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Disease Profiles Flashcards

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1
Q

Psoriasis

A

Chronic inflammatory dermatosis

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2
Q

Psoriasis: Sex incidence

A

Equal

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3
Q

Psoriasis: Peaks in incidence

A

20s and 50s

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4
Q

Psoriasis: Risk Co-morbidities (6)

A

Psoriatic Arthritis
Metabolic Syndrome
Crohn’s Disease
Cancer
Depression
Uveitis

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5
Q

Psoriasis: Increased risk of what?

A

Cardiovascular MI

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6
Q

Psoriasis: Drugs that precipitate Psoriasis (4)

A

Beta blockers
Lithium
Anti-malarial drugs
Swift withdrawal of topical or systemic steroids

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7
Q

Psoriasis: What cytokines are involved? (3)

A

TNF-Alpha
IL-17
IL-23

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8
Q

Psoriasis: Types (4)

A

Psoriasis vulgaris
Guttate
Palmoplantar Pustular
Erythrodermic pustular

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9
Q

Psoriasis: Koebner phenomenon

A

New lesions arise at the sites of trauma

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10
Q

Psoriasis: Pathological changes

A

Epidermal hyperplasia

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11
Q

Psoriasis: Epidermal Hyperplasia

A

Increased epidermal turnover

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12
Q

Psoriasis: What is the name for the chronic plaques?

A

Psoriasis vulgaris

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13
Q

Psoriasis: Pathology - Initiating event

A

Keratinocytes under stress release factors that stimulate plasmacytoid dendritic cells to produce IFN-alpha, IL-1beta, IL-6 and TNF

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14
Q

Psoriasis: Pathology - Chemical signals activate what cells?

A

Dendritic cells

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15
Q

Psoriasis: Pathology - What happens to dendritic cells?

A

Migrate to the lymph nodes and present to and activate TH1 and TH17 cells

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16
Q

Psoriasis: Pathology - What reaction occurs in the dermis?

A

T cells stimulate an inflammatory cascade involving anti-microbial peptide release and neutrophil attracting chemokines

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17
Q

Psoriasis: Pathology - What enables the formation of munro micro abscesses?

A

Complement attracting neutrophils to the keratin layer

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18
Q

Psoriasis: Pathology - Complement attracting neutrophils in the keratin layer enable the formation of what?

A

Munro micro abscesses

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19
Q

Psoriasis: Pathology - What CD cells are involved?

A

CD8+

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20
Q

Psoriasis: Pathology - Function of dermal fibroblasts

A

Release keratinocytes and epidermal growth factors

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21
Q

Psoriasis: Pathology - What occurs to keratinocytes?

A

Proliferation

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22
Q

Psoriasis: Typical clinical presentation

A

Symmetrically distributed red scaly plaques with well defined edges

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23
Q

Psoriasis: Location of plaques

A

Extensors - Elbow and Knee
Scalp
Sacrum
Hands, Feet and Nails
Trunk

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24
Q

Psoriasis: How does it present on dark skin?

A

More white with silver scale

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25
Q

Psoriasis: Scratching can lead to what?

A

Lichenification

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26
Q

Psoriasis: Auspitz Sign

A

Removal of surface scale reveals tiny dilated capillaries in elongated dermal papillae that bleed

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27
Q

Psoriasis: Nail Disease Changes seen (3)

A

Nailbed pitting
Onycholysis
Subungual Hyperkeratosis

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28
Q

Psoriasis: Nail bed pitting

A

Superficial depressions in the nailbed

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29
Q

Psoriasis: Onycholysis

A

Separation of the nail plate from the nail bed

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30
Q

Psoriasis: Subungual hyperkeratosis

A

Thickening of the nail bed

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31
Q

Psoriasis: Most common type

A

Psoriasis Vulgaris

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32
Q

Psoriasis: Psoriasis Vulgaris

A

Symmetrical plaques on the extensor surfaces of the limbs, scalp and lower back

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33
Q

Psoriasis: Flexural Psoriasis

A

Smooth erythematous plaques without scale in flexures and skin folds that are colonised by candida yeast

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34
Q

Psoriasis: Guttate psoriasis

A

Mutliple small tear-drop shaped erythematous plaques on the trunk after a streptococcal infection in young adults

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35
Q

Psoriasis: Pustular psoriasis

A

Multiple petechiae and pustules on the palms and soles

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36
Q

Psoriasis: Generalised Erythrodermic Psoriasis

A

Rare and serious form characterised by erythroderma and systemic illness

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37
Q

Psoriasis: Unstable plaque psoriasis

A

Rapid extension of existing or new plaques induced by infection, stress, drugs or drug withdrawal

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38
Q

Psoriasis: Sebopsoriasis

A

Overlap of seborrheic dermatitis and psoriasis affecting the scalp, face, ears, chest due to colonisation by malassezia

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39
Q

Psoriasis: Palmoplantar Psoriasis

A

Psoriasis of the palms and soles with keratoderma and fissuring

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40
Q

Psoriasis: What investigation can aid diagnosis?

A

Biopsy

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41
Q

Psoriasis: Histology - Epidermis appearance

A

Thickened epidermis

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42
Q

Psoriasis: Histology - Impact on the keratin layer

A

Increased keratin content

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43
Q

Psoriasis: Histology - Impact on keratinocytes

A

Parakeratosis - retention of nuclei in keratinocytes due to rapid and abnormal differentiation of keratinocytes

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44
Q

Psoriasis: Histology - What occurs in the upper epidermis?

A

Accumulation of neutrophils to form micro-abscesses

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45
Q

Psoriasis: Histology - What occurs in the dermis?

A

Elongated Rete pegs - project into the dermis

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46
Q

Psoriasis: Management - Examples of Vitamin D Analogues (2)

A

Caclipotriol
Calcitriol

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47
Q

Psoriasis: Management - Vitamin D Analogues - What is used for localised plaques?

