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MRCP Combined > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What malignancy is Acanthosis nigricans assoc. with?

A

Acanthosis nigricans - Gastric cancer

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2
Q

what malignancy is Acquired ichthyosis and erythroderma assoc with?

A

Acquired ichthyosis and erythromderma - Lymphoma

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3
Q

what malignancy is Acquired hypertrichosis lanuginosa assoc. with?

A

Acquired hypertrichosis lanuginosa - Gastrointestinal and lung cancer

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4
Q

what malignancy is Erythema gyratum repens assoc with?

A

Erythema gyratum repens - Lung Ca

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5
Q

what malignancy is Dermatomyositis assoc with?

A

Dermatomyositis - Bronchial and breast ca

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6
Q

what malignancy is Migratory thrombophlebitis assoc. wit?

A

Migratory thrombophlebitis - Pancreatic cancer

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7
Q

what malignancy is Necrolytic migratory erythema assoc. with?

A

Necrolytic migratory erythema - Glucagonoma

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8
Q

what malignancy is Pyoderma gangrenosum assoc. with?

A

Pyoderma gangrenosum - Myeloproliferative disorders

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9
Q

what malignancy is Sweet’s syndrome assoc with?

A

Sweet’s syndrome - Hematological Ca e.g. Myelodysplasia - tender, purple plaques

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10
Q

What malignancy is Tylosis assoc. with?

A

Tylosis - Oesophageal cancer

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11
Q

what is polymorphic eruption of pregnancy?
-what trimester is this seen in?
-where do lesions appear?
-what is the management?

A

Polymorphic eruption of pregnancy
• Pruritic condition associated with last trimester
• Lesions often first appear in abdominal striae
• Management depends on severity: emollients, mild potency topical steroids and oral steroids
may be used

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12
Q

what is pemphigoid gestionus?
-where do these develop?
-what trimester is this assoc. with?
-what is the management?

A

Pemphigoid gestationis
• Pruritic blistering lesions
• Often develop in peri-umbilical region, later spreading to the trunk, back, buttocks and arms
• Usually presents 2nd or 3rd trimester and is rarely seen in the first pregnancy
• Oral corticosteroids are usually required

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13
Q

• Lupus vulgaris (accounts for 50% of cases)
• Erythema nodosum
• Scarring alopecia
• Scrofuloderma: breakdown of skin overlying a tuberculous focus
• Verrucosa cutis
• Gumma
are all assoc with…

A

TB

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14
Q

what is the most common form of cutaneous TB? describe the lesion?

A

Lupus vulgaris is the most common form of cutaneous TB seen in the Indian subcontinent. It generally occurs on the face and is common around the nose and mouth. The initial lesion is an erythematous flat plaque which gradually becomes elevated and may ulcerate later

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15
Q

Describe skin condition in hypothyroid

A

• Dry (anhydrosis), cold, yellowish skin
• Non-pitting oedema (e.g. hands, face)
• Dry, coarse scalp hair, loss of lateral
aspect of eyebrows
• Eczema
• Xanthomata

Pruritus in both

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16
Q

Describe skin condition in hyperthyroid

A

• Pretibial myxoedema: erythematous, oedematous lesions above the lateral malleoli
• Thyroid acropachy: clubbing
• Scalp hair thinning
• ↑ sweating

Pruritus in both

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17
Q

Describe the lesions in erythema multiforme

A

• Target lesions (typically worse on peripheries e.g. Palms and soles)
• Severe = stevens-johnson syndrome (blistering and mucosal involvement)

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18
Q

• Idiopathic
• Bacteria: mycoplasma, Streptococcus
• Viruses: herpes simplex virus, Orf
• Drugs: penicillin, sulphonamides,
carbamazepine, allopurinol, NSAIDs,
oral contraceptive pill, nevirapine
• Connective tissue disease e.g.
Systemic lupus erythematosus
• Sarcoidosis
• Malignancy

are all causes of…

A

erythema multiforme

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19
Q

what may alopecia be subdivided into?

A

Alopecia may be divided into scarring (destruction of hair follicle) and non-scarring (preservation of hair follicle)

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20
Q

describe the causes of scarring alopecia

A

• Trauma, burns
• Radiotherapy
• Lichen planus
• Discoid lupus
• Tinea capitis - scarring would develop in untreated tinea capitis if a kerion develops
• TB

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21
Q

what are the causes of non-scarring alopecia?

A

• ♂-pattern baldness
• Drugs: cytotoxic drugs, carbimazole,
heparin, oral contraceptive pill,
colchicine
• Nutritional: iron and zinc deficiency
• Autoimmune: alopecia areata
• Telogen effluvium (hair loss following stressful period e.g. Surgery)
• Trichotillomania “hair loss from a patient’s repetitive self-pulling of hair”

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22
Q

what is alopecia areata? what does this cause?

A

Alopecia areata is a presumed autoimmune condition causing localised, well demarcated patches of hair loss. At the edge of the hair loss, there may be small, broken ‘exclamation mark’ hairs

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23
Q

what is the prognosis of alopecia areata?

A

Hair will regrow in 50% of patients by 1 year, and in 80-90% eventually. Careful explanation is therefore sufficient in many patients.

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24
Q

list the treatment options of alopecia areata?

A

Other treatment options include:
• Topical or intralesional corticosteroids
• Topical minoxidil
• Phototherapy
• Dithranol
• Contact immunotherapy • Wigs

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25
Q

what are 4 types of shin lesion?

A

• Erythema nodosum
• Pretibial myxedema
• Pyoderma gangrenosum
• Necrobiosis lipoidica diabeticorum

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26
Q

what is the lesion:
• Symmetrical, erythematous, tender, nodules which heal without scarring
• Most common causes are streptococcal infections, sarcoidosis, inflammatory bowel disease and
drugs (penicillins, sulphonamides, oral contraceptive pill)

A

erythema nodosum

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27
Q

what is the lesion:
• symmetrical, erythematous lesions seen in Graves’ disease
• shiny, orange peel skin

A

pretibial myxoedema

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28
Q

what is the lesion:
• Initially small red papule
• Later deep, red, necrotic ulcers with a violaceous border
• Idiopathic in 50%, may also be seen in inflammatory bowel disease, connective tissue disorders
and myeloproliferative disorders

A

pyoderma grangrenosum

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29
Q

what is the lesion:
• Shiny, painless areas of yellow/red skin typically on the shin of diabetics
• Often associated with telangiectasia

A

Necrobiosis lipoidica diabeticorum

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30
Q

erythema nodosum:
-what is this the inflammation of?
-where are the lesions?
-what is the prognosis?
-do they scar?

