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disease profiles Flashcards

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1
Q

autoimmune skin condition which antibodies are produced against hemi desmosomes proteins that are involved in the maintenance of the dermo epidermal junction

A

bullous pemphigoid

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2
Q

what does bullous pemphigoid result in

A

interuption of the dermo epidermal junction and the formation of sub epidermal blisters

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3
Q

presentation of bullous pemphigoid

A

elderly, well dermarcated plaques may present 1 year prior to blisters, large tense itchy blisters on skin or erythemous base typically trunk or proximal limbs

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4
Q

nikolsky sign what in bullous pemphigoid

A

negative

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5
Q

what is nikolski sign

A

skin finding in which the top layers of the skin slip away from the lower layers when rubbed

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6
Q

how to diagnose bullous pemphigoid

A

biopsy - sub epidermal blisters and inflammatoru infiltrates within blister and immunodluorescence - linerar IgG + complement along the basement membrane

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7
Q

management of bullous pemphigoid (local disease)

A

high potency topical steroids

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8
Q

management of bullous pemphigoid (systemic disease

A

oral steroids +/- tetracycline +/- antihostamine

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9
Q

why is an antihistamine used in bullous pemphigoid ?

A

for sedating and antu pruritic properties

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10
Q

why is tetracycline used in bullous pemphigoid

A

steroid sparing agents

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11
Q

how to treat bullous pemphigoid if there is no response ti antihistamine or tetracycline

A

immunosuppression

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12
Q

autoimmune condition in which there is antibodies produced against desmoglein 3

A

pemphigus vulgaris

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13
Q

what is desmoglein 3

A

one of the desmosome proteins involved in cell-cell adhesion

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14
Q

what does pemphigus vulgaris result in

A

intra epidermal blisters and acantholysis

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15
Q

what is acantholysis

A

seperatiion of indiduals keratinocytes

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16
Q

presentation of pemphigus vulgaris

A

middle aged, multiple painful, flaccid, fragile blisters and erosions of the skin and mucous membranes

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17
Q

pemphigous vulgaris nikolsky sign

A

positive

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18
Q

diagnosis of pemphigous vulgaris

A

biopsy intra epidermal blister with accumulation of inflammatory cells within the dermis and immunofluorescence - chicken wire depositation of IgG within the epidermis

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19
Q

management of local pemphigous vulgaris

A

topical steroids and topical anaesthetics

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20
Q

management of systemic pemphigous vulgaris

A

high dose steroids and immuno suppresion + /- rituximab

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21
Q

what immunosuppressant is used in the management of pemphigois vulgaris

A

mycophenolate, azathioprine, dapsone or cyclophosphamide

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22
Q

autoimmune skin condition caused by auto antibodies against TTG caues sub epidermal blisters in skin

A

dermatitis herpetiformis

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23
Q

what is TTG

A

the antibody implacated in ceoliac disease

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24
Q

presentation of dermititis herpetiformis

A

small intenesly itchy blisters on an erythemous swollen base

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25
Q

diagnosis of dermititis herpetiformis

A

blood anti TTG, biopsy of sub epidermal blitsers with papillary micro abseceses, immunofluorescence - granular deposits of IgA within papillae of epidermis

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26
Q

management of dermititis herpetiformis

A

gluten free diet +/- dapson

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27
Q

rare complication of dermititis herpitiformis

A

increased risk of small bowel lymphoma

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28
Q

incidence of psoriasis in men and women

A

equal

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29
Q

incidence of psoriasis age wise

A

peaks in 20s and 50s

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30
Q

precipitating factors of psoriasis

A

stress, trauma, alcohol, smoking , strep throat, drugs

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31
Q

drugs putting people at risk of psoriasis

A

B blockers, lithium, anti malarial drugs, swift withdrawal of topical or systemic steroids

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32
Q

underlying pathological processes of psoriasis

A

increased epidermal proliferation, dilation and proliferation of dermal blood vessels, inflammation and accumulation of immune cells especially T cells in teh dermis and epidermis

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33
Q

what does increased epidermal proliferation result in

A

hyperkeratosis and para keratosis

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34
Q

what is parakeratosis

A

retention of nuclei in corneocytes due to increased proliferation redcing time cells are are allowed for migration and differentation

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35
Q

histological changes in psoriasis

A

hyperkeratotis stratum corneum with parakeratosis, absence of granual layer, thicking of prickle cells layer, munroabscesses, large dilated papillary blood vessels

