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4th year presentations > Dermatology > Flashcards

Dermatology Flashcards

1
Q

What is a vesicle?

A

Fluid-filled blister less than 0.5 cm in diameter

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2
Q

What is a bulla?

A

Fluid-filled blister more than 0.5 cm in diameter

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3
Q

What is a skin fissure?

A

Deep crack/crevice into skin

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4
Q

What is a macule?

A

Flat pigmented lesion less than 1 cm in diameter

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5
Q

What is a patch?

A

Flat pigmented lesion more than 1 cm in diamter

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6
Q

What is a papule?

A

Raised lesion less than 0.5 cm in diameter

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7
Q

What is a nodule?

A

Raised lesion more than 0.5 cm in diameter

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8
Q

What is a pustule?

A

Pus-filled lesion

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9
Q

What is a plaque?

A

Raised lesion more than 1 cm in diameter

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10
Q

What is lichenification?

A

Thickened skin

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11
Q

What is purpura?

A

Purple pigmentation that does not blanche

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12
Q

What is petechiae?

A

1-2 mm of purpura

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13
Q

What is erythema?

A

Red pigmentation that does blanche

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14
Q

What is an erosion?

A

Superficial break in epidermis

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15
Q

What is an ulcer?

A

Deep break in epidermis and dermis

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16
Q

What is a wheal?

A

Compressible dermal swelling

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17
Q

List skin manifestations of diabetes

A 
Flexural candidiasis
Folliculitis, infection
Necrobiosis lipoidica
Acanthosis nigricans
Ulcers
Xanthomata
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18
Q

What is necrobiosis lipoidica?

A

Waxy, shiny red-brown plaques with atrophic yellow lesions on shins

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19
Q

What is acanthosis nigricans?

A

Velvety thickening of skin, usually in the axillae

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20
Q

What is the main skin manifestation of Coeliac disease?

A

Dermatitis herpetiformis

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21
Q

List skin manifestations of inflammatory bowel disease

A

Erythema nodosum

Pyoderma gangrenosum

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22
Q

What is erythema nodosum?

A

Tender, ill-defined nodules usually found on shins

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23
Q

What is pyoderma gangrenosum?

A

Recurring nodulo-pustular ulcers that have a red-blue necrotic edge

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24
Q

List skin manifestations of systemic lupus erythematosus

A

Butterfly rash
Photosensitivity
Alopecia

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25
Q

What is the main skin manifestation of herpes simplex infection?

A

Erythema multiforme

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26
Q

List skin manifestations of vasculitis

A

Purpura (may be palpable)
Nodules
Livedo reticularis

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27
Q

What is livedo reticularis?

A

Mottled red-blue lesions that don’t blanche

Usually triggered in the cold

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28
Q

List skin manifestations of dermatomyositis

A

Heliotrope rash
Gottron’s papules
Scaly red plaques over neck (V-sign)
Periungual redness

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29
Q

List aetiology/risk factors for atopic dermatitis

A

Genetic mutation in filaggrin gene
Overactive TH2 cells results in more circulating IL-4, IL-5, IgE
Infection (Staph aureus)
Exacerbators (dust, temperature, allergies)

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30
Q

List clinical features of atopic dermatitis

A 
Itchy, dry skin
Flexural scale and erythema
Weepy vesicles
Lichenification
Hyperlinear pals
Eczema herpeticum (HSV infection)
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31
Q

What investigations would you do for atopic dermatitis?

A

Serum IgE

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32
Q

What is the clinical criteria for diagnosing childhood eczema?

A 
Itch + 3 of:
Flexural rash
Onset before 2 years of age
History of atopy
Dry skin
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33
Q

Outline treatment options for atopic dermatitis

A

Allergen/trigger avoidance
Emollients (Epaderm, Diprobase)
Topical steroid (hydrocortisone, clobetasone, betametasone, mometasone, clobetasol)
Immunomodulator (tacrolimus, ciclosporin)
Antibiotic if infection
Antihistamine
Paste bandaging
Phototherapy/systemic therapy if non-responsive

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34
Q

Ointments are more effective than emollients for dry skin. True/False?

A

True

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35
Q

What is contact allergic dermatitis?

A

Type IV hypersensitivity skin reaction to environmental allergens

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36
Q

List aetiology/risk factors for contact allergic dermatitis

A

Nickel
Chemicals, creams
Rubber
Occupational substances

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37
Q

List clinical features of contact allergic dermatitis

A

Localised rash with cut-off patern
Itch
Rhinitis
Wheal

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38
Q

What is contact irritant dermatitis?

A

Non-specific skin reaction to environmental substances

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39
Q

List aetiology/risk factors for contact irritant dermatitis

A 
Soap, detergents
Oil
Bleach
Trauma
Occupational substances
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40
Q

List clinical features of contact irritant dermatitis

A

Localised rash/redness
Weeping
Dry fissures
Usually hands affected

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41
Q

How would you differentiate between contact allergic and irritant dermatitis?

