Dermatology

Question 1

macule

Answer 1

a flat area of altered colour e.g. freckle or naevi

Question 2

patch

Answer 2

a larger area of altered colour or texture compared to a macule

e.g. naevus flammeus/port wine stain - a congenital lesion consisting of small blood vessels in the skin that are open all the time

Question 3

papule vs pustule

Answer 3

papule = solid raised lesion <0.5cm in diameter (some sources say <1cm)
e.g. xanthomata or some moles

pustule = similar to papule but have a white centre due to pus build up

Question 4

nodule

Answer 4

solid raised lesion >0.5cm in diameter

e.g. pyogenic granuloma (a vascular lesion) or a wart

Question 5

plaque

Answer 5

palpable scaling raised lesion >0.5cm

e.g. psoriasis

Question 6

vesicle vs bulla

Answer 6

vesicle = <0.5cm

bulla = >0.5cm e.g. a burn blister

Question 7

wheal

Answer 7

transient raised lesion due to dermal oedema

the fluid is within the dermis layer rather than higher up - like in a vesicle or bulla

are characteristically evanescent (i.e. lasting less than 24 hours)

e.g. urticaria

Question 8

boil/furuncle vs carbuncle

Answer 8

boil/furuncle = staphylococcal infection around or within a hair follicle

carbuncle = staphylococcal infection of adjacent hair follicles as well (multiple boils/furuncles)

Question 9

lichenification

Answer 9

Thickening (and hyperpigmentation) of the epidermis in response to excessive itching or rubbing of the skin (a secondary skin lesion)

Question 10

crust

Answer 10

• Rough surface consisting of dried serum, blood, bacteria and cellular debris
• That has exuded through an eroded epidermis e.g. from a burst blister
• E.g. impetigo

Question 11

types of scar

Answer 11

May be atrophic (thinning), hypertrophic (hyperproliferation within wound boundary), or keloidal (hyperproliferation beyond wound boundary)

Question 12

hirsutism vs hypertrichosis

Answer 12

hirsutism - androgen-dependent hair growth in a female

hypertrichosis - non-androgen dependent pattern of excessive hair growth e.g. in pigmented naevi

Question 13

onycholysis associations

Answer 13

associated with trauma, psoriasis, fungal nail infection, hyperthyroidism

Question 14

pitting associations

Answer 14

psoraisis, eczema and alopecia acreata

Question 15

medication risk factors for acne vulgaris

Answer 15

androgens, corticosteroids, antiepileptics, isoniazid, lithium, ACTH

Question 16

pathophysiology of acne vulgaris

Answer 16

1. abnormal follicular differentiation - in acne keratinocytes are retained and accumulate due to increased cohesiveness instead of being shed
2. sebaceuous gland hyperplasia and excess sebum production (due to stimulation by androgens)
3. propionibacterium acnes colonisation (gram positive non-motile rods)
4. inflammation and immune response

Question 17

open vs closed comedone

Answer 17

open = blackhead
closed = whitehead

Question 18

cysts in acne vulgaris

Answer 18

most severe type of acne spot
look similar to boils
carry the greatest risk of permanent scarring

Question 19

acne vulgaris grading

Answer 19

mild
moderate
severe

depending on comedone count, number of inflammatory lesions and number of pseudocysts and scars

Question 20

acne vulgaris treatment

Answer 20

PATIENT EDUCATION
- e.g. emphasise it doesn’t mean skin is dirty
CONSERVATIVE
- don’t over wash face, use fragrance free/paraben free products, SPF, role of diet is controversial (emerging data suggests high GI diets may exacerbate)
MEDICAL
- topical retinoid alone (adapalene, tretinoin) or in combination with benzoyl peroxide
- topical antibiotic (e.g. clindamycin 1%)
- azelaic acid
- cream or lotions preferable with dry/sensitive skin and less greasy gels in oily skin
- if not responding to topical then consider oral Abx
- COC
- refer to derm if all failed for consideration of oral isotretinoin

Question 21

oral antibiotic for acne vulgaris

Answer 21

lymecycline or doxycycline for a max of 3 months

NB a topic retinoid or benzoyl peroxide should always be co-presrcibed with oral or topical ABx to reduce the risk of antibiotic resistance occuring

Question 22

follow up in acne vulgaris

Answer 22

review each treatment step at 8-12 weeks

If acne has cleared or almost cleared — consider maintenance therapy with topical retinoids (first line, if not contraindicated) or azelaic acid

Question 23

acne rosacea

Answer 23

chronic disorder of blood vessels and sebaceuos glands in central face regions

primarily affects the convexities of the face, cheeks, chin, nose and central forehead (but may also extend to the upper trunk)

symptoms; flushing, telangiectasia, erythema, rhinophyma, irritated eyes. episodes of remission and recurrence

