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Clinical Flashcards

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Dermatology Board Prep flashcards
1
Q

What is a macule?

A

hyperpigmented flat lesion which is <1cm

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2
Q

what is a patch?

A

hyperpigmented flat lesion which is >1cm

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3
Q

what is a papule?

A

raised well defined lesion which <0.5cm

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4
Q

what is a nodule?

A

raised well defined lesion which >0.5cm

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5
Q

what is a plaque?

A

raised flat top lesions that grow horizontal which is > 1cm

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6
Q

what is a wheal?

A

a raised compressible dermal swelling

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7
Q

what is a vesicle?

A

a fluid filled lesion <0.5 cm

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8
Q

what is a bulla?

A

fluid filled lesion >0.5 cm

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9
Q

what is a pustule?

A

pus filled lesion

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10
Q

what is a cyst?

A

nodule with semi solid material

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11
Q

what is an erosion?

A

superficial skin break in the epidermis

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12
Q

what is an ulcer?

A

deep skin break down to the dermis

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13
Q

what is a fissure?

A

linear split in the epidermis

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14
Q

what is lichenification?

A

increased appearance of skin markings

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15
Q

what is atrophy?

A

loss of epidermis +/- dermis

surface remains in tact

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16
Q

what is scale?

A

accumulated fragments of keratin layer

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17
Q

what is crust?

A

dried exudate

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18
Q

what is a scar?

A

normal tissue replaced by fibrous tissue

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19
Q

what are the characteristics of hypopigmented rashes?

A

paler - lack melanin

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20
Q

what are the characteristics of hyperpigmented rashes?

A

increased melanin

contain hemosiderin

direct chemical staining

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21
Q

what is psoriasis?

A

a chronic inflammatory skin condition characterised by scaly erythematous plaques, which typically follows a relapsing course

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22
Q

what is the pathogenesis of psoriasis?

A

epidermis in psoriatic plaques is hyperproliferative. there is proliferation and dilation of blood vessels in the dermis and infiltration of inflammatory cells

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23
Q

what are “trigger” factors associated with psoriasis?

A

streptococcus infection

stress

skin trauma (Koebener phenomenon)

alcohol

obesity

smoking

drugs: lithium, NSAIDs, beta blockers , antimalarials and sudden oral or potent topical corticosteroid withdrawal

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24
Q

what types of psoriasis are there?

A
  1. Pustular psoriasis

may be generalized or localized.

Generalised pustular psoriasis (a potentially life-threatening medical emergency)

Rapidly developing widespread erythema, followed by the eruption of white, sterile non-follicular pustules which coalesce to form large lakes of pus.
Lesions associated with systemic illness, such as fever, malaise, tachycardia, weight loss, and arthralgia.
Usually presents in people with existing or previous chronic plaque psoriasis, but can also occur in people without a history of psoriasis.

Localized (palmoplantar) pustular psoriasis
Lesions on the palms and soles, such as yellow-brown pustules within established psoriasis plaques, or redness, scaling, and pustules at the tips of the fingers and toes.

2.Erythrodermic psoriasis

Erythrodermic psoriasis is a potentially life-threatening medical emergency.

Diffuse, widespread severe psoriasis that affects more than 90% of the body surface area

It can develop gradually from chronic plaque psoriasis or appear abruptly, even in people with mild psoriasis

Lesions may feel warm, and may be associated with systemic illness, such as fever, malaise, tachycardia, lymphadenopathy, and peripheral oedema

3.Chronic plaque psoriasis (psoriasis vulgaris)

most common type

Monomorphic, erythematous plaques covered by adherent silvery-white scale, usually on the scalp, behind the ears, trunk, buttocks, periumbilical area, and extensor surfaces (such as forearms, shins, elbows, and knees).

Lesions which are typically distributed symmetrically and can coalesce to form larger lesions.

  1. Scalp psoriasis

affects 75–90% of people with psoriasis.

It typically presents as chronic plaque psoriasis affecting the scalp area.
The whole scalp can be affected, or individual plaques may be visible. Plaques may be very thick, particularly in the occipital region.

5.Facial psoriasis

Well-demarcated plaques on the face, similar to those of chronic plaque psoriasis.
Lesions which may affect the hairline.
Possible mild scaling around the eyebrows and nasolabial folds, which may be due to co-existent seborrhoeic dermatitis (so-called ‘sebo-psoriasis’)

6.Flexural psoriasis

Itchy psoriasis lesions affecting areas such as the groin, genital area, axillae, inframammary folds, abdominal folds, sacral and gluteal cleft.

The elderly, immobile, and people who are overweight or obese are at increased risk of being affected

Lesions of chronic plaque psoriasis which are well-defined, but there may be little or no scaling, due to friction and occlusion at these sites.
Lesions are often red and glazed in appearance, and there may be a fissure in the skin crease.

7.Guttate psoriasis

Small, scattered, round or oval (2 mm to 1 cm in diameter) scaly papules, which may be pink or red.
Multiple lesions which may occur all over the body over a period of 1–7 days, particularly on the trunk and proximal limbs. Lesions may occur on the face, ears, and scalp, but rarely affect the soles of the feet.
A first presentation of psoriasis (classically after acute streptococcal upper respiratory tract infection), or as an acute exacerbation of plaque psoriasis.

8.Nail psoriasis

Nail psoriasis more commonly affects fingernails than toenails and may affect all parts of the nail and surrounding structures.

Nail changes can occur with any type of psoriasis, and are particularly common in people with psoriatic arthritis (up to 90% of people are affected). The incidence of nail involvement increases with the duration of psoriasis.

Nail pitting (depressions in the nail plate) is the most common finding.

Discolouration (for example the ‘oil drop sign’) — orange-yellow discolouration of the nail bed.

Subungual hyperkeratosis — hyperproliferation of the nail bed, with accumulation of keratinocytes under the nail.

Onycholysis — detachment of the nail from the nail bed, which may allow bacteria and fungi to enter and cause infection.

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25
Q

what other conditions can also develop due to psoriasis?

A

a seronegative arthropathy:

  1. asymmetrical mono/oligoarthritic
  2. symmetrical polyarthritis
  3. psoriatic spondylitis
  4. distal predominant
  5. arthritis mutilans
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26
Q

how do you manage psoriasis?

A
  1. education
  2. Topical treatments:

vitamin D analogues: first line topical therapy e.g. calcipotriol

emollients: should be used liberally by all patients. greasy ointments such as olive oil may need to used on the scalp
diathranol: used in short contact regimens for stable chronic plaque disease as it burns and stains normal skin

coal tar: only used as in patient due to smell and mess

steroids: mild steroids are used flexural and palmar plantar disease

salicylate - is used to break down particularly hyper keratotic skin

n. b. Dovobet - gel which contains both calcipotriol and betamethasone dipropionate
3. phototherapy: most suitable for guttate (first line) or plaque psoriasis. best for more severe disease. can use UVB or PUVA.