A

Caclipotriol

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48
Q

Psoriasis: Management - Vitamin D Analogues - What is used for flexures?

A

Calcitriol

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49
Q

Psoriasis: Management - First line management

A

Potential corticosteroid + topical vitamin D + Emollient

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50
Q

Psoriasis: Management - Treatment for scalp psoriasis

A

Greasy ointments to soften scale
Steroids
Vitamin D analogues

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51
Q

Psoriasis: Management - Treatment for Psoriasis of the Axilla

A

Topical steroids for the face, flexures and groin
Calcineurin Inhibitors

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52
Q

Atopic Dermatitis

A

Itchy skin lesions

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53
Q

Atopic Dermatitis: Most common in what population?

A

Children

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54
Q

Atopic Dermatitis: Genetic predisposition

A

Mutations within the fillagrin gene impairs the skin barrier function

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55
Q

Atopic Dermatitis: Immunopathology - Initiating factor

A

Langerhans cells in the epidermis process the antigen

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56
Q

Atopic Dermatitis: Immunopathology - Processed antigen is presented to what by Langerhans cells?

A

T Helper Cells

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57
Q

Atopic Dermatitis: Immunopathology - Sensitised T Helper Cells have what action?

A

Migrate into lymphatics and then to regional nodes where antigen presentation is amplified

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58
Q

Atopic Dermatitis: Immunopathology - What is the final stage that causes the dermatitis?

A

Antigen challenges cause T cell proliferation that migrate and infiltrate the skin

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59
Q

Atopic Dermatitis: Acute - Presentatio of lesiosn

A

Papulovesicular erythematous lesions with oedema
Scaling and crusting may be present

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60
Q

Atopic Dermatitis: Acute -Dyshidriotic eczema

A

Spongiosis coalesces into vesicles or bullae

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61
Q

Atopic Dermatitis: Acute - What histological feature is present in the upper dermis?

A

Inflammatory infiltrate

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62
Q

Atopic Dermatitis: Acute - Spongiosis description

A

Fluid accumulates around the keratinocytes

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63
Q

Atopic Dermatitis: Acute - What can develop from spongiosis?

A

Blister or vesicle development

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64
Q

Atopic Dermatitis: What does crust indicate?

A

Staphylococcus aureus

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65
Q

Atopic Dermatitis: What does eczema herpeticum indicate?

A

Herpes simplex virus infection

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66
Q

Atopic Dermatitis: Clinical presentation of Eczema Herpeticum

A

Monomorphic punched out lesions

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67
Q

Atopic Dermatitis: Presentation of Adult Eczema

A

Generalised dryness and itching with a primary manifestation of hand eczema

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68
Q

Atopic Dermatitis: Presentation of Childhood Eczema

A

Predominantly flexural eczema

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69
Q

Atopic Dermatitis: Presentation of Infantile Eczema

A

Eczema primarily involving the face, scalp and extensor surfaces of the limbs

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70
Q

Atopic Dermatitis: Contact Allergic Dermatitis - What type of reaction is this?

A

Type IV Hypersensitivity reaction

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71
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Example of triggers (4)

A

Nickel
Chemicals
Topical therapies
Plants

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72
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Routes of exposure (3)

A

Direct skin contact
Airborne contact
Injection

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73
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Sensitisation Phase Description

A

Generation of memory T cells following exposure to an antigen via Langerhan cells in the epidermis

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74
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Allergic Phase Description

A

Activated of sensitised Th cells in response to an antigen, causing activation of cell-mediated cytotoxicity and release of inflammatory cytokines

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75
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Investigation

A

Patch Testing

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76
Q

Atopic Dermatitis: Contact Allergic Dermatitis - Description of Patch Testing

A

Allergens prepared on a FinnChamber which are applied on the back and removed after 48 hours - the results are read between 48-96 hours

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77
Q

Atopic Dermatitis: Contact Irritant Dermatitis

A

Non-specific physical irritation due to e.g. soap, cleaning products and nappy rash

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78
Q

Atopic Dermatitis: Atopic Eczema - 3 causative factors

A

Reduced skin barrier function
Environment
Immunological changes

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79
Q

Atopic Dermatitis: Atopic Eczema - What is fillagrin?

A

A filament aggregating protein

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80
Q

Atopic Dermatitis: Atopic Eczema - Function of fillagrin protein?

A

Reduces AMP in the skin

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81
Q

Atopic Dermatitis: Atopic Eczema - What cells are involved?

A

TH2 cells
Dendritic Cells
Keratinocytes
Macrophages
Mast Cells

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82
Q

Atopic Dermatitis: Atopic Eczema - Typical Presentation

A

Ill-defined erythema with scaling with dry skin

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83
Q

Atopic Dermatitis: Atopic Eczema - Location

A

Flexors

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84
Q

Atopic Dermatitis: Atopic Eczema - Associated with what other diseases? (3)

A

Asthma
Allergic Rhinitis
Food Allergy

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85
Q

Atopic Dermatitis: Atopic Eczema - What is the presentation of this in black individuals?

A

Nodular pruigo - well-defined lichenification with itchy nodules

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86
Q

Atopic Dermatitis: Atopic Eczema - Diagnostic Criteria is 3 or more of what? (5)

A

Visible flexural rash - cheeks and extensors in infants
History of flexural rash - cheeks and extensors in infants
Personal history of atopy - of first degree relative if under 4
Generally dry skin
Onset before the age of 2

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87
Q

Atopic Dermatitis: Drug Related Eczema - what type of reactions are these?

