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Focused 2 > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is the classic presentation of a dermoid cyst?

A

= cystic teratoma - tumour of mature skin cells; contains skin, sweat glands, hair follicles; sometimes teeth, fat, bone, thyroid tissue. commonly occurs in young child at lateral aspect of eyebrow

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2
Q

What investigation might be required for dermoid cysts and why?

A

if appears close to midline - to look for intracranial extension if excision considered

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3
Q

What are the commonest histological findings in seborrhoeic keratosis?

A

localised proliferation of basal layer of epidermis

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4
Q

What are the characteristic features of a sebaceous cyst?

A

considered same as epidermoid cyst (type of trichilemmal cyst) - closed sac/cyst with lining resembling upper part of hair follicle, produces sebum, may have visible punctum

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5
Q

What is the management of the following manifestations of herpes simplex virus?

A
  1. gingivostomatitis: oral aciclovir, chlorhexidine mouthwash
  2. cold sores: topical aciclovir (?limited benefit)
  3. genital herpes: oral aciclovir
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6
Q

What is the guidance for herpes simplex infection during pregnancy?

A
  • elective caesarean if primary attack of herpes >28 weeks gestation
  • pregnant + BG recurrent herpes: suppressive therapy, reassure low risk of fetal transmission
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7
Q

What organism causes pityriasis versicolor?

A

Malassezia furfur

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8
Q

What are the features of pityriasis versicolor?

A
  • red when occur in white skin, paler than surrounding skin on brown/black skin
  • more noticeable following sun tan
  • scale common
  • may be itchy
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9
Q

What is first line treatment for pityriasis versicolor?

A

ketoconazole shampoo - useful for covering large surface area of body

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10
Q

What viruses causes Kaposi’s sarcoma?

A

Human herpes virus 8

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11
Q

What is the treatment of kaposi’s sarcoma?

A

radiotherapy + resection

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12
Q

Do most melanomas arise in normal skin or pre-existing moles?

A

most in normal skin

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13
Q

What is the treatment of acute urticaria?

A
  • First line - non-sedating antihistamine (cetirizine, loratidine, fexofenadine)
  • if inadequate response to treatment - doubel standard dose of antihistamine / switch to alternative / use sedating AH at night
  • If severe/resistant - prednisolone + AH
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14
Q

What makes incisions less likely to cause keloid scars?

A

Making incisions along relaxed skin tension lines

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15
Q

What are two options for the treatment of keloid scars?

A

Intra-lesional steroids e.g. triamcinolone injection
Excision - but be wary may create more scars

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16
Q

What treatment options exist for a port wine stain?

A

cosmetic camouflage or laser therapy

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17
Q

What are 3 genetic factors that play a role in psoriasis?

A
  1. HLA-B13
  2. HLA-B17
  3. HLA-Cw6
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18
Q

What immunological factors play a role in psoriasis?

A

T helper cells, Th17, which produce IL-17 - stimulates keratinocyte proliferation

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19
Q

What is the most common subtype of psoriasis?

A

plaque psoriasis

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20
Q

What are 4 types of psoriasis?

A
  1. plaque psoriasis
  2. flexural psoriasis (smooth)
  3. guttate psoriasis (triggered by strep)
  4. pustular psoriasis (palms + soles)
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21
Q

What are the diagnostic criteria for malignant melanoma?

A

Glasgow 7 -
3 major: change in size, shape and colour
4 minor: diameter >7mm, inflammation, oozing/bleeding, itch/ odd sensation

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22
Q

What are the commonest sites for melanoma in males vs females?

A

Males - trunk
Females - lower leg

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23
Q

What 2 dermatological side effects may be seen on the face from anabolic steroids?

A
  1. acne conglobata - severe form of acne with burrowing + interconnecting abscesses, irregular scars (keloidal and atrophic)
  2. acne fulminans - severe, painful, haemorrhagic acne
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24
Q

What are 6 treatment options for actinic keratoses?

A
  1. Topical fluorouracil (2-3 week course)
  2. Topical diclofenac
  3. Imiquimod
  4. Cryotherapy
  5. Curettage
  6. Cautery
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25
Q

What are 6 types of drugs which can exacerbate plaque psoriasis?

A
  1. Beta blockers
  2. Lithium
  3. ACE inhibitors
  4. NSAIDs
  5. Antimalarials - chloroquine and hydroxychloroquine
  6. Infliximab
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26
Q

What are 3 non-drug causes which can exacerbate plaque psoriasis?

A
  1. Alcohol
  2. Trauma
  3. Withdrawal of systemic steroids
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27
Q

When does BCC require referral to dermatology on 2ww?

