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Finals Revision > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is pemphigus vulgaris?

A

Autoimmune condition characterised by IgG antibodies against desmoglein 3

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2
Q

When does pemphigus vulgaris normally occur?

A

Middle age

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3
Q

What are risk factors for pemphigus vulgaris?

A

Jewish descent, drugs (NSAIDs, ACEis)

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4
Q

How does pemphigus vulgaris present?

A

Flaccid blisters that are easily ruptured to form shallow erosions. Not itchy. Seen in face, scalp, axilla, mucosa

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5
Q

Is pemphigus vulgaris Nikolsky sign +ve or -ve?

A

Positive

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6
Q

What does immunofluorescence of Pemphigus Vulgaris show?

A

Intracellular IgG deposits

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7
Q

‘Crazy paving/chicken wire appearance on immunofluorescence’

A

Pemphigus vulgaris

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8
Q

What is the treatment of pemphigus vulgaris?

A

Topical steroids and pain relief

Prednisolone +/- azaithioprine, dapsone, ciclosporin

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9
Q

What is the prognosis of pemphigus vulgaris?

A

Remits in 3-6 years, mortality rate of 10-20%

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10
Q

What is bullous pemphigoid?

A

Autoimmune condition characterised by antibodies against the BM

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11
Q

What age group commonly get bullous pemphigoid?

A

Elderly

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12
Q

How does bullous pemphigoid present?

A

Itchy tense bullae, around flexures, on an urticarial base. Usually without scarring, mouth spared

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13
Q

Is bullous pemphigoid Nikolsky sign +ve or -ve?

A

Negative

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14
Q

What is seen on immunofluorescence in bullous pemphigoid?

A

IgG and c3 deposits at dermoepidermal junction

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15
Q

How is bullous pemphigoid managed?

A

Topical steroids

Oral prednisolone, tetracyclines, azaithioprine, dapsone

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16
Q

What is the prognosis of bullous pemphigoid?

A

Chronic self limiting course, most achieve remission in 3-6 months

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17
Q

What is dermatitis herpetiformis?

A

Autoimmune blistering skin condition caused by IgA deposition in the dermis

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18
Q

What is dermatitis herpetiformis associated with?

A

Coeliac disease

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19
Q

How does dermatitis herpetiformis present?

A

Itchy, vesicular skin lesions on extensor surfaces, buttocks, face and scalp. On erythematous bases

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20
Q

What is seen on histology in dermatitis herpetiformis?

A

Papillary dermal microabscesses

IgA deposits in dermal papillae

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21
Q

How is dermatitis herpetiformis treated?

A

Gluten free diet

Dapsone, tetracyclines

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22
Q

What is acne vulgaris?

A

Common chronic inflammatory condition of the pilosebaceous unit

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23
Q

What percentage of teenagers does acne vulgaris affect?

A

80-90%

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24
Q

What are the 4 main pathogenesis’ of acne vulgaris?

A

Duct occlusion
Increased sebum production
Bacterial colonisation
Inflammation

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25
Q

What bacteria commonly colonise in acne vulgaris?

A

P. Acnes, staph epidermidis

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26
Q

What are aggravating factors for acne vulgaris?

A

Diet, premenstrual, sweating, UV radiation, job (Steam/oil), stress

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27
Q

What atrophic scarring is seen in acne vulgaris?

A

‘Ice pick lesions’

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28
Q

What hypertrophic scarring is seen in acne vulgaris?

A

Keloid

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29
Q

What is mild acne?

A

Scattered papules and pustules

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30
Q

What is moderate acne?

A

Numerous papules, pustules, atrophic scarring

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31
Q

What is severe acne?

A

Papules, pustules, nodules, significant scarring

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32
Q

What is the first line management of acne?

A

Single topical treatment

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33
Q

What topical treatments are there?

A

Topical antibiotics
Topical retinoids
Benzoyl Peroxide

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34
Q

What is second line management of acne?

A

Combined topical treatment

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35
Q

What is 3rd line management of acne?

A

Oral antibiotics or OCP

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36
Q

What oral antibiotics are used for management of acne vulgaris?

A

Erythromycin, oxytetracycle, lymecycline, doxycycline

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37
Q

What are side effects of oral antibiotics?

A

Gi upset, thrush, photosensivity

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38
Q

What type of COCP is used for acne vulgaris?