A

Type I or IV hypersensitivity reactions

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88
Q

Atopic Dermatitis: Photo-induced Eczema - Cause

A

Reaction to UV light
Secondary to photosensitising drugs

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89
Q

Atopic Dermatitis: Photo-induced Eczema - Presentation

A

Well defined eczema e.g. cuff of collar

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90
Q

Atopic Dermatitis: Lichen Simplex

A

Chronic skin condition as a result of repetitive scratching

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91
Q

Atopic Dermatitis: Stasis Dermatitis

A

Eczema induced by physical trauma to the skin due to venous insufficiency - increases the hydrostatic pressure of the blood

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92
Q

Atopic Dermatitis: Stasis Dermatitis - where does this affect?

A

Lower legs

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93
Q

Atopic Dermatitis: Discoid Eczema

A

Eczema that occurs in circular or oval patches - often due to infection

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94
Q

Atopic Dermatitis: Seborrheic Eczema - Alternate name

A

Cradle cap

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95
Q

Atopic Dermatitis: Seborrheic Eczema - What areas are affected?

A

Nose
Eyebrows
Ears
Scalp

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96
Q

Atopic Dermatitis: Dyshidriotic Eczema

A

Sudden acute flare up of eczema in which spongiotic vesicles join together

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97
Q

Atopic Dermatitis: Dyshidriotic Eczema - Presentation

A

Tiny blisters form on the hands, side of the fingers and feet that are severely itchy

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98
Q

Atopic Dermatitis: General Management

A

Remove triggers or irritants
Emollients

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99
Q

Atopic Dermatitis: Management of Mild Eczema

A

Topical steroid

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100
Q

Atopic Dermatitis: Management of Moderate Eczema

A

Moderate topical steroid - Bethamethasone valerate or Clobetasone butyrate
Use mild steroid in face area

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101
Q

Atopic Dermatitis: Management of Severe Eczema

A

Potent topical steroid - Bethamethasone valerate
Reduced potency on sensitive areas

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102
Q

Atopic Dermatitis: Dupixent Mechanism of Action

A

Blocks Type II IL-4 and IL-13 receptors

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103
Q

Atopic Dermatitis: Lebrikzumab Mechanism of Action

A

Blocks IL-13

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104
Q

Atopic Dermatitis: Tralokinumab Mechanism of Action

A

Blocks IL-13

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105
Q

Atopic Dermatitis: Pascolinumab Mechanism of Action

A

Blocks IL-4 (ineffective as IL-13 also needs to be blocked)

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106
Q

Haploinsufficiency

A

Only one copy of the gene is working causing a reduced protein production

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107
Q

Tuberous Sclerosis

A

Autosomal dominant condition of benign tumours in organ systems of the body

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108
Q

Tuberous Sclerosis: What genetic pattern is observed?

A

Autosomal dominant

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109
Q

Tuberous Sclerosis: What chromosomes are affected? (2)

A

9q34
16p13.3

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110
Q

Tuberous Sclerosis: What genes are involved?

A

TSC1 and TSC2

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111
Q

Tuberous Sclerosis: What do TSC1 and 2 code for?

A

Tubers and Hamartin - tumour regulating genes

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112
Q

Tuberous Sclerosis: Penetrance

A

High

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113
Q

Tuberous Sclerosis: How may this present in infants?

A

Infantile seizures

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114
Q

Tuberous Sclerosis: Earliest cutaneous sign

A

Ash-leaf Macule - depigmented macules can be observed by Woods Lamp

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115
Q

Tuberous Sclerosis: Presentation on nails (2)

A

Periungual Fibromata
Longitudinal ridging

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116
Q

Tuberous Sclerosis: Presentation on the skin (2)

A

Shagreen patch - leather texture
Facial angiofibroma

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117
Q

Tuberous Sclerosis: Presentation in teeth

A

Enamel pitting

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118
Q

Tuberous Sclerosis: What may occur to the falx cerebri?

A

Cortical tubers or calcification - may induce seizures

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119
Q

Tuberous Sclerosis: Impact on the organs

A

Angiomyolipomas - Heart, Lungs and Kidneys

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120
Q

Tuberous Sclerosis: What may be seen on X-ray?

A

Bone Cysts

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121
Q

Epidermolysis Bullosa

A

Group of inherited disorders with blister formation in response to mechanical trauma

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122
Q

Epidermolysis Bullosa: How many genes are involved?

A

10

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123
Q

Epidermolysis Bullosa: What type of condition is this?

A

Autoimmune

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124
Q

Epidermolysis Bullosa: Examples of genes involved? (4)

A

Keratin 5 and 14
Laminin
Integrins
Collagen 17

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125
Q

Epidermolysis Bullosa: 3 Types

A

Simplex
Junctional
Dystrophic

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126
Q

Epidermolysis Bullosa: Keratin - Type I Keratins

A

K9-K20

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127
Q

Epidermolysis Bullosa: Keratin - Type II Keratins

A

K1-K8

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128
Q

Epidermolysis Bullosa: Simplex - What layer is affected?

A

Epidermal layer affected

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129
Q

Epidermolysis Bullosa: Junctional - What layer is affected?

A

Dermoepithelial layer affected

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130
Q

Epidermolysis Bullosa: Dystrophic - What layer is affected?

A

Upper dermis affected

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131
Q

Epidermolysis Bullosa: Clinical presentation

A

Skin fragility
Blistering at birth with skin loss

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132
Q

Epidermolysis Bullosa: Investigation

A

Skin Biopsy

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133
Q

Neurofibromatosis

A

Genetic condition that causes tumours along the nervous system

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134
Q

Neurofibromatosis: Aetiology

A

Mutations in the NF1 gene

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135
Q

Neurofibromatosis: What signs are shown in the skin? (2)

A

Cafe au lait macules - more than 5
Axillary or inguinal freckles

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136
Q

Neurofibromatosis: What tumour presents?