PUVA more suitable for extensive large plaque psoriasis or localised pustular

  1. Pharmacological

can also give drugs for more severe or non responsive

Methotrexate, Ciclosporin or aciterin

biological drugs: inhibit T cell activation and function or neutralise cytokines

first line: ustekinumab, adalimab, secukinumab

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27
Q

what is dermatitis (acute eczema)?

A

condition which causes a rash with inflamed red skin that is poorly demarcated and less scaly than psoriasis.

the barrier function of the pidermis is abnormal and skin is easily irritated

it is itchy

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28
Q

what is the clinical presentation of dermatitis?

A

essentially:

itchy, ill-defined, erythematous and scaly

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29
Q

give examples of endogenous dermatitis:

A

Atopic

seborrheic

varicose

discoid

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30
Q

give examples of exogenous dermatitis:

A

contact allergic

contact irritant

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31
Q

state the pathogenesis and histology for the following types of dermatitis:

contact allergic

contact irritant

atopic

drug-related

photo-induced

lichen simplex

stasis dermatitis

A

Pathogenesis histology

  1. delayed type 4 reaction spongiotic dermatitis
  2. Trauma e.g. soap and water spongiotic dermatitis
  3. Genetic and environmental factors spongiotic dermatitis
  4. Type 1 or 4 spongiotic dermatitis & eosinophils
  5. Reaction to UV light spongiotic dermatitis
  6. physical trauma e.g. scratching spongiotic dermatitis & external trauma
  7. physical trauma - hydrostatic pressure spongiotic dermatitis & extravasation of RBCs
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32
Q

what are the causes of atopic eczema/dermatitis?

A

Genetic: family history of atopy is common . include mutations in the filaggrin protein which is a protein involved in maintaining the waterproof

infection: staph colonise lesions
allergens: difficult to avoid

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33
Q

how do you diagnose atopic eczema?

A

child must have itchy skin and 3 or more of the following factors:

  1. onset before 2 years old
  2. past flexural involvement
  3. history of dry skin
  4. personal history of other atopy ( or first degree relative if under 4 year old)
  5. visible flexural dermatitis
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34
Q

what are the chronic changes of atopic eczema?

A

lichenification - chronic thickening and increased marking of the skin caused by scratching

excoriation - scratch marks self induced, often due to itching

secondary infection: crusting indicated staph aureus

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35
Q

what is the rash distribution of atopic dermatitis?

A

infants: face and scalp extensor surfaces involved, flexor surfaces and napkin area spared

children & adults: flexor surfaces, especially the wrist, cubital fossa, popliteal fossa and ankles

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36
Q

how do you manage atopic dermatitis?

A

DANGER : manage any severe weeping rash around the mouth: this could be eczema herpeticum which can be fatal

atopic eczema treatment in general:

  1. Emollients and soap substitutes: dry skin itches and is susceptible to irritants. Use emollients liberally even when eczema is less active
  2. anti histamine for pruritus e.g. hydroxyzine
  3. topical corticosteroids:
    mild: hydrocortisone
    moderate: betnovate, eumovate
    potent: betnovate, elocon

very potent: dermovate, etrivex

  1. phototherapy mainly UVB
  2. systemic immunosuppressants
  3. biological agents
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37
Q

what is seborrheic dermatitis?

A

common inflammatory skin condition occurring in areas rich in sebaceous glands (such as the scalp, nasolabial folds, eyebrows, and chest). In infants the scalp is most commonly affected (‘cradle cap’).

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38
Q

what is the cause of seborrheic dermatitis?

A

over-growth of skin yeasts (malassezia)

also associated with immunosuppression - severe if HIV +ve or if patient uses drugs e.g. ciclosporin

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39
Q

what is the clinical presentation of seborrheic dermaititis?

A

adults and adolescent:

Red, itchy, scaly rash affects the following areas:

  1. Scalp - mainly causes dandruff
  2. Face - in particular the nasolabial nodes, behind the ear, eyebrows and cheeks
  3. upper chest and back
  4. Flexures and skin folds

child:

  1. cradle cap
  2. face
  3. ears
  4. neck
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40
Q

how do you manage seborrheic dermatitis

A

Infantile cradle cap: emollients +/- topical steroids

Adults: emollients + topical steroids + topical antifungal (ketoconazole) - if non responsive or more wide spread, oral antifungal can be given (daktacort or ketoconazole)

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41
Q

what does hyperkeratosis mean?

A

increased thickness of keratin layer

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42
Q

What does parakeratosis mean?

A

persistence of nuclei in the keratin layer

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43
Q

What does acanthosis?

A

increased thickness of epidermis

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44
Q

what is spongiosis?

A

oedema between keratinocytes

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45
Q

what types of contact dermatitis are there?

A

contact irritant – non specific physical irritation

contact allergic - specific allergic reaction

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46
Q

give example of allergens which cause contact allergic dermatitis.

A

cosmetic ingredients – such as preservatives, fragrances, hair dye and nail varnish hardeners

metals – such as nickel or cobalt in jewellery

some topical medicines (medicines applied directly to the skin) – including topical corticosteroids, in rare cases

rubber – including latex, a type of naturally occurring rubber

textiles – particularly the dyes and resins that are contained in them

strong glues – such as epoxy resin adhesives

plants – such as chrysanthemums, sunflowers, daffodils, tulips and primula

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47
Q

what is the pathogenesis of contact allergic dermatitis?

A
  1. Langerhans cell in epidermis process the antigen - this increases immunogenicity
  2. processed antigen is then presented to Th cells in dermis
  3. sensitised Th cells migrate into lymphatics and then to regional nodes where antigen presentation is amplified
  4. on subsequent antigen challenge specifically sensitised T- cells proliferate and migrate to and infiltrate the skin
  5. Rash and skin changes take 48-96 hours
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48
Q

How do you diagnose contact allergic dermatitis?

A

patch testing

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49
Q

how do you manage contact allergic dermatitis?

A

allergen avoidance

regular emollients

topical steroids during flares

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50
Q

what are the causes of contact irritant dermatitis?

A

soaps and detergents

antiseptics and antibacterial

perfumes and preservatives in toiletries or cosmetics
solvents

oils used in machines

disinfectants

acids and alkalis

cement

powders, dust and soil

water – especially hard, chalky water or heavily chlorinated water

plants – such as Ranunculus, spurge, Boraginaceae and mustards

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51
Q

give examples of professions which are more at risk from irritant contact dermatitis?