A

Patch testing to check for allergic trigger

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42
Q

Outline treatment for contact dermatitis

A

Avoid allergen/trigger

Topical steroid

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43
Q

What is stasis dermatitis?

A

Chronic venous insufficiency/hypertension causes blood pooling and skin disease

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44
Q

List aetiology/risk factors for stasis dermatitis

A

Obesity
Varicose veins
History of DVT

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45
Q

List clinical features of stasis dermatitis

A

Haemosiderin staining (brown pigments)
Ulcers
Hair loss
Painless scale, itch

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46
Q

Outline treatment for stasis dermatitis

A

Emollients
Topical steroid
Compression stockings, leg elevation

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47
Q

What is lichen simplex dermatitis?

A

Self-induced eczema due to repeated physical trauma

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48
Q

What is acne vulgaris?

A

Inflammation of pilosebaceous unit that causes a rash, typically in areas high in concentration of these glands (face, neck, chest, back)

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49
Q

What causes comedones in acne?

A

Abnormal keratinisation/desquamation within pilosebaceous unit causes blockage of secretions and comedone formation

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50
Q

Open comedones are white/black heads and closed comedones are white/black heads

A

Open comedones are blackheads and closed comedones are whiteheads

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51
Q

List aetiology/risk factors for acne vulgaris

A

Increased sebum production (increased androgens, CRH)
P. acnes infection
Occlusion of pilosebaceous unit
Dermal inflammation

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52
Q

List clinical features of acne

A

Comedones
Seborrhoea
Inflammatory papules and pustules, nodules
Scars and cysts in severe acne
Psych disturbance
Develop keloid scars: thick inflamed lesions on trunk and shoulders

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53
Q

Outline treatment for mild, moderate and severe acne

A

Education and psych support, dispel myths
Mild: topical benzoyl peroxide +/- azelaic acid, antibiotic
Moderate: topical doxycycline/erythromycin + benzoyl peroxide
Severe: oral isotretinoin

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54
Q

What is acne rosacea?

A

Chronic relapsing-remitting facial rash usually affecting convex areas

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55
Q

List aetiology/risk factors for acne rosacea

A 
Largely unknown
Chlamydia
Demodex mite
Spicy food
Alcohol
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56
Q

List clinical features of acne rosacea

A 
Rhinophyma
Facial flushing
NO COMEDONES
Telangiectasia
Erythema
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57
Q

Outline treatment of acne rosacea

A

Avoid irritants
Topical azelaic acid + metronidazole
Oral azithromycin for chlamydia

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58
Q

What is pemphigus vulgaris?

A

Autoimmune blistering condition caused by IgG produced against desmoglein 3, causing loss of adhesion of epidermis to basal layer

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59
Q

List aetiology/risk factors for pemphigus vulgaris

A

Autoimmunity
Genetics
Drugs (ACEi, NSAID, phenobarbitol, levodopa)

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60
Q

List clinical features of pemphigus vulgaris

A

Flaccid, superficial, fluid-filled blisters
Rupture leaves erosions
Nikolsky sign +ve
Oral mucosal ulcers

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61
Q

What investigation would you do for pemphigus vulgaris?

A

Skin biopsy for immunofluorescence shows IgG crazy-paving/chicken-wire pattern in epidermis

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62
Q

Outline treatment for pemphigus vulgaris

A

High-dose oral prednisolone

Immunosuppression (rituximab, azathioprine)

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63
Q

What is bullous pemphigoid?

A

Autoimmune blistering condition caused by IgG produced against hemidesmosomes and basement membrane, causing sub-epidermal separation

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64
Q

Which is more common - bullous pemphigoid or pemphigus vulgaris?

A

Bullous pemphigoid

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65
Q

List clinical features of bullous pemphigoid

A

Large, tense bullae
Urticated base
Nikolsky sign -ve

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66
Q

What investigation would you do for bullous pemphigoid?

A

Skin biopsy for immunofluorescence shows linear IgG deposition along basement membrane

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67
Q

Outline treatment for bullous pemphigoid

A

High-dose oral steroid

Clobetasol propionate cream

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68
Q

What is dermatitis herpetiformis?

A

Rare autoimmune blistering condition caused by IgA cross-reacting with connective tissue matrix proteins, causing sub-epidermal separation

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69
Q

Which condition is associated with dermatitis herpetiformis?

A

Coeliac disease (HLA DQ2)

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70
Q

List clinical features of dermatitis herpetiformis

A

Small, intense itchy blisters usually on elbow/scalp/shoulders/ankles
Crusting

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71
Q

What investigation would you do for dermatitis herpetiformis?