A

• Inflammation of subcutaneous fat
• Typically causes tender, erythematous,
nodular lesions
• Usually occurs over shins, may also occur
elsewhere (e.g. Forearms, thighs)
• Usually resolves within 6 weeks
• Lesions heal without scarring

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31
Q

what are different causes of erythema nodosum?

A

• Infection: streptococci, TB, brucellosis
• Systemic disease: sarcoidosis, inflammatory
bowel disease, Behcet’s
• Malignancy/lymphoma
• Drugs: penicillins, sulphonamides,
combined oral contraceptive pill
• Pregnancy

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32
Q

what are the features of pyoderma gangrenosum:
-where are these?
-how does this develop?
-assoc. symptoms?

A

• Typically on the lower limbs
• Initially small red papule
• Later deep, red, necrotic ulcers with a violaceous border
• May be accompanied systemic systems e.g. Fever, myalgia

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33
Q

long list of causes of pyoderma gangrenosum:
-name a few

A

• Idiopathic in 50%
• IBD: ulcerative colitis, crohn’s
• Rheumatoid arthritis, SLE
• Myeloproliferative disorders
• Lymphoma, myeloid leukemias
• Monoclonal gammopathy (IgA)
• Primary biliary cirrhosis

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34
Q

what is the management of pyoderma gangrenosum?

A

• The potential for rapid progression is high in most patients and whilst topical and intralesional steroids have a role in management most doctors advocate oral steroids as first-line treatment
• Other immunosuppressive therapy, for example Cyclosporin and infliximab, have a role in
difficult cases

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35
Q

what is seborrhoeic dermatitis?
-what is this caused by?
-is this common and what patients are commonly affected?

A

Seborrhoeic dermatitis in adults is a chronic dermatitis thought to be caused by an inflammatory reaction related to a proliferation of a normal skin inhabitant, a fungus called Malassezia (formerly known as Pityrosporum ovale). It is common, affecting around 2% of the general population. Seborrhoeic dermatitis is more common in patients with Parkinson’s disease

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36
Q

describe common features of seborrhoeic dermatitis

A

• Eczematous lesions on the sebum-rich areas: scalp (may cause dandruff), periorbital, auricular and nasolabial folds
• Otitis externa and blepharitis may develop

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37
Q

what are two assoc. conditions with seborrhoeic dermatitis?

A

Associated conditions include
• HIV
• Parkinson’s disease

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38
Q

what is the management for scalp disease in seborrhoeic dermatitis?

A

• Over the counter preparations containing zinc pyrithione (‘Head & Shoulders’) and tar (‘Neutrogena T/Gel’) are first-line
• The preferred second-line agent is ketoconazole
• Selenium sulphide and topical corticosteroid may also be useful

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39
Q

what is the management for face and body disease in seborrheoic dermatitis?

A

Face and body management
• Topical antifungals: e.g. Ketoconazole
• Topical steroids: best used for short periods
• Difficult to treat - recurrences are common

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40
Q

where is venous ulceration typically seen?

A

Venous Ulceration is typically seen above the medial malleolus

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41
Q

what are the investigations for venous ulceration?

A

Investigations
• Ankle-brachial pressure index (ABPI) is important in non-healing ulcers to assess for poor arterial flow which could impair healing
• A ‘normal’ ABPI may be regarded as between 0.9 - 1.2. Values below 0.9 indicate arterial disease. Interestingly, values above 1.3 may also indicate arterial disease, in the form of false- negative results secondary to arterial calcification (e.g. In diabetics)

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42
Q

what is the management for venous ulceration?

A

• Compression bandaging, usually four layer (only treatment shown to be of real benefit)
• Oral pentoxifylline (Trental®), a peripheral vasodilator, improves healing rate
• Small evidence base supporting use of flavinoids
• Little evidence to suggest benefit from hydrocolloid dressings, topical growth factors,
ultrasound therapy and intermittent pneumatic compression

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43
Q

what is the most important factor in determining prognosis in malignant melanoma

A

Malignant Melanoma: the invasion depth of a tumour (Breslow depth) is the single most important factor in determining prognosis of patients with malignant melanoma

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44
Q

What is the approx 5 year survival for malignant melanoma with a breslow thickness of:
< 1 mm -
1 - 2 mm -
2.1 - 4 mm -
> 4 mm -

A

< 1 mm - 95-100%
1 - 2 mm - 80-95%
2.1 - 4 mm - 60-75%
> 4 mm - 50%

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45
Q

describe the general treatment of impetigo

A

Impetigo - topical fusidic acid → oral flucloxacillin / topical mupirocin

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46
Q

what is the treatment of impetigo and Limited, localised disease

A

• Topical fusidic acid is first-line
• Topical retapamulin is used 2nd-line if
fusidin is ineffective or not tolerated
• MRSA is not susceptible to either fusidic acid or retapamulin. Topical mupirocin (Bactroban) should be used in this
situation

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47
Q

what is the treatment of extensive disease in impetigo?

A

Extensive disease
• Oral flucloxacillin
• Oral erythromycin if penicillin allergic

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48
Q

what is erythema ab igne?
-what can this develop into?

A

Erythema ab igne is a skin disorder caused by over exposure to infrared radiation. Characteristic features include erythematous patches with hyperpigmentation and telangiectasia. A typical history would be an elderly women who always sits next to an open fire (ovens)
If the cause is not treated then patients may go on to develop squamous cell skin cancer

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49
Q

what is actinic keratoses and what does this develop as a consequence of?

A

Actinic keratoses, or solar, keratoses (AK) is a common premalignant skin lesion that develops as a consequence of chronic sun exposure

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50
Q

what are the features of actinic keratoses?

A

• Small, crusty or scaly, lesions
• May be pink, red, brown or the same color as the skin
• Typically on sun-exposed areas e.g. Temples of head
• Multiple lesions may be present

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51
Q

what are different management options of actinic keratoses?

A

Management options include
• Prevention of further risk: e.g. Sun avoidance, sun cream
• Fluorouracil cream: typically a 2 to 3 week course. The skin will become red and inflamed -
sometimes topical hydrocortisone is given following fluorouracil to help settle the inflammation
• Topical diclofenac: may be used for mild AKs. Moderate efficacy but much fewer side-effects
• Topical imiquimod: trials have shown good efficacy
• Cryotherapy
• Curettage and cauter

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52
Q

what is Necrobiosis lipoidica? what condition is this assoc. with?