A

If in areas at high risk of causing damage - eyelids, nasal ala

otherwise routine

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28
Q

What are 6 management options for BCC?

A
  1. Surgical removal
  2. Radiotherapy
  3. Cryotherapy
  4. Curettage
  5. Fluorouracil
  6. Imiquimod
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29
Q

What is the autoimmune process happening in bullous pemphigoid?

A

antibodies to hemidesmosome proteins BP180 and BP230 - causes subepidermal blistering

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30
Q

What are 3 features of blistering disease in bullous pemphigoid?

A
  1. itchy, tense blisters around flexures
  2. blisters heal without scarring
  3. in exams: no mucosal involvement
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31
Q

How should bullous pemphigoid be managed if suspected in primary care?

A

refer to secondary care (dermatology)

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32
Q

How is bullous pemphigoid investigated?

A
  • skin biopsy
  • histopathological examination + immunofluorescence testing
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33
Q

What does immunofluorescence testing show in bullous pemphigoid?

A

IgG and C3 at the dermoepidermal junction

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34
Q

What is the treatment of bullous pemphigoid?

A

mainstay = oral corticosteroids; topical steroids, immunosuppressants, antibiotics also used

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35
Q

What is the approximate risk of someone having another seizure after a first episode unprovoked seizure with normal investigations?

A

30-50%

70-80% after second unprovoked seizure - as suggests epilepsy

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36
Q

In what proportion of dermatomyositis is there associated underlying malignancy?

A

20-25%

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37
Q

What are 3 types of malignancy associated with dermatomyositis?

A
  1. Ovarian
  2. Breast
  3. Lung cancer
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38
Q

What is polymyositis?

A

variant of dermatomyositis where skin manifestations are not prominent

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39
Q

What are 5 less common features of dermatomyositis?

A
  1. proximal muscle weakness +- tenderness
  2. raynaud’s
  3. respiratory muscle weakness
  4. ILD e.g. fibrosing alveolitis or organising pneumonia
  5. dysphagia, dysphonia
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40
Q

What are are 4 types of blood tests which may be positive in dermatomyositis?

A
  1. ANA positive (80%)

antibodies to aminoacyl-tRNA synthetases including:
1. anti-tRNA ligase aka Jo-1
2. anti-signal recognition particle (SRP)
3. anti-Mi-2

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41
Q

What are 8 complications of extensive burns?

A
  1. haemolysis due to damage of erythrocytes by heat and microangiopathy
  2. loss of capillary membrane integrity causing plasma leakage into interstitial space
  3. extravasation of fluids from burn site causing hypovolaemic shock
  4. protein loss
  5. secondary infection e.g. Staph aureus
  6. ARDS
  7. Curlings ulcer
  8. compartment syndrome - full thickness circumferential burns in an extremity
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42
Q

What is the method of healing for superificial burns?

A

kertinocytes migrate to form a new layer over burn site

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43
Q

What is the method of healing of full thickness burns?

A

dermal scarring; need keratinocytes from skin grafts to provide optimal coverage

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44
Q

What are the 3 criteria that must be met for post-exposure prophylaxis treatment for VZV?

A
  1. significant exposure (if limited, covered up shingles doesn’t count)
  2. clinical condition increasing risk of severe varicella - immunosuppressed, neonates, pregnant
  3. no antibodies
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45
Q

What timing should be met for blood tests for varicella antibdies in PEP for VZV?

A

ideally all patients should have blood test, bus shouldn’t delay post-exposure prophylaxis past 7 days after initial contact

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46
Q

What treatment is given for post-exposure prophylaxis for VZV if they meet the criteria?

A

varicella zoster immunoglobulin

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47
Q

What is the usual age of onset of vitiligo?

A

20-30 years

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48
Q

Which areas tend to be most affected by vitiligo?

A

Peripheries

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49
Q

What are 4 aspects of management of vitiligo?

A
  1. Sun block
  2. Camouflage makeup
  3. Steroids if applied early
  4. Tacrolimus + phototherapy may have role
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50
Q

How are fracture NOFs divided anatomically?

A
  • intracapsular
  • extracapsular - divided into trochanteric and subtrochanteric
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51
Q

What is granuloma annulare?

A

papular lesions that are often sligthyl hyperpigmented and depressed central

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52
Q

Where does granuloma annulare most commonly occur?

A

dorsal surfaces of hands and feet, and extensor aspects of arms and legs

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53
Q

What is a possible association of granuloma annulare?

A

diabetes mellitus (weak evidence)

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54
Q

What are 7 systemic disease causes of pruritus?

A
  1. Liver disease
  2. Iron deficiency anaemia
  3. Polycythaemia
  4. Chronic kidney disease
  5. Lymphoma
  6. Hyper/hypothyroidism
  7. Diabetes
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55
Q

What is the causative organism of molluscum contagiosum?