A

Neurofibromas

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137
Q

Neurofibromatosis: What signs are observed in the eyes? (2)

A

Optic glioma
>2 Lisch Nodules - present on the iris

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138
Q

Necrotising Fasciitis

A

Rapidly progressive infection resulting in extensive necrosis of the superficial fascia and overlying subcutaneous fat that can develop into a life-threatening condition

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139
Q

Necrotising Fasciitis: Type I causative organisms

A

Mixed anaerobes
Coli forms

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140
Q

Necrotising Fasciitis: When does Type I typically occur?

A

Post-abdominal surgery

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141
Q

Necrotising Fasciitis: Type II Causative Organisms

A

Group A streptococcus infection

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142
Q

Necrotising Fasciitis: Risk Factors (4)

A

Immunosuppressed
Obesity
PWID
Peripheral arterial disease

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143
Q

Necrotising Fasciitis: Systemic Symptoms (3)

A

Fever
Chills
Altered mental state

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144
Q

Necrotising Fasciitis: Skin manifestation (2)

A

Manifests as suspected cellulitis - diffuse erythema that doesn’t respond to antibiotic therapy
Purple skin discolourisation

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145
Q

Necrotising Fasciitis: Investigation

A

Microbiology - blood culture with gram staining and cultures from deep tissue

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146
Q

Necrotising Fasciitis: Management

A

Surgical debridement and antibiotics

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147
Q

Acne Vulgaris

A

Inflammatory condition of the pilosebaceous unit

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148
Q

Acne Vulgaris: Typical age in Females

A

14-17

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149
Q

Acne Vulgaris: Associated with what disorders? (2)

A

Endocrine disorders - PCOS and Hyperandrogenism

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150
Q

Acne Vulgaris: Typical age in Males

A

16-19

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151
Q

Acne Vulgaris: What are the potential triggering events for this? (2)

A

Increased androgens at puberty
Patients have increased androgen sensitivity of the sebaceous glands

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152
Q

Acne Vulgaris: What event induces plugging of the pilosebaceous units?

A

Hypercornification causes keratin plugging of the pilosebaceous units

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153
Q

Acne Vulgaris: What produces comodones?

A

Keratin and sebum build up

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154
Q

Acne Vulgaris: What can increase sebum production?

A

Androgens

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155
Q

Acne Vulgaris: What can rupture cause?

A

Acute inflammation and foreign body granulomas to produce inflammatory lesions - papules, pustules, cysts and nodules

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156
Q

Acne Vulgaris: Distribution

A

Sebaceous gland sites - Face, Upper back and Anterior chest

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157
Q

Acne Vulgaris: What is a comodone?

A

White and blackheads

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158
Q

Acne Vulgaris: What is the difference between white heads and black heads?

A

Black heads have oxidised pus

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159
Q

Acne Vulgaris: Complications of Chronic Acne (2)

A

Atrophic scares - ice pick scars or hypertrophic keloid scars
Skin hyperpigmentation

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160
Q

Acne Vulgaris: Mild grading

A

Scattered papules and pustules with comedones

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161
Q

Acne Vulgaris: Moderate grading

A

Numerous papules, pustules and mild atrophic scarring

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162
Q

Acne Vulgaris: Severe grading

A

Cysts, nodules and significant scarring

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163
Q

Acne Vulgaris: Aim of treatment

A

Control and prevent scarring

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164
Q

Acne Vulgaris: Topical treatment options (3)

A

Benzoyl peroxide
Topical vitamin A derivatives - Retinoids
Topical antibiotics

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165
Q

Acne Vulgaris: Action of Benzoyl Peroxide (2)

A

Keratolytic
Anti-bacterial

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166
Q

Acne Vulgaris: Action of Vitamin A Derivatives

A

Drying effect

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167
Q

Acne Vulgaris: Action of Vitamin A Derivatives

A

Drying effect

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168
Q

Acne Vulgaris: Systemic Treatment Options (2)

A

Antibiotics - for at least 6 months
Isotretinoin

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169
Q

Acne Vulgaris: Effect of Isotretinoin

A

Effects sebaceous gland activity

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170
Q

Acne Vulgaris: Initial management

A

Oral Antibiotic or Topical Retinoid

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171
Q

Acne Vulgaris: Second Line Management

A

Oral Isotretinoin - must be hospital only prescribing

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172
Q

Acne Vulgaris: Effect of oral isotretinoin

A

Usually causes an initial flare up for 2-3 weeks then steadily improves at 16 weeks

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173
Q

Acne Vulgaris: Contraindication of Isotretinoin

A

Pregnancy - causes congenital defects

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174
Q

Acne Vulgaris: What can antibiotics be combined with to reduced antimicrobial resistance? (3)

A

Benzoyl peroxide
Retinoids
Zinc

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175
Q

Acne Vulgaris: Examples of Retinoids (3)

A

Adapalene
Isotretinoin
Tretinoin

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176
Q

Acne Vulgaris: If there is a poor response to topical treatment what is administered to those under 12?

A

Erythromycin or Clarithromycin

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177
Q

Acne Vulgaris: If there is a poor response to topical treatment what is administered to those over 12?

