    • Dermatophytes: terbinafine
    • Candida: itraconazole
105
Q

What is kerion?

A

Abscess caused by fungal infection which most commonly occurs in tinea capitis. Will require urgent referral to dermatologist and prolonged treatment with oral terbinafine

106
Q

For pityriasis versicolor, discuss:

  • What is is
  • Aetiology/pathophysiology
  • Epidemiology
A
  • Supeficial fungal infection of skin caused by yeast (of the genus Malassezia). They are normal skin flora but can cause disease when converted to thei pathogenic hyphal form
  • Common in teens & young adults (due to increased sebum production) and more common in tropical countries and in summer
107
Q

Discuss how pityriasis versicolor presents

A
  • Well demarcated thin plaques with fine scaling
  • Plaques may be hyperpigmented, hypopigmented or erythematous
  • Usually involves torso (can involve face)
  • Can become confluent & widespread
  • Post-inflammatroy pigmentary changes may persist for months despite eradication of infection
108
Q

Discuss whether you do any investigations for pityriasis versicolor

A
  • Diagnosis usually clinical
  • Can do microscopy to help if uncertain- seee spaghetti & meatballs appearance
109
Q

Discuss the management of pityriasis versicolor

A
  • Education: condition is not contagious & skin discolouration may persist for weeks
  • Pharmacological:
    • Antifungals
      • For large areas= antifungal shampoo e.g. ketoconazole shampoo. Make into lather and apply to body, leave for 5 mins, rinse
      • For smaller areas= topical imidazole e.g. clotrimazole
      • Consider second topical therapy before using oral antifungal e.g. itraconazole or fluconazole
      • If topical antifungal ineffective, consider oral antifungal e.g. itraconazole
110
Q

For viral warts, discuss:

  • What they are
  • Who common in
  • Transmission
  • Risk factors
  • Different subtypes and presentation
A
  • Papillomas (remember papilloma is a benign epithelial tumour) caused by HPV
  • Common in childhood
  • Spread via direct contact or via environment
  • Risk factors: immunosupression, walking bare foot in public/shared spaces, biting nails etc…
  • Subtypes & presentation:
    • Plantar warts: thick hyperkeratotic plaques beneach pressure points on sole
    • Verruca vulgaris: hyperkeratotic papules often on hands
    • Planar warts: flat topped papules commonly occuring on face
    • Condyloma acuminata (anogenital warts): cauliflower like plaques over anogential area

** Presence of thrombosed capillaries especially after paring is charcteristic of viral warts

111
Q

Discuss the prognosis of viral warts

A
  • Can persist for years and are generally asymptomatic
  • Spontaenous clearance in children within 1-2yrs is common; much slower in adults
112
Q

Discuss the management of viral warts

A
  • Educate pt on how to lower risk of transmission e.g. don’t share towels, avoid scratching or biting, cover with plaster when swimming
  • If aymptomatic and in non-cosmetically sensitive area consider no treatment
  • If treatment is required:
    • First line= topical salicyclic acid for up to 12 weeks
    • Second line= cyrotherapy with liquid nitrogen every 2 weeks up to 6 times. Can also continue to use salicyclic acid & parring once scabbing from cyrotherapy has resolved
    • Third line= topical imiquimod, intralesion bleomycin, cautery etc…
  • Patients with anogenital warts should be reffered to genitourinary medicine
113
Q

For erythema multiforme, discuss:

  • What it is
  • Who it commonly affects
  • Causes
A
  • Immune mediated mucocutaenous condition most commonly caused by HSV. EM major refers to EM with mucosal involvement, EM minor only involves skin
  • Young adults, slight female predilection
  • Infection causes around 90% of EM; most common infectious agent is HSV followed by Mycoplasma pneumoniae. Drug induced EM <10% cases; common drug causes are NSAIDs, sulphonamides, anti-epileptics & antibiotics
114
Q

Describe the presentation of erythema multiforme

A
  • Classically presents as acrally (affecting peripheries- typically hands)
  • Targetoid lesions with 3 zones: dusky central disc, pale oedematous ring, erythematous outermost ring (some lesions may only have 2 zones)
  • May have mild prodromal symptoms
  • Lesions may coalesce
  • May have mucsosal erosions
  • May be slightly pruritic
115
Q

Discuss the management of erythema multiforme

A
  • Antihistamine & emollients for itching
  • If HSV associated or idiopathic recurrent EM= antiviral therapy for 6 months e.g. aciclovir
  • Identify & remove any causes e.g. if drug induced stopping causative drugs, abx for Mycoplasma pneumoniae infection
  • If there is mucosal involvement:
    • Mild: high potency topical steroids, oral antiseptic wases or oral anaesthetic solutions
    • Severe: systemic steroids
  • In treatment ressitant recurrent EM consider immunosupression
116
Q

What is an alternative name for Stevens-Johnson syndrome (SJS)?

A

Toxic epidermal necrolysis (TEN)

117
Q

What is SJS/TEN?

A

SJS and TEN are considered two ends of spectrum of severe epidermolytic adverse cutanous drug reactions.

  • SJS <10% body surface area involved
  • TEN >30% of body surface involved

*(when inbetween 10 and 30% conditions overlap)

118
Q

Incidence of SJS/TEN is higher in what patients?

A

HIV positive patients

119
Q

Drugs are the most common cause of SJS/TEN (infections are occasionally reported as the sole cause); state some common drugs that cause SJS/TEN

A
  • Allopurinol
  • Sulphnoamides
  • Antibiotics
  • Anticonvulsants
  • NSAIDS (oxicam-type)
120
Q

Discuss the clinical features of SJS/TEN

A
  • Onset within 2 months of commencing causative drug
  • Painful, dusky erythema with blisters & erosions
  • Rapidly progress into confluent erythema with sheet-like epidermal detachment
  • Nickolsky sign (epidermis detached by mechanical pressure)
  • Prodromal symptoms
  • Mucosal involvement is common
121
Q

In primary care you would urgently admit to secondary care if suspect SJS/TEN. What investigations would they do in secondary care?

A
  • Skin biopsy: confirm SJS/TEN
  • Direct immunofluorescence to rule out autoimmune blistering diseases
  • Blood tests to identify complications & prognosis:
    • FBC
    • U&Es
    • LFTs
    • ABG
    • Blood cultures
    • Magnesium
    • Phosphate
122
Q

Discuss the management of SJS/TEN

A
  • Stop causative drug
  • Supportive care best delivered in ICU or burns unit (e.g. fluids, electrolyte management, wound mangement)
  • Dressings, topical antibacterials& emollients
  • Analgesia
  • IV immunoglobulin for TEN
  • Treatment of sequale e.g. opthalmoloy review for eye involvement
123
Q

Discuss the mortality of SJS and TEN

A
  • SJS= 1-5%
  • TEN= 25-35%