A

MCV, a member of Poxviridae family

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56
Q

In which patient group does molluscum contagiosum most commonly occur?

A

children (often with atopic eczema)

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57
Q

What is the prognosis of molluscum contagiosum?

A

spontaneous resolution usually occurs within 18 months; self-limiting condition

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58
Q

What are 3 types of treatment, if required, for molluscum contagiosum?

A
  1. squeezing (fingernails) or piercing (orange stick) may be tried, following bath (a few lesions at a time only)
  2. cryotherapy - by experienced HCP
  3. if eczema/inflammation around lesions - emollient + mild topical corticosteroid for itch, topical abx if looks infected e.g. fusidic acid
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59
Q

What are 3 situations when referral is required for molluscum contagiosum?

A
  1. HIV positive + extensive lesions - HIV specialist (URGENT)
  2. eyelid-margin or ocular lesions + red eye - ophthalmology (URGENT)
  3. anogenital lesions - GUM for STI screening
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60
Q

What is the presentation of acne rosacea?

A
  • flushing of nose, cheeks, forehead
  • telangiectasia
  • later develops into persistent erythema + papules + pustules
  • rhinophyma, blepharitis
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61
Q

What are 4 things that can trigger / exacerbate symptoms of acne rosacea?

A
  1. alcohol
  2. spicy foods
  3. hot drinks
  4. sunlight
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62
Q

What are 4 aspects of the management of acne rosacea?

A
  1. sunscreen, camouflage creams
  2. topical brimonidine - for predominant flushing
  3. topic ivermectin - for mild-moderate papules/pustules
  4. topical ivermectin + oral doxycycline - moderate-severe papules / pustules
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63
Q

How quickly does topical brimonidine work to treat flushing in acne rosacea?

A

reduces redness within 30 minutes, reaches peak action at 3-6 hours, then redness returns

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64
Q

What are 2 second-line alternatives to topical ivermectin for mild-moderate papules/pustules in acne rosacea?

A

topical metronidazole, topical azelaic acid

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65
Q

What are 2 organisms which most commonly cause cellulitis?

A
  1. Streptococcus pyogenes
  2. Staphylococcus aureus
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66
Q

What classification is used for cellulitis to guide management and what are the classes?

A

Eron classification
1. No signs of systemic toxicity, no uncontrolled comorbidities
2. systemically unwell or systemically well with comorbidity (e.g. PAD, chronic venous insufficiency, morbid obesity)
3. significant systemic upset e.g. acute confusion, tachycardia, tachypnoea, hypotension, or unstable comorbidities
4. sepsis syndrome or severe life-threatening infection e.g. necrotising fasciitis

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67
Q

What are 6 criteria recommended by NICE for admission for IV treatment of cellulitis?

A
  1. Eron class III or IV
  2. severe or rapidly deteriorating cellulitis (e.g. extensive areas of skin)
  3. very young (<1year) or frail
  4. immunocompromised
  5. significant lymphoedema
  6. facial cellulitis or periorbital cellulitis
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68
Q

Which antibiotics can be given in cellulitis, Eron grade I-II in penicillin allergic patients?

A

clarithromycin, erythromycin (pregnancy), doxycycline

flucloxacillin normally first line

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69
Q

What is the recommended management of Eron grade III-IV cellulitis?

A
  • admit
  • oral/IV co-amoxiclav, oral/IV clindamycin, IV cefuroxime or IV ceftriaxone
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70
Q

What 3 groups can urticaria be classed into?

A
  1. idiopathic (30-40%)
  2. immunological: autoimmune, allergic, immune complex, complement-dependent
  3. non-immunological: drugs, dietary pseudoallergens
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71
Q

What are 4 types of immunological urticarias?

A
  1. autoimmune - autoantibodies against FcεRI or IgE
  2. allergic - IgE mediated type I
  3. immune complex (urticarial vasculitis)
  4. complement-dependent (c1 esterase inhibitor deficiency)
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72
Q

What are 4 drugs that can cause non-immunological urticaria?

A
  1. direct mast cell-releasing agents e.g. opiates
  2. aspirin
  3. NDSAIDs
  4. ACE inhibitors
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73
Q

When should patients with urticaria be referred to secondary care?

A

refer to a dermatologist or immunologist if symptoms are not well-controlled on treatment, or antihistamines required continuously for >6 weeks to control sx

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74
Q

What is the recommended management of a first presentation of alopecia areata?

A

topical corticosteroid + refer to dermatologist

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75
Q

What is the presentation of alopecia areata?

