Medicine - Dermatology Flashcards

1
Q

How can you differentiate between SJS and TEN?

A
SJS = up to 10% skin involvement
TEN = \>30% skin involvement
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2
Q

What is Nikolsky’s sign?

A

Epidermis separates with mild lateral pressure - secondary to adverse drug reaction

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3
Q

How should SJS or TEN be managed?

A

Stop the cause
Transfer to ITU
IV Ig
Immunosuppression (eg ciclosporin and cyclophosphamide)

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4
Q

Which drugs are most likely to cause SJS?

A

Never Press Skin As It Can Peel
NSAIDs
Phenytoin
Sulphonamides
Allopurinol
IV Ig
Carbemazapine
Penicillins

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5
Q

What is erythroderma?

A

Any rash involving >95% of the body

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6
Q

Recall 3 possible complications of erythroderma

A

Dehydration
High output heart failure
Infection

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7
Q

What is the cause of adult seborrhoeic dermatitis?

A

Fungus called malassezia furfur

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8
Q

What 2 skin conditions can be caused by malassezia furfur?

A

Seborrhoeic dermatitis
Pityriasis versicolor

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9
Q

What are the 1st and 2nd line options for treating scalp seborrhoeic dermatitis?

A

1st line = zinc pyrithione (‘head and shoulders’)
2nd line = ketoconazole

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10
Q

Which pathogen is the most common cause of impetigo?

A

Staphylococcus aureus

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11
Q

What are the 3 classes of impetigo and their respective management?

A

Localised, non-bullous: topical H2O2 1% cream / topical fusidic acid

Widespread, non-bullous: oral flucloxacillin or topical fusidic acid

Widespread, bullous: oral flucloxacillin

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12
Q

How long should children with impetigo be excluded from school?

A

Until lesions crusted over or 48 hours after antibiotics started

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13
Q

Describe the pathophysiology of acne

A

Obstruction of pilosebaceous follicle with keratin plugs which result in comedones, inflammation + pustules

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14
Q

Epidemiology of acne

A

Affects 80-90% Teenagers

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15
Q

What are the lay terms for open and closed comedones?

A

Open = blackheads
Closed = whiteheads

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16
Q

5 features of acne

A

Comedones
Inflammatory lesions: papules + pustules / nodules + cysts
Scarring
Pigmentation
Seborrhoea (oily skin)

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17
Q

What to enquire about in acne history? (8)

A

Duration, type + distribution
Previous Tx
Exacerbating factors: menstruation, cosmetics
Systemic features: fever, myalgia
Psychological impact
FH: acne, PCOS
DH: steroids, lithium
Hyperandrogenism: irregular periods, hirsutism

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18
Q

Recall 3 conservative recommendations for acne

A

Avoid over-cleaning face: BD with gentle soap is okay
Avoid oil-based cosmetics
Avoid picking + squeezing (scarring)

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19
Q

How long should each acne medication be tried for to give it chance to work?

A

8 weeks

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20
Q

Describe treatment for mild to moderate acne

A

12w course topical combination therapy
Adapalene + Benzoyl peroxide TOP
or
Tretinoin + Clindamycin TOP
or
Benzoyl peroxide + Clindamycin TOP
or
Benzoyl peroxide TOP monotherapy

Adapalene + Tretinoin = Retinoids

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21
Q

Describe treatment for moderate- severe acne

A

12w course:
Adapalene + Benzoyl peroxide TOP
or
Tretinoin + Clindamycin TOP
or
Adapalene + Benzoyl peroxide TOP + Lymecycline/ Doxycycline PO
or
Azelaic acid TOP + Lymecycline/ Doxycycline PO

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22
Q

In which patients should tetracyclines be avoided? What can be used instead?

A

Pregnant, breastfeeding + <12y

Erythromycin

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23
Q

What should always be prescribed with antibiotics (TOP + PO) for acne? Why?

A

Retinoid or Benzoyl peroxide TOP to reduce risk of abx resistance developing

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24
Q

Give an alternative to oral antibiotics for acne in females. How should these be used?

A

COCP
Used in combination with TOP agents

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25
Q

What form of acne requires urgent same day referral to the on-call dermatologists? What is this? Give 3 signs of this

A

Acne fulminans
Sudden severe inflammatory reaction that precipitates deep ulceration + erosions
Fever
Arthralgia
Myalgia

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26
Q

5 indications for referral for acne

A

Mild-mod not responded to 2 completed courses
Mod-severe not responded to Tx inc. an Abx
Scarring
Persistent pigmentation
Acne contributing to psychological distress/ MH disorder

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27
Q

What can be prescribed by specialists for acne?