A

agricultural workers

beauticians and hairdressers

chemical workers

cleaners

construction workers

cooks and caterers

metal and electronics workers

health and social care workers

machine operators

mechanics and vehicle assemblers

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52
Q

what is acne vulgaris?

A

Acne vulgaris is a chronic inflammatory skin condition affecting mainly the face (99% of cases), back (60% of cases) and chest (15% of cases).

is characterised by blockage and inflammation of the pilosebaceous unit

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53
Q

what is the pathogenesis of acne vulgaris?

A
  1. sebum produced by sebaceous gland plugs pilosebaceous unit
  2. keratin and sebum build up to produce comedones (blackheads/whiteheads). basal kertinocyte proliferation in pilosebaceous follicles caused by androgen and corticotropin release hormones
  3. Rupture causes acute inflammation ( caused by colonisation of Propionibacterium acne) + foreign body granulomas
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54
Q

what is the clinical presentation of acne vulgaris?

A

face, chest and upper back are most affected areas

Non-inflammatory lesions (comedones) which may be open (blackheads) or closed (whiteheads).

Inflammatory lesions such as:
Papules and pustules – superficial raised lesions

Nodules or cysts- deeper, palpable lesions which are often painful and may be fluctuant.

may also have scars

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55
Q

what are the risk factors of acne vulgaris?

A

Age 12-24

greasy skin

endocrine disorders - Hyper androgenism

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56
Q

how do you classify acne vulgaris?

A

Mild acne - mainly facial comedones

moderate acne - inflammatory lesions (papules and pustules) dominate, affecting face +/- torso

severe acne - nodules, cysts scars and inflammatory papules and pustules

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57
Q

how do you manage acne vulgaris?

A

mild acne:

topical benzoyl peroxide or topical retinoid

if poorly tolerated try azelaic acid

Moderate acne:

oral antibiotic combined with topical benzoyl peroxide or topical retinoid

contraceptive pill can be used in women

severe acne:

topical therapies and isotretinoin

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58
Q

what is rosacea?

A

a chronic relapsing/remitting disorder of blood vessels and pilosebaceous units in central facial areas typically in fair skinned people.

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59
Q

what is the clinical presentation of rosacea?

A

more common in women

pre-rosacea features:

  1. flushing triggered by stress, alcohol, spices and sunlight

Rosacea signs and symptoms:

central facial rash with:

  1. erythema
  2. telangiectasia
  3. papules and pustules
  4. inflammatory nodules +/- facial lymphoedema
  5. men have risk of rhinophyma ( swelling + soft tissue overgrowth of the nose)
  6. ocular rosacea - conjunctivitis/blepharitis
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60
Q

how do you manage rosacea?

A

Use soap substitutes and avoid sun overexposure

  1. topical metronidazole
  2. topical therapies + oral antibiotics (doxycycline)
  3. Isotretinoin - causes dry skin and lips and photosensitivity
  4. talangectasia + rhinopyma: laser therapy
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61
Q

What is bullous pemphigoid?

A

the chief autoimmune blistering disorder in the elderly - due to IgG autoantibodies to the basement membrane

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62
Q

what are the signs and symptoms of bullous pemphigoid?

A

Patient is typically elderly

blisters are localised to one area, or widely spread on the trunk and proximal limbs

can have large tense bullae on normal skin on erythematous base

blisters burst to leave erosions but are non scarring

itchy erythematous plaques and papules may be presenting feature

A history of itch in the months preceding the onset of blistering

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63
Q

How do you diagnose Bullous pemphigoid?

A

Immunofluorescence +ve - Linear IgG and C3 along the basement membrane

skin biopsy: sub epidermal blisters + inflammatory infiltrates within blisters

Nikolsky sign negative

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64
Q

how do you manage bullous pemphigoid?

A

very potent topical steroids applied to lesions (prednisolone) - slowly reduced over 4 weeks

tetracycline antibiotics - steroid sparing agents better than oral steroids

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65
Q

what are the main causes of bullous (blistering) diseases?

A

infection (e.g. herpes)

insect bite

friction

eczema

drugs (e.g. ACE or furosemide)

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66
Q

Name the two main examples of bullous disorders.

A

Bullous Pemphigoid - split is deeper through DEJ

Pemphigus vulgaris - split is more superficial, intra-epidermal

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67
Q

what is pemphigus vulgaris?

A

a bullous disorder due to IgG antibodies against desmosomal components ( desmoglein 1&3) which leads to acantholytsis (keratinocytes separate from each other)

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68
Q

what is the clinical presentation of pemphigus vulgaris?

A

more common in younger people (<40)

typically affects scalp, face, axillae and groins

flaccid vesicles/bullae - thin roofed and leave eroded raw areas

lesions rupture to leave raw areas - increased infection risk

Mucosal involvement (eyes, genitals) : very common.

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69
Q

how do you diagnose pemphigus vulgaris?

A

Nikolsky sign positive

+ve immunofluorescence - intracellular IgG giving a crazy paving effect

skin biopsy of blisters

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70
Q

how do you manage pemphigus vulgaris?

A

prednisolone

steroid sparing agents: mycophenolate mofetil and azathioprine

use rituximab and IV immunoglobulin in resistant cases

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71
Q

what is nikolsky’s sign?

A

top layers of the skin slip away from the lower layers when slightly rubbed

indicates plane of cleavage within the epidermis

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72
Q

what is dermatitis herpetiformis?

A

autoimmune skin condition caused by auto antibodies against tissue transglutaminase (TTG), which is the antibody implicated in coeliac disease and causes sub epidermal blisters in the skin

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73
Q

what is the clinical presentation of dermatitis herpetiformis?

A

small, intensely itchy blisters on an erythematous and swollen base.

itch can precede the blisters

lesions tend to be found on extensor aspects of elbows, forearms, knees, buttocks, scapulae, face and scalp. it is symmetrical

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74
Q

how do you diagnose dermatitis herpetiformis?

A

blood Anti TTG

biopsy: sub epidermal blisters with papillary micro abscesses
immunofluorescence: granular deposits of IgA within papillae of epidermis

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75
Q

how do you manage dermatitis herpetiformis?

A

Gluten free diet +/- dapsone

rare complication: increased risk of small bowel lymphoma

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76
Q

what is lichen Planus?

A

an inflammatory skin condition , characterized by an itchy, non-infectious rash on the arms and legs

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77
Q

what are the signs and symptoms of Lichen planus?