A

Skin biopsy histology shows dermal papillary microabscesses

IgA immunofluorescence

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72
Q

Outline treatment for dermatitis herpetiformis

A

Oral dapsone

Gluten-free diet

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73
Q

List skin manifestations of hyperthyroidism

A 
Moist smooth skin
Facial flushing
Palmar erythema
Fine, thin hair/alopecia
Hyperhidrosis
Nail changes
Hyperpigmentation
Pretibial myxoedema
Urticaria
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74
Q

List skin manifestations of hypothyroidism

A 
Cold, dry, pale skin
Coarse, brittle hair
Thickened nails
Generalised myxoedema
Peri-orbital oedema
Facial puffiness
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75
Q

List skin manifestations of Addison’s disease

A

Palmar crease pigmentation

Buccal pigmentation

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76
Q

List skin manifestations of endocrine tumours

A

Hyperpigmentation
Hirsutism
Acne
Baldness

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77
Q

List skin manifestations of systemic sclerosis

A 
Pinched mouth
Radial furrows
Beaked nose
Facial telangiectasia
Raynaud's phenomenon
Dysphagia
Sclerodactyly
Calcinosis
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78
Q

What is pityriasis rosea?

A

Common skin rash tending to occur in epidemics, presenting with solitary herald patch with subsequent truncal eruption of pink oval lesions with scale

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79
Q

What is vitiligo?

A

Acquired de-pigmentation caused by loss of melanocytes

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80
Q

List aetiology/risk factors for generalised hair loss

A 
Telogen effluvium
Endocrine disease (thyroid)
Drugs
Dietary deficiency (iron, zinc, vit D)
Alopecia areata
Malnutrition
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81
Q

What investigations would you do for hair loss?

A 
Skin scraping, hair plucking
Woods lamp examination
Dermoscopy
Scalp biopsy
Bloods: hormones, FBC, thyroid
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82
Q

What is alopecia areata?

A

Autoimmune cause of hair loss in round/spotty distribution all over the body

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83
Q

What is hirsutism?

A

Male-pattern hair growth in response to increased androgenic drive/levels

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84
Q

List aetiology/risk factors of hirsutism

A 
Familial, genetics
Adrenal hyperplasia/tumour
PCOS
Hyperprolactinaemia
Drugs (danazol, glucocorticoids)
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85
Q

What investigations would you do for hirsutism?

A

Hormones: testosterone, DHEA, SHBG, LH, FSH

Ovarian USS if indicated

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86
Q

What is hypertrichosis?

A

Excessive hair growth in a non-androgenic distribution

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87
Q

List aetiology/risk factors for hypertrichosis

A 
Naevi
Chronic scarring/inflammation
Malnutrition
Anorexia
Porphyria cutanea tarda
Occult malignancy
Drugs (minoxidil, phenytoin, ciclosporin)
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88
Q

What is the most common type of drug skin eruption?

A

Maculopapular/Exanthematous - up to 2-3 weeks after administration

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89
Q

List some drugs that cause exanthematous skin eruptions

A 
Penicillin
Carbamazepine
Allopurinol
NSAID
Cephalosporins
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90
Q

When does drug-induced urticaria usually onset?

A

Within 36 hours of administration but may develop within minutes when re-challenged

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91
Q

What is Steven-Johnson syndrome?

A

Full-thickness epidermal necrolysis, involving mucosal erosions, occurring in response to drugs and/or illness

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92
Q

List some drugs that cause Steven-Johnson syndrome

A

Allopurinol
Antibiotics
Anticonvulsants
NSAID

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93
Q

What is the difference between Steven-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)?

A

SJS involves up to 30% epidermal detachment

TEN involves more than 30% epidermal detachment

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94
Q

List some drugs that cause erythroderma/exfoliative dermatitis

A 
Barbiturates
Gold
Quinine
Sulphonamides
Carbamazepine
Allopurinol
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95
Q

Fixed drug eruptions are mediated by what cells and occur when?

A

Mediated by T memory cells

Occur 1-2 weeks after exposure and may persist and reappear with further exposure

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96
Q

List some drugs that cause fixed drug eruptions

A 
Tetracyclines
Phenolphthalein
NSAIDs
Quinine
Oral contraceptive
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97
Q

List some drugs that cause lichenoid eruptions

A

B blockers
Captopril
Thiazides
Furosemide

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98
Q

Outline general management of drug eruptions

A 
Stop likely drug offender
Regular emollients for dryness and itch
Topical steroid
IV hydrocortisone + antihistamine for urticaria
Specialist/ICU management if severe
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99
Q

Outline management of an insect bite

A

Prevent with insect repellant
Topical steroid
Antihistamine
Treat affected animals and environment

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100
Q

What disease can tick bites cause and why?