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36
Q

what are munro absesses

A

neutrophil filled abscesses with stratum corneum

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37
Q

most common type of psoriasis

A

chronic plaque

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38
Q

appeaace of chronic plaque psoriaces

A

often symetrical and scale may be silvery

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39
Q

rash on chronic plaque psoriasis

A

midly itchy, palpable, scaly, erythematois plaques

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40
Q

what is auspitz sign

A

removing scale causes pin point bleeding

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41
Q

auspitz sign in chronic plaque psoriasis

A

positive

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42
Q

where does chronic plaque psoriasis preferentially develop

A

on extensor aspect on knees, elbows, sacrum and scalp

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43
Q

where is scap psoriasis most commonly seen

A

posterior aspect of the scalp

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44
Q

what is koebner phenomenon

A

plaques of psoriasis develop at site of trauma 2-6 weeks after a trauma

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45
Q

what types of trauma can induce koebner phenomenon

A

physical, sunlight or caused by another skin condition

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46
Q

what age group is guttate psoriasis usually seen in

A

15-25 year olds

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47
Q

when is the onset of guttae psoriasis

A

7-10 days after infection

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48
Q

most common infection caising guttae psoriasis

A

strep throat

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49
Q

what is the appearance of guttae psoriasis

A

well demarcated, scaly, erythematous plaques that are pear drop in shape and develop on the trunk

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50
Q

where is fexural psoriasis seen (age group)

A

elderly patients

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51
Q

where does flexural psoriasis develop

A

in groin, axilla or under breasts

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52
Q

appearance of flexural psoriasis

A

erythematous, glazed, well demarcated plaques with out scale

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53
Q

how can erythrodermic psoriasis develop

A

de novo or in patients who have deterioating psoriasis

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54
Q

what can the onset of erythrodermic psoriasis be precipitated by

A

removal of potent steroids

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55
Q

what can erythrodermic psoriasis lead to

A

complete failure of skin

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56
Q

appearance of erythrodermic psoriasis

A

well demarcated plaques with absent scale with confluent full body erythema

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57
Q

what is generalised pustular psoriasis associated with

A

pain, fever and malaise

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58
Q

appearance of pustular psoriasis

A

sterile pustules within plaques of psoriasis and widespread erythema

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59
Q

what is palmo plater pustulosis

A

a distinct condition that is related to psoriasis

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60
Q

who does palmo plantar pustulosis effect (age and gender)

A

typically women over 50

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61
Q

what does palmo plantar pustulosis have a strong association with

A

smoking

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62
Q

what is the appearnace of palmo plantar pustulosis

A

multiple sterile yellow pustules that develop into brown macules then develop scale

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63
Q

nail disease associated with psoriasis

A

pitting, onchyoysis, subungual hyperkeratosis, sydtrophy, oil drop lesion

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64
Q

what is a risk of those with severe psoriasis

A

cardiovascular provlems

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65
Q

use of emollients in patients with psoriasis

A

used liberally by all pateints - great ointments may need to be used on scalp

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66
Q

what is generally considered the first line topical therapy in psoriasis

A

vit D analogues

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67
Q

examples of vit D analogues

A

calciptriol/calcitriol

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68
Q

how is dithranol used in psoriasis

A

in short term regimes for stable chronic plaque disease

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69
Q

why is dithranol only used in short term regimes for stable chronic plaque disease

A

as it burns and stains normal skin

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70
Q

where is coal tar used in psoriasis

A

only in inpatient and smelly and messy

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71
Q

what is used for flexural disease and palmer plantar disease

A

steroids

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72
Q

when is used to break down hyperkeratotis skin

A

salicylate

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73
Q

when is photodynamic therapy used in psoriasis

A

in severe widespread disease and as a first line for guttae psoriasis

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74
Q

what UV can be used in photodynamic therapy for psoriasis

A

UVB or PUVA

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75
Q

side effects of photo dynamic therapy

A

sunburn, conjunctivitis, excerbatoion of HSV

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76
Q

when in systemic therapy used in psoriasis

A

in severe or non responsive disease

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77
Q

options for systemic therapy in psoriasis

A

methrotrexate, ciclosporin terinoids, biologics (infliximab)

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78
Q

what is synomonous with eczema

A

dermatitis

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79
Q

what is dermatitis

A

an umbrella term used to describe a group of inflammatory skin conditions that share similar clinical and histological presentations

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80
Q

shared histological finidngs of dermatitis

A

spongiosis, ancanthosis, hyperkeratosis, dilation of blood vessels, eosinophilic infiltration

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81
Q

shared general clinical features of dermatitis

A

itchy, ill defined, erythematous rash +/- scale, sxcoriations, papules, vesicles, ooze and crust

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82
Q

chronic features of dermatitis

A

scale, skin thickening pigment changes and lichenification

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83
Q

what is atopic dermatitis

A

endogenous dermatitis associated in defective barrier function of the skin

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84
Q

what is the genetic contribution to atopic dermatitis

A

fillagrin protein mutations

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85
Q

what is fillagrin protein

A

a. protein involved in maintaining the waterproof protective nature of the keratin layer

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86
Q

what does mutation in the fillagrin gene lead to

A

predisposition to all atopic disease

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87
Q

prevelenec of atopic dermatitis in urban area and high socio economic class

A

higher

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88
Q

immunological influences of atopic dermatitis

A

overactive T cells

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89
Q

risk factors for atopic dermatitis

A

age <5, family/personal history of atopy

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90
Q

what does the atopic march describe

A

clinical progession of patients with atopy with eczema in infancy, asthma at 2 years old and hay fever at 7

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91
Q

presentation of atopic dermatitis

A

usually between 6 months and 5 years, associated with dry skin, will follow relapsing and remitting course