A

localised, well-demarcated patches of hair loss; at edge there may be exlamation mark hairs

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76
Q

What is the prognosis of alopecia areata?

A

hair will regrow in 50% of patients by 1 year, and 80-90% of patients eventually

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77
Q

What are 7 treatment options in alopecia areata?

A
  1. watchful waiting
  2. topical or intralesional corticosteroids
  3. topical minoxidil
  4. phototherapy
  5. dithranol
  6. contact immunotherapy
  7. wigs
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78
Q

What are the 2 types of necrotising fasciitis?

A
  1. type 1 caused by mixed anaerobes and aerobes (post surgery in diabetics)
  2. type 2 caused by Streptococcus pyogenes
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79
Q

Which type of necrotising fasciitis is more common?

A

type 1

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80
Q

Which patient group is more typically affected by type 1 necrotising fasciitis?

A

post-surgery in diabetics

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81
Q

What are 5 risk factors for necrotising fasciitis?

A
  1. skin factors: trauma, burns, soft tissue infections
  2. diabetes mellitus
  3. diabetic treated with SGLT2 inhibitors
  4. IV drug use
  5. immunosuppression
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82
Q

What is the body site most commonly affected by necrotising fasciitis?

A

perineum (Fournier’s gangrene)

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83
Q

What are the clinical features of necrotising fasciitis?

A
  • acute onset
  • pain, swelling, erythema
  • may present as rapidly worsening cellulitis, POOP with physical features
  • extreme tenderness
  • hypoaesthesia to light touch
  • skin necrosis + crepitus/gas gangrene - late
  • fever and tachycardia
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84
Q

What is the management of necrotising fasciitis?

A

urgent surgical referral for debridement, IV antibiotics

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85
Q

What is the average mortality of necrotising fasciitis?

A

20%

86
Q

Of bullous pemphigoid and pemphigus vulgaris, which features mucous membrane involvement?

A

pemphigus vulgaris

87
Q

What is the difference between the blisters formed in pemphigus vulgaris vs bullous pemphigoid?

A
  • pemphigus vulgaris: flaccid blisters, easily ruptures vesicles, bullae, painful (not itchy)
  • bullous pemphigoid: tense blisters, rsistant to rupture
88
Q

What is the pathophysiology of pemphigus vulgaris?

A

autoimmune disease caused by antibodies directed against desmoglein 3, a cadherin-type epithelial cell adhesion molecule

89
Q

Which ethnicity is pemphigus vulgaris more common in?

A

Ashkenazi Jewish population

90
Q

What is Nikolsky’s sign in pemphigus vulgaris?

A

describes the spread of bullae following application of horizontal, tangential pressure to the skin

91
Q

What will be seen on biopsy in pemphigus vulgaris?

A

acantholysis

92
Q

What is the management of pemphigus vulgaris?

A

steroids first line, immunosuppressants

93
Q

What are 4 associationns of spider naevi?

A
  1. liver disease
  2. pregnancy
  3. COCP
  4. childhood
94
Q

What are 10 associations of acanthosis nigricans?

A
  1. T2DM
  2. PCOS
  3. Hypothyroidism
  4. Cushing’s disease
  5. obesity
  6. acromegaly
  7. GI cancer
  8. familial
  9. Prader-Willi syndrome
  10. Drugs - COCP, nicotinic acid
95
Q

What are 2 drugs that can cause acanthosis nigricans?

A
  1. COCP
  2. nicotinic acid
96
Q

What is suggestive of malignancy as a cause of acanthosis nigricans?

A

rapid development, atypical locations such as oral cavity - think malignancy (esp. gastric)

97
Q

What is the pathophysiology of acanthosis nigricans?

A

insulin resistance - hyperinsulinaemia - stimulation ofkeratinocytes and dermal fibroblast proliferation via interaction with insulin-like growth factor receptor-1 (IGFR1)

98
Q

What are 8 side effects of isotretinoin?

A
  1. dry skin, eyes and lips/mouth (commonest)
  2. teratogenicity
  3. low mood
  4. raised triglycerides
  5. hair thinning
  6. nose bleeds
  7. IIH (don’t combine w/ tetracyclines)
  8. photosensitivity
99
Q

What abx is first line to treat human or animal bite?

A

co-amoxiclav (doxy + metronidazole if allergic)

100
Q

What abx is first line to treat mastitis during breast feeding?

A

flucloxacillin

101
Q

What organism causes eczema herpeticum?

A

herpes simplex virus 1 or 2 - most common in children with atopic eczema

102
Q

What is the management of eczema herpeticum?

A

admit for IV aciclovir (potentially life-threatening)

103
Q

What is the pathophysiology of pyoderma gangrenosum?