A

Lyme disease

Ticks transmit Borrelia Burgdorferi, a spirochaete responsible for lyme disease

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101
Q

Describe the first clinical stage of lyme disease

A

Erythema chronicum migrans, usually up to 14 days after bite, seen as a solitary macule or annular lesion
May have mild systemic symptoms

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102
Q

Describe the second clinical stage of lyme disease

A

Borrelia lymphocytoma occurs up to 6 months after the bite, involving firm blue-red swelling or earlobes/nipples
Tender local lymphadenopathy
Associated numbness/arthralgia/myalgia/paralysis

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103
Q

Describe the third clinical stage of lyme disease

A

Acrodermatitis chronica atrophicans up to 8 years after initial infection, involving blue-red discolouration and atrophy
Early inflammation, late atrophy
Associated arthritis/neuropathy/pain

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104
Q

List non-cutaneous features of lyme disease

A 
Fever, malaise, lymphadenopathy
Cough
Headache
Conjunctivitis, keratitis, iritis
Meningitis, encephalitis, GBS
Heart block, arrhythmia, cardiomyopathy
Arthralgia, tendonitis
Orchitis, proteinuria, haematuria
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5
Perfectly
105
Q

Outline treatment of lyme disease

A

Doxycycline + amoxicillin/cefuoroxime/erythromycin

IV penicillin/ceftriaxone if severe

106
Q

What systemic reaction may be caused in treating lyme disease in the 1st 24 hours?

A

Jarisch Herxheimer reaction involving release of endotoxin due to large numbers of organisms being killed

107
Q

What is scabies?

A

Contagious skin infestation caused by Sarcoptes scabei

108
Q

List aetiology/risk factors for scabies

A

Poor hygiene
Prolonged close/sexual contact
Hotel bedding

109
Q

When do symptoms of scabies typically onset?

A

Individuals can be asymptomatic for up to 6 weeks, then delayed hypersensitivity reaction develops

110
Q

List clinical features of scabies

A 
Intensely itchy
Red papules
Rubbery nodules
Burrow lines
Vesicles, pustules
Involves finger webs, wrist flexures, axillae, abdomen, palms, soles
111
Q

How would you make the diagnosis of scabies?

A

Clinical diagnosis

Skin scraping and microscopy

112
Q

Outline treatment of scabies

A 
Permethrin cream
Symptom relief (steroid, anti-pruritic)
113
Q

What are headlice?

A

Tiny flightless insects that feed on blood from the scalp

Infestation common in school children

114
Q

List clinical features of headlice

A

Eggs in scalp hair
Itch
Papular rash on nape of neck
Secondary infection

115
Q

Outline treatment of headlice

A

Physical removal using fine-tooth comb and shampoo

Anti-parasitic (malathion, dimeticone)

116
Q

What is furunculosis?

A

Acute deep infection of hair follicles

117
Q

What is staphylococcal scalded skin syndrome?

A

Epidermolytic exotoxin produced by Staph that causes splitting between desmosomes in granular layer

118
Q

What are the three phases in the growth cycle of a hair?

A

Anagen (growth)
Catagen (involution)
Telogen (rest)

119
Q

Most hair is in the anagen phase. True/False?

A

True

120
Q

What is telogen effluvium?

A

Reversible/transient hair loss due to stress

121
Q

What treatment may be tried for androgenetic hair loss?

A

Minoxidil

Anti-androgenic drugs

122
Q

What is Beau’s line?

A

White horizontal line on nail caused by transient arrest in nail growth due to stress/trauma/illness

123
Q

What are main causes of acute paronychia? (inflammation of the nail)

A

Staph or Strep infection

124
Q

What are the main causes of chronic paronychia?

A

Candida

Mould

125
Q

What are characteristic histological features of acute eczema?

A

Spongiosis
Acanthosis
Inflammatory infiltrate

126
Q

List the main endogenous dermatitis conditions

A 
Atopic dermatitis
Seborrhoeic dermatitis
Discoid eczema
Nodular prurigo
Lichen simplex chronicus
127
Q

What is impetigo?

A

Highly contagious infection mostly seen in children caused by Staph aureus

128
Q

List clinical features of impetigo

A

Well-defined honey-coloured crusting on face/nose
Erythematous base
Superficial flaccid blisters
Weeping

129
Q

Outline treatment for impetigo

A

Topical fusidic acid
Oral flucloxacillin
Avoid school/close contact

130
Q

What is erysipelas?

A

Localised cellulitis usually affecting the face caused by Strep pyogenes

131
Q

List clinical features of erysipelas

A

Sharply defined superficial rash, usually on face
Unilateral
Associated fever

132
Q

Which antibiotic is used to treat erysipelas?

A

Penicillin

133
Q

What is cellulitis?

A

Acute severe infection of skin and soft tissues that is deeper and less well-defined than erysipelas

134
Q

List aetiology/risk factors for cellulitis

A 
B-haemolytic Strep (pyogenes)
Staph aureus
Trauma
Vascular disease, poor healing
Immunosuppression
135
Q

List clinical features of cellulitis

A 
Severe pain
Swelling
Erythema
Systemic upset
Lymphadenopathy
136
Q

Outline treatment of cellulitis

A

IV benzylpenicillin + PO flucloxacillin

Erythromycin if penicillin-allergic

137
Q

What is necrotising fasciitis?