A

Dianette, triphasic pills

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39
Q

How will progesterone only contraception affect acne vulgaris?

A

May exacerbate it

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40
Q

What is 4th line acne treatment?

A

Oral retinoids

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41
Q

How doe oral isotretinoin (roaccutane) work?

A

Reduces sebaceous gland activity

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42
Q

What are side effects of roaccutane?

A

Dry skin, lips, eyes, skin fragility, hyperlipidaemia, abnormal LFTs, teratogenic, mood alteration, hair thinning,

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43
Q

What is acne rosacea?

A

Chronic skin condition of unknown aetiology

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44
Q

How does acne rosacea present?

A

papules, pustules and erythema, prominent facial flushing (worsened by spicy food/alcohol)

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45
Q

What is acne rosacea associated with?

A

Blepharitis

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46
Q

How is acne rosacea managed?

A

Avoid dietary triggers
Topical metronidazole
Telangactasia - laser therapy
Rhinophyma - surgery/laser shaving

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47
Q

What is eczema?

A

Inflammatory skin condition often starting in early infancy

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48
Q

What are causes of eczema?

A

Multifactorial - genetics, allergens, diet, overwashing, poor barrier, filaggrin deficiency, dryness, heat, cold, stress, infection

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49
Q

Which social class is there a higher incidence of eczema in?

A

Higher social classes

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50
Q

How does eczema present?

A

Itchy, red, flexural rash. Chronic scratching causes lichenification, scarring, infection

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51
Q

How is eczema diagnosed?

A

Itching PLUS 3 OF

visible flexural rash, history of flexural rash, personal/family history of atopy, dry skin, onset before 2

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52
Q

What is step 1 in eczema management?

A

Emollients

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53
Q

What is step 2 in eczema management?

A

Emollients + mild steroid

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54
Q

What is step 3 in eczema management?

A

Emollients + mild steroid + calcineurin inhibitor

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55
Q

What is step 4 in eczema management?

A

Emollients + potent/very potent steroid

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56
Q

How should emollients be used?

A

Liberally (500g/week), also bath and shower emollients

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57
Q

What are the effects of topical steroids?

A

Anti-inflammatory
Vasoconstrictive
Antiproliferative

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58
Q

What are side effects of topical steroids?

A

Skin thinning, increased infections, telangastasia, cushings

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59
Q

How much steroid does one finger tip unit cover?

A

Two hands

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60
Q

What is an example of a mild topical steroid?

A

Hydrocortisone

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61
Q

What is an example of a moderate topical steroid?

A

Eumovate

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62
Q

What is an example of a potent topical steroid?

A

Betnovate

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63
Q

What is an example of a very potent topical steroid?

A

Dermovate

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64
Q

What are examples of calcineurin inhibitors?

A

Tacrolimus, pimecromilus

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65
Q

What can be used if eczema is severe and does not respond to topical treatments?

A

Phototherapy, systemic agents (e.g. azaithioprine, methotrexate, mycopentolate)

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66
Q

What organism is the cause of infected eczema?

A

Staph Aureus

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67
Q

How is infected eczema treated?

A

Fusidic acid

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68
Q

What is eczema herpeticum?

A

Herpes simplex infection of eczema

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69
Q

How does eczema herpeticum present and how is it treated?

A

Monomorphic rash with circular blisters

EMERGENCY - admit for IV aciclovir

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70
Q

What is psoriasis?

A

Chronic relapsing remitting condition

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71
Q

When is the peak incidence of psoriasis?

A

20s-50s

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72
Q

What is the underlying pathophysiology of psoriasis?

A

Hyperproliferation of epidermal cells

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73
Q

What is the normal skin turnover?

A

25 days ish

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74
Q

What is the skin turnover in psoriasis?

A

5 days

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75
Q

What does histology show in psoriasis?

A

Parakeratotic statum corneum
Absence of granular layer
Extended prickle cell layer

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76
Q

How does chronic plaque psoriasis present?

A

Erythematous, scaly plaques on extensor aspects of skin. Palpable and shiny with silvery scale. Koebner phenomenon

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77
Q

What is the Koebner phenomenon?

A

Skin lesions arising in areas of trauma

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78
Q

How does guttate psoriasis present?

A

Usually occurs 2-4 weeks post strep infection. ‘Tear drop’ scaly patches. Resolves spontaneously in 2-4 months

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79
Q

How does flexural psoriasis present?