A

common with middle age

  1. lesions are distributed at flexor aspect of wrists, forearms, ankles and legs
  2. the lesions are described as:
  3. purple
  4. pruritic
  5. poly-angular
  6. planar (flat-topped)
  7. papules
  8. white lacy markings (Wickham’s striae) found on papules and buccal mucosa

associated with Hep C

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78
Q

How do you manage Lichen planus?

A

symptomatic treatment

  1. topical steroids are 1st line
  2. oral steroids if extensive

can use emollients

phototherapy (UVB or PUVA)

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79
Q

what is tuberose sclerosis?

A

a multi-gene disorder which is autosomal dominant and effects virtually every organ system

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80
Q

what are the causes of tuberose sclerosis?

A

mutations on chromosomes 9q34 and 16p13.3

tumour suppressing genesTSC1 and TSC2 are the genes affected - code for hamartin and tuberin

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81
Q

what are the signs and symptoms of tuberose sclerosis?

A

skin:

ash leaf macules - oval shaped areas of hypopigmentation. earliest cutaneous sign of tuberose sclerosis

Periungal fibroma: fibroma’s of the nail bed . they are small fleshy tumours which grow aroun and under the toenails or finger nails

sebaceous adenoma: angiofibroma of the sebaceous glands on the face

shagreen patches: leathery texture nodules and is found most commonly in the lower back region

other:

hamartomas - angiomyolipomas found on hear,lung and kidneys

bone cysts seen on x-ray

enamel pitting

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82
Q

what is Neurofibromatosis type 1?

A

an autosomal dominant genetic condition that causes tumours to grow along your nerves. The tumours are usually benign.

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83
Q

what are the sign and symptoms of neurofibromatosis type 1 ?

A

cafe au lait macules

neurofibromas

plexiform neuroma

axillary or inguinal freckling

optic glioma

2 or more lisch nodules on iris

a distinctive bony lesion

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84
Q

what are the 4 main subtypes of inflammatory skin diseases?

A
  • spongiotic
  • psoriasiform
  • lichenoid
  • vesiculobollous
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85
Q

what happens to the epidermis in psoriasiform inflammation?

A

acanthosis due to elongation of rete ridges

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86
Q

what happens in lichenoid inflammation?

A

basal layer damage

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87
Q

what happens in vesiculobullous inflammation?

A

blistering

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88
Q

what subtype of inflammatory skin disease does eczema, contact allergic dermatitis and photosensitivity come under?

A

spongiotic inflammation

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89
Q

what subtype of inflammatory skin disease does psoriasis come under?

A

psoriasiform inflammation

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90
Q

what subtype of inflammatory skin disease does lichen planus and lupus come under?

A

lichenoid inflammation

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91
Q

what subtype of inflammatory skin disease does pemphigoid pemphigus and dermatitis herpetiformis come under?

A

vesiculobullous inflammation

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92
Q

what type of nerve fibres transmit itch?

A

C fibres

unmyelinated

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93
Q

what are salmon patches?

A

non vascular birthmarks found on the face or nuchal area

It is a central erythematous macule - majority will regress with time

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94
Q

what are port wine stains?

A

capillary malformations that are present at birth and are permanent

they are usually found in the head and neck region

the lesions are pink/red macule that is unilateral which tend to darken and thicken with age

location on the nerve is described in relation to the distribution of the trigeminal nerve

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95
Q

what is klippel-trenaunay syndrome?

A

rare congenital vascular disorder in which a limb may be affected by port wine stains, varicose veins, and bone and soft tissue growth

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96
Q

what is infantile haemangioma (strawberry naevi)?

A

benign vascular tumours that usually appears within the first month of life in the head or neck region

more common in females and premature babies

lesion: superficial, red plaque - majority undergo complete or partial resolution

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97
Q

where do melanocytes arise from?

A

neural crest

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98
Q

What are the three main types of skin cancers?

A

Basal cell carcinoma - most common

squamous cell carcinoma

Melanoma

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99
Q

what happens when melanoblasts settle in the skin?

ii. what is the normal melanocyte: basal keratinocyte?

A

they form melanocytes

ii. 1:5 - 1:10

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100
Q

what are the risk factors of malignant melanoma?

A
  1. UV exposure
  2. sunburn
  3. fair complexion
  4. many melanocytes or dysplastic naevi
  5. +ve family history - MC1R defect leads to freckling
  6. old age
  7. had a previous melanoma
101
Q

what are actinic lentigines?

A

also called ‘age’ or ‘liver’ spots

spots found on face, forearms and dorsal hands

related to UV exposure

these spots have an increase melanin and basal melanocytes

102
Q

what are dysplastic naevi?

A

variegated pigment spots which are generally >6mm in dimeter

they are either sporadic (low risk of malignant melanoma) or familial (high risk of malignant melanoma)

103
Q

what are the signs and signs and symptoms of malignant melanoma?

A

signs
ABCDEF:

Asymmetry in the outline of lesion

Border irregularity or blurring

Colour variation with shades of black, brown, blue or pink

Diameter >6mm

Evolution - all changing moles in size, elevation and/or colour are suspect

Funny looking mole - the lesion stands out

nodular melanomas: much more dangerous

Elevated

Firm

Growing

104
Q

what types of malignant melanomas are there?

A

four main types:

  1. superficial spreading (most common) - found on trunks and limbs it presents as a slowly enlarging pigmented lesion with colour variation and irregular border
  2. Nodular - most aggressive type. rapid growing, varied sites but often trunk
  3. Acral lentiginous - occur on the palms, soles and subungual areas
  4. Lentigo maligna - arises within a lentigo maligna
105
Q

how do you diagnose malignant melanomas?

A

Clinical

biopsy

check Breslow’s thickness to determine prognosis:

the measurement of the depth of the melanoma from the granular layer of the epidermis down through to the deepest point of the tumour

106
Q

how do you manage malignant melanomas?

A

initial:

primary excision to give clear margins (2mm)

sentinel node biopsy - if positive then do a regional lymphadenectomy

Main:

depends on assessment of Breslow :

  1. if in-situ then clear by circa 5mm
  2. if invasive but <1mm thick: 1 cm clearance
  3. if invasive >1mm thick: 2 cm clearance
  4. sentinel node biopsy if >1mm thick or thinner with mitoses

advanced treatment: difficult to manage

chemotherapy

immunotherapy

Genetic therapy

107
Q

Give examples of epidermal tumour causing cancers.

A
  1. Basal cell carcinoma (malignant)
  2. squamous cell carcinoma (malignant)
  3. Dysplasias-bowen’s disease (pre-malignant)
  4. Actinic keratosis (pre-maligant)
  5. Viral lesions (pre-malignant)
  6. seborrhoeic keratosis (benign)
108
Q

what is seborrhoeic keratosis?