A

neutrophilic dermatosis - skin condition characterised by dense iniltration of neutrophils in affected tissue

104
Q

What are 6 causes of pyoderma gangrenosum?

A
  1. idiopathic 50%
  2. IBD
  3. rheum - RA, SLE
  4. haematological - myeloproliferation, lymphoma, myeloid leukaemias, IgA monoclonal gammopathy
  5. GPA
  6. PBC
105
Q

What is the typical site of pyoderma gangrenosum?

A

lower limb - site of minor injury (pathergy)

106
Q

What is the management of pyoderma gangrenosum?

A
  • oral steroids
  • other immunosuppressive therpay in difficult cases - e.g. ciclosporin + infliximab
  • postpone any surgery until disease process controlled
107
Q

What should be done if there is failure to respond to treatment of pityriasis versicolor with ketoconazole shampoo?

A

consider alternative diagnosis - send skin scrapings, and oral itraconazole

108
Q

What is a pyogenic granuloma?

A

a.k.a. eruptive haemangioma - benign, vascular skin lesions that grow rapidly over weeks or months

109
Q

What are 3 factors linked to pyogenic granulomas?

A
  1. trauma
  2. pregnancy
  3. more common in women and young adults
110
Q

What are the most common sites affected by pyogenic granulomas?

A
  • head/neck
  • upper trunk
  • hands
  • oral mucosa lesions - common in pregnancy
111
Q

What is the usual progression of pyogenic granulomas?

A

rapidly progress within days to weeks forming raised, red/brown lesions which are often spherical in shape; may bleed profusely or ulcerate

112
Q

What is the management of pyogenic granulomas?

A
  • pregnancy - usually resolve postpartum
  • others - persist; curettage and cauterisation, cryotherapy, excision
113
Q

What most commonly causes toxic epidermal necrolysis (TEN)?

A

drug reactions

114
Q

What are 7 key drugs known to induce TEN?

A
  1. phenytoin
  2. sulphonamides
  3. allopurinol
  4. penicillins
  5. carbamazepine
  6. NSAIDs
115
Q

What are 3 key features of the skin changes in TEN?

A
  1. extensive detachment of epidermis leading to large fluid-filled blisters
  2. blisters easily separate upon pressure
  3. scalded appearance over extensive area
116
Q

What is the management of TEN?

A
  • stop precipitating factor
  • supportive care (manage in ICU)
  • IVIG - first line
  • other options: immunosuppressive (ciclosporin + cyclophosphamide), plasmaphresis
117
Q

What are 3 types of organisms that cause onychomycosis (fungal nail infections)?

A
  1. dermatophytes (90%) - mainly Trichophyton rubrum
  2. Yeasts e.g. Candida
  3. Non-dermathophyte moulds
118
Q

What investigations are done in suspected onychomycosis?

A

nail clippings +- scrapings of affected nail - microscopy + culture

should be done for all patients if antifungal tx considered

119
Q

What is the false negative rate for fungal nail clippings / scrapings?

A

around 30% - repeat samples may be needed

120
Q

What are the maangement options for fungal nail infection?

A
  • treatment not necessary if asymptomatic / not concerned re appearance
  • limited involvement: topical amorolfine 5% lacquer
  • extensive involvement due to dermatophyte infection: oral terbinafine
  • extensive involvement due to Candida: oral intraconazole
121
Q

What is the course of treatment for a fungal nail infection with amorolfine?

A

6 months for fingernails, 9-12 months for toenails

122
Q

What is the course of treatment for a fungal nail infection with terbinafine?

A
  • 6 weeks - 3 months for fingernails
  • 3 - 6 months for toenails
123
Q

How is oral itraconazole used in the treatment of fungal nail infections?

A

‘pulsed’ weekly therapy

124
Q

What is the treatment of allergic contact dermatitis?

A

potent topical steroid

125
Q

What are milia?

A

small, benign, keratin-filled cysts that typically appear around the face. occur any age but more common in newborns

126
Q

What is thought to cause pityriasis rosea?

A

human herpes virus 7 thought to have a role

127
Q

Which type of rash typically has a herald patch and fir tree appearance with a distribution in parallel to the lines of Langer?

A

pityriasis rosea

128
Q

What is the management of pityriasis rosea?

A

self-limiting - usually disappears after 6 - 12 weeks

129
Q

What is leukoplakia?

A

white patches in the oral cavity that cannot be rubbed off and not attributed to any other identifiable cause

130
Q

What proportion of cases of leukoplakia progress to squamous cell carcinoma?

A

20%

131
Q

Which patient group is leukoplakia more common in?

A

smokers

132
Q

How is a diagnosis of leukoplakia made?