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92
Q

rash distribution of atopic dermatitis in infants

A

face, scalp, extensor surfaces and flexor surfaces and napkin area spares

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93
Q

rash distribution of atopic dermatitis in children and adults

A

flexor surfaces, especially wrist, cubital fossa, popliteal fossa and ankles

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94
Q

triggers of atopic dermatitis

A

stress, non compliance with treatment, allergens

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95
Q

diagnostic criteria of atopic dermatitis

A

itch + 3 or more of visible flexure rash, history of flexure rash, personal history of atopy, dry skin in past year, onset before age of 2

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96
Q

associated bacterial infection with atopic dermatitis

A

staph A and produces yellow weeping crust over the eczema

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97
Q

viral infections associated with atopic dermatitis

A

eczema herpeticum - infection with herpes simplex - emergency

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98
Q

presentation of eczema herpeticum

A

monomorphic punched out lesions

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99
Q

management of eczema herpeticum

A

IV aciclovir

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100
Q

management of atopic dermatitis

A

everyone - emollients
for itch - anti histamines
flare - topical steroids
mild - mild topical steoirds
moderate - moderate topical steroids
severe - potent topical steroids +/- UV light therapy +/- systemic immunosuppressio

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101
Q

example of mild topical steroids

A

hydrocortisones, eumovate

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102
Q

examples of moderate topical steroids

A

betnovate +/- tacrolimus

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103
Q

examples of potent tpoical steroids

A

Dermovate

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104
Q

what to use in patienst relying on continual us of sterois

A

tacrolimus

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105
Q

what vit D analogue to use for plaques in psoriasis

A

calcipqotriol

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106
Q

what vit D analogue to use of flexures in psoriasis

A

calcitriol

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107
Q

what is seborrheic dermatitis considered

A

endogenous dermatitis

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108
Q

what is seborrheic dermatitis caused by

A

commensal yeast on skin

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109
Q

what is the development of seborrheoic dermatitis associated with

A

immunosuppression due to the likes of HIV or drugs such as ciclosporin

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110
Q

presentation of seborrhoeic dermatitis rash

A

itchy rash, erythematous and scaly

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111
Q

distribution of seborrhoeic dermatitis on newborns

A

cradle cap, flexural surfaces abd napkin area

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112
Q

distribution of seborrhoeic dermatitis on adults

A

forhead, nasolabial folds, behind ear and anterior chest

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113
Q

management of seborrhoeic dermatitis in infants

A
  • emoillients +/- topical steroids
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114
Q

management of seborrhoeic dermatitis in adults

A

emollients + topical steroids + antifungal

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115
Q

example of anti fungal

A

ketocanozole

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116
Q

what is pompolyx

A

a type of eczema that effects the hands and soles of the feet

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117
Q

what is the rash on pompholyx present as

A

erythematous rash with intensely itchy vesicles that burst to produce superficial erosions

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118
Q

what is azteototic

A

a type of eczema seen in elderly patients

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119
Q

what is the rash associated with azteototic like

A

dry skin with polyhedral fissures creating a crazy paving pattern seen on the lower limbs

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120
Q

treatment of azteototic

A

emollients

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121
Q

what is venous eczema

A

a type of eczema presenting in elderly pateints that develops due to venous insuffieicency of lower limbs

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122
Q

what is the managemnet for venous eczema

A

compression to treat venous insuffiency

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123
Q

what does discoid develop as a result of

A

chronic itch

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124
Q

what is discoid associated with

A

atopic eczema and other conditions that cause itch sich as renal failure

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125
Q

what is the rash of discoid like

A

often widespread, disc shaped, intensely itchy lesions

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126
Q

what is irritant contact dermatitis

A

a non immune form of dermatitis

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127
Q

what is irritant contact dermatitis caused by

A

repeated exposure to substances that abrade irrtate and aggrevate skin

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128
Q

what occupations commonly cause irrtant contact dermatitis

A

hairdressers, cleanerd and hospital workers

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129
Q

what is the mechanism of contact allergic dermatitis

A

is a type 4 T cell mediated hypersensitivity reaction in response to an antigen that they have had exposure to

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130
Q

when do rash a skin changes occur in contact allergic dermatitis

A

48-96 hours after exposure to the antigen

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131
Q

whatputs people at risk of contact allergic dermatitis

A

an increased risk in those with chronic skin conditions such as leg ulcers due to exposure of topical therapyies

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132
Q

how to diagnose contact allergic dermatitis

A

patch testing

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133
Q

management of contact allergic dermatitis

A

antigen avoidance, regular emollients, topical steroids during flares

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134
Q

what is acne

A

an inflammatory condition of the pilosebaceous unit

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135
Q

what are the pathological changes seen in acne

A

duct occlusion, increased sebum production, bacterial colonisation, duct rupture

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136
Q

whatis duct occlusion due to

A

hyper cornification

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137
Q

what does hypercornification produce

A

comedones

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138
Q

what are black heads

A

open comedones

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139
Q

what are white heads

A

closed comedones

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140
Q

what can worsen occlusion in acne

A

cosmetics and pre menstral oedema

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141
Q

what is sebum

A

oil used to lubricate the skin in an androgen sensitive manner

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142
Q

how can sebum production be increased

A

due to increased androgen production, increased availability of androgens and increased sensitivity of androgen receptors