Question 24

management of acne rosacea

Answer 24

PATIENT EDUCATION
- avoid irritants and sun over-exposure, CBT proven to help avoid facial flushing
CONSERVATIVE
- don’t overwash face
- use fragrance free/paraben free products, SPF
- review medications as some drugs may aggrevate flushing symptoms (CCBs) and flares (topical steroids)
MEDICAL
- topical metronidazole or azelaic acid
- if with papules then prescribe an oral Abx
EXTREME MEDICAL
- isoretrinoin
- IPL (intense pulsed light) for erythema with telangiectasia
- prominent rhinophyma –> plastic surgeon

for ocular - eyelid hygeine measures, ocular lubricants for dry eye

Question 25

oral antibiotic for acne rosacea

Answer 25

lymecycline, erythromycin, doxycycline or tetracycline

Question 26

follow up on those on isotretinoin

Answer 26

``` depression screen LFTs lipids - pancreatitis risk photosensitivity (SE) dry mucus membranes PPP - double contraception - condom + OCP ```

Question 27

solar keratosis (actinic keratosis)

Answer 27

small scaly macules or plaques localised in sun-exposed areas of the body - ill-defined typically in middle-aged men with fair skin

Question 28

what can solar keratosis (actinic keratosis) progress into

Answer 28

sqaumous cell carcinoma (SCC)

Question 29

removal of actinic keratosis

Answer 29

o Can be with cryotherapy o 5-FU (5-flurouracil – a chemotherapy drug) creams where the lesions are widespread o imiquimod cream (Diclofenac and retinoic acid are other drugs in cream or ointment form that are helpful when applied to milder actinic keratoses) o excision as an alternative to cryotherapy for large lesions o chemical peels o photodynamic therapy o curettage and cautery (where the affected skin is scraped away under LA)

Question 30

another name for Bowen's disease

Answer 30

squamous cell carcinoma in situ 1 in 20 – 1 in 30 will progress to cancer in untreated Bowen’s disease

Question 31

appearance of Bowen's disease vs actinic keratosis

Answer 31

bowen's disease = red or pink, scaly or crusty, flat or raised, possibly itchy area actinic keratosis = skin coloured, yellowish or erythematous ill defined small scaly macules or papules

Question 32

ABCDE

Answer 32

``` asymmetry border irregulatiry colour variation diameter >6mm evolution of the lesion ```

Question 33

name for melanoma in situ

Answer 33

lentigo maligna

Question 34

lentigo maligna

Answer 34

consists of malignant cells but does not show invasive growth - is confined to the epidermis unlike other types of melanoma, it is related to chronic sun exposure rather then infrequent intense exposure

Question 35

management of lentigo maligna

Answer 35

excision biopsy with a 2mm margin followed by WLE oe Mohs surgery to remove all the cells the other option is to watch the lesion carefully and biopsy if it becomes more suspicious

Question 36

seborrheic keratosis

Answer 36

benign skin tumour frequently found on the torso 75% of those aged 70 are affected - often arise in middle age cause unknown but HPV and sunlight are risk factors stuck on, brown/black appearance, painless but can cause itching

Question 37

management of seborrheic keratosis

Answer 37

diagnosed by clinical appearance (can use dermoscopy) or biopsy if unsure (e.g. isolated dark SK) manage - usually none required - Corticosteroids (topical betamethasone) can be used on irritated and itching seborrhoeic keratosis - They can also be removed if there are unsightly or rubbing against clothing with cryotherapy, curettage and cautery, cryotherapy, and laser therapy

Question 38

treatment of viral warts

Answer 38

watchful waiting debridement + salicyclic acid (an adjunct to this is duct tape occlusion) cryotherapy silver nitrate solution - applied every other day for 3-6 weeks curretage and cautery can be used for larger warts under LA

Question 39

dermatofibroma

Answer 39

nodules of the dermis that can develop in reaction to insect bites or trauma but exact cause is not clear ranges from pink to brown more common in women - often on the LL of young or middle ages adults treat if causing problemss (e.g. if unsightly)

Question 40

epidermoid cyst management

Answer 40

can safely be left alone - Can have Abx if become infected - Both epidermoid and pilar cysts can be removed under LA – but will leave a scar - Reasons for removal o If the cyst is unsightly and easily seen by others o If it interferes with everyday life, for example by catching on your comb o If the cyst becomes infected

Question 41

pyogenic granuloma

Answer 41

Vascular lesion that occurs on both mucosa and skin Rapidly developing bright-red or blood -crusted, pedunculated nodule Are an acquired form of haemangioma typically present at the site of localised trauma and are prone to bleeding usually managed with curettage and cautery, followed by histological examination to exclude melanoma recurrence is common

Question 42

layers split with a blisters

Answer 42

intra-epidermal split - causes blisters to rupture easily sub-epidermal split (between the epidermis and dermis) - blisters are less fragile

Question 43

epidermolysis bullosa

Answer 43

includes >30 inherited (usually dominant) conditions characterised by mechanical fragility of the skin and epithelial lined tissues like the mouth results from mutations within genes encoding for any of at least 20 structural skin proteins that hold the skin cells together