A

diagnosis of exclusion - biopsy should be performed to rule out lichen planua, squamous cell carcinoma, candidiasis

133
Q

What are 4 management options for hyperhidrosis?

A
  1. topical aluminium chloride (first line)
  2. iontophoresis (electric current to skin)
  3. botulinum toxin (axillary)
  4. surgery e.g. endoscopic transthoracic sympathectomy
134
Q

How can a ganglion cyst be identified clinically?

A

most commonly seen on dorsal aspect of the wrist, firm and well circumscribed, transilluminate

135
Q

What is the management of ganglion cysts?

A

most can reassure + do nothing; if causing severe problems e.g. neurovascular involvement, refer for surgical excision

136
Q

What is Sweet’s syndrome?

A

also known as acute febrile neutrophilic dermatosis; strong association with acute myeloid leukaemia.

137
Q

What is the difference between Stevens-Johnson syndrome and toxic epidermal necrolysis?

A

SJS: rash affects < 10% of body and mucosal involvement
TEN: at least 30% body surface area (also involves MMs)

138
Q

What are 8 drugs which can cause Stevens Johnson syndrome?

A
  1. penicillin
  2. sulphonamides
  3. lamotrigine
  4. carbamazepine
  5. phenytoin
  6. allopurinol
  7. NSAIDs
  8. oral contraceptive pill
139
Q

What are the typical features of SJS?

A
  • maculopapular rash
  • target lesions
  • may develop vesicles or bullae
  • Nikolsky sign - blisters and erosions appear when rub skin
  • mucosal involvement
  • fever
  • arthralgia
140
Q

What is the management of SJS / TEN?

A

admission for supportive management

141
Q

What is the single most important prognostic factor in determining prognosis of patients with malignant melanoma?

A

Breslow thickness (depth of tumour)

142
Q

What is the difference between irritant and allergic contact dermatitis?

A
  • irritant: non-allergic due to weak acids or alkalis e.g. detergents, often hands, erythematous
  • allergic: type IV hypersensitivity, seen on head from hair dye. acute weeping eczema at hairline
143
Q

What is a material that can cause both irritant and allergic contact dermatitis?

A

cement (alkaline - irritant, also dichromates can cause allergic reaction)

144
Q

What is geographic tongue?

A
  • benign, chronic condition of unknown cause
  • presents with erythematous areas with white-grey border (irregualr smooth red areas look like map outline)
  • some patients report burning after eating certain food
145
Q

What is the management of geographic tongue?

A

reassurance about benign nature

146
Q

What is another name for dermatofibromas?

A

histiocytomas

147
Q

What is the cause of dermatofibromas?

A

abnormal growth of dermal dendritic histiocyte cells, often following precipitating injury

148
Q

Which areas of the body are often affected by dermatofibroma?

A

arms and legs

149
Q

What is the classical sign of a dermatofibroma?

A

skin dimples on pinching the lesion

150
Q

What is thought to cause seborrhoeic dermatitis?

A

inflammatory reaction related to proliferation of normal skin inhabitant, fungus Malassezia furfur

151
Q

What are 2 complications related to seborrheic dermatitis?

A
  1. otitis externa
  2. blepharitis
152
Q

What are 2 conditions associated with seborrhoeic dermatitis?

A
  1. HIV
  2. Parkinson’s disease
153
Q

What is the management of scalp seborrhoeic dermatitis?

A
  • first line: ketoconazole 2% shampoo
  • OTC preparations with zinc pyrithione (Head + Shoulders)
  • OTC preparations containing tar (e.g. Neutrogena T/Gel)
  • selenium sulphide
  • topical corticosteroid
154
Q

What are 2 options for the treatment of face + body seborrhoeic dermatitis?

A
  • topical antifungals e.g. ketoconazole
  • topical steroids (short periods)
155
Q

What is the name given to uniform hair loss / thinning of the hair caused by stress?

A

telogen effluvium

156
Q

What is alopecia totalis?

A

complete loss of all hair of head and face

157
Q

Which 2 organisms cause impetigo?

A
  1. Staphylococcus aureus
  2. Streptococcus pyogenes
158
Q

What is first line treatment for limited, localised impetigo without systemic illness?

A

hydrogen peroxide 1% cream

159
Q

If hydrogen peroxide is ineffective as first line treatment for localised impetigo what are 2 alternatives?

A
  • topical fusidic acid
  • topical mupirocin if resistance to fusidic acid suspected
160
Q

What is the treatment for extensive impetigo?

A
  1. oral flucloxacillin
  2. oral erythromycin (penicillin allergic)
161
Q

What are the school exclusion rules for children with impetigo?

A

excluded from school until lesions crusted and healed OR 48h after commencing abx treatment

162
Q

What is the difference between Janeway lesions and Osler nodes?