A

Necrobiosis lipoidica
o Shiny, painless areas of yellow/red/brown skin typically on the shin o Often associated with surrounding telangiectasia

Diabetes mellitus

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53
Q

what is granuloma annulare?
what is this assoc. with?

A

• Granuloma annulare*
o Papular lesions that are often slightly hyperpigmented and depressed centrally
*it is not clear from recent studies if there is actually a significant association between diabetes mellitus
and granuloma annulare, but it is often listed in major textbooks

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54
Q

• Infection
o Candidiasis
o Staphylococcal • Neuropathic ulcers
• Vitiligo
• Lipoatrophy

are all assoc with…

A

diabetes

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55
Q

what is lichen planus?

A

Planus: Purple, Pruritic, Papular, Polygonal rash on flexor surfaces. Wickham’s striae over
surface. Oral involvement common

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56
Q

what is lichen sclerosus?

A

Sclerosus: itchy white spots typically seen on the vulva of elderly women

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57
Q

what is lichen planus most likely caused by?

A

Is a skin disorder of unknown etiology; most probably being immune mediated

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58
Q

describe the features of lichen planus

A

• Itchy, papular rash most common on the
palms, soles, genitalia and flexor surfaces
of arms
• Rash often polygonal in shape, ‘white-lace’
pattern on the surface (wickham’s striae)
• Koebner phenomenon seen
• Mucous membrane involvement
• Nails: thinning of nail plate, longitudinal
ridging

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59
Q

what 3 different drugs can causes lichenoid drug eruptions?

A

Lichenoid drug eruptions - causes:
• Gold
• Quinine
• Thiazides

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60
Q

what is lichen sclerosus caused by?

A

Was previously termed lichen sclerosus et atrophicus. It is an inflammatory condition which usually affects the genitalia and is more common in elderly ♀s. Lichen sclerosus leads to atrophy of the epidermis with white plaques forming

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61
Q

what are the features of lichen sclerosus
-what investigation may need to be performed

A

Features
• Itch is prominent
A biopsy is often performed to exclude other diagnoses

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62
Q

what is the management of lichen sclerosus?

A

Management
• Topical steroids and emollients
• ↑ risk of vulval cancer

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63
Q

what is scabies caused by?

A

Scabies is caused by the mite Sarcoptes scabiei and is spread by prolonged skin contact. It typically affects children and young adults.

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64
Q

what is the pathophysiology of scabies?

A

The scabies mite burrows into the skin, laying its eggs in the stratum corneum. The intense pruritus associated with scabies is due to a delayed type IV hypersensitivity reaction to mites/eggs which occurs about 30 days after the initial infection.

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65
Q

what are the features of scabies?

A

Features
• Widespread pruritus
• Linear burrows on the side of fingers, interdigital webs and flexor
aspects of the wrist
• In infants the face and scalp may also be affected
• Secondary features are seen due to scratching: excoriation, infection

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66
Q

what is the management of scabies?

A

Management
• Permethrin 5% is first-line
• Malathion 0.5% is second-line
• Give appropriate guidance on use
• Pruritus persists for up to 4-6 weeks post eradication

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67
Q

what is appropriate patient guidance on the treatment of scabies?

A

• Avoid close physical contact with others until treatment is complete
• All household and close physical contacts should be treated at the same time, even if
asymptomatic
• Launder, iron or tumble dry clothing, bedding, towels, etc., on the first day of treatment to kill
off mites.

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68
Q

how is insecticide used in scabies?

A

• Apply the insecticide cream or liquid to cool, dry skin
• Pay close attention to areas between fingers and toes, under nails, armpit area, creases of the
skin such as at the wrist and elbow
• Allow to dry and leave on the skin for 8–12 hours for permethrin, or for 24 hours for malathion,
before washing off
• Reapply if insecticide is removed during the treatment period, e.g. If wash hands, change
nappy, etc
• Repeat treatment 7 days later

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69
Q

what is type 1 vs type 2 psoriasis?
-age of presentation
-family history
-HLA assoc.

A

Type 1
• Presents < 40 years old
• Positive family history
• Associated with HLA-CW6
Type 2
• Presents > 50 years old
• No family history

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70
Q

what are the features of psoriasis?

A

• Red, scaly plaques
• Scalp, extensor surfaces elbows/knees, sacrum
• Nail signs: pitting, onycholysis
• Arthritis

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71
Q

what is the pathophysiology of psoriasis?

A

• Abnormal T cell activity stimulates keratinocyte proliferation (rather than an actual primary keratinocyte disorder)
• Mediated by type 1 helper T cells

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72
Q

describe 6 topical treatments in psoriasis?

A

• Simple emollients
• Coal tar: probably inhibit DNA synthesis
• Topical corticosteroids: particularly flexural disease.
Mild steroids are useful in facial psoriasis
• Calcipotriol: vitamin D analogue which ↓ epidermal
proliferation and restores a normal horny layer
• Dithranol: inhibits DNA synthesis, wash off after 30
mins, SE: burning, staining

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73
Q

what is the management of flexural psoriasis?

A

Flexural psoriasis
• emollients
• topical steroids

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74
Q

Describe phototherapy used in psoriasis?
-what are the adverse effect?

A

• Narrow band ultraviolet B light (311-313nm) is now
the treatment of choice
• Photochemotherapy is also used - psoralen +
ultraviolet A light (PUVA)
• Adverse effects: skin ageing, squamous cell cancer
(not melanoma)

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75
Q

what is the treatment of scalp psoriasis?

A

• Calcipotriol lotion
• Steroid lotion + shampoo
• Combination shampoo:
betamethasone with vitamin D
analogues
• Coconut oil compound
shampoos (combination of coal
tar, salicylic acid and sulphur) • Tar shampoo

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76
Q

what systemic therapy can be used in psoriasis?

A

• Methotrexate: useful if associated joint disease
• Biological agents: infliximab, etanercept and adalimumab, Ustekinumab (IL-12 and IL-23
blocker) is showing promise in early trials.
• Cyclosporin
• Systemic retinoids

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77
Q

who is guttate psoriasis common in? what may precipitate this?