A

Isotretinoin (PO)
(aka roaccutane = synthetic vitamin A)

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28
Q

Once acne has cleared, how should this be maintained?

A

Topical retonoids and azelaic acid

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29
Q

What pregnancy prevention plan should be in place for Roaccutane?

A

1 highly effective e.g. IUD/ Implant
or
2 user dependent forms e.g. OCP + Condoms

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30
Q

Recall 7 side effects of Roaccutane

A

Dry skin, eyes, lips, mouth
Teratogenicity
Low mood
Raised triglycerides
Hair-thinning
Intracranial HTN
Photosensitivity

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31
Q

What is the progression of symptoms of rosacea?

A
1st = flushing 
2nd = symmetrical facial rash with telangiectasia 
3rd = persistent pustulopapular erythema
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32
Q

How should rosacea be managed?

A
Mild-moderate = topical metronidazole 
Severe = oral tetracycline
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33
Q

What is the aetiology of hidradenitis supparativa?

A

Chronic inflammatory occlusion of folliculopilosebaceous units that obstructs the apocrine glands and prevents keratinocytes from properly shedding the follicular epithelium

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34
Q

In lay terms, what is hidradenitis supparativa?

A

Abscesses that form near hair follicles in places where we tend to sweat more

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35
Q

What are the 2 biggest risk factors for hidradenitis supparativa?

A

Smoking and obesity

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36
Q

Rarely, what inflammatory disease is associated with
hidradenitis supparativa?

A

Crohn’s

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37
Q

How can hidradenitis supparativa be managed?

A

Conservative: weight loss, stop smoking, hygeine
Acutely: steroids PO, flucloxacillin, I&D
Chronically: topical clindamycin

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38
Q

What pathogen causes pityriasis versicolor?

A

Malassezia furfur

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39
Q

How does pityriasis versicolor appear?

A

Hypopigmented patches on trunk
Mild pruritis

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40
Q

How is pityriasis versicolor managed?

A

Topical ketoconazole

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41
Q

How does vitiligo appear?

A

Well demarctaed, depigmented skin patches usually affecting the peripheries

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42
Q

Recall some associations of vitiligo (don’t need to know in detail)

A

T1DM, Addison’s, autoimmune thyroid, pernicious anaemia, alopecia areata

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43
Q

How can vitiligo be managed?

A
Sunblock 
Topical corticosteroids (reverses changes if applied early)
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44
Q

What pathogen causes pityriasis rosea?

A

HHV-7

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45
Q

Describe the presentation of pityriasis rosea

A

Recent viral infection –> herald patch
Then erythematous, oval scaly patches

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46
Q

How should pityriasis rosea be managed?

A

It is self-limiting (6-12w) so no need

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47
Q

Broadly describe the 4 types of psoriasis

A

Plaque - most common, is well-demarcated red and scaly - affects scalp, back, extensors
Guttate - following a strep infection, “tear drop” lesions
Pustular - affects palms and soles
Flexural - skin is smooth

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48
Q

Recall some factors that exacerbate psoriasis

A

Trauma
EtOH
Certain drugs

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49
Q

Which drugs can exacerbate psoriasis?

A

INFLAME
Infliximab
NSAIDs
For HTN (beta blockers)
Lithium
ACE inhibitors
Malarial drugs
EtOH

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50
Q

How should chronic plaque psoriasis be managed in primary care? (give 1st, 2nd and 3rd line)

A

1st line: 4w trial of OM potent corticosteroid and ON vitamin D analogue

2nd line: after 8w (so 4w break): OM potent corticosteroid and BD vitamin D analogue

3rd line: 4w trial of BD potent corticosteroid OR coal tar

Use emollients as an adjunct

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51
Q

What is the maximum duration of use of topical potent and very potent steroids before a break is needed?

A

Potent = 8w
Very potent = 4w

52
Q

How can chronic plaque psoriasis be managed in secondary care?

A
Phototherapy/photochemotherapy 
Systemic immunosuppression (eg infliximab, etanercept, ustekinumab)
53
Q

Describe the distribution of eczema in infants vs children vs young adults

A

Infants: face and trunk
Child: extensors
Young adult: flexures

54
Q

Describe the different severities of eczema in terms of physical symptoms

A

Mild: infrequent itching, some areas of dry skin and a little redness
Moderate: frequent itching, lots of redness and some excoriation
Severe: widespread dryness, incessant itching, redness, excoriation, thickening, cracking, alteration of pigmentation

55
Q

How should eczema be investigated?