A

benign proliferation of epidermal keratinocytes

it is common on face and trunk and occurs usually in ageing skin

lesions: tuck on appearance - greasy hyperkeratotic surface. warty and rough

109
Q

what is basal cell carcinoma?

A

it is the commonest skin cancer

best outcome for skin cancers

basal cells sprout from epidermis. the cells then invade the dermis, peripheral palisading.

slowly growing and locally destructive - never metastasises

110
Q

what are the risk factors for basal cell carcinoma?

A

Fair skin

UV light exposure

intermittent sun damage during childhood

111
Q

what are the three main types of BCC?

A

Nodular

superficial

infiltrative - most worrying

112
Q

what is the clinical presentation of BCC?

A

Infiltrative:

prominent desmoplastic fibrous stroma

margins are poorly defined

may spread along nerves

Nodular:

pearly nodule with rolled telangiectatic edge on the face or a sun exposed site +/- central ulcer

causes local destruction if left untreated

Superficial:

lesions appear as red scaly plaques with raised smooth edge often on the trunk or shoulders

113
Q

how do you diagnose BCC?

A

clinical presentation

biopsy

114
Q

how do you manage BCC?

A

conservative: leave it and monitor

surgical :Excision (first line)

medical: topical imiquimod or fluorouracil - reasonable options for superficial lesion at low risk sites

can also do: cryotherapy, cutterage, radiotherapy, photodynamic therapy

115
Q

What is squamous cell carcinoma?

A

second most common form of skin cancer

generally good prognosis

locally invasive

low but definite risk of metastasis

116
Q

what are the main precursors for SCC?

A
  1. Bowen’s disease
  2. Actinic keratosis
  3. Viral lesions

all display squamous dysplasia

117
Q

what is Bowen’s disease?

A

it is SCC in SITU

118
Q

what is the clinical presentation of Bowen’s disease?

A

Scaly plaque that is well defined and has a flat edge and it slowly enlarges

Mainly presents in women on their lower leg

119
Q

how do you manage Bowen’s disease?

A

cryotherapy

topical fluorouracil or imiquimod

photodynamic therapy

curettage + cautery

120
Q

what is actinic keratosis?

A

Pre malignant lesions associated with partial thickness intra-epidermal proliferation of atypical keratinocytes

121
Q

what is clinical presentation of actinic Keratosis

A

lesions found on sun exposed area, especially somewhere on the head

lesions: pre-malignant crumbly yellow white scaly crusts

122
Q

which virus are viral precursors of SCC associated with?

A

HPV

123
Q

what are the riskfactors of SCC?

A

HPV

fair skin

cumulative sun damage over the years

immunosuppression

124
Q

what is the clinical presentation of SCC?

A

Lesion:

ulcerated or crusted

firm and irregular

locally invasive can metastasise

seen on sun exposed sites (face, ears, dorsal hands)

can have chronic leg ulcers (uncommon)

can have xeroderma pigmentosum (rare)

sites with poorer prognosis:

scalp

ear

nose

125
Q

how do you diagnose SCC?

A

biopsy

126
Q

how do you manage SCC?

A

local complete excision in primary SCC

127
Q

what does photosensitivity mean?

A

denotes conditions triggered by light

128
Q

what are the two types of UV is the skin exposed to?

A

UVA - longer wave - penetrates glass

UBV - smaller wave length, main contributing type to sunburn and skin cancer

129
Q

what is xeroderma pigmentosum?

A

group of autosomal recessive genetic disorders caused by deficiency in the DNA repairs mechanisms in the skin

130
Q

what is the clinical presentation of xeroderma pigmentosum?

A

severe photosensitivity

accelerated photoaging

ocular damage

early formation of skin cancers

131
Q

How do you manage xeroderma pigmentosum

A

patients required to undertake strict sun avoidance

most die in teenage years due to skin cancer

132
Q

what is porphyria?

A

a group of cutaneous and systemic conditions associated with deficiency of enzyme involved in the synthesis of haem

133
Q

what is porphyria cutanea tarda?

A

the most common type of porphyria

usually seen in middle aged men

commonly associated with liver disease - seen in patients often with haemochromatosis, hepatitis or alcohol misuse

134
Q

what enzyme deficiency occurs with porphyria cutanea tarda?

A

Uroporphyrinogen decarboxylase -the porphyrin type accumulated is uroporphyrinogen 3

135
Q

what is the rash of porphyria cutanea tarda?

ii. what other presentations are there?

A

blistering lesions on sun exposed sites that heal with scarring and are associated with hyper pigmentation

skin affected is fragile

ii. lot of hair growing on cheeks

136
Q

how do you diagnose porphyria cutanea tarda?

A

bloods - porphyrin studies

woods lamp: urine shines pink instead of blue

137
Q

what is acute intermittent porphyria?

A

form of porphyria where the enzyme deficiency is porphobilinogen deaminase. Therefore the porphyrin accumulated is porphobilinogen

commonly presents in females around the age of 30

138
Q

what is erythropoietic protophopyria?

A

an autosomal dominant condition - most commonly seen in children

the enzyme deficiency is Ferrochelatase - leads to accumulation of the porphyrin: protoporphyrin IX

rash: sometimes no evidence of rash but there will be burning and itching on the skin with

139
Q

what drugs can cause photosensitiviy?

A

NSAIDs

Diuetics

Amiodarone

Antibiotics: Tetracyclines, ciprofloxacin

140
Q

what type of hypersensitivity reaction causes chronic actinic dermatitis?

A

type IV

141
Q

what is the clinical presentation of chronic actinic dermatitis?

A

Most commonly seen in men over 50

develop eczematous type rash on sun exposed sites

often associated with contact allergic dermatitis

142
Q

How do you manage chronic actinic dermatitis?

A

sun protection

standard eczema treatment of emollients and topical steroids

143
Q

what is solar urticaria?

A

a photosensitivity condition where sunlight causes a Type I

144
Q

what is the clinical presentation of solar urticaria?

A

immediate onset of erythema, urticaria and itchy rash upon exposure to sunlight

rash resolves in a few hours

145
Q

how do you manage solar urticaria?

A

Sun avoidance

anti-histamines

146
Q

what is urticaria (hives)?

A

a transient rash caused by oedema from mast cell degranulation and release of inflammatory mediators

147
Q

what are the causes of urticaria?