A

Guttate psoriasis is more common in children and adolescents. It may be precipitated by a streptococcal infection (tonsillitis) 2-4 weeks prior to the lesions appearing

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78
Q

what are the features of guttate psoriasis?

A

Features
• Tear drop papules on the trunk and limbs

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79
Q

what is the management of guttate psoriasis?

A

Management
• Most cases resolve spontaneously within 2-3 months
• There is no firm evidence to support the use of antibiotics to eradicate streptococcal infection
• Topical agents as per psoriasis
• UVB phototherapy
• Tonsillectomy may be necessary with recurrent episodes

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80
Q

what is toxic epidermal necrolysis?
-when is this most commonly seen?

A

Toxic Epidermal Necrolysis (TEN) A potentially life-threatening skin disorder that is mostly seen secondary to a drug reaction. In this condition the skin develops a scalded appearance over an extensive area. Some authors consider TEN to be the severe end of a spectrum of skin disorders which includes erythema multiforme and Stevens- Johnson syndrome

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81
Q

what are the features of TEN?

A

Features
• Systemically unwell e.g. Pyrexia, tachycardic
• Positive Nikolsky’s sign: the epidermis
separates with mild lateral pressure

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82
Q

what is the management of TEN

A

• Stop precipitating factor
• Supportive care, often in intensive care unit
• Intravenous immunoglobulin has been shown
to be effective and is now commonly used
first-line
• Other treatment options include:
immunosuppressive agents (Cyclosporin and cyclophosphamide), plasmapheresis

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83
Q

Phenytoin
Sulphonamides
Allopurinol
Penicillins
Carbamazepine
NSAIDs
are all assoc. with…

A

TEN

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84
Q

what is a keloid scar?

A

Keloid scars are tumour-like lesions that arise from the connective tissue of a scar and extend beyond the dimensions of the original wound

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85
Q

what are predispositions to keloid scars?

A

• More common in young, black, male adults, rare in the elderly
• Common sites (in order of decreasing frequency): sternum, shoulder, neck, face, extensor
surface of limbs, trunk
• Keloid scars are less likely if incisions are made along relaxed skin tension lines

86
Q

what is the treatment of keloid scars?

A

Treatment
• Early keloids may be treated with intra-lesional steroids e.g. Triamcinolone
• Excision is sometimes required

87
Q

what is acanthosis nigrans?

A

Acanthosis nigricans: describes symmetrical, brown, velvety plaques that are often found on the neck, axilla and groin

88
Q

• Internal malignancy (esp. Gastrointestinal)
• Insulin-resistant diabetes mellitus
• Obesity
• Acromegaly
• Cushing’s disease
• Hypothyroidism
• Polycystic ovarian syndrome
• Familial
• Prader-Willi syndrome
• Drugs: oral contraceptive pill, Nicotinic acid
are all assoc with…

A

acanthosis nigrans

89
Q

what is the diagnosis of eczema?

A

UK Working Party Diagnostic Criteria for Atopic Eczema An itchy skin condition in the last 12 months
Plus three or more of
• Onset below age 2 years*
• History of flexural involvement**
• History of generally dry skin
• Personal history of other atopic disease***
• Visible flexural dermatitis
not used in children under 4 years
**or dermatitis on the cheeks and/or extensor areas in children aged 18 months or under
**in children aged under 4 years, history of atopic disease in a first degree relative may be included

90
Q

topical steroids mild/potent/v potent:
Topical steroids
Clobetasone butyrate 0.05%
Clobetasol propionate 0.05%
Betamethasone valerate 0.1%

A

Topical steroids
• moderate: Clobetasone butyrate 0.05%
• potent: Betamethasone valerate 0.1%
• very potent: Clobetasol propionate 0.05%

91
Q

what is a mild topical steroid?

A

Hydrocortisone 0.5-2.5%

92
Q

what are 2 moderate topical steroids?

A

Betamethasone valerate 0.025% (Betnovate RD)
Clobetasone butyrate 0.05% (Eumovate)

93
Q

what are 2 potent steroids?

A

Betamethasone dipropionate 0.025% (Propaderm)
Betamethasone valerate 0.1% (Betnovate)

94
Q

what is a very potent steroid?

A

Clobetasol propionate 0.05% (Dermovate)

95
Q

what is the finger tip rule?

A

Finger tip rule
• 1 finger tip unit (FTU) = 0.5g, sufficient to treat area about twice that of flat adult hand

96
Q

how much finger tip units are used for:
Hand and fingers (front and back)
A foot (all over)
Front of chest and abdomen
Back and buttocks
Face and neck
An entire arm and hand
An entire leg and foot

A

Hand and fingers (front and back) 1.0
A foot (all over) 2.0
Front of chest and abdomen 7.0
Back and buttocks 7.0
Face and neck 2.5
An entire arm and hand 4.0
An entire leg and foot 8.0

97
Q

how many grams of steroid needed to cover each area if using daily for two weeks?
Face and neck
Both hands
Scalp
Both arms
Both legs
Trunk
Groin and genitalia

A

Face and neck 15 to 30 g
Both hands 15 to 30 g
Scalp 15 to 30 g
Both arms 30 to 60 g
Both legs 100 g
Trunk 100 g
Groin and genitalia 15 to 30 g

98
Q

what is pomphoyx eczema?

A

Pompholyx is a type of eczema which affects both the hands (cheiropompholyx) and the feet (pedopompholyx). It is also known as dyshidrotic eczema

99
Q

what are the features of pompholyx eczema?

A

Features
• Small blisters on the palms and soles
• Pruritic, sometimes burning sensation
• Once blisters burst skin may become dry and crack

100
Q

what is the management for pompholyx eczema?

A

Management
• Cool compresses
• Emollients
• Topical steroids

101
Q

pityriasis rosacea:
-what is the cause?
-who does this affect?

A

Pityriasis rosea Overview
• Cause unknown, herpes hominis virus 7 (HHV-7) is a possibility
• Tends to affect young adults

102
Q

what are the features of pityriasis rosacea?

A

Features
• Herald patch (usually on trunk)
• Followed by erythematous, oval, scaly
patches which follow a characteristic distribution with the longitudinal diameters of the oval lesions running parallel to the line of Langer. This may produce a ‘fir-tree’ appearance

103
Q

what is the management of pityriasis rosacea

A

Management
• Self-limiting, usually disappears after 4-6 weeks

104
Q

what is pityriasis versicolor caused by?