A

Lymecycline, Doxycycline or Erythromycin

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178
Q

Rosaecea

A

Condition in which the facial blood vessels dilate to produce a flushed appearance of the cheeks and nose

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179
Q

Rosaecea: Peak Age

A

30-60 years

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180
Q

Rosaecea: Sex epidemiology

A

More common in females

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181
Q

Rosaecea: Presentation of rash

A

Vascular ectasia
Patchy inflammation with plasma cells
Pustules and Papules
Erythema

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182
Q

Rosaecea: Triggers

A

Alcohol
Heat
Spicy food
Stress
Sunlight

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183
Q

Rosaecea: Location

A

Nose
Chin
Cheeks
Forehead
Spares the naso-labial folds

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184
Q

Rosaecea: Impact on the nose

A

Rhinophyma - enlarged unshapely nose due to thickening of skin

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185
Q

Rosaecea: Impact on the eyes

A

Conjunctivitis

186
Q

Rosaecea: First line treatment

A

Topical Metronidazole

187
Q

Rosaecea: Action of Ivermectin

A

Reduce the demodex mite

188
Q

Rosaecea: Second Line Management

A

Topical Metronidazole + Oral Tetracycline

189
Q

Rosaecea: Second Line Management for severe cases

A

Low dose Isotretinoin

190
Q

Rosaecea: Management of Telangiectasia

A

Vascular laser

191
Q

Lichen Planus

A

Rash impacting the skin causing swelling and irritation

192
Q

Lichen Planus: Age epidemiology

A

Mainly impacts middle aged individuals

193
Q

Lichen Planus: Immunopathology

A

T-cell mediated inflammation to an unknown protein in the skin and mucosal keratinocytes

194
Q

Lichen Planus: Characterised by damage to what?

A

The basal epidermis

195
Q

Lichen Planus: Associated with what virus?

A

Hepatitis C

196
Q

Lichen Planus: Diagnostic Test

A

Biopsy - useful to differentiate SCC and Lichen Planus

197
Q

Lichen Planus: Histological features (5)

A

Irregular sawtooth acanthosis
Hypergranulosis
Orthohyperkeratosis
Band-like upper dermal infiltrate of lymphocytes
Basal damage with formation of Cytoid bodies

198
Q

Lichen Planus: Duration

A

12-18 months

199
Q

Lichen Planus: Nail presentation

A

Nail ridges

200
Q

Lichen Planus: Location

A

Volar wrists and forearms
Shins
Ankles

201
Q

Lichen Planus: Wickhams Striae

A

Fine lace-like pattern on the surface of papules and buccal mucosa

202
Q

Lichen Planus: Presentation

A

Itchy Violaceous pink or purple flat-topped shiny papules

203
Q

Lichen Planus: Management

A

Topical or Oral Steroids with Emollients

204
Q

Lichen Planus: Must check for what?

A

Drug precipitant - can cause lichenoid drug eruption

205
Q

Bullous Disorder

A

Autoimmune diseases where damage to adhesion mechanisms in the skin result in blistering

206
Q

Bullous Pemphigoid

A

Sub-epidermal blister caused by an autoimmune reaction

207
Q

Bullous Pemphigoid: Typical age

A

> 60 years

208
Q

Bullous Pemphigoid: Main pathophysiological mechanism

A

Anti-hemidesmosome antibodies react with major or minor antigens of the hemidesmosomes anchoring basal cells to the basement membrane

209
Q

Bullous Pemphigoid: What type of hypersensitivity reaction is this?

A

Type II

210
Q

Bullous Pemphigoid: What type of antibodies are anti-hemidesmosome antibodies?

A

IgG

211
Q

Bullous Pemphigoid: Antigen-Antibody complex results in what?

A

Complement activation and tissue damage

212
Q

Bullous Pemphigoid: Complement activation and tissue damage causes what to occur?

A

Interruption of the dermo-epidermal junction and formation of the sub-epidermal blister

213
Q

Bullous Pemphigoid: Diagnostic Test

A

Biopsy - With Immunofluorescence and Histology

214
Q

Bullous Pemphigoid: Immunological findings

A

Linear IgG and complement deposited around the basement membrane

215
Q

Bullous Pemphigoid: Histological findings

A

Subepidermal blisters and inflammatory infiltrates (mainly eosinophils) within the blister

216
Q

Bullous Pemphigoid: What forms the roof of the blister?

A

Epidermis

217
Q

Bullous Pemphigoid: What happens to older lesions on histology?

A

Shows re-epithelialisation of the floor to mimic pemphigus vulgarus

218
Q

Bullous Pemphigoid: Distribution

A

Localised to one area or widespread on the trunk and proximal limbs

219
Q

Bullous Pemphigoid: Morphology of bullae

A

Large tense bullae on the erythematous base

220
Q

Bullous Pemphigoid: What happens when blisters burst?

A

Leaves erosions

221
Q

Bullous Pemphigoid: Is it scarring?

A

No

222
Q

Bullous Pemphigoid: Early in disease presentation

A

Urticated itchy plaques

223
Q

Bullous Pemphigoid: Nilkolsky sign

A

Negative

224
Q

Nilkolsky Sign

A

Top layers of the skin slip away from the lower layers when rubbed

225
Q

Bullous Pemphigoid: Diagnosis

A

Skin Biopsy with Immunofluorescence studies

226
Q

Bullous Pemphigoid: Treatment for local disease

A

High potency topical steroids

227
Q

Bullous Pemphigoid: Treatment for systemic disease

A

Oral steroids +/- Tetracycline Antibiotics +/- antihistamines

228
Q

Bullous Pemphigoid: What if there is no response to treatment?

A

Administer immunosuppression - Azathioprine or Methotrexate

229
Q

Pemphigus Vulgaris

A

Autoimmune bullous disease

230
Q

Most common subtype of the pemphigus group?

A

Pemphigus vulgaris

231
Q

Pemphigus Vulgaris: Sex incidence

A

Equal

232
Q

Pemphigus Vulgaris: Age presentation

A

Middle age - 40-60

233
Q

Pemphigus Vulgaris: What type of reaction is this?

A

Type II Hypersensitivity

234
Q

Pemphigus Vulgaris: Mechanism of pathophysiology

A

IgG antibodies against desmoglein 3 - this is responsible for maintaining the desmosomal attachments

235
Q

Pemphigus Vulgaris: What occurs once antigen-antibody complexes are generated?