A

1.Acute causes:

Allergy (most common cause for acute) - Type 1

Infections

parasites (helminths)

chemicals (insect bites, lates, drugs or food)

systemic disease

2.Chronic: urticaria which lasts more than >6 weeks

idiopathic

histamine releasing autoantibodies

  1. Physical causes:

solar

cold

dermographism

cholinergic: after exercise or shower
autoimmune: SLE

148
Q

what are the sign and symptoms of urticaria?

A

smooth, erythematous, itchy hives and wheals (localised swellings)

associated with angioedema

149
Q

how do you diagnose urticaria?

A

skin prick test

Blood RAST tests

150
Q

how do you manage urticaria?

A

Non sedating antihistamines

avoid allergen avoidance

UVB phototherapy - stabilises mast cells

151
Q

when do angioedema develop?

A

oedema within the subcutaneous or sub mucosal tissues

152
Q

what type of swelling does angioedema cause?

A

non pitting swelling

153
Q

what is the the primary varicella zoster infection?

A

Chickenpox

154
Q

how is chickenpox spread?

A

via droplets/vesicle fluid

incubation 11-21 days

155
Q

what is the sign and symptoms of chickenpox?

A

crops of skin vesicles of different ages

often starts on face, scalp or trunk

the rash is more concentrated on the torso than the extremities

rash starts 2 days after infection - often starts on the back: macule - papuple to vesicle with a red surround leads to ulcers. crusting may then occur

156
Q

how do you manage chickenpox?

A

Live attenuated vaccine for non-immune people and pregnant women

supportive - calamine lotion

if immunocompromised or on steroids give aciclovir

157
Q

what is shingles?

A

also called herpes zoster

158
Q

what is the pathophysiology of shingles?

A

following chicken pox, the varicella zoster virus can lay dormant in sensory nerve roots. Shingles is caused by reactivation of the dormant virus

159
Q

what is the clinical presentation of shingles?

A

burning tingling pain and itch along dermatomal distribution which may preced rash

Rash: erythematous macules/ papules that develop into vesicles before crusting over and healing

160
Q

what are the specific location of shingles?

A

ophthamlic (V1): reactivation of the virus in the trigeminal nerve. rash develops unilaterally over the forehead and around the eyes.

ramsay hunt syndrome: reactivation of the virus within the geniculate nucleus of the facial nerve. Rash and pain experienced in the auditory canal associated with:

Bell palsy
Deafness
Vertigo
Tinnitus

161
Q

How do you manage shingles?

A

anti viral

if admission or immediate specialist advice is not indicated, consider the need for oral antiviral treatment (aciclovir, valaciclovir, or famciclovir).

pain management:

  1. For adults with mild pain, offer a trial of paracetamol alone or in combination with codeine or a nonsteroidal anti-inflammatory drug (NSAID), such as ibuprofen.
  2. Consider oral corticosteroids in the first 2 weeks following rash onset in immunocompetent adults with localized shingles if pain is severe, but only in combination with antiviral treatment.
162
Q

What strains of herpes simplex are there?

A

Type 1: primary causes oral lesions but can Genital lesions

Type 2: only causes genital lesions

163
Q

what is the clinical presentation of herpes simplex?

A

Rash: grouped painful, itch vesicles on an erythematous base that burst to form ulcers, crust over and then heal without scarring

oral: gingiva-stomatitis

additional symptoms: tingling, malaise, dysuria for genital lesions

can be acute or recurrent with recurrence happening due to virus laying dormant and not being eradicated with treatment

recurrent disease can present with erythema multiforme

164
Q

give specific examples of herpes simplex?

A

Herpetic whitlow: inoculation of virus in the finger to produce a solitary painful lesion

Eczema Herpeticum: typically occurs in children with atopic eczema. Is a disseminated infection that presents with monomorphic, punched out lesions

165
Q

how do you manage herpes simplex?

A

High dose acyclovir (oral or IV)

analgesia

education about spread

166
Q

what does HPV cause?

A

Cervical cancer

warts: raised papules with a firm, roughened surface. Can also be described as papillomatous

167
Q

what strains of HPV are there?

A

HPV 1-4: cause common warts

HPV 6/11: genital warts

HPV 16/18: cervical cancer

168
Q

what is the management of HPV?

A

common: salicylic acid, cryotherapy and imiquimod

Genital: Podophyllin and imiquimod

169
Q

what is the causative organism of molluscum contagiousum?

A

pox virus

170
Q

what is the causative organism of erythema infectiosum?

A

Parvovirus B19 - can be detected by B19 IgM

171
Q

what is the clinical presentation of molluscum contagiousum?

A

Self limiting viral infection seen in children, with lesions typically developing on head, neck and trunk

more commonly seen in those with atopic eczema

Rash: itchy, solid, pearly pink papules with umbilicated centre

172
Q

what is the clinical presentation of erythema infectiosum?

A

self limiting infection, most commonly in children

Rash:

initially: bilateral macular erythema on cheeks
subsequent: maculopapular with lacy ertyhema on trunk and limbs

173
Q

what is the causative organism of Orf?

A

parapox virus - found in sheep

174
Q

what is the clinical presentation of Orf?

A

usually seen in farmers

Lesion: single, firm fleshy nodules on hand

Self limiting

175
Q

what is the causative organism of Hand, foot and mouth disease?

A

coxsackie virus

176
Q

what are the clinical presentation of Hand, foot and mouth disease?

A

Prodromal fever malaise

rash: grey vesicles surrounded by erythema and mouth ulcers

self limiting

177
Q

what are the causative organisms of Dermatophyte infections?

A

Trichophyton rubrum – 70%. (only infects humans)
Trichophyton mentagraphytes – 20%.
Microsporum canid – rare.

178
Q

what are dermatophyte infections?

A

fungal infections that invade and grow in dead keratin

spread is mainly indirect (man to man)

179
Q

what are the sign and symptoms of dermatophyte infections?

A

lesion: round scaly itchy whose edge is inflamed than its centre

wet maceration in flexural areas

it is called tinea followed by the part affected:

  1. Tinea capitis - scalp
  2. Tinea barbae - beard
  3. Tinea corpis - body
  4. Tinea mannum - hand
  5. Tinea unguium - nail
  6. Tinea cruris - groin
  7. Tinea pedis - foot: often only one foot involved
180
Q

how do you diagnose dermatophyte infections?

A

skin scrapings from the active edge of a lesion or nail clippings

either used for microscopy or culture

181
Q

how do you manage dermatophyte inefections?

A

Localised: topical antifungal e.g. terbinafine or imidazole creams twice daily for 2 weeks

Nails: difficult to treat - use terbinafine

toe nails is 3-6 months finger nails - 6-12 weeks

182
Q

what is candida albicans?