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143
Q

what is the bacteria that causes bacterial colonisation in acne

A

propionobacterium which is a normal bacteria natirally found in the skin

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144
Q

what aids bacterial colonistaion

A

sebum

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145
Q

what causes the duct of the hair follicle to rupture in acne

A

presence of propianobacterium acne which prodces inflammation of the dermis and formation of lesions such as papules, pustules, cysts and nodules

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146
Q

risk factors for acne

A

age between 12-25, family history, greasy skin, endocrine disorders

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147
Q

aggregating factors of acne

A

stress, sweating, pre menstural period

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148
Q

distribution fo acne

A

face, chest and upper back

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149
Q

examples of non inflammatory lesions in acne

A

black heads and white heads

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150
Q

examples of inflammatory lesions in acne

A

papules, pustules, cysts, nodules on erythematous base

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151
Q

complications of chronic acne

A

scars and skin hyper pigmenation

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152
Q

describe acne scars

A

ice pick scars of hypertrophic keloid scars

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153
Q

mild acne classification

A

scattered comedones, papules and pustules

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154
Q

moderate acne classification

A

numberous papules, pustules and mild atrophic scarring

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155
Q

severe classification of acne

A

numerous papules, pustules, mild atrophic scarring, cysts, nodules and significant scarring

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156
Q

how to treat mild acne

A

topical only - retinoid, benzyl peroxide +/- antibiotic

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157
Q

what antibiotic to use in mild acne

A

erythromycine or clindamycin

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158
Q

how to treat moderate acne

A

topical therapies + oral antibiotic (erythromycin or oxytetracycline, contraceptive pill can be used in women

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159
Q

how to treat severe acne

A

topical therapies + isotretinoin

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160
Q

what gender is acne rosacea more common in

A

women

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161
Q

what age range does acne rosacea spike in

A

30 and 40s

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162
Q

presenation of acne rosacea

A

facial flushing, rash - erythema with papules and pustules on nose chin, cheeks and forehead wuth sparing of nasolabial folds

163
Q

complications of acne rosacea

A

talangectasia, rhinopyma

164
Q

what is facial flushing in acne rosacea triggered by

A

alcohol, hot drinks, stress, spicy food

165
Q

first line management of acne rosacea

A

topical metronidazole

166
Q

second line for acen rosacea

A

topical therapies + doxycycline

167
Q

third line for acne rosacea

A

isotrenanoin

168
Q

how to treat talangectasia and rhinopyma

A

laser therapy

169
Q

what is talangectasia

A

“spider veins”, dilated or broken bood vessels lacyer near surface or mucous membranes

170
Q

what is pityraisis rosea

A

a spontaneous inflammatory skin condition

171
Q

what may bring on pityraisus rosea

A

virus

172
Q

what age group pityraisis rosea seen in

A

teenages and young adukts

173
Q

presentation of pityraisus rosea

A

sudeen onset, hearald patch, subsequent rash

174
Q

what is hearald patch

A

oval shaped erythematous scaly patch usually on trunk or neck that is larger than other lesion

175
Q

what is the rash like in pityraisis rosea

A

smaller oval shaped scaly lesions on trunk and extremities that spread along skin cleavages which gives a christmas tree appearance

176
Q

what is the management of pityraisis rosea

A

self limiting - emmolients and anti histamines

177
Q

distribution of lichen planus

A

flexor surfaces of wrist/foreaerm, ankles, legs and oral mucosa - can develop at site of trauma

178
Q

describe rash associated with lichen planus

A

intensely itchy rash purple, flat topped papules or plaques that are rhomboid or poly angular in shage +/- white lacy markings