A

Life-threatening subcutaneous/soft tissue infection

138
Q

List aetiology/risk factors for necrotising fasciitis

A

Type 1: polymicrobial (mixed aerobes-anaerobes)

Type 2: group A Strep (pyogenes)

139
Q

List clinical features of necrotising fasciitis

A 
Extreme pain
Paraesthesia
Systemic upset
SEPSIS
Spreading erythema
140
Q

Outline treatment of necrotising fasciitis

A

Surgical debridement

IV benzylpenicillin + clindamycin

141
Q

Which strain of HPV causes viral warts?

A

HPV 6 and 11

142
Q

List clinical features of viral warts

A 
Skin-coloured/brown lesions
Affect large confluence areas on soles
Highly infectious
May affect genitals
Koebner phenomenon
143
Q

Outline treatment of viral warts

A 
Resolve spontaneously
Topical keratolytic (salicyclic acid)
Liquid nitrogen cryotherapy
Cautery/laser therapy
Imiquimod
Antiviral if severe
144
Q

List aetiology/risk factors for herpes infection

A

Triggers (sunlight, fever)
Immunosuppression
Close contact with infected person

145
Q

List clinical features of herpes infection

A

Burning
Itching
Grouped, painful vesicles
Erythematous base

146
Q

Outline treatment of herpes

A

Self-limiting

Topical aciclovir

147
Q

What is shingles?

A

Reactivation of Varicella zoster in dorsal root ganglion of spine causes skin rash in unilateral dermatomal distribution

148
Q

List clinical features of shingles

A 
Polymorphic eruption
Red papules, vesicles, pustules, crusting
Dermatomal distribution
May heal with scarring
Post-herpetic neuralgia
149
Q

Outline treatment of shingles

A

Analgesia

Oral aciclovir

150
Q

What is molluscum contagiosum?

A

Pox virus causes chronic infection usually in children

151
Q

List clinical features of molluscum contagiosum

A

Pink papules with central puntum
Expressed white discharge
Painless nodules

152
Q

Outline treatment of molluscum contagiosum

A

Self-resolving
Cryotherapy
Curettage

153
Q

What are dermatophyte infections?

A

Fungal infections caused by ringworm organisms (Epidermophyton, Trichophyton, Microsporum)

154
Q

List clinical features of dermatophyte infections

A

Round, itchy lesions with inflamed border
Tinea corporis/cruris/pedis/capitis/unguium
Well-demarcated red plaques
Between toe clefts
Whitening of nails
Scale
Alopecia

155
Q

How would you investigate fungal skin infections?

A

Skin scraping microscopy/culture

Wood’s lamp fluoresecence

156
Q

Outline treatment for fungal skin infections

A 
Antifungal cream (terbinafine, clotrimazole)
Oral terbinafine for scalp involvement
157
Q

List aetiology/risk factors for Candida infection

A

Immunosuppression
Long-term steroid/inhaler use
Poor hygiene

158
Q

List clinical features of Candida infection

A

Pink, moist “satellite” lesions
Peeling
Pustules, papules
Oral white patches

159
Q

Outline treatment of Candida infection

A 
Topical clotrimzaole/terbinafine
Oral nystatin
Vaginal imidazole
Steroid cream if itchy/finalmed
Oral fluconazole if not improving
160
Q

List clinical features of lichen planus

A 
Purple pruritic polyangular planar papules
Usually on flexor aspects
White lacy markings (Wickham's striae)
Scarring alopecia
Longitudinal ridges, pterygium on nails
Oral/genital lesions
161
Q

Outline treatment of lichen planus

A

Topical steroid

Antifungal (topical, spray)

162
Q

What is a hemangioma?

A

Benign vascular dilation typically in neonates

163
Q

List clinical features of hemangioma

A

Strawberry naevus: rapidly enlarging red spot

Pyogenic granuloma: moist red lesion on finger that bleeds easily

164
Q

Outline treatment for hemangioma

A

Self-resolving
Curettage
B-blocker
Steroid

165
Q

List the main non-melanoma skin cancers

A

Actinic keratosis
Bowen’s disease
Basal cell carcinoma
Squamous cell carcinoma

166
Q

What is actinic keratosis?

A

Pre-malignant partial thickness dysplasia involving intra-epidermal porliferation of atypical keratinocytes

167
Q

List aetiology/risk factors for actinic keratosis

A

Sun damage

Fair skin

168
Q

List clinical features of actinic keratosis

A

Erythematous crumbly yellow-white scale
Crusts
Tense skin
Actinic lentinges

169
Q

Outline treatment for actinic keratosis

A

Education, sun protection
Cryotherapy
Surgical excision/curettage if suspect SCC
Topical 5-fluoracil/imiquimod/diclofenac

170
Q

What is bowen’s disease?