A

a yeast infection

183
Q

what are the signs and symptoms of candida albicans?

A

often pink and most satellite lesions

mainly affect the following areas:

  1. mouth
  2. vagina
  3. glans of penis
  4. skin folds (under breasts, groin areas, abdominal and nappy area in babies)
  5. toe web
  6. nail areas
184
Q

how do you diagnose candida albicans?

A

swab for culture

oral candida wipes off with a spatula - unlike lichen planus

185
Q

how do you manage candida albicans?

A

Skin: imidazole creams

mouth: Nystatin
vagina: imidazole cream +/- pessary

186
Q

what is pityriasis versiocolor?

A

yeast infection caused by malassezia species

187
Q

what is the clinical presentation of pityriasis versiocolor

A

hypopigmented or hyperpigmented scaly macules on the upper back trunk and back

risk factors:

living or staying in a warm, moist environment, including the UK, in the summer

sweating excessively (hyperhidrosis)

creams, dressings or clothing that do not allow your skin to breathe

being malnourished

having a weakened immune system

being a teenager or in your early 20s

188
Q

how do you manage pityriasis versicolor?

A

imidazole cream for localised disease

antifungal shampoo

oral antifungals for resistant disease

189
Q

what is impetigo?

A

contagious superficial skin infection caused by staph aureus (+/- strep pyogenes)

190
Q

what is the clinical presentation of impetigo?

A

normally presents in ages 2-5

Lesions:

normally starts around nose and face

well defined lesions with honey-coloured crust on erythematous base (+/- superficial flaccid blisters)

191
Q

how do you manage impetigo?

A

1st:topical fusidic acid for localised infection

severe: Flucloxacillin IV/PO (5-7 days)
Clarithromycin IV/PO if penicillin allergic

192
Q

what is cellulitis?

A

acute infection of skin and soft tissues

193
Q

what are the causes of cellulitis?

A

Beta haemolytic streps +/- staphs

194
Q

what is erysipelas?

A

superficial form of cellulitis caused by strep pyogenes

usually affects the face and is a spreading rash with a fever

195
Q

what is the clinical presentation of cellulitis?

A

Rash often seen on legs

signs:

pain

swelling

erythema

warmth

systemic upset

local lymphadenopathy

196
Q

how do you manage cellulitis?

A

Flucloxacillin 1g qds (If penicillin allergic: Doxycycline 100mg bd PO)

severe: Iv flucloxacillin or vancomycin if allergic

197
Q

what is scabies?

A

a highly contagious common disorder particularly affecting children and young adults

caused by sarcoptes scabei

198
Q

How does scabies occur?

A

usually direct spread (person to person)

female mite digs a burrow and lays eggs which hatch as lave - the itch and rash is due to allergic sensitivity to the mite or its products

199
Q

what is the clinical presentation of scabies?

A

very itchy papules, vesicles, pustules and nodules affecting finger-webs, wrist flexures, abdomen, buttocks and groins

itch is often worst at night

young infants: palms and soles are characteristically involved

Norwegian scabies: highly contagious which is normally seen in the elderly or immunocompromised

200
Q

how do you manage scabies?

A

1st Permethrin - most effective topical agent

2nd choice: ,malathion - don’t use if pregnant or <6months old

severe: oral ivermectin

201
Q

what is the clinical presentation of head lice?

A

itch and papular rash on the nape (back of head)

lice can be visible

202
Q

how do you manage headlice?

A

lotion options:

Malathion

Dimeticone

Isopropyl myristate

203
Q

what is lyme diease?

A

a disease caused by a tick bite

the causative organism is Borrelia Burgdorferi

204
Q

what is the clinical presentation of Lyme disease?

A
  1. erythema chornicium migrans - annular erythematous lesions that looks like a bullseye. take 2 weeks to form after bite
  2. systemic symptoms of malaise and arthralgia and firm bluish/red swelling on ears and nipples. occurs after 6 months
  3. bluish discolouration and atrophy of the skin. systemic symptoms can be variable and include chronic pain
205
Q

how do you diagnose lyme disease?

A

serology

206
Q

how do you manage lyme disease?

A

remove tick

Doxycycline 100mg 2-3 weeks

amoxicillin 500mg TDS 2-3 weeks

207
Q

what is the definition of a leg ulcer?

A

any break in the skin of the lower leg above the ankle

which has been present for more than 4 weeks

208
Q

what are the normal ranges of ABPI?

A

0.8 - 1.3

209
Q

what ranges of ABPI show vascular disease?

A

less than 0.8

210
Q

compare venous and arterial ulcer in terms of the border?

A

venous have a much more shallow edge/border

211
Q

where do venous ulcers tend to develop?

A

around the malleoli

212
Q

what are the 5 layers of the scalp?

A 
Skin
Connective tissue
Aponeurosis
Loose connective tissue
Parietal bone
213
Q

which skin condition is alopecia areata associated with?

A

atopic dermatitis

214
Q

what is alopecia totoalis?

A

baldness effecting the whole scalp

215
Q

what is alopecia universalis?

A

baldness effecting the whole body

216
Q

what skin condition is behcet disease associated with?

A

erythema nodosum

other symptoms:

ophthalmic lesions e.g. uveitis and retinitis

recurrent painful genital ulcers

217
Q

what is steven Johnston syndrome/ toxic epidermal necrolysis (TEN)?

A

conditions which are type IV hypersensitivity reactions characterised by necrosis and detachment of the epidermis

SJS is more mild than TEN

SJS only covers <10% of the body

TEN covers >30% of the body

218
Q

what are the causes of SJS/TEN?

A

mainly drugs:

sulfonamides

antiepileptics

penicillins

cephalosporins

allopurinol

NSAIDs

trimoxazole

219
Q

what are the signs and symptoms of SJS/TEN?

A

May have Flu like symptoms by skin involvement:

widespread painful dusky erythema

then necrosis of large sheets of epidermis

ulcerations - conjunctivae, oral cavity, labia and urethra

220
Q

how do you diagnose SJS/TEN?

A

classified via SCORTEN score - measures extent of skin desquamation

221
Q

how do you manage SJS/TEN?

A
  • Cessation of causative drug.
  • Supportive care.
  • Emollients.
  • Iv Ig.
222
Q

what is erythema nodosum?

A

it is a pannicuitis and typically occurs on the shins and is raised in nature (nodular)

it is painful

it is associated with TB and sarcoidosis and IBD

chest radiograph can be used for diagnosis to exclude serious causes.

use NSAIDs for skin rash

223
Q

what is erythema multiforme?

A

skin immune reaction which causes target lesions

first found on hands and feet and then limbs and trunk

fades over 2-4 weeks but recurrence is common

224
Q

what condition are Kaposi sarcomas associated with?