179
Q

describe oral lesions associated with lichen planus

A

lacy white lesions on inside of cheek

180
Q

what is lichen planus associated with

A

Hep C

181
Q

management of lichen planus

A

topical steroid + anti histamine

182
Q

what is tuberose sclerosis

A

a multi system autosomal dominant genetic condition

183
Q

what is the most common genetic skin condition

A

tuberose sclerosis

184
Q

what are the skin manifestations of tuberose sclerosis

A

ash leaf macules, perigungal fibroma, sebaceus adenoma, shagreen patches

185
Q

what are ash leaf macules

A

oval shaped areas of hyper pigmentation

186
Q

what is perigingal fibroma

A

fibroma of the nail bed

187
Q

sebaceous adenoma

A

angiofibroma of the sebaceous glands on the face

188
Q

what are shagreen patches

A

sir, skin coloured nodules

189
Q

what is neurofibromatosis type 1

A

a multisystem autosomal dominant genetic condition

190
Q

what are the skin manifestations of neurofirbomatosis type 1

A

neurofibromas, axillary or inguinal freckles, cafe au lait macules

191
Q

how many cafe au lait macules do you need to diagnose

A

over 6

192
Q

what are cafe au lait macules

A

light briown macules

193
Q

what are the systemic manifestations of type 1 neurofibromatosis

A

optic glioma, lisch nodules on iris

194
Q

histology of lichen planus

A

saw tooth

195
Q

what are salmon patches

A

non vascular birth marks usually found on face or nuchal area

196
Q

why are salmon patches thought to develop

A

persistant fetal circulation

197
Q

appearance of salmon patches

A

central erythemous macule

198
Q

what happens to salmon patches over time

A

vast majority regress

199
Q

what are port wine stains

A

capillary malformations that are present at birth and are permanent

200
Q

where are portwine stains usually found

A

in head and neck region

201
Q

appearance of portwine stains

A

red macule usually unilateral

202
Q

what happens to portwine stains overtime

A

darken and thicken

203
Q

how do port wine stains grow

A

proportionally with the face and dont extend from the original site

204
Q

how to describe the locations of portwine stains on the face

A

in relation to the distribution of the trigeminal nerve

205
Q

associated conditions with portwine stains

A

sturge- weber syndrome, klippel- trenaunay

206
Q

what is associated with struge weber syndrome

A

V1 portwine stain, seizures, learning disability, hemi paresis, glaicoma, vascular malformation is found in the cerebral cortex on the ipsilateral side to the port wine stain

207
Q

what are infantile haemangioma also called

A

strawberry neavi

208
Q

what are infantile haemangiomas

A

benign vascular tumours that usually appear in the first moneth of life in the head and neck region

209
Q

who are infantile haemangiomas most common in

A

woman and premature babies

210
Q

appearance of infantile haemangiomas

A

superficial red plaque

211
Q

what happens to infantile haemangiomas

A

they mostly undergo complete or partial resolution

212
Q

presentation of erythema multiforme

A

target lesions

213
Q

severe erythema multiforme

A

steven johnstone synfrome or toxic epidermal necrolysis

214
Q

what is erythema multiforme major associated with

A

mucosal involvement

215
Q

what are the causes of erythema multiforme

A

herpes, mycoplasma, hep b, ebv, cmv, thiazide diuretics, anti malarials, sulphonylureas, penicillins, allopurinol

216
Q

management of erythema multiforme

A

supportive care and treat underlying cause

217
Q

systemic disease associated with diabetes

A

necrobiosis lipoidica

218
Q

presentation of necrobiosis lipoidica

A

firm waxy, red brown or yellpw plaques on anterior shin associated with increased risk of ulceration

219
Q

what is associated with diabetes, addisons and malignancy

A

acanthosis nigricans

220
Q

what does acantosis nigricans look like

A

thickened brown hyperpigmented velvety skin in flexural areas

221
Q

what is associated with graves

A

pretibial myxoedema

222
Q

what does pretibial myxoedema look like

A

purple brow, indurated waxy plaques on anterior shins

223
Q

what is erythema nodosum associated with

A

IBD, TB, sarcoids, OCP use

224
Q

presentation of erythema nodosum

A

painfl, erythematous nodules on shins

225
Q

what is pyoderma gangrenosum associated with

A

IBD and rheumatoid

226
Q

presentation of pyoderma gangernosum

A

pustules and blisters that break down to form necrotic ulcer with purplish margins

227
Q

what is kaposi sarcoma associated with

A

HIV

228
Q

what does kaposi sarcomas look like

A

brown/purple nodules

229
Q

what is the difference between SJS and TENS

A

the extent of skin invlovement

230
Q

extent of skin involvement in SJS

A

<10%

231
Q

extent of skin invlovement in TENS

A

> 30%

232
Q

presentatin of SJS/TENS

A

widespread erythema and blistering of the skin and mucousal surfaces - the blisters merge and undergo necrosis and large sheets of skin are lost

233
Q

causes of SJS and TENS

A

penicillins, NSAIDs, anti-convulsants

234
Q

management of TENS and SJS

A

cessation of causative drug, supportive care, emollients, Iv Ig

235
Q

what is the most common type of porphyria

A

PCT - cutanea tarda

236
Q

what is porphyria

A

a group of diseases caused by errors in haem and accumulation of toxic precursors

237
Q

what is the pathophysiology of PCT

A

caused by deficiency in the enzyme uroporphyrinogen decarboxylate.