A

Complement activation and protease release causes disruption to desmosomes to cause acantholysis

236
Q

Pemphigus Vulgaris: Clinical presentation

A

Fluid-filled blisters that rupture to form shallow erosions

237
Q

Pemphigus Vulgaris: What process is involved?

A

Pacantholysis

238
Q

Pemphigus Vulgaris: Pacantholysis definition

A

Lysis of intercellular adhesion sites

239
Q

Pemphigus Vulgaris: Has no involvement with what cells?

A

Basal cells

240
Q

Pemphigus Vulgaris: There is a loss in the integrity of what?

A

Epidermal cell adhesion

241
Q

Pemphigus Vulgaris: Distribution

A

Scalp
Axilla
Face
Groin

242
Q

Pemphigus Vulgaris: Splits through what?

A

Intra-epidermal space

243
Q

Pemphigus Vulgaris: Nikolsky sign

A

Positive

244
Q

Pemphigus Vulgaris: Mucosal involvement effects what areas?

A

Eyes
Genitals

245
Q

Pemphigus Vulgaris: Diagnosis tool

A

Skin biopsy with immunofluorescence

246
Q

Pemphigus Vulgaris: Hallmark on Biopsy

A

Chicken wire deposition of IgG within the epidermis

247
Q

Pemphigus Vulgaris: Management of local disease

A

Topical steroids and anaesthetics

248
Q

Pemphigus Vulgaris: Management of systemic disease

A

High dose oral steroids with immunosuppression +/- Rituximab

249
Q

Pemphigus Vulgaris: How long does remission take with treatment?

A

3-6 months

250
Q

Dermatitis Herpetiformis

A

Autoimmune bullous disorder associated with coeliac disease

251
Q

Dermatitis Herpetiformis: Strong association with what disease?

A

Coeliac Disease

252
Q

Dermatitis Herpetiformis: 90% of patients have what disorder?

A

Gluten sensitive enteropathy

253
Q

Dermatitis Herpetiformis: Associated with what gene?

A

HLA-DQ2 haplotype

254
Q

Dermatitis Herpetiformis: Peak Incidence

A

15-40 years

255
Q

Dermatitis Herpetiformis: Pathophysiology

A

IgA antibodies target the gliadin component of gluten but cross-reacts with connective tissue matrix proteins - tissue transglutaminase

256
Q

Dermatitis Herpetiformis: Where do the immune complexes form?

A

In the dermal papillae

257
Q

Dermatitis Herpetiformis: What does immune complex formation do?

A

Activate complement and generates neutrophil chemotaxins to induce sub-epidermal blisters

258
Q

Dermatitis Herpetiformis: Clinical presentation

A

Intensely itchy symmetrical lesions on an erythematous and swollen base followed by blisters

259
Q

Dermatitis Herpetiformis: Locations

A

Elbows
Knees
Buttocks
Scalp
Shoulders

260
Q

Dermatitis Herpetiformis: Diagnostic blood tests

A

Anti-TTG

261
Q

Dermatitis Herpetiformis: Biopsy findings

A

Immunofluorescence showing granular IgA deposts in the dermal papillae
Histology shows sub-epidermal blisters with papillary micro-abscesses

262
Q

Dermatitis Herpetiformis: Management

A

Gluten free diet

263
Q

Dermatitis Herpetiformis: Complications

A

Small bowel lymphoma

264
Q

Dermatitis Herpetiformis: Hallmark

A

Papillary dermal microabscesses

265
Q

Skin Cancer: Risk Factors

A

Sun exposure
Skin type
Immunosuppression - Chronic inflammatory diseases or organ transplants
Environmental carcinogens

266
Q

Skin Cancer: Genetic Susceptibility examples (4)

A

Xeroderma Pigmentosum
Albinism
Naevoid Basal Cell Carcinoma
Epidermolysis Bullosa

267
Q

Skin Cancer: What is Xeroderma Pigmentosum?

A

Defect in XPA-G nucleotide excision repair gene to cause skin cancer on a UV exposed site with neurological degeneration

268
Q

Skin Cancer: What is Epidermolysis Bullosa?

A

Deficiency in Type VII collagen to cause skin fragility and blistering leading to chronic wounding with inflammation and scarring

269
Q

Skin Cancer: Examples of encironmental carcinogens (5)

A

Ionising radiation
Arsenic
Coal tar
Trauma
Chronic wounding

270
Q

Skin Cancer: Examples of Immunosuppression that increase the risk (4)

A

Organ transplant patients
Haematological malignancies
Inflammatory conditions receiving immunosuppressive therapy e.g. IBS, Crohns or RA
HIV

271
Q

Skin Cancer: 2 Main types

A

Keratinocyte skin cancer
Melanoma

272
Q

Skin Cancer: Examples of Keratinocyte Skin Cancer (4)

A

Basal cell carcinoma
Squamous Cell Carcinoma
Actinic Keratoses
Bowen’s Disease

273
Q

Skin Cancer: Melanoma is in what layer?

A

The basal layer of the epidermis

274
Q

Skin Cancer: What layer do basal cell carcinomas arise from?

A

Basal layer of the epidermis

275
Q

Skin Cancer: What layer do the squamous cell carcinomas arise from?

A

Suprabasal layers

276
Q

Skin Cancer: Most common skin cancers?

A

Keratinocyte

277
Q

Skin Cancer: What % of skin cancers are BCCs?