A

Consider food allergy and contact dermatitis
Skin prick tests
Patch tests

56
Q

How long should flares of eczema be treated for?

A

Treat ASAP and for 48 hours after resolution of symptoms

57
Q

Recall the management of mild, moderate and severe eczema

A

Mild: emollients, mild potency topical corticosteroids

Moderate: emollients, moderate potency topical corticosteroids, topical calcineurin inhibitors and bandages

Severe: emollients, potent topical corticosteroids, topical calcineurin inhibitors, bandages and phototherapy

58
Q

How should infected eczema (not herpeticum) be managed?

A

Skin swab and culture
Flucloxacillin PO

59
Q

How should eczema herpeticum be managed?

A

Oral aciclovir
If around eyes, same day referral to ophthalmologist
Looks similar to impetigo so ALSO treat for that with oral aciclovir

60
Q

How should topical emollients and steroids be applied

A

Emollients applied liberally
Wait 30 mins
then apply steroids

61
Q

Recall 2 examples of topical calcineurin inhibitors that can be used to manage eczema

A

Mild-moderate - pimecrolimus
Moderate - severe - tacrolimus

62
Q

Recall some points for PACES counselling for eczema

A

Explain diagosis (dry, itchy skin)
Explain epidemiology (very common, many grow out of it)
Explain management
Encourage frequent, liberal use of emollients and use of emollients as a soap substitute
Advise avoidance of triggers
Avoid scratching if poss (eg mittens for infants)
Safety ned about signs of infection
Info: itchysneezywheezy.co.uk shows how to apply emollients

63
Q

What type of pathogen causes tinea?

A

Dermatophyte fungi

64
Q

What pathogen causes tinea?

A

Trichophytum rubrum

65
Q

How should scabies be managed?

A

Permethrin - full body treatment that you wash off after 8-12 hours - treat all household/close contacts

66
Q

How should headlice be managed?

A

Malathion

67
Q

How should tinea be managed?

A

Mild –> topical antifungals (terbinafine)
Mod–> hydrocortisone 1%
Severe–> oral antifungals (eg terbinafine)
If tinea capitis –> oral antifungal

68
Q

How long should children with tinea be excluded from school?

A

No need

69
Q

Recall 2 risk factors for shingles

A

Increasing age
Immunosuppression

70
Q

Describe the symptoms of shingles

A

Prodromal burning pain over the affected dermatome for 2-3 days +/- fever, headache, lethargy
Rash begins erythematous, macular –> vesicular

71
Q

For how long is shingles infectious?

A

Until vesicles have crusted over (about 5-7 days)

72
Q

How should shingles be managed?

A

PO aciclovir if <72 hours from symptom onset and >50y/in lots of pain/ immunocompromised

Analgesia: paracetamol/ NSAIDs –>amitriptyline

Emergency referral if serious complications suspected

73
Q

Recall 3 possible complications of shingles

A

Post-herpetic neuralgia
Herpes zoster ophthalmicus (affects ocular division of CNV)
Herpes zoster oticus (Ramsay Hunt syndrome)

74
Q

What are the 2 pre-malignant conditions for squamous cell carcinoma known as?

A

Actinic keratoses and keratocanthomas

75
Q

Where do actinic keratoses appear?

A

sun-exposed areas

76
Q

How can actinic keratoses be managed medically?

A

Fluorouracil + topical hydrocortisone
Topical diclofenac/imiquimod

77
Q

What are some surgical options for managing actinic keratoses?

A

Cryotherapy
Curettage and cautery

78
Q

What is a keratocanthoma?

A

Pre-malignant skin condition (for SCC) with rapid growth (around 1 week)

79
Q

How should keratocanthomas be managed?

A

Excision

80
Q

What is the causative organism in fungal nail infections 90% of the time?

A

Trichophytum rubrum (dermatophyte)

81
Q

How can fungal nail infections be investigated?

A

Nail clipping MC&S

82
Q

How should fungal nail infections be managed?

A

Must first confirm infection by MC&S in order to commence treatment
- Can do nothing (if pt not bothered)

  • Can do PO terbinafine (2nd line itraconazole)
  • finger = 6w-3m
  • toe = 3-6m
  • If candida infection –> topical antifungals
83
Q

How does lichen planus appear?