A

Pityriasis Versicolor, also called tinea versicolor, is a superficial cutaneous fungal infection caused by Malassezia furfur (formerly termed Pityrosporum ovale)

105
Q

what are the features of pityriasis versicolor?

A

Features
• Most commonly affects trunk
• Patches may be hypopigmented, pink or
brown (hence versicolor)
• Scale is common
• Mild pruritus

106
Q

what are predisposing factors for pityriasis versicolor?

A

Predisposing factors
• Occurs in healthy individuals
• Immunosuppression
• Malnutrition
• Cushing’s

107
Q

what is the management of pityriasis versicolor?

A

Management
• Topical antifungal e.g. Terbinafine or selenium sulphide
• If extensive disease or failure to respond to topical treatment then consider oral itraconazole

108
Q

what are the features of acne rosacea?

A

• Typically affects nose, cheeks and forehead
• Flushing is often first symptom
• Telangiectasia are common
• Later develops into persistent erythema with papules and pustules
• Rhinophyma
• Ocular involvement: blepharitis

109
Q

what is the management of acne rosacea?

A

• Topical metronidazole may be used for mild symptoms (i.e. Limited number of papules and pustules, no plaques)
• More severe disease is treated with systemic antibiotics e.g. Oxytetracycline
• Recommend daily application of a high-factor sunscreen
• Camouflage creams may help conceal redness
• Laser therapy may be appropriate for patients with prominent
telangiectasia

110
Q

what is acne vulgaris?

A

Acne vulgaris is a common skin disorder which usually occurs in adolescence. It typically affects the face, neck and upper trunk and is characterized by the obstruction of the pilosebaceous follicle with keratin plugs which results in comedones, inflammation and pustules.

111
Q

who does acne vulgaris affect?

A

Epidemiology
• Affects around 80-90% of teenagers, 60% of whom seek medical advice
• Acne may also persist beyond adolescence, with 10-15% of ♀s and 5% of ♂s over 25 years old
being affected

112
Q

describe the pathophysiology of acne vulgaris

A

Pathophysiology is multifactorial
• Follicular epidermal hyperproliferation resulting in the formation of a keratin plug. This in turn
causes obstruction of the pilosebaceous follicle. Activity of sebaceous glands may be controlled
by androgen, although levels are often normal in patients with acne
• Colonisation by the anaerobic bacterium propionibacterium acnes
• Inflammation

113
Q

describe mild acne

A

Acne may be classified into mild, moderate or severe:
• Mild: open and closed comedones with or without sparse inflammatory lesions.

114
Q

describe moderate acne

A

• Moderate acne: widespread non-inflammatory lesions and numerous papules and pustules

115
Q

describe severe acne

A

• Severe acne: extensive inflammatory lesions, which may include nodules, pitting, and scarring

116
Q

describe the management of acne

A

A simple step-up management scheme often used in the treatment of acne is as follows:
• Single topical therapy (topical retinoids, benzyl peroxide)
• Topical combination therapy (topical antibiotic, benzoyl peroxide, topical retinoid)
• Oral antibiotics: e.g. Oxytetracycline, doxycycline. Improvement may not be seen for 3-4
months. Minocycline is now considered second line treatment due to the possibility of irreversible pigmentation. Gram negative folliculitis may occur as a complication of long-term antibiotic use - high-dose oral trimethoprim is effective if this occurs
• Oral isotretinoin: only under specialist supervision

117
Q

how effective in isotretinoin?

A

Isotretinoin is an oral retinoid used in the treatment of severe acne. Two-thirds of patients have a long term remission or cure following a course of oral isotretinoin

118
Q

what are the adverse effects of retinoids?

A

• Teratogenicity: ♀s MUST be using two forms of contraception (e.g. Combined oral
contraceptive pill and condoms)
• Dry skin, eyes and lips: the most common side-effect of isotretinoin
• Nose bleeds (caused by dryness of the nasal mucosa)
• Low mood
• Raised triglycerides
• Hair thinning
• Benign intracranial hypertension: isotretinoin treatment should not be combined with
tetracyclines for this reason

119
Q

Features of ?
• Perioral dermatitis: red, crusted lesions
• Acrodermatitis
• Alopecia
• Short stature
• Hypogonadism
• Hepatosplenomegaly
• Geophagia (ingesting clay/soil)
• Cognitive impairment

A

zinc deficiency

120
Q

what is Koebner phenomenon seen in?

A

• Psoriasis
• Vitiligo
• Warts
• Lichen planus
• Lichen sclerosus
• Molluscum contagiosum

121
Q

describe cafe-au lait spots

A

Café-au-lait spots: Hyperpigmented lesions that vary in color from light brown to dark brown, with borders that may be smooth or irregular

122
Q

what are 4 causes of cafe-au lait spots?

A

• Neurofibromatosis type I & II
Tuberous sclerosis
Fanconi anemia
Mccune-Albright syndrome

123
Q

what are causes of skin bulla?

A

Bullous disorders causes of skin bullae:
• Congenital: epidermolysis bullosa
• Autoimmune: bullous pemphigoid, pemphigus
• Insect bite, Trauma, friction
• Drugs: barbiturates, furosemide

124
Q

what is bullous pemphigoid?
-what proteins are antibodies developed against

A

Bullous pemphigoid is an autoimmune condition causing sub-epidermal blistering of the skin. This is secondary to the development of antibodies against hemidesmosomal proteins BP180 and BP230

125
Q

what are the features of bullous pemphigoid?

A

Bullous pemphigoid is more common in elderly patients. Features include
• Itchy, tense blisters typically around flexures
• Mouth is usually spared

126
Q

what is seen on skin biopsy of bullous pemphigoid?

A

Skin biopsy
• Immunofluorescence shows IgG and C3 at the dermoepidermal junction

127
Q

what is the management of bullous pemphigoid?

A

Management
• Referral to dermatologist for biopsy and confirmation of diagnosis
• Oral corticosteroids are the mainstay of treatment
• Topical corticosteroids, immunosuppressants and antibiotics are also used

128
Q

what is pemphigus vulgaris caused by?

A

Pemphigus vulgaris is an autoimmune disease caused by antibodies directed against desmoglein, a cadherin-type epithelial cell adhesion molecule. It is more common in the Ashkenazi Jewish population

129
Q

Blisters/bullae
• No mucosal involvement: ?
• Mucosal involvement: ?