Question 44

diagnostic factors for epidermolysis bullosa

Answer 44

``` FHx mechanical fragility of the skin recurrent blisters and erosions poorly healing wounds onset of cutaneous signs at birth or early infancy ```

Question 45

diagnosis of epidermolysis bullosa

Answer 45

can be made on history alone if other family members are affected or take a skin biopsy and perform immunofluorescene antigenic mapping or just transmission electron microscopy

Question 46

treatment of epidermolysis bullosa

Answer 46

dressings, sterile drainage of large blisters, topical antibacterial agents, nutritional supplementatoin

Question 47

bullous pemphigoid

Answer 47

a chronic acquired autoimmune blistering disease characterised by autoantibodies against hemidesmosomal antigens (BP180 and BP230)

Question 48

presentation of bullous pemphigoid

Answer 48

may be preceded by a non-specific itchy rash | presents with tense blisters on the skin - usually affecting the trunk and limbs

Question 49

investigations for bullous pemphigoid

Answer 49

usually clinical but can skin biopsy a blister | look at with light micrscopy or direct immunofluorescne testing

Question 50

treatment of bullous pemphigoid (v similar to pemphigus vulagris)

Answer 50

wound dressings to prevent infection topical steroids or topical tacrolimus oral steroids + Abx for widespread disease sedating antihistamines for itch

Question 51

3 categories of pemphigus

Answer 51

pemphigus vulgaris pemphigus foliaceus paraneoplastic pemphigus

Question 52

pemphigus vs pemphigoid pemphigus e.g. pemphigus vulgaris pemphigoid - bullous pemphigoid

Answer 52

pemphigoid affects a lower layer of skin between the epidermis and dermis --> TENSE blisters that do not break easily pemphigus affects the epidermis --> easily rupture pemphigus vulgaris is more common

Question 53

pemphigus vulgaris presentation

Answer 53

easily ruptured blistering of the skin, mucosa or both (mucosal involvement can preceded skin involvement) Nikolsky’s sign - The skin is very fragile, and the top layer is often easily removed with lateral pressure Pruritic scalp, Bloody nose, Painful skin

Question 54

pemphigus foliaceus

Answer 54

blisters are more superficial than in pemphigus vulgaris - the antibody targets a desmoglein which links keratinocytes at a higher level confined to SKIN - does not affect mucus membranes like pemphigus vulgaris causes scaly, crusty lesions (blisters themselves are rarely seen)

Question 55

Dermatitis herpetiformis

Answer 55

blistering skin condition related to coeliac disease - IgA antibodies against gliadin

Question 56

presentation and diagnosis of dermatitis herpetiformis

Answer 56

intensely itchy blisters are distributed symmetrically on extensor surfaces come and go often misdiagnosed - need a skin biopsy and blood test for anti-tTG (tissue transglutaminase)

Question 57

treatment for dermatitis herpetiformis

Answer 57

strict gluten-free diet steroid creams dapsone (oral) - an antibiotic that alleviates the rash and itching

Question 58

erythroderma define

Answer 58

intense and widespread reddening of the skin (at least 90%) due to inflammatory skin disease often preceded with exfoliation of the skin (peeling off)

Question 59

another word for idiopathic erythroderma

Answer 59

red man syndrome

Question 60

causes of erythroderma

Answer 60

``` 30% idiopathic drug eruption dermatitis, especially atopic dermatitis psoriasis (especially after the withdrawal of systemic steroids) pityriasis rubra pilaris eczema lymphoma ``` systemic diseases: haematological malignancies, GvHD, HIV

Question 61

presentation of erythroderma

Answer 61

warm skin itchiness eyelid swelling may result in ectropion scaling that may lead to hair loss

Question 62

complications of erythroderma

Answer 62

heat loss dehydration and electrolyte abdnormalities secondary skin infection - impetigo or cellulitis hypoalbuminaemia from protein loss and increased metabolic rate causes oedeam high-output HF

Question 63

urticaria vs angiodema

Answer 63

urticaria (hives) = red, blanching, oedematous 9confined to DERMAL layer), pruritic lesions approximately 40% of urticaria is associated with angiodema angiodema = swelling involving the deeper layers of the subdermis (subcutaneous tissue)

Question 64

acute vs chronic angiodema

Answer 64

acute = <6 weeks causes - allergic (drug, foods), insect bites chronic = >6 weeks causes - more difficult to tell - approx 40% are thought to be autoimmune in nature - while many cases are thought to be idiopathic

Question 65

pathophysiology of urticaria

Answer 65

mast cells activation --> release vasoactive mediators that lead to vasodilation and increased permability --> pruritus and oedema NB angiodema due to same response but may also involve the kinin system

Question 66

investigations for urticaria

Answer 66

FBC - infection, anaemic, or findings of chronic illness and establishes a baseline for monitoring CRP anti-IgE receptor antibody skin biopsy - may show urticarial vasculitis in setting of atypical urticarial lesions complement levels - low C4 suggests hereditary or acquired angiodema. C1 esterase inhibitor level decreased in hereditary. C1q is normal in hereditary but low in acquired

Question 67

treatment of acute urticaria without airway involvement

Answer 67

trigger identification and avoidance plus H1 receptor antagonist (antihistamine) e.g. loratadine, desloratadine plus systemic steroids for severe acute urticaria and angiodema

Question 68

SE of oral steroids

Answer 68

adrenal suppression, weight gain, osteoporosis, hyperglycaemia, acne, easy bruising, hypertension, swollen puffy face, difficulty sleeping