A

Rash is:
Purple
Pruritic
Papular
Polyglonal
Also can get thin, white lines in the mouth

84
Q

Where does lichen planus tend to affect?

A

Flexor surfaces

85
Q

Recall some causes of lichen planus

A

Gold
Thiazides
Quinine

86
Q

How should lichen planus be managed?

A

Topical steroids

87
Q

How does lichen sclerosus appear?

A

Itchy white spots typically on the vulva of elderly womenn

88
Q

How should lichen sclerosus be managed?

A

1st: clobetasol proprionate ointment
2nd: tacrolimus and biopsy

89
Q

Which 2 pathogens are most likely to cause cellulitis?

A

Strep pyogenes
Staph aureus

90
Q

What classification system is used for cellulitis?

A

Eron classification

91
Q

How should cellulitis be managed?

A

Mild/mod: flucloxacillin
Severe: co-amox

92
Q

Describe the 4 severities of cellulitis under the Eron classification

A

I - no signs of systemic toxicity, person has no uncontrolled comorbidities
II - systemically unwell OR systemically well with an uncontrolled comorbidity
III - significant systemic upset such as acute confusion, tachycardia/tachypnoea, hypotension, unstable comorbidity
IV - sepsis/ necrotising fasciitis

93
Q

What is the cause of erysipelas?

A

Strep pyogenes

94
Q

How should erysipelas be managed?

A

PO flucloxacillin

95
Q

What is the cause of erythrasma?

A

corynebacterium minitissimu

96
Q

How can erythrasma be investigated?

A

Wood’s slit lamp –> coral-red fluorescence

97
Q

How should erythrasma be managed

A

Topical miconazole

98
Q

Recall some causes of pyoderma gangrenosum

A

IBD
Connective tissue disorders
Myeloproliferative disorders

99
Q

Describe the classical natural history of pyoderma gangrenosum

A

Small red papule –> later deep, red, necrotic ulcers with a violaceous border

100
Q

How should pyoderma gangrenosum be managed?

A

PO steroids

101
Q

In what patient population is necrobiosus lipoidica diabeticorum seen and how does it appear?

A

Diabetics
Shiny, painless area of yellow/red skin on shins

102
Q

What are antibodies directed against in bullous pemphigoid?

A

Basement membrane (dermo-epidermal junction)

103
Q

How can bullous pemphigoid be managed?

A

Oral corticosteroids

104
Q

How can bullous pemphigoid and pemphigus vulgaris be differentiated?

A

Bullous pemphigoid = tense blisters with no oral involvement
Pemphigus vulgaris = flaccid blisters with oral involvement

105
Q

What are antibodies directed against in pemphigus vulgaris?

A

Desmosomes

106
Q

What is this?

(Source: Derm Net NZ)

A

Guttate psoriasis

107
Q

What is this?

(source: Derm Net NZ)

A

Pityriasis versicolor

108
Q

What is this?

(source: Derm net NZ)

A

Impetigo

109
Q

What is this?

(source NHS)

A

Hidradenitis supparativa

110
Q

What is this?

(source: Derm Net NZ)

A

Vitiligo

111
Q

What is this?

(source: Derm Net NZ)

A

Pityriasis rosea

112
Q

What is this?

(source: NHS)

A

Plaque psoriasis

113
Q

What is this?

A

Guttate psoriasis

114
Q

What is this?

(Source: Derm Net NZ)

A

Pustular psoriasis

115
Q

What is this?

(Source: Derm Net NZ)

A

Flexural psoriasis

116
Q

What is this?

(Source: Derm Net NZ)

A

Tinea corporis

117
Q

What is this?

(Source: Derm Net NZ)

A

Scabies

118
Q

What is this?

(Source: Derm Net NZ)

A

Actinic keratosis

119
Q

What is this?

(Source: Derm Net NZ)

A

Keratocanthoma

120
Q

What is this?

(Source: Derm Net NZ)

A

Lichen planus

121
Q

What is this?

(Source: Derm Net NZ)

A

Erysipelas

122
Q

What is this?

(Source: Derm Net NZ)

A

Erysipelas

123
Q

What is the recommended margin for excision of a malignant melanoma?

A

When the breslow thickness is known = 2mm

124
Q

Recall 3 causes of Koebner’s phenomena

A

Vitiligo

Psoriasis

Lichen planus

125
Q

Which type of skin lesion commonly appears in response to traume eg an insect bite?

A

Dermatofibroma