A

Shiny red well demarcated plaques in flexural surfaces

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80
Q

How does erythrodermic psoriasis present?

A

90% of skin surface goes red. Usually occurs in patients with psoriasis and is due to UV burns/withdrawal of steroids

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81
Q

What nail changes may be seen in psoriasis?

A

Pitting, onycholysis, oil drop lesions, sublingual hyperkeratosis, deformity

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82
Q

How is psoriasis managed 1st line?

A

Topical treatment

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83
Q

What topical treatments are available for psoriasis?

A

Emollients, tar, vitamin D analogues, salicylic acid, dithranol, steroids

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84
Q

How does coal tar work?

A

Reduces DNA synthesis and epidermal proliferation

85
Q

What is an example of a vitamin D analogue?

A

Calcitriol

86
Q

What does salicyic acid do in psoriasis?

A

Removes hyperkeratosis

87
Q

How does dithranol cream work?

A

Anti-mitotic - used in short regimes as can burn skin

88
Q

What is second line treatment for psoriasis after topical agents?

A

Phototherapy

89
Q

What are the options of phototherapy?

A

UVB treatment or PUVA (psoralen topical.oral and UVA)

90
Q

What is the 3rd line treatment for psoriasis after phototherapy?

A

Systemic treatment

91
Q

What systemic treatments are available for psoriasis?

A

Methotrexate, ciclosporin, retinoids, biologics

92
Q

What are causes of venous ulcers?

A

Venous hypertension secondary to venous insufficiency

93
Q

What is the pathogenesis of venous ulcers?

A

Ulcers form due to capillary fibrin cuff or leucocyte sequestration

94
Q

What are features of venous insufficiency?

A

Oedema, brown pigmentation, lipatodermatosclerosis, eczema

95
Q

What are features of venous ulcers?

A

Superficial, above ankle (Gaiter area), painless

96
Q

What investigations should be done for venous ulcers?

A

Doppler USS

ABPI

97
Q

How are venous ulcers managed?

A

4 layer compression bandaging

98
Q

What should the pressure of a bandage be for venous ulcer at the ankle?

A

Around 40mmHg

99
Q

What should the pressure of a bandage be fore venous ulcers at the knee?

A

Around 25mmHg

100
Q

How long should you aim to heal a venous ulcer in?

A

12 weeks

101
Q

What should the ABPI be to be suitable for compression bandaging?

A

Over 0.8

102
Q

What are causes of arterial ulcers?

A

Hypertension, atherosclerosis

103
Q

What are the features of arterial insufficiency?

A

Hairless, pale, cold, unable to palpate pulses

104
Q

What are features of arterial ulcers?

A

Deep, punched out, may see tendon, over heels/toes, painful

105
Q

What investigations are done for an arterial ulcer?

A

Doppler USS

ABPI

106
Q

What is the management of an arterial ulcer?

A

Pain relief, lifestyle changes, aspirin, treat infections, Soffban + crepe bandages to reduce oedema. Vascular surgery if needed

107
Q

What does ABPI measure?

A

Ratio of systolic blood in the lower leg compared to the arms

108
Q

What does a decreased pressure in the legs indicate?

A

Peripheral arterial disease

109
Q

What is a normal ABPI?

A

1-1.2

110
Q

What does an ABPI of 0.8-0.9 indicate?

A

Mild peripheral arterial disease

111
Q

What does an ABPI of 0.5-0.79 indicate?

A

Moderate PAD

112
Q

What does an ABPI less than 0.5 indicate?

A

Severe PAD

113
Q

What does an ABPI above 1.2 indicated?

A

Calcification of artery

114
Q

What is a Marjolins ulcer?

A

SCC occuring at a site of chronic inflammation

115
Q

Who and where do neuropathic ulcers occur?

A

In diabetics. commonly on points on pressure (e.g. metatarsal head)

116
Q

What is pyoderma gangrenosum?

A

Erythematous nodules than can ulcerate, associated with IBD, RA. may occur at stoma sites

117
Q

What are symptoms of venous eczema?

A

Red, scaly rash that is intensely itchy. Often misdiagnosed as cellulitis

118
Q

What are the causative organisms of impetigo?

A

Staph aureus, strep pyogenes

119
Q

How does impetigo present?