A

Pre-malignant full thickness dysplasia (carcinoma in-situ)

171
Q

List clinical features of bowen’s disease

A

Slow-growing red scaly plaque
Erythema
Ill-defined
Usually on lower legs of females

172
Q

Outline treatment of bowen’s disease

A

Cryotherapy
Topical 5-fluoracil/imiquimod
Photodynamic therapy

173
Q

What is the most common skin cancer?

A

Basal cell carcinoma

174
Q

List aetiology/risk factors for basal cell carcinoma

A

Sun exposure
Mutated TP53 gene
PTCH1 mutation causes Gorlin’s syndrome

175
Q

List clinical features of basal cell carcinoma

A

Slow-growing pearly translucent lump with rolled telangiectatic edge
Well-define
May have central ulceration

176
Q

Outline treatment of basal cell carcinoma

A 
Excision
Mohs' surgery if recurrent/difficult
Photodynamic therapy
Radiotherapy if big
Cryotherapy/curettage
Imiquimod
177
Q

List aetiology/risk factors for squamous cell carcinoma

A 
Sun exposure
Actinic keratosis
Bowen's disease
Marjolin's ulcer
Smoking
Chronic inflammation
178
Q

List clinical features of squamous cell carcinoma

A

Ulcerating, hyperkeratotic lesion
Firm and irregular
Ill-defined
Crusted

179
Q

Outline treatment of squamous cell carcinoma

A

Excision
Topical imiquimod/5-fluoracil
Radiotherapy

180
Q

What is basal cell papilloma?

A

Common benign lesion involving overgrowth of basal cell layer
AKA seborrhoeic keratosis

181
Q

List aetiology/risk factors for basal cell papilloma

A

Chronic UV damage
Genetics
Idiopathic
FGR3 mutation

182
Q

List clinical features of basal cell papilloma

A

Brown greasy “stuck-on” appearance

Irritating, catch on clothes etc.

183
Q

Outline treatment of basal cell papiloma

A

Leave if asymptomatic
Cryotherapy/curettage
Excision

184
Q

What are lentigos?

A

Brown macules/papules that may be pre-malignant

185
Q

What is lentigo maligna?

A

Precursor to invasive melanoma

melanoma in-situ

186
Q

What are melanocytic naevi?

A

Benign overgrowth of melanocytes that are mostly not pre-malignant

187
Q

What are the different histological types of melanocytic naevi?

A

Junctional: at DEJ
Compound: into dermis from DEJ
Intradermal: in dermis

188
Q

List aetiology/risk factors for melanocytic naevi

A

Congenital “birthmark”
Idiopathic
Sun/UV exposure

189
Q

When would you be worried about a melanocytic naevus?

A

If greater than 5-6mm and irregular and growing

190
Q

What is the fastest increasing skin cancer?

A

Malignant melanoma

191
Q

List aetiology/risk factors for malignant melanoma

A 
Sun/UV exposure
Sunburn
Sunbed use
Sun, sun, suuuuun, all over our bodies
Fair skin type
More than 50 melanocytic naevi
Lentigo maligna
Family history
BRAF gene mutation
192
Q

What are the different histological types of melanoma?

A

Superficial spreading (most common)
Lentigo maligna
Acral lentiginous
Nodular

193
Q

List clinical features of melanoma

A 
Rapidly growing/evolving irregular lesion
Varied pigmentation, generally brown
Associated ulceration
Asymmetry
Diameter greater than 6mm
194
Q

Outline treatment of melanoma

A

Excision
Sentinel node biopsy
Chemotherapy
Education and protection from sun

195
Q

Define a chronic leg ulcers

A

Open lesion between knee and ankle joint that remains unhealed for 4 weeks

196
Q

List aetiology/risk factors for leg ulcers

A 
Venous/arterial insufficiency
Diabetes
DVT
Malignancy
Vasculitis
Inflammation
Obesity
197
Q

List clinical features of venous ulcers

A 
Superficial
Venous disease (varicose veins)
Haemosiderin staining
Venous eczema
Lipidodermatosclerosis
Atrophie blanche
Generally painless
198
Q

List clinical features of arterial ulcers

A 
Deep, punched out
Tendon exposure
Foot/toes/pressure points
Hair loss
Cold limb
Generally painful
199
Q

What measurement is essential to make before applying pressure bandaging?

A

ABPI

200
Q

State the cut-offs for ABPI

A

0.8 - 1.3 is normal
Less than 0.8 indicates vascular disease
Greater than 1.5 indicates calcificiation

201
Q

Outline treatment of venous ulcers

A 
De-slough agent
Graduated compression greater at ankle than below knee
Non-adherent dressing
Weekly/daily changing
Aim to heal by 12 weeks
Emollients/steroid for eczema
202
Q

Outline treatment of arterial ulcers

A 
Pain relief
Lifestyle changes
Aspirin
Treat infection
Soffban, crepe bandage toe to knee to reduce oedema
Vascular surgery
Topical -ve pressure treatment
203
Q

What are port-wine stains?