238
Q

what can cause PCT

A

genetic, alcohol, iron and oestrogen replacement

239
Q

clinical features of PCT

A

photo sensitivity of dorsum of hands, blisters and bullae that easily rupture and cause erosions, hyperpigmentation and hypertrichosis - especially at the top of the cheek

240
Q

diagnosis of PCT

A

by testeting elevated urine porphyrins or through skin biopsy

241
Q

management of PCT

A

avoid sunlight and triggers, phlebotomy to reduce iron levels and antimalarials such as chloroquine

242
Q

what are seborrhoeic keratoses also known as

A

basal cell papillomas

243
Q

what are seborrhoeic keratoses

A

benign proliferations of epidermal keratinocytes

244
Q

presenation of seborrhoeic keratoses

A

usually elderly patients, on head forearms, back of hands and trunk, well demarcated raised usually brown coloured lesion with well defined edges warty granular surface and stuck on appearance, no pain or itch

245
Q

management of seborrhoeic keratoses

A

non surgical - cryotherapy, curettage

246
Q

what are actinic lentinges also known as

A

sun or liver spots

247
Q

where do actinic lentinges develop

A

in sun exposed sites

248
Q

pathophysiology of actinic letinges

A

melanocyte proliferation as a protective mechanism against sun exposure

249
Q

appearance of actinic lentinges

A

flat brown macule

250
Q

what are melanocytic neavi

A

moles

251
Q

how can moles develop

A

can be congenital or acquired

252
Q

what is a mongolian blue spot

A

a large blue coloured congenital neavi that is found on the back and buttocks

253
Q

what is spitz

A

fleshy pink papule seen in children

254
Q

appearance of halo

A

surrounded by an area of depigmentation

255
Q

what is dermatofibroma

A

benign tumour of fibroblasts

256
Q

location of dermatofibroma

A

anywhere but usually on the lower limb

257
Q

development of dermatofibroma

A

associated with trauma such as an insect bite

258
Q

appearance of a dermatofibroma

A

firm, hyperpigmented or pink papule +/- associated pain and itch

259
Q

what is pyogenic granuloma

A

capillary haemangioma most that develops at the site of trauma especially on fingers

260
Q

appearance of pyogenic granuloma

A

well defined papule, red papule associated with bleeding

261
Q

management of pyogenic granuloma

A

surgical excision

262
Q

what is the most common type of skin cancer

A

basal cell

263
Q

what is the least dangerous type of skin cancer

A

basal cell

264
Q

does basal cell carcinoma metastasize

A

rarely, but it can be locally destructive

265
Q

who usually presents with basal cell carcinoma

A

middle ages patients on sun exposed areas

266
Q

risk factors for basal cell carcinoma

A

fair skin, UV light exposure, intermittent sun damage during childhood

267
Q

presentation of basal cell carcinoma

A

slow growing

268
Q

3 types of basal cell carcinoma

A

nodular, superficial and infiltrative

269
Q

characteristics of nodular basal cell carcinoma

A

raised lesion that has a pearly shine, rolled edges and a picket fence border, may also be associated with central depression or ulceration and talangectasia

270
Q

diagnosis of basal cell carcinoma

A

clinical - biopsy

271
Q

management of basal cell carcinoma

A

conservative, surgical or topical imquimod or 5 - fluro uracil

272
Q

what are actinic keratosis

A

pre malignant lesions associated with partial thickness intra epidermal proliferation of atypical keratinocytes

273
Q

where are actinic keratosis found

A

sun exposed areas, especially on the head

274
Q

presentation of actinic keratosis

A

slow growing macules or plaques that have associated erythema, scale and a crumbly yellow crust

275
Q

diagnosis of actinic keratosis

A

clinical +/- biopsy

276
Q

what is bowens disease

A

pre malignant lesions associated with full thickness dysplasia within the epidermis

277
Q

what is SCC that has not broken through the dermis

A

bowens disease

278
Q

location of bowens disease lesions

A

on legs - especially the shins of older woman

279
Q

presentation of bowens disease

A

usually a solitary lesion, slow growing, red scaly plaques

280
Q

what is the second most common skin cancer

A

squamous cell

281
Q

what does squamous cell carcinoma have the potential to do

A

metastasize

282
Q

who and where does squamous cell carcinoma present

A

in middle aged patients on sun exposed sites

283
Q

risk factors for squamous cell carcinoma

A

HPV, fair skin, cumulative sun damage over the years, immunosuppresson especially in post transplant patients

284
Q

presentation of squamous cell carcinoma

A

growth of lesion over months, firm erythematois plaque on sun exposed site, associated scale, crust, bleeding, ulceration, itch and tenderness

285
Q

diagnosis of squamous cell carcinoma

A

biopsy

286
Q

management of squamous cell carcinoma

A

screen for mets, surgical

287
Q

risk factors for melanoma

A

fair skin, sun bed use, immunosuppression, family or personal history, history of intermittent sun damage in childhood

288
Q

growth phases of melanoma

A

radial and vertical

289
Q

radial growth phase of melanoma

A

melanoma grows horizontally within the epidermis - catch at this stage as there is no risk of metastasis

290
Q

vertical growth phase of melanoma

A

occurs after the radial growth and is when the lesion will become elevated. once it invades the dermis there is a risk of metastasis

291
Q

types of melanomas

A

superficial spreading, nodular, lentigo maligna, amelanotic

292
Q

superficial spreading melanoma

A

most common relatively long radial growth phase

293
Q

nodular melanoma

A

enters straight into vertical growth phase and has worse prognosis

294
Q

lentigo maligna melanoma

A

usually on face of old women, within a lentigo

295
Q

amelanotic melanoma

A

non pigmented lesions

296
Q

how does melanoma occur

A

usually de novo but can develop from dysplastic neavi

297
Q

how does a patient usually present with melanoma

A

usually after noticing a change in what they thought was a mole

298
Q

assessment of melanoma

A

ABCDE

299
Q

diagnosis of melanoma

A

clinical and biopsy

300
Q

management of melanoma

A

surgical excision with 2mm margins, check breslows thickness, follow up for wide local excision