A

Blisters/bullae
• No mucosal involvement: bullous pemphigoid
• Mucosal involvement: pemphigus vulgaris

130
Q

what are the features of bullous pemphigus?

A

• Mucosal ulceration is common and often the presenting symptom. Oral involvement is seen in 50-70% of patients
• Skin blistering - flaccid, easily ruptured vesicles and bullae. Lesions are typically painful but not itchy. These may develop months after the initial mucosal symptoms. Nikolsky’s describes the spread of bullae following application of horizontal, tangential pressure to the skin
• Acantholysis on biopsy

131
Q

what is the management of bullous pemphigus?

A

Management
• Steroids
• Immunosuppressants

132
Q

what is molluscum contagiosum caused by?
who are these common in?

A

Molluscum contagiosum: caused by poxvirus, common in immunocompermised patients, flesh-white or colored, dome-shaped, and pearly in appearance. They are often 1–5 millimeters in diameter, with a dimpled center. They are generally not painful, but they may itch or become irritated. Picking or scratching the bumps may lead to further infection or scarring.

133
Q

Dermatitis herpetiformis - caused by ? in the dermis

A

Dermatitis herpetiformis - caused by IgA deposition in the dermis

134
Q

what is dermatitis herpetiformis caused by?

A

Dermatitis herpetiformis is an autoimmune blistering skin disorder associated with coeliac disease. It is caused by deposition of IgA in the dermis.

135
Q

what are the features of dermatitis herpetiformis?

A

itchy, vesicular skin lesions on the extensor surfaces (e.g. Elbows, knees buttocks)

136
Q

what is the diagnosis of dermatitis herpetiformis?

A

skin biopsy: direct immunofluorescence shows deposition of IgA in a granular pattern in the upper dermis

137
Q

what is the management of dermatitis herpetiformis?

A

Gluten-free diet Dapsone

138
Q

describe irritant contact dermatitis?

A

• Irritant contact dermatitis: common - non-allergic reaction due to weak acids or alkalis (e.g.
Detergents). Often seen on the hands. Erythema is typical, crusting and vesicles are rare

139
Q

describe allergic contact dermatitis
-what is this caused by
-what is the treatment

A

• Allergic contact dermatitis: type IV hypersensitivity reaction. Uncommon - often seen on the head following hair dyes. Presents as an acute weeping eczema which predominately affects the margins of the hairline rather than the hairy scalp itself. Topical treatment with a potent steroid
is indicated

140
Q

how does cement cause dermatitis?

A

Cement is a frequent cause of contact dermatitis. The alkaline nature of cement may cause an irritant contact dermatitis whilst the dichromates in cement also can cause an allergic contact dermatitis

141
Q

what is nickel dermatitis caused by?
-how is this diagnosed?

A

Nickel Dermatitis: is a common cause allergic contact dermatitis and is an example of a type IV
hypersensitivity reaction. It is often caused by jewellery such as watches. It is diagnosed by a skin
patch test

142
Q

what is porphyrea cutanea tarda?
-what is this due to?

A

Porphyria Cutanea Tarda is the most common hepatic porphyria. It is due to an inherited defect in uroporphyrinogen decarboxylase or caused by hepatocyte damage e.g. alcohol, estrogens

143
Q

what are the features of porphyria cutanea tarda?

A

Features
• Classically presents with photosensitive rash with blistering and skin fragility on the face and dorsal aspect of hands (most common feature)
• Hypertrichosis
• Hyperpigmentation

144
Q

what is the investigation for porphyria cutanea tarda?

A

• Urine: elevated uroporphyrinogen and pink fluorescence of urine under Wood’s lamp

145
Q

what is the management of porphyria cutanea tarda?

A

Management
• Chloroquine • Venesection

146
Q

what is keratoacanthoma?
-when are these more frequently seen?

A

Keratoacanthoma is a benign epithelial tumour. They are more frequent in middle age and do not become more common in old age (unlike basal cell and squamous cell carcinoma)

147
Q

what are the features of keratoacanthoma?

A

Features - said to look like a volcano or crater
• Initially a smooth dome-shaped papule
• Rapidly grows to become a crater centrally-filled with keratin

148
Q

what is the management of keratoacanthoma?

A

Spontaneous regression of keratoacanthoma within 3 months is common, often resulting in a scar. Such lesions should however be urgently excised as it is difficult clinically to exclude squamous cell carcinoma. Removal also may prevent scarring.

149
Q

what is grauloma annulare?

A

• Papular lesions that are often slightly hyperpigmented and depressed centrally
• Typically occur on the dorsal surfaces of the hands and feet, and on the extensor aspects of the
arms and legs

150
Q

when is the term erythroderma used?

A

Erythroderma is a term used when more than 95% of the skin is involved in a rash of any kind

151
Q

what are causes of erythroderma?

A

Causes of erythroderma
• Eczema
• Psoriasis
• Drugs e.g. Gold
• Lymphoma, leukemia
• Idiopathic

152
Q

erythrodermic psoriasis:
-what may this result from?
-how may acute deterioration be triggered and how is this managed?

A

• May result from progression of chronic disease to an exfoliative phase with plaques covering most of the body. Associated with mild systemic upset
• More serious form is an acute deterioration. This may be triggered by a variety of factors such as withdrawal of systemic steroids. Patients need to be admitted to hospital for management

153
Q

what is erythrasma?

A

Erythrasma is a generally asymptomatic, flat, slightly scaly, pink or brown rash usually found in the groin or axillae. It is caused by an overgrowth of the diphtheroid Corynebacterium minutissimum

154
Q

what does examination with wood light show in erythrasma?

A

Examination with Wood’s light reveals a coral-red fluorescence

155
Q

what is the management of erythrasma?

A

Topical miconazole or antibacterial are usually effective. Oral erythromycin may be used for more extensive infection

156
Q

• Systemic lupus erythematosus, discoid lupus
• Porphyria (not acute intermittent)
• Herpes labialis (cold sores)
• Pellagra
• Xeroderma pigmentosum
• Solar urticaria
• Polymorphic light eruption
are all…

A

photosensitive skin disorders

157
Q

what is tinea?

A

Tinea is a term given to dermatophyte fungal infections. Three main types of infection are described depending on what part of the body is infected

158
Q

where does:
• Tinea capitis
• Tinea corporis
• Tinea pedis

A

• Tinea capitis - scalp
• Tinea corporis - trunk, legs or arms
• Tinea pedis - feet

159
Q

tinea capitis:
-what is this caused by?
-what is the diagnosis?