A

Naevus flammeus
Capillary malformation results in macular lesion that is lifelong and usually unilateral
Do not extend but may get hyperplasia

204
Q

What is the commonest genodermatosis?

A

Neurofibromatosis type 1

205
Q

What is neurofibromatosis type 1?

A

Autosomal dominant defect in NF1 amino acid which inactivates oncogenes, causing neuroectodermal disorder

206
Q

List clinical features of neurofibromatosis

A 
Cafe au lait macules
Axillary freckles
Lisch nodules in iris
Learning difficulty
Skeletal dysplasia
Fleshy skin tags/neurofibromas
207
Q

What is tuberous sclerosis?

A

Autosomal dominant defect in TSC1 (hamartin) or TSC2 (tuberin) that allows hamartoma development

208
Q

List clinical features of tuberous sclerosis

A 
Ash leaf (depigmented) macules
Dental pits
Periungual fibromata
Adenoma sebaceum
Shagreen patch
Epilepsy
Mental retardation
Autism
Lipoma
209
Q

Outline treatment for neurofibromatosis type 1 and tuberous sclerosis

A

Surgical removal of skin lesions
Laser therapy
Surveillance
Treat symptoms/complications

210
Q

What is epidermolysis bullosa?

A

Inherited skin fragility involving mutated skin structure proteins

211
Q

What are the histological subtypes of epidermolysis bulosa?

A

Simplex: involves epidermis
Junctional: involves DEJ
Dystrophic: involves dermis

212
Q

List clinical features of epidermolysis bullosa

A 
Recurrent blisters and erosions
Poor healing
Milia
Scarring
Dystrophic nails
213
Q

Outline treatment of epidermolysis bullosa

A

Dressing wounds
Topical antibacterial
Sterile drainage

214
Q

List hazards of UV exposure

A

Sunburn
Eye damage
Skin cancer
Photosensitivity

215
Q

Sort the different types of UV radiation from longest to shortest wavelength (most penetrating to least penetrating)

A

UVA
UVB
UVC

216
Q

What are the main forms of therapeutic UV radiation?

A

Phototherapy (UVB)
Photochemotherapy (Psoralen UVA) (PUVA)
Photodynamic therapy

217
Q

List Fitzpatrick skin types

A 
I: always burns
II: usually burns, can tan
III: usually tans, can burn
IV: always tans
V: brown skin
VI: black skin
218
Q

When does UVB “sunburn” erythema onset? What mediates the erythema?

A

Onset 2-4 hours
Peak 12-24 hours
Mediated by prostaglandins

219
Q

When does PUVA erythema onset? What mediates the erythema?

A

Onset 24 hours
Peak 96 hours
Mediated by oxygen/free radicals

220
Q

It is more likely to develop squamous cell carcinoma with cumulative sunburn and melanoma with acute sunburn. True/False?

A

True

221
Q

List the main immunological photodermatoses

A 
Polymorphic light eruption
Actinic prurigo
Solar urticaria
Chronic actinic dermatitis
Hydro vacciniforme
222
Q

What is polymorphic light eruption?

A

Delayed reaction to sunlight involving non-scarring papulo-vesicular rash and hardening of skin

223
Q

When does actinic prurigo typically onset?

A

Childhood

224
Q

What is solar urticaria?

A

Rare acute type 1 hypersensitivity reaction to sunlight

225
Q

List the main genetic photodermatose

A

Xeroderma pigmentosum

226
Q

What is xeroderma pigmentosum?

A

Rare, autosomal recessive failure of DNA repair, causing rapid photo-ageing of skin and skin cancer
Often death in teens

227
Q

List common drugs that cause photosensitivity

A 
Psoralens (lime, celery)
Antibiotics (sulfonamides, tetracycline, fluoroquinolones)
Diuretics
NSAIDs
Quinine
Amiodarone
228
Q

What are porphyrias?

A

Inherited/acquired photosensitivty caused by deficit in enzymes in the haem pathway, resulting in build-up of porphyrins that react to light

229
Q

Which enzyme is deficient in porphyria cutanea tarda?

A

Uroporphyrinogen decarboxylase

230
Q

List aetiology/risk factors for porphyria cutanea tarda

A 
Haemochromoatosis
HIV
Hepatitis C
Alcohol
Oestrogen excess
Iron excess
231
Q

List clinical features of porphyria cutanea tarda

A 
Vesicles/bullae in sun-exposed sites
Hypertrichosis
Hyperpigmentation
Skin fragility
Scarring
232
Q

What investigations would you do for porphyria cutanea tarda?