A

Well defined lesions with a honey coloured crust and erythematous base

120
Q

How is impetigo treated?

A

Topical fusidic acid

If sevre - oral flucloxicillin

121
Q

What are complications of impetigo?

A

Bullous impetigo

Staphylococcal scolded skin syndrome

122
Q

What is staphylococcal scaled skin syndrome?

A

Loss of epidermis secondary to exotoxin release

123
Q

What is folliculitis?

A

Superficial infection of hair follicle

124
Q

What is a boil?

A

Deep infection of a single hair follicle

125
Q

What is a carbuncle?

A

Deep infection of multiple hair follicles

126
Q

How does folliculitis/boils/carbuncles present?

A

Discrete erythematous papules/pustules on hair bearing sites, itch

127
Q

How are boils and carbuncles treated?

A

Oral flucloxacillin

128
Q

What is cellulitis?

A

Acute infection of skin and soft tissues

129
Q

What are causes of cellulitis?

A

Strep pyogenes, staph aureus

130
Q

How does cellulitis present?

A

Usually in legs, macular hot erythema with ill defined margins that is often spreading. Associated fever, malaise, leg pain, swelling, local lymphadenopathy

131
Q

How is cellulitis managed?

A

Flucloxacillin orally

132
Q

If a patient gets recurrent cellulitis, what should you consider swabbing for?

A

Panton-Valentine-Leucocidin

133
Q

What is erysipelas?

A

Superficial form of cellulitis

134
Q

What is erysipelas caused by?

A

Strep Pyogenes

135
Q

How does erysipelas present?

A

Spreading rash, commonly on face. Well demarcated, erythematous plaque, systemic upset

136
Q

How is erysipelas treated?

A

IV flucloxacillin

137
Q

What is necrotising fasciitis?

A

Infection of soft tissue and fascia

138
Q

What causes type 1 necrotising fasciitis?

A

Mixed aerobe/anaerobe

139
Q

What causes type 2 necrotising fasciitis?

A

Strep pyogenes

140
Q

What causes type 3 necrotising fasciitis?

A

Clostridia

141
Q

How does necrotising fasciitis present?

A

Acute onset, painful, erythematous lesions, extremely tender over tissue

142
Q

How is necrotising fasciitis managed?

A

Surgical debridement, IV antibiotics

143
Q

What causes skin warts?

A

HPV types 1-4

144
Q

How do warts present?

A

Raised papules with firm, rough surface, cauliflower appearance

145
Q

How are warts managed?

A

Salicylic acid, cryotherapy, imiquimod

146
Q

What causes molluscum contagiosum?

A

Pox virus

147
Q

How does molluscum contagiosum present?

A

Itchy, solid, pearly pink papules with umbilicated centre

148
Q

How is molluscum contagiosum managed?

A

Self limiting

149
Q

What causes coldsores?

A

Herpes Simplex Virus 1

150
Q

How does herpes simplex virus (coldsores) present?

A

Single or grouped painful itchy vesicles on erythematous base that burst without scarring

151
Q

What is herpetic whitlow?

A

HSV lesion on finger

152
Q

How is HSV managed?

A

Analgesia

Topical/oral aciclovir

153
Q

What causes chicken pox?

A

Varicella Zoster virus

154
Q

How does chicken pox present?

A

Macules -> papules -> vesicles that crust over and recover. Intensely itchy

155
Q

What is the cause of shingles?

A

Herpes Zoster - reactivation of VZV in dorsal root ganglion

156
Q

How does shingles present?

A

Erythematous macules, burning and tingling pain, dermatomal distribution

157
Q

How is shingles managed?

A

Oral aciclovir + analgesia

158
Q

How does a dermatophyte infection present?

A

Erythematous, scaly itchy ring shaped lesion with expanding edge and resolving centre. Named by body site.

159
Q

How is a dermatophyte infection treated?

A

Topical/oral antifungals

160
Q

What causes thrush?

A

Candida albicans

161
Q

How does thrush present?

A

Itchy scale, ragged peeling edges. In mouth - white lesion that can be scraped off.

162
Q

How is thrush treated?

A 
Oral = miconazole
Skin = topical clotrimazole or oral antifungal
163
Q

What causes pityriasis vesicular?

A

Melassezia yeast

164
Q

How does pityriasis vesicular present?