A

AIDS

they are nodules, papules or macules which can be red, purple, brown or black

225
Q

what is a rodent ulcer?

A

basal cell carcinoma

226
Q

what is cutaneous larva migrans?

A

most common tropical dermatosis

caused by percutaneous penetration and subsequent migration of various nematode species

presentation: tupical snake like speriginous lesions

topical or oral thiobendazole is treatment of choice

227
Q

what is hyperlipidaemia type 3 caused by?

A

mutation in the apo-E gene resulting in increased chylomicron remnants

228
Q

A 3 year old boy presents on a sunny day in June. His mother reports he keeps crying and rubs at his skin when playing outside and this has been going on for a few weeks. His skin is sometimes a bit red, but there is never a rash and his skin is clear on examination now. He is skin type 1 with a few freckles evident, generally well, on no medication and there is no family history of skin problems?

A

Erythropoietic protoporphyria

229
Q

what does the virulence factor cytotoxin leukocidin do?

ii. which bacteria is it associated with?

A

causing necrolytic skin infections by directly killing leukocytes

ii. staph aureus

230
Q

State how the following four virulence act on the body :
Invasin

Adhesin

Aggressin

Modulin

Impedin

A

invasin → enables the organism to invade a host tissue,

Adhesin → enables binding of the organism to host tissue

Aggressin → causes damage to the host directly

Modulin → causes damage to the host indirectly

Impedin → enables the organism to avoid host defense mechanisms

231
Q

what is skin failure?

A

loss of normal temperature control with inability to:

maintain the core body temperature

failure to prevent percutaneous loss of fluid, electrolytes and protein, with resulting imbalance

failure of the mechanical barrier to prevent penetration of foreign materials

232
Q

Regarding topical steroids, which ONE of the following is TRUE?

Select one:
They have a vaso-dilatory effect

They cross the plasma membrane by endocytosis

They increase cell proliferation

They are lipophilic

Absorption is greater across hyperkeratotic than atrophic skin

A

lipophilic

233
Q

Which of the following is a component of the strain of MRSA (Methicillin Resistant Staphylococcus Aureus) which causes severe skin infection such as necrotising fasciitis?

Select one:
Hyaluronidase
Coagulase 
Protein A
Panton Valentine Leukocidin
Fibrinolysin
A

panton valentine leukocidin

234
Q

Acute intermittent porphyria is due to impaired function of which enzyme?

A

Porphobilinogen deaminase

235
Q

topical steroids are lipophilic true or false?

A

true

236
Q

what type of infection are the following conditions:

Ring worm

Shingles

Head lice

Necrotising fasciitis

A

ring worm - fungal

shingles - viral

head lice - parasitic

necrotising fasciitis - bacterial

237
Q

Describe the following topical treatments:

creams

Ointments

Lotions

Gels

Pastes

A

Creams → Semisolid emulsion of oil in water, contains preservative, cosmetically acceptable, non greasy

Ointments → Semisolid grease/oil, no preservative, less cosmetically attractive, greasy

Lotions → Liquid Formulation

Gels → Thickened aqueous solutions,

Pastes → Semisolids, stiff, greasy, difficult to apply, often used in cooling, drying, soothing bandages

238
Q

how do you diagnose scabies?

A

Skin scrapings for microscopy

239
Q

how do you diagnose impetigo?

A

Swab of lesion sent in bacterial container for microscopy and culture

240
Q

how do you diagnose shingles?

A

Swab of lesion fluid sent in Viral container for PCR

241
Q

how do you diagnose ringworm?

A

Skin scraping for microscopy and culture, and woods light

242
Q

Which ONE of the following is true regarding topical therapies?

Select one:

A typical adult body requires 10g of ointment for one all over application

Creams are more likely than ointments to cause contact sensitisation

Ointments are more cosmetically acceptable to patients than creams

Occluding a treated area with clingfilm will reduce topical therapy penetration

Lotions are useful for very dry and hyperkeratotic eczema

A

Creams are more likely than ointments to cause contact sensitisation

243
Q

what conditions make up the atopic triad?

A

hayfever

asthma

atopic eczema

244
Q

The woman is a 20 year old waitress. She is already very conscious of her skin at work and does not want to have to put any greasy or smelly treatment on as it may show on her shirt.

Which of the following therapies would be best suited for her?

Select one:

Coal tar solution

Topical antibiotic gel

Very potent steroid ointment

Dithranol cream

Vitamin D analogue cream

A

vitamin D analogue

this is because:

Coal tar solution smells and can stain.

Topical antibiotics are not indicated as her condition is not caused by bacteria.

Very potent steroid ointment is not recommended due to the long term affects of steroid use.

Dithranol cream is a short contact therapy, time consuming to use and can stain.

Vitamin D analogue cream would be the 1st line treatment in her case as it is effective, easy to apply, non greasy and non-smelly.

245
Q

what is “The disposition to judge things as being more likely, or frequently occurring, if they readily come to mind”.

A

availability

246
Q

what is “The tendency to perceptually lock onto salient features in the patient’s initial presentation too early in the diagnostic process, and failing to adjust this initial impression in the light of later information”.

A

anchoring

247
Q

Which of the following statements are TRUE in patients with leg ulcers? (Must select ALL correct answers to gain marks)
Select one or more:

Ulcers can lead to malignant change

Contact sensitivity to topical treatments and bandages frequently develops

Systemic antibiotics are needed in all ulcers as
infection is inevitable

Compression bandages should be used to treat all ulcers that occur below the knee

Ankle exercises are important to maintain joint mobility with ulcers near the ankle

A

ankle exercises are important to maintain joint mobility with ulcers near the ankle

Ulcers can lead to malignant change

Contact sensitivity to topical treatments and bandages frequently develops

248
Q

When excising skin, which of the following methods provides the best aesthetic result.

Select one:

An elliptical excision with the scalpel cutting at 45 degrees to the surface of the skin

An elliptical excision with the scalpel cutting at 90 degrees to the surface of the skin

A circular excision with the scalpel cutting at 90 degrees to the surface of the skin

A circular excision with the scalpel cutting at 45 degrees to the surface of the skin

A

An elliptical excision with the scalpel cutting at 90 degrees to the surface of the skin

249
Q

Malignant melanomas can usually be effectively treated with combined therapy of chemotherapy and radiotherapy true or false?

A

false - Due to their embryological origins and the high amount of melanin within them, malignant melanomas do not respond well to chemotherapy or radiotherapy even when used in combination. The most effective treatment is early radical surgery

My Dermatology (3 decks)

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