A

LFTs typically deranged
High serum ferritin
Plasma/faecal/urinary porphyrins

233
Q

Which enzyme is deficient in erythropoietic porphyria?

A

Ferrochelatase

234
Q

List clinical features of erythropoietic porphyria

A

Swelling
Burning pain
Young kid tingling/itchy skin in sunlight
Gallstones

235
Q

Which enzyme is deficient in acute intermittent porphyria?

A

PBG deaminase

236
Q

List aetiology/risk factors for acute intermittent porphyria

A

Autosomal dominant
Alcohol
Contraception (increased progesterone)

237
Q

List clinical features of acute intermittent porphyria

A

Neuro + autonomic upset
Nausea
Pain

238
Q

Outline treatment of porphyrias

A 
Avoid sunlight
Remove precipitants
Venesection if ferritin high
Support and education
Haemarginate in AIP
239
Q

What is psoriasis?

A

Chronic inflammatory skin condition involving uncontrolled epidermal proliferation (parakeratosis) and T-cell-driven inflammatory infiltration of epidermis and dermis

240
Q

List aetiology/risk factors for psoriasis

A

Genetics, strong family history
Triggers (stress, infection, trauma, alcohol, obesity)
Smoking
Drugs (B-blockers, lithium, antimalarials)
TH1 + TH17 cells

241
Q

List clinical features of psoriasis

A 
Symmetrical well-defined itchy red plaques
Scale
Usually affects extensors
Nail changes (pitting, onycholysis, subungual keratosis)
Koebner phenomenon
Auspitz sign
Small plaques (guttate) in young
Pustules if severe
Psoriatic arthritis
Erythroderma with systemic upset
242
Q

What investigations would you do for psoriasis?

A

Skin biopsy for histology shows parakeratosis, epidermal proliferation and microabscesses with inflammatory infiltrate

243
Q

Outline treatment for psoriasis

A 
Education, avoid triggers/stressors
Emollients for cooling
Vitamin D analogue (calcipotriol)
Topical steroid
Coal tar preparations
Short-term retinoid (Acitretin)
Dithranol, tazarotene if unresponsive
Immunosuppression (methotrexate, etanercept, infliximab)
Phototherapy
244
Q

List infective skin manifestations of HIV

A 
HIV seroconversion disease
Thrush
Molluscum contagiosum
Herpes
Varicella zoster
Cryptococcus
Oral hairy leukoplakia
245
Q

List inflammatory manifestations of HIV

A

Seborrhoeic dermatitis
Psoriasis
Eosinophillic folliculitis

246
Q

What malignancy associated with HIV has prominent skin features?

A

Kaposi sarcoma

247
Q

What causes Kaposi’s sarcoma?

A

Herpes hominis virus (HHV-8)

248
Q

List clinical features of Kaposi’s sarcoma

A

Purpule macules
Papules, nodules
Plaques affecting skin and mucosa
Periorbital purpura (racoon eyes)

249
Q

Outline treatment of Kaposi’s sarcoma

A

HAAR
Radiotherapy
Interferon-alpha

250
Q

Dermatitis to latex is type 1 hypersensitivity. True/False?

A

True

Do skin prick IgE test, not patch test

251
Q

What are halo naevi?

A

Immune reponse to a mole

Has a “fried egg” appearance

252
Q

What are blue naevi?

A

Result due to melanocytes that failed to fully migrate from neural cell crest

253
Q

What is Sturge Weber syndrome?

A

Port wine staining affects CN V1 nerve distribution

Associated with vascular malformations on ipsilateral side, including in the brain

254
Q

What is Klippel Trenauney syndrome?

A

Capillary + venous malformation that causes progressive limb overgrowth with purpuric rash

255
Q

If a strawberry naevus affects the eye in children, what might develop?

A

Ambliopia or other visual field defects - refer urgently to ophthalmology

256
Q

How long do individual lesions of urticaria normally last?

A

Up to 24 hours
Acute urticaria: up to 6 weeks
Chronic urticaria: over 6 weeks

257
Q

Which cell is responsible for releasing inflammatory mediators that cause urticaria?

A

Mast cell

258
Q

List causes of urticaria

A 
Allergy (not usually chronic)
Direct chemicals
Physical (dermographism, vibration, cold, solar)
Autoimmune conditions
Infection
Dermatitis
259
Q

What treatments are available to block the effects of mediators released from mast cells?

A

Antihistamines
Leukotriene antagonists
Serotonin antagonists

260
Q

Which histamine receptors are relevant in urticaria?

A

H1
H2
H4

261
Q

What is anaphylaxis?

A

Acute angioedema, often with urticaria, with respiratory compromise and hypotension
Life-threatening!

262
Q

Outline treatment of anaphylaxis

A 
Ensure airway patent (ABCDE)
IM adrenaline
IV antihistamine
IV hydrocortisone
IV fluids if hypotensive

4th year presentations (22 decks)

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