A

75%

278
Q

Skin Cancer: Basal Cell Carcinoma - Age of incidence

A

30-40

279
Q

Skin Cancer: Basal Cell Carcinoma - Pathophysiology

A

Epidermal keratinocyte dNA is damaged by solar UV radiation to cause mutations in tumour suppressor genes, loss of apoptotic function and mutations in proto-oncogenes
Clonal selection of non-apoptosing, mutated cells
Solar UV suppresses normal cell-mediated immune response against tumour cells

280
Q

Skin Cancer: Basal Cell Carcinoma - Description of growth

A

Slow with local destruction

281
Q

Skin Cancer: Basal Cell Carcinoma - 4 types

A

Nodular
Superficial
Infiltrative
Pigmented

282
Q

Skin Cancer: Basal Cell Carcinoma - Description of Nodular BCC

A

Slow growing, shiny pearly nodule with superficial telangiectasia

283
Q

Skin Cancer: Basal Cell Carcinoma - Location of nodular BCC

A

Face

284
Q

Skin Cancer: Basal Cell Carcinoma - Name if ulcerated nodular BCC

A

Rodent ulcer

285
Q

Skin Cancer: Basal Cell Carcinoma - Description of Superficial BCC

A

Erythematous well-demarcated scaly plaques with a slightly raised whipcord margin

286
Q

Skin Cancer: Basal Cell Carcinoma - Superficial BCC size

A

Larger than 20mm at presentation

287
Q

Skin Cancer: Basal Cell Carcinoma - Growth description for superficial BCC

A

Slow growth over months or years

288
Q

Skin Cancer: Basal Cell Carcinoma - Description of Infiltrative BCC

A

Thickened yellowish plaques with a poorly defined margin

289
Q

Skin Cancer: Basal Cell Carcinoma - Description of spread of infiltrative BCC

A

May infiltrate tissues widely and along nerves

290
Q

Skin Cancer: Basal Cell Carcinoma - Description of Pigmented BCC

A

Brown, blue or greyish lesion of nodular or superficial histology

291
Q

Skin Cancer: Basal Cell Carcinoma - Pigmented BCC more common in what patients?

A

Those with dark skin

292
Q

Skin Cancer: Basal Cell Carcinoma - Pigmented BCC may resemble what?

A

Malignant melanoma

293
Q

Skin Cancer: Basal Cell Carcinoma - Investigation

A

An incisional biopsy - must be sent to histology before treatment

294
Q

Skin Cancer: Basal Cell Carcinoma - Treatment of choice

A

Wide excision with histology to ensure complete removal of the tumour with adequate margins

295
Q

Skin Cancer: Basal Cell Carcinoma - Treatment for infiltrative BCC and tumours of the nasal creases

A

Mohs Microscopic Surgery

296
Q

Skin Cancer: Basal Cell Carcinoma - Treatment options for non-surgical treatment

A

Cryotherapy
Photodynamic therapy
Topical Imiquimod

297
Q

Skin Cancer: Basal Cell Carcinoma - Targeted treatment for advanced cancers or those unable to tolerate surgery

A

Vismodegib

298
Q

Skin Cancer: Basal Cell Carcinoma - MOA of Vismodegib

A

Hedgehog inhibitor that binds to SMO

299
Q

Skin Cancer: Squamous Cell Carcinoma

A

Malignant tumour that arises from supra-basal keratinocytes

300
Q

Skin Cancer: Squamous Cell Carcinoma - Occasionally arises from sites of what conditions? (3)

A

Chronic leg ulcers
Site of burns
Chronic lupus vulgaris

301
Q

Skin Cancer: Squamous Cell Carcinoma - Genetic Factors that increase the risk (3)

A

Fair skin type
Xeroderma pigmentosum
Oculocutaneous albinism

302
Q

Skin Cancer: Squamous Cell Carcinoma - Most common skin cancer in what populations?

A

Immunosuppressed patients

303
Q

Skin Cancer: Squamous Cell Carcinoma - Associated with what first line risk factor?

A

Lifetime cumulative UV exposure

304
Q

Skin Cancer: Squamous Cell Carcinoma - Pattern of growth and spread

A

Locally invasive with low risk of metastasis

305
Q

Skin Cancer: Squamous Cell Carcinoma - Description of presentation

A

Warty or hyperkeratotic crusted lump or ulcer

306
Q

Skin Cancer: Squamous Cell Carcinoma - Arises on what skin type?

A

Sun-damaged

307
Q

Skin Cancer: Squamous Cell Carcinoma - Which age range at risk?

A

Elderly

308
Q

Skin Cancer: Squamous Cell Carcinoma - 90% of presentations are where?

A

Head
Neck
Hands
Forearms

309
Q

Skin Cancer: Squamous Cell Carcinoma - Growth pattern

A

Fast growth - may be painful or bleed

310
Q

Skin Cancer: Squamous Cell Carcinoma - Precursor lesions

A

Actinic keratoses
Bowen’s Disease

311
Q

Skin Cancer: Squamous Cell Carcinoma - What metastases are most common?

A

Loco-regional spread with nodal metastases

312
Q

Skin Cancer: Squamous Cell Carcinoma - Management

A

Complete surgical excision with biopsy

313
Q

Skin Cancer: Melanoma

A

Proliferation of atypical melanocytes with potential for dermal invasion and widespread metastases

314
Q

Skin Cancer: Melanoma - Age of incidence

A

Increases with age

315
Q

Skin Cancer: Melanoma - Associated with what main risk factor?

A

Intermittent intense sun exposure or sunburn in childhood

316
Q

Skin Cancer: Melanoma - Risk factors (4)

A

Fair skin
Multiple melanocytic naevi
Family history of melanoma
Immunosuppression

317
Q

Skin Cancer: Melanoma - 60% have what associated genetic mutation?

A

Activating BRAF mutation

318
Q

Skin Cancer: Melanoma - Acral melanomas are associated with what mutation?