A

• A cause of scarring alopecia mainly seen in children
• Most common cause is trichophyton tonsurans in the UK and the USA
• May also be caused by microsporum canis acquired from cats or dogs
• Diagnosis: lesions due to microsporum canis green fluorescence under wood’s (lesions due to Trichophyton species do not readily fluoresce under Wood’s lamp) However the most useful investigation is scalp scrapings

160
Q

tinea corporis:
-what are the causes?
-what does this cause?
-how is this treated?

A

• Causes include Trichophyton rubrum (also causes fungal nail infection) and Trichophyton verrucosum (e.g. From contact with cattle)
• Well-defined annular, erythematous lesions with pustules and papules
• May be treated with oral fluconazole

161
Q

tinea pedis: AKA
-what is this characterised by?

A

athletes foot
• Characterized by itchy, peeling skin between the toes
• Common in adolescenc

162
Q

what is stevens johnson syndrome?

A

Stevens-Johnson syndrome severe form of erythema multiforme associated with mucosal involvement and systemic symptoms

163
Q

what are the features of stevens johnson syndrome?

A

Features
• Rash is typically maculopapular with target lesions being characteristic. May develop into vesicles or bullae
• Mucosal involvement
• Systemic symptoms: fever, arthralgia

164
Q

• Idiopathic
• Bacteria: mycoplasma, streptococcus
• Viruses: herpes simplex virus, orf
• Drugs: penicillin, sulphonamides, carbamazepine, allopurinol, nsaids, oral contraceptive pill
• Connective tissue disease e.g. Sle
• Sarcoidosis
• Malignancy

are all causes of…

A

stevens johnson syndrome

165
Q

what is the causes of pruritus:
History of alcohol excess
Stigmata of chronic liver disease: spider naevi, bruising, palmar erythema, gynaecomastia etc
Evidence of decompensation: ascites, jaundice, encephalopathy

A

liver disease

166
Q

what is the cause of pruritus:
Pallor
Other signs: koilonychia, atrophic glossitis, post-cricoid webs, angular stomatitis

A

iron deficiency anaemia

167
Q

what is the cause of pruritus:
Pruritus particularly after warm bath ‘Ruddy complexion’
Gout
Peptic ulcer disease

A

polycythaemia rubra vera

168
Q

what is the cause of pruritus:
Lethargy & pallor
Edema & weight gain
Hypertension

A

CKD

169
Q

what is the cause of pruritus:
Night sweats
Lymphadenopathy
Splenomegaly,
hepatomegaly
Fatigue

A

lymphoma

170
Q

what is hirsutism? what is hypertrichosis?

A

Hirsuitism & Hypertrichosis: hirsuitism is often used to describe androgen-dependent hair growth in women, with hypertrichosis being used for androgen-independent hair growth

171
Q

what are causes for hirsutism?

A

• Polycystic ovarian syndrome
• Cushing’s syndrome
• Congenital adrenal hyperplasia
• Androgen therapy
• Adrenal tumour
• Androgen secreting ovarian tumour
• Drugs: phenytoin

172
Q

what are causes of hypertrichosis?

A

• Drugs: minoxidil, Cyclosporin, diazoxide
• Congenital hypertrichosis lanuginosa,
congenital hypertrichosis terminalis
• Porphyria cutanea tarda
• Anorexia nervosa
• GI and Lung malignancies.

173
Q

how is hirsutism assessed?

A

Assessment of hirsuitism
• Ferriman-Gallwey scoring system: 9 body areas are assigned a score of 0 - 4, a score > 15 is considered to indicate moderate or severe hirsutism

174
Q

how is hirsutism managed?

A

• Advise weight loss if overweight
• Cosmetic techniques such as waxing/bleaching - not available on the NHS
• Consider using combined oral contraceptive pills such as co-cyprindiol (Dianette) or ethinylestradiol and drospirenone (Yasmin). Co-cyprindiol should not be used long-term due to the increased risk of venous thromboembolism
• Facial hirsuitism: topical eflornithine - contraindicated in pregnancy and breast-feeding

175
Q

what is yellow nail syndrome?

A

Yellow nail syndrome: Slowing of nail growth leads to the characteristic thickened and
discolored nails seen in yellow nail syndrome

176
Q

what are 4 association with yellow nail syndrome?

A

Associations:
• Congenital lymphedema
• Pleural effusions
• Bronchiectasis
• Chronic sinus infections

177
Q

what is Onychomycosis?

A

Onychomycosis is fungal infection of the nails.

178
Q

what are 3 causes of onychomycosis

A

• Dermatophytes - mainly Trichophyton rubrum, 90% of cases
• Yeasts - such as Candida
• Non-dermatophyte moulds

179
Q

what are the features of onychomycosis?

A

• ‘Unsightly’ nails are a common reason for presentation
• Thickened, rough, opaque nails are the most common finding

180
Q

what is involved in investigations of onychomycosis?

A

• Nail clippings
• Scrapings of the affected nail

181
Q

how is onychomycosis managed?

A

• Treatment is successful in around 50% of people
• Diagnosis should be confirmed by microbiology before starting treatment
• Dermatophyte infection: oral terbinafine is currently recommended first-line with oral
itraconazole as an alternative. Six weeks therapy is needed for fingernail infections whilst
toenails should be treated for 12 weeks
• Candida infection: mild disease should be treated with topical antifungals (e.g. Amorolfine)
whilst more severe infections should be treated with oral itraconazole for a period of 12 weeks

182
Q

what is a myxoid cyst?

A

Myxoid cysts (also known as mucous cysts) are benign ganglion cysts usually found on the distal, dorsal aspect of the finger. There is usually osteoarthritis in the surrounding joint. They are more common in middle-aged women

183
Q

Causes of?
• Idiopathic
• Trauma e.g. Excessive manicuring
• Infection: especially fungal
• Skin disease: psoriasis, dermatitis
• Impaired peripheral circulation e.g. Raynaud’s
• Systemic disease: hyper- and hypothyroidism

A

onycholysis

184
Q

what are risk factors for SCC

A

excessive exposure to sunlight / psoralen UVA therapy
actinic keratoses and Bowen’s disease
immunosuppression e.g. following renal transplant, HIV
smoking
long-standing leg ulcers (Marjolin’s ulcer)
genetic conditions e.g. xeroderma pigmentosum, oculocutaneous albinism

185
Q

what is the treatment for SCC?