A

Well defined macular lesions with fine scale that are hypo or hyperpigmented. Often noticed after being on holiday

165
Q

How is pityriasis vesicular treated?

A

Topical ketoconazole

166
Q

What is the most common skin cancer?

A

BCC

167
Q

What are risk factors for BCC?

A

Fair skin, UV exposure, intermittant sun damage

168
Q

How does a nodular BCC present?

A

Raised lesion with pearly shiny papule, rolled edge, central ulceration, telangactasia

169
Q

‘Rodent ulcer’

A

BCC

170
Q

How is BCC diagnosed?

A

Clinical suspicion and biopsy

171
Q

How is BCC managed?

A

Leave and monitor
Topical imiquimod
Cryotherapy
Surgery/MOHS

172
Q

What is actinic keratosis?

A

Premalignant lesion, develops as a consequence of sun exposure

173
Q

How does an actinic keratosis present?

A

Small crusty or scaly lesion. May be pink/brown/red/same colour as skin. Typically on sun exposed sites

174
Q

How is actinic keratosis’ managed?

A 
Prevention of further risk
Fluorauricil cream
Topical diclofenac
Topical imiquimod
Cryotherapy/Currettage/Cautery
175
Q

What is Bowens disease?

A

Intraepidermal SCC

176
Q

How does Bowens disease present?

A

Slow growing red scaly plaque, typically on shin

177
Q

How is Bowens disease managed?

A

Topical fluoracil
Topical Imiquimod
Cryotherapy
Excision

178
Q

What is the commonest skin cancer post transplant?

A

SCC

179
Q

What are risk factors for SCC?

A

Excessive sunlight exposure, PUVA, actinic keratosis, Bowens disease, immunosuppression, smoking, long standing ulcers

180
Q

How does an SCC present?

A

Grows slowly over months, firm erythematous plaque over sun exposed site. Associated scale, crust bleeding, tenderness, itch

181
Q

How is SCC managed?

A

Surgical excision

182
Q

What is a malignant melanoma?

A

Tumour derived from melanocytes

183
Q

What are risk factors for malignant melanoma?

A

Personal/family history, large number of moles, excess sun exposure, sunbed use, immunosuppression

184
Q

What are the two growth phases of melanomas?

A

Radial and vertical

185
Q

What is the radial growth phase of a melanoma?

A

Grows horizontally within the epidermis

186
Q

What is the vertical growth phase of a melanoma?

A

Lesion becomes elevated and invades dermis

187
Q

What is the commonest type of melanoma?

A

Superficial spreading

188
Q

How does superficial spreading melanoma present?

A

Growing, changing mole

189
Q

How does a nodular melanoma present?

A

Red/black lump that oozes and bleeds

190
Q

Who do lentigo malignas occur in?

A

Elderly sun exposed skin

191
Q

What is an acral lenitgo?

A

A melanoma arising on the palms, nails or soles of feet

192
Q

How is assessment of a melanoma done?

A

Asymmetry, Border, Colour, Diameter >6mm, evolving

193
Q

How is a melanoma managed?

A

Surgical excision with 2mm margins +/- sentinel node biopsy

If advanced can do chemo/radio/immunotherapy

194
Q

What is a prognostic indicator in melanoma?

A

Breslow thickness

195
Q

What is breslow thickness?

A

Measure of tumour thickness/depth, measured from basal layer of epidermis

196
Q

‘Herald patch’

A

Pityriasis rosea

197
Q

How is scabies treated?

A

Malathion lotion/permethrin cream

198
Q

What is the cause of sebhorroeic dermatitis?

A

Malassezia

199
Q

‘Hypersensitity reaction triggered by infections’

A

Erythema multiforme

200
Q

What is ertythema ab igne caused by?

A

Infra-red exposure

201
Q

‘Itchy white spots on vulva of elderly woman’

A

Lichen scleorsis

202
Q

‘Pruritic purple pustular rash on flexors. Itchy’

A

Lichen planus

203
Q

‘Wickhams striae’

A

Lichen planus

204
Q

How is lichen planus treated?

A

Topical steroids

205
Q

How is erythrasma treated?

A

Erythromycin

206
Q

‘Exclamation mark hairs’

A

Alopecia areata

207
Q

What drugs can commonly trigger psoriasis?

A

Betablockers and lithium

208
Q

Lupus pernio

A

Sarcoidosis

Finals Revision (22 decks)

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