A
  • Janway lesions - painless erythematous haemorrhagic lesions on palms and soles - septic emobli
  • Osler nodes -painful erythematous lesions caused by immune complex deposition
163
Q

What is a kerion?

A

in tinea capitis (Scalp ringworm) when untreated can caused raised, pustular spongy/boggy mass = kerion

164
Q

How can a diagnosis of tinea capitis be made?

A
  • most useful investigation is scalp scrapings
  • lesions due to Microsporum canis show green fluorescence under Wood’s lamp
165
Q

What is the management of tinea capitis (scalp ringworm)?

A

oral antifungals
* terbinafine for Trichophyton tonsurans
* griseofulvin for Microsporum infections
* topical ketoconazole shampoo - first 2 weeks

166
Q

What is the treatment of tinea corporis (ringworm)?

A

oral fluconazole

167
Q

What is tinea pedis?

A

athlete’s foot

168
Q

What are 4 aspects of the management of guttate psoriasis?

A
  1. most cases resolve spontaneously in 2-3 months
  2. topical agents per psoriasis
  3. UVB phototherapy
  4. tonsillectomy if recurrent (as can be triggered by streptococcal infection)
169
Q

What are are 9 associations with erythema nodosum?

A
  1. streptococcal infection
  2. TB
  3. brucellosis
  4. sarcoidosis
  5. IBD
  6. Behcet’s
  7. malignancy / lymphoma
  8. drugs - penicillins, sulphonamides, COCP
  9. pregnancy
170
Q

What is the classical appearance of chronic plaque psoriasis?

A

erythematous plaques covered with a silvery-white scale

171
Q

What areas does chronic plaque psoriasis affect?

A
  • extensor surfaces such as the elbows and knees.
  • scalp
  • trunk
  • buttocks
  • periumbilical area
172
Q

What is Auspitz’s sign?

A

if the scale is removed, a red membrane with pinpoint bleeding points may be seen (chronic plaque psoriasis)

173
Q

What are 4 key features of erythema multiforme?

A
  1. target lesions
  2. initially back of hands / feet -> torso
  3. upper limbs > lower limbs
  4. pruritus occasionally seen - mild
174
Q

What is the most common cause of erythema multiforme?

A

herpes simplex virus

175
Q

What are 7 causes of erythema multiforme?

A
  1. viruses: herpes simplex virus, Orf
  2. idiopathic
  3. bacteria: mycoplasma, streptococcus
  4. drugs: penicillin, sulphonamides, COCP, NSAIDs, carbamazepine, allopurinol, nevirapine
  5. connective tissue disease e.g. SLE
  6. sarcoidosis
  7. malignancy
176
Q

What are 2 viral causes of erythema multiforme?

A
  1. herpes simplex cirus
  2. orf
177
Q

What are 2 bacterial causes of erythema multiforme?

A
  1. Mycoplasma
  2. Streptococcus
178
Q

What are 7 causes of erythema multiforme?

A
  1. Penicillin
  2. Sulphonamides
  3. Carbamazepine
  4. Allopurinol
  5. NSAIDs
  6. COCP
  7. Nevirapine
179
Q

What is erythema multiforme major?

A

erythema multiforme associated with mucosal involvement

180
Q

What distinguishes mild / moderate / severe acne?

A
  • mild: open and closed comedones + sparse inflammatory lesions
  • moderate: widespread non-inflammatory lesions + numerous papules + pustules
  • severe: extensive inflammatory lesions, may include nodules, pitting scarring
181
Q

What is the first line treatment for mild-moderate acne?

A

12 week course topical combination therapy
* adapalene+benzoyl peroxide
* tretinoin+clindamycin
* benzoyl peroxide + clindamycin)
benzoyl peroxide monotherapy - if contraindicated / avoiding retinoids + abx

182
Q

What are 4 options for treating moderate - severe acne vulgaris?

A
  1. topical combination therapy - abx + BP OR tretinoin
  2. oral antibiotic - plus topical therapy (must not use oral + topical abx together)
  3. COCP in women
  4. oral isotretinoin
183
Q

What oral antibiotic can be used for acne in pregnancy?

A

erythromycin

184
Q

What is usually the maximum period to use topical or oral abx for acne vulgaris?

A

6 months - except under exceptional circumstances

185
Q

What should always be co-prescribed with oral antibiotics for acne and why?

A

topical benzoyl peroxide or retinoid - reduce risk of resistance

186
Q

What is a possible complication of long-term antibiotic use for acne vulgaris (other than resistance)?

A

gram-negative folliculitis

187
Q

What is the treatment of gram-negative folliculitis secondary to long-term antibiotic use for acne?