301
Q

what is berslows thickness

A

the depth of tumour from basal layer of the epidermis

302
Q

what does photosensitivity describe

A

a group of skin disorders that result from exposure to normal levels of UV light exposure

303
Q

UVA

A

longer wave can penetrate glass

304
Q

UBV

A

smaller wave length main contributing type to sunburn and skin cancer

305
Q

factors affecting photosensitivity

A

intensity of UV light, genetics, drugs and skin type

306
Q

always burns never tans

A

type 1

307
Q

usually burns sometimes tans

A

type 2

308
Q

sometimes burns usually tans

A

type 3

309
Q

rarely burns always tans

A

type4

310
Q

never burns always tans

A

type 5 and 6

311
Q

what is xeroderma pigmentosum

A

autosomal recessive genetic disorders caused by. adefiecincy in the DNA repairs mechanisms in the skin

312
Q

presentation of xeroderma pigmentosum

A

severe photosensitivity, accelerated photo aging, early formation of skin cancers

313
Q

management of xeroderma pigmentosum

A

patients are required to undertake strict sun avoidance

314
Q

what is porphyria

A

a group of cutaneous and systemic conditions associated with deficiency of enzymes involved in the synthesis of haem

315
Q

where does acute intermittent porphyria usually present

A

females around the age of 30

316
Q

presentation of acute intermittent porphyria

A

acute abdomen, mood disturbance, neurological, seizures

317
Q

enzyme deficiency associated with acute intermittent porphyria

A

prophobilinogen deaminase

318
Q

what accumulates in acute intermittent porphyria

A

porphobilinogen

319
Q

what is the most common type of porphyria

A

prophyria cutanea tarda

320
Q

who is PCT most commonly seen in

A

middle aged men

321
Q

what is PCT commonly associated with

A

liver disease therefore often seen in those with haemochromatosis, hepatitis or alcohol misuse

322
Q

enzyme deficiency in PCT

A

uroporphyrinogen decarboxylase

323
Q

what accumulates in PCT

A

uroporphyrinogen

324
Q

what js the rash like in PCT

A

blistering lesions on sun exposed sites that heal with scarring and are associated with hyper pigmentation

325
Q

investigations of PCT

A

bloods - porphyrin studies, woods lamp - urine shines pink instead of blue

326
Q

what is erthropoetic protopohphyria mode of inheritance

A

autosomal dominant

327
Q

who is erthropoetic protopohphyria most commonly seen in

A

children

328
Q

what is the rash associated with erthropoetic protopohphyria like

A

may be no rashbut there will be burning and itching on the skin with sun exposure

329
Q

typical presentation of erthropoetic protopohphyria

A

child screaming when placed out in the sun

330
Q

what is the enzyme deficient in erthropoetic protopohphyria

A

ferrochelatase

331
Q

what accumulates in erthropoetic protopohphyria

A

protoporphyrin IX

332
Q

common causative drugs of photosensitivity

A

NSAIDs, Diuretics, amiodarone, antibiotics - tetracyclines, ciprofloxacin

333
Q

what is polymorphic light eruption

A

a photosensitive disorder whose mechanism is thought to be type4 hypersensitivity

334
Q

who does polymorphic light eruption usually present in

A

women around the age of 30

335
Q

presentation of polymorphic light eruption

A

usually after a few hours of sunlight exposure, erythema lesions of varying morphology but usually blisters and papules - severe itch

336
Q

management of polymorphic light eruption

A

topical steroids and desensitizing using UVB prior to sunlight exposure

337
Q

chronic actinic dermatitis is what type of reaction

A

type 4

338
Q

who is chronic actinic dermatitis usually seen in

A

men over 50

339
Q

presentation of chronic actinic dermatitis

A

develop on eczematous type rash on sun exposed sites, often associated with contact allergic dermatitis

340
Q

management of chronic actinic dermatitis

A

sun protection and standard eczema treatments of emollients and topical sterids

341
Q

what types of reaction is solar urticaria

A

type1

342
Q

what. is the presentation of solar urticaria

A

immediate onset of erythema, urticaria and itchy rash upon exposure to sunlight - rash will resolve within a few hours

343
Q

management of solar urticaria

A

sun avoidance and anti histamines

344
Q

what are urticaria and angioedema

A

transient rashes caused by oedema caused by mast cell degranulation and release of inflammatory mediators