A

Surgical excision with 4mm margins if lesion <20mm in diameter. If tumour >20mm then margins should be 6mm. Mohs micrographic surgery may be used in high-risk patients and in cosmetically important sites.

186
Q

what is assoc with good prognosis in SCC?

A

Well differentiated tumours
<20mm diameter
<2mm deep
No associated diseases

187
Q

what is assoc. with poor prognosis in SCC?

A

Poorly differentiated tumours
>20mm in diameter
>4mm deep
Immunosupression for whatever reason

188
Q

what are 4 types of melanoma?

A

Superficial spreading
Nodular
Lentigo maligna
Acral lentiginous

189
Q

Superficial spreading melanoma:
-frequency
-where does this affect?
-what is the appearance?

A

70% of cases
Arms, legs, back and chest, young people
A growing moles with diagnostic features listed above

190
Q

Nodular melanoma:
-frequency
-where does this affect?
-what is the appearance?

A

Second commonest
Sun exposed skin, middle-aged people
Red or black lump or lump which bleeds or oozes
MOST AGGRESSIVE

191
Q

Lentigo maligna
-frequency
-where does this affect?
-what is the appearance?

A

Less common
Chronically sun-exposed skin, older people
A growing mole with diagnostic features listed above

192
Q

Acral lentiginous
-frequency
-where does this affect?
-what is the appearance?

A

Rare form
Nails, palms or soles, African Americans or Asians
Subungual pigmentation (Hutchinson’s sign) or on palms or feet

193
Q

what are the main diagnostic features of melanoma?

A

The main diagnostic features (major criteria):

Change in size
Change in shape
Change in colour
194
Q

what are the minor criteria in the diagnosis of melanoma?

A

Secondary features (minor criteria)

Diameter >6mm
Inflammation
Oozing or bleeding
Altered sensation
195
Q

what is the treatment for melanoma?

A

Treatment

Suspicious lesions should undergo excision biopsy. The lesion should be removed in completely as incision biopsy can make subsequent histopathological assessment difficult.
Once the diagnosis is confirmed the pathology report should be reviewed to determine whether further re-excision of margins is required

Further treatments such as sentinel lymph node mapping, isolated limb perfusion and block dissection of regional lymph node groups should be selectively applied.

196
Q

what margin of excision is needed in each:
Lesions 0-1mm thick
Lesions 1-2mm thick
Lesions 2-4mm thick
Lesions >4 mm thick

A

Lesions 0-1mm thick 1cm
Lesions 1-2mm thick 1- 2cm (Depending upon site and pathological features)
Lesions 2-4mm thick 2-3 cm (Depending upon site and pathological features)
Lesions >4 mm thick 3cm

197
Q

what is pellagra?

A

Pellagra is a caused by nicotinic acid (niacin) deficiency. The classical features are the 3 D’s - dermatitis, diarrhoea and dementia.

198
Q

what may pellagra occur as a consequence of?

A

Pellagra may occur as a consequence of isoniazid therapy (isoniazid inhibits the conversion of tryptophan to niacin) and it is more common in alcoholics.

199
Q

what are the features of pellagra?

A

Features

dermatitis (brown scaly rash on sun-exposed sites - termed Casal's necklace if around neck)
diarrhoea
dementia, depression
death if not treated
200
Q

what is eczema herpiticum?

A

Eczema herpeticum describes a severe primary infection of the skin by herpes simplex virus 1 or 2.

201
Q

who is affected most by eczema herpiticum?

A

It is more commonly seen in children with atopic eczema and often presents as a rapidly progressing painful rash.

202
Q

what is the appearance of eczema herpiticum?

A

On examination, monomorphic punched-out erosions (circular, depressed, ulcerated lesions) usually 1–3 mm in diameter are typically seen.

203
Q

what is the treatment of eczema herpeticum?

A

As it is potentially life-threatening children should be admitted for IV aciclovir.

204
Q

what factors may exacerbate psoriasis?

A

trauma
alcohol
drugs: beta blockers, lithium, antimalarials (chloroquine and hydroxychloroquine), NSAIDs and ACE inhibitors, infliximab
withdrawal of systemic steroids

205
Q

what is hereditary haemorrhagic telangiectasia?

A

Also known as Osler-Weber-Rendu syndrome, hereditary haemorrhagic telangiectasia (HHT) is an autosomal dominant condition characterised by (as the name suggests) multiple telangiectasia over the skin and mucous membranes. Twenty percent of cases occur spontaneously without prior family history.

206
Q

what is the diagnosis of hereditary haemorrhagic telangiectasia?

A

There are 4 main diagnostic criteria. If the patient has 2 then they are said to have a possible diagnosis of HHT. If they meet 3 or more of the criteria they are said to have a definite diagnosis of HHT:

epistaxis : spontaneous, recurrent nosebleeds
telangiectases: multiple at characteristic sites (lips, oral cavity, fingers, nose)
visceral lesions: for example gastrointestinal telangiectasia (with or without bleeding), pulmonary arteriovenous malformations (AVM), hepatic AVM, cerebral AVM, spinal AVM
family history: a first-degree relative with HHT
207
Q

what does systemic mastocytosis result from?

A

Systemic mastocytosis results from a neoplastic proliferation of mast cells

208
Q

what are the features of mastocytosis?

A

Features

urticaria pigmentosa - produces a wheal on rubbing (Darier's sign)
flushing
abdominal pain
monocytosis on the blood film
209
Q

what is the diagnosis of mastocytosis?

A

Diagnosis

raised serum tryptase levels
urinary histamine
210
Q

BCC:
-what are lesions AKA
-how does this progress?
-does this metastasize?

A

Basal cell carcinoma (BCC) is one of the three main types of skin cancer. Lesions are also known as rodent ulcers and are characterised by slow-growth and local invasion. Metastases are extremely rare. BCC is the most common type of cancer in the Western world.

211
Q

what are the features of a BCC

A

Features

many types of BCC are described. The most common type is nodular BCC, which is described here
sun-exposed sites, especially the head and neck account for the majority of lesions
initially a pearly, flesh-coloured papule with telangiectasia
may later ulcerate leaving a central 'crater'
212
Q

what are management options for BCC?

A

surgical removal
curettage
cryotherapy
topical cream: imiquimod, fluorouracil
radiotherapy

MRCP Combined (58 decks)

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