A

high dose oral trimethoprim

188
Q

What is an example of a COCP used for acne and what is a key risk?

A

Dianette (co-cyprindiol) - VTE

189
Q

How long should dianette (co-cyprindiol) be continued for as a maximum for acne?

A

3 months

190
Q

What are 3 things done ot reduce the risk of antibiotic resistance from antibiotics used to treat acne?

A
  1. avoid monotherapy with topical abx
  2. avoid monotherapy with oral abx
  3. avoid combination of topical and oral abx
191
Q

What are 2 situations when patients must be referred to dermatology for acne?

A
  1. patients with acne conglobata: extensive inflammatory papules, suppurative nodules, sinuses, cysts on trunk
  2. nodulo-cystic acne
192
Q

What are 5 situations when referral to dermatology for acne should be considered?

A
  1. mild-moderate acne not responded to 2 completed courses of treatment
  2. moderate - severe acne not responded to previous treatment including oral abx
  3. acne with scarring
  4. acne with persistent pigmentary changes
  5. acne causing / contributing to persistent psychological distress / mental health disorder
193
Q

What are 5 causes of scarring alopecia?

A
  1. trauma, burns
  2. radiotherapy
  3. lichen planus
  4. discoid lupus
  5. tinea capitis (if kerion develops)
194
Q

What are 6 causes of non-scarring alopecia?

A
  1. male-pattern baldness
  2. drugs: cytotoxic, carbimazole, heparin, COCP, colchicine
  3. nutritional: iron and zinc deficiency
  4. alopecia areata
  5. telogen effluvium (hair loss after stress)
  6. trichotilliomania (pulling out hair)
195
Q

What are the dermatomes most commonly affected by shingles?

A

T1 - L2

196
Q

When are patients with shingles infectious?

A

until vesicles have crusted over - usually 5-7 days following onset

197
Q

What are the analgesia options for shingles?

A
  • paracetamol + NSAIDs first line
  • neuropathic if not responding e.g. amitryptiline
  • oral corticosteroids in first 2 weeks if immunocompetent if severe
198
Q

When should antivirals be initiated for shingles?

A

within 72 h for majority - if < 50 y with mild truncal rash + mild pain + no risk factors, may not require

199
Q

How long can post-herpetic neuralgia last?

A

6 months (sometimes longer)

200
Q

What scoring system is used in the assessment of hirsutism?

A

Ferriman-Gallwey scoring system
9 body areas assigned score 0 - 4, >15 is moderate or severe

201
Q

What are 4 treatment options for hirsutism?

A
  1. weight loss if overweight
  2. cosmetic - waxing/bleaching
  3. COCP e.g. Dianettes or Yasmin
  4. topical eflornithine (for facial hirsutism)
202
Q

What are 2 drugs which can cause hirsutism?

A
  1. phenytoin
  2. corticosteroids
203
Q

What is the stepwise management of chronic plaque psoriasis?

A
  • first line: potent corticosteroids OD + vitamin D analogue OD for up to 4 weeks
  • second line: vitamin D analogue BD for up to 8-12 weeks
  • third line: potent corticosteroid BD up to 4 weeks OR coal tar preparation OD or BD

also short-acting dithranol

204
Q

What are 7 secondary care options for the treatment of refractory chronic plaque psoriasis?

A
  1. phototherapy - narrowband UVB
  2. photochemothreapy - psoralen + UVA (PUVA)
  3. oral methotrexate
  4. ciclosporin
  5. systemic retinoids
  6. biological agents: infliximab, etanercept, adalimumab
  7. ustekinumab (IL-12 and IL-23 blocker)
205
Q

What do NICE recommend as the treatment for scalp psorasis first + second line?

A
  1. potent topical steroids OD 4 weeks
  2. different formulation of potent corticosteroid (eg. shampoo or mousse) and/or topical agents to remove scale (e.g. salicylic acid, emollients, oils) before aplication
206
Q

What is the management of face, flexural and genital psoriasis?

A

mild or moderate potency corticosteroid OD or BD for max 2 weeks

207
Q

What is the mechanism of action of topical vitamin D analogues to treat psoriasis?

A

reducing cell divsion and differentiation to reduce epidermal proliferation

208
Q

What is the mechanism of action of dithranol to treat psoriasis?

A

inhibits DNA synthesis (wash off afer 30 min)

209
Q

What is the likely diagnosis in someone with widespread discoid (coin-shaped) scaly lesions that develop in cold weather and ooze serum and crust over?

A

discoid (nummular) eczema

210
Q

What is anagen effluvium?

A

chemotherapy / immunosuppression / radiotherapy causes rapid hair loss

211
Q

What is the incubation period of impetigo?

A

4-10 days

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