345
Q

where is oedema when urticaria develops

A

within the dermis

346
Q

presentation of urticaria

A

erythematous localised swellings of various shapes that can be itchy and stingy

347
Q

how long does urticaria typically last for

A

less than 24 hours

348
Q

where is oedema when angioedema develops

A

in the subcutaneous or sub mucousal tissues

349
Q

presentation of angioedema

A

non pitting swelling

350
Q

how long does angioedema last for

A

24-48 hours

351
Q

acute angioedema / urticaria classification

A

recurrent daily episodes for less than 6 weeks

352
Q

chronic angioedema/urticaria classification

A

recurrent daily episodes for longer than 6 weeks

353
Q

what is the most common cause of acute urticaria

A

allergy

354
Q

gold standard investigation for urticaria

A

skin prick testing

355
Q

drugs that cause angioedema/urticaria

A

ACEi, NSAIDs, Codeine /morphine

356
Q

physical causes of angioedema/urticaria

A

solar, cold, dermographism, cholinergic(shower/exercise), antoimmune (SLE)

357
Q

management of angioedema and urticaria

A

antihistamines, allergen avoidance, UVB phototherapy

358
Q

what does UVB phototherapy do

A

stabilises mast cells

359
Q

what. isa primary varicella zoster infection

A

chicken pox

360
Q

presentation of chicken pox

A

fever, malaise, intense itch, macules that develop into pustulesthen vesicles that crust over and recover

361
Q

where does chicken pox usually start

A

face then trunk / limbs

362
Q

management of chicken pox

A

supportive, vaccination

363
Q

who is the chicken pox vaccine available for

A

non immune health workers, pregnant women, those in regular contact with immunosuppressed patients

364
Q

what type of vaccine is the chicken pox vaccine

A

live attenuated

365
Q

what is shingles also called

A

herpes zoster

366
Q

how is shingles caused

A

reactivation of dormant chicken pox virus which is dormant in sensory nerve roots

367
Q

what is the presentation of shingles

A

burning, tingling pain and itch along dermatological distribution which may precede rash - rash is erythematous macules, papules that develop into vesicles before crusting over and healing

368
Q

specific locations of shingles

A

ophthalmic, ramsay hunt

369
Q

shingles on the forehead and around the eyes means

A

reactivation of the virus in the trigeminal nerve

370
Q

shingles on the forehead requires

A

urgent ophthalmology referral

371
Q

what is ramsay hunt syndrome

A

reactivation of the virus within the geniculate nucleus of the facial nerve

372
Q

what does ramsey hunt syndrome cause

A

rahs and pain in the auditory canal associated with bells palsy, deafness, vertigo, tennitus

373
Q

management of shingles

A

oral aciclovir and analgesia

374
Q

complications of shingles

A

post herpetic neuralgia - which is chrnic dermatomal pain following resolution of shingles

375
Q

type 1 herpes simplex causes what

A

primarily oral lesions but also can cause genital lesion s

376
Q

type 2 herpes simplex causes what

A

only genital lesions

377
Q

presentation of herpes

A

grouped painful, itchy vesicles on an erythematous base that burst to form ulcers crust over and then heal without scarring - oral - gingiva stomatitis

378
Q

hat can recurrent herpes present with

A

erythema multiforme

379
Q

what is herpetic whitlow

A

inoculation of the virus in the finger to produce a solitary painful lesion

380
Q

what is eczema herpeticum

A

a disseminated infection that presents with monomorphic punched out lesions

381
Q

who gets eczema herpeticum

A

children with atopic eczema

382
Q

management of herpes

A

analgesia, aciclovir, education

383
Q

what is HPV

A

causitive organism of warts and cervical cancer

384
Q

what are warts caused by

A

infection of keratinocytes by HPV

385
Q

what are warts

A

raised papules with a firm roughened surface

386
Q

what can warts be described as

A

papillomatous

387
Q

what does HPV 1-4 cause

A

common warts

388
Q

what does HPV 6/11 cause

A

genitcal warts

389
Q

what does HPV 16/18 cause

A

cervical cancer

390
Q

management of HPV - general

A

salicylic acid, cryotherapy imiquimod

391
Q

management of genetal warts

A

podophyllin, imiquimod

392
Q

causative organism of molluscum contagiousum

A

pox virus

393
Q

presentation of molluscum contagiousum

A

self limiting viral infection seen in children with lesions developing on head neck and trunk - rash is itchy, solid pink papules witha umbilicated centre

394
Q

who. ismolluscum contagiousum seen in

A

those with atopic eczema

395
Q

what is erythema infectiosum called

A

slapped cheek disease

396
Q

causative organism of erythema infectiosum

A

parvovirus B19

397
Q

how to detect parvovirus B19

A

B19 IgM

398
Q

presentation of erythema infectiosum

A

self limiting infection commonly seen in children, rash is initially bilateral erythema on cheeks but then turns into a maculopapular rash with lacy erythema on trunk and limbs

399
Q

associated symptoms of erythema infectiosum

A

fever, poly arthritis

400
Q

causative organism of Orf

A

parapox virus

401
Q

where is parapox virus found

A

in sheep

402
Q

presentation. of orf

A

in farmers, single firm fleshy nodules on the hands, self limiting

403
Q

causative organism of hand foot and mouth

A

coxsackie virus

404
Q

presentation. of hand foot and mouth

A

promdormal fever malaise, grey vesicles surrounded by erythema and ulcers - self limiting

dermatology (12 decks)

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