A

c-kit

319
Q

Skin Cancer: Melanoma - Rare genetic conditions that are associated? (2)

A

Xeroderma pigmentosum
Oculocutaneous albinism

320
Q

Skin Cancer: Melanoma - 4 types

A

Superficial spreading
Acral lentiginous malignant melanoma
Lentigo maligna melanoma
Nodular malignant melanoma

321
Q

Skin Cancer: Melanoma - Superficial spreading description

A

Large flat irregularly pigmented lesion

322
Q

Skin Cancer: Melanoma - Superficial spreading most common sites

A

Trunk
Limbs

323
Q

Skin Cancer: Melanoma - Superficial spreading description of growth

A

Grows laterally before vertical invasion develops

324
Q

Skin Cancer: Melanoma - Acral letiginous malignant melanoma presentation

A

Pigmented lesions on the palm, sole or under the nail

325
Q

Skin Cancer: Melanoma - Lentigo maligna melanoma presentation

A

Invasive tumour that develops with pre-existing lentigo maligna

326
Q

Skin Cancer: Melanoma - Lentigo maligna melanoma location

A

Sun-damaged face, neck or scalp

327
Q

Skin Cancer: Melanoma - Nodular malignant melanoma location

A

Trunk

328
Q

Skin Cancer: Melanoma - Nodular malignant melanoma presentation

A

Rapidly growing pigmented nodule that bleeds or ulcerates

329
Q

Skin Cancer: Melanoma - RGP

A

Radial Growth Phase

330
Q

Skin Cancer: Melanoma - VGP

A

Vertical growth phase

331
Q

Skin Cancer: Melanoma - RGP description

A

Melanomas grow as macules either entirely in situ or with dermal microinvasion

332
Q

Skin Cancer: Melanoma - VGP description

A

Melanoma cells invade. thedermis forming an expasnile mass with mitosis

333
Q

Skin Cancer: Melanoma - Only what type of melanomas can metastasies?

A

Those in VGP

334
Q

Skin Cancer: Melanoma - Why are nodular melanomas considered more aggressive?

A

They do not have an RGP

335
Q

Skin Cancer: Melanoma - Why are melanomas more likely to metastasises than keratinocyte skin cancers?

A

As melanocytes are motile cells

336
Q

Skin Cancer: Melanoma - Sites

A

Common on sun-exposed sites - Scalp, Face, Neck, Arm, Trunk and Leg

337
Q

Skin Cancer: Melanoma - What appearance would suggest a melanoma?

A

Change in shape
Irregular pigmentation
Bleeding
Satellite nodules
Ulceration
New adult pigmented lesion

338
Q

Skin Cancer: Melanoma - First Line Management

A

Narrow complete excision

339
Q

Skin Cancer: Melanoma - What is used to determine prognosis?

A

Breslow Criteria

340
Q

Skin Cancer: Melanoma - Breslow Criteria

A

Determines the prognosis based on tumour depth

341
Q

Skin Cancer: Melanoma - <1mm Breslow Criteria

A

5 year survival of 95-100%

342
Q

Skin Cancer: Melanoma - >4mm Breslow Criteria

A

5 year survival of 50%

343
Q

Skin Cancer: Melanoma - Metastasis Bresow Criteria

A

5 year survival of 5%

344
Q

Skin Cancer: Melanoma - Where is the Breslow Criteria measured from?

A

Granular layer of the epidermis down to the deepest point of invasion

345
Q

Skin Cancer: Melanoma - Treatment for advanced disease with c-kit mutation?

A

Imatinib

346
Q

Skin Cancer: Melanoma - Treatment for advanced disease with BRAF mutations?

A

Debrafenib or Vemurafenib

347
Q

Skin Cancer: Melanoma - How to reduce resistance to BRAF inhibitors?

A

Add a MEK inhibitor

348
Q

Melanoyctic Lesions: Melanocytes are derived from what?

A

The neural crest

349
Q

Melanoyctic Lesions: Early in embryogenesis the melanoblasts migrate from the neural crest to where?

A

Skin
Uveal Tract
Leptomeniges

350
Q

Melanoyctic Lesions: Where are melanocytes located?

A

Basal layer

351
Q

Melanoyctic Lesions: Involves what gene?

A

Melanocortin 1 Receptor Gene

352
Q

Melanoyctic Lesions: Melanocortin 1 Receptor Gene encodes what?

A

MC1R protein

353
Q

Melanoyctic Lesions: MC1R determines what?

A

Balance of pigment in the skin and hair

354
Q

Melanoyctic Lesions: Eumelanin has what impact?

A

Causes any hair colour other than red

355
Q

Melanoyctic Lesions: Phaeomelanin has what impact?

A

Causes red hair

356
Q

Melanoyctic Lesions: MC1R has what action?

A

Converts Phaeomelanin into Eumelanin

357
Q

Melanoyctic Lesions: One defective MC1R copy has what impact?

A

Freckling

358
Q

Melanoyctic Lesions: Two defective MC1R copy has what impact?

A

Red hair and freckling

359
Q

Biological word for freckles

A

Ephilides

360
Q

Melanoyctic Lesions: Ephilides - What are these?

A

Patchy increases in melanin production (Freckles)

361
Q

Melanoyctic Lesions: Ephilides - Occurs after what?

A

UV exposure

362
Q

Melanoyctic Lesions: Ephilides - Reflects an increased what?

A

Density of melanocytes

363
Q

Melanoyctic Lesions: Actinic lentigines

A

Age or liver spots related to UV exposure on the face, forearms and dorsal hands

364
Q

Melanoyctic Lesions: Actinic lentigines - Refects increased what>

A

Melanin and basal melanocytes

365
Q

Melanoyctic Lesions: Actinic lentigines - Impact on the epidermis

A

Elongated rete ridges

366
Q

Melanoyctic Lesions: Naevi - Types (4)

A

Usual
Dysplastic
Spitz
Blue

367
Q

Melanoyctic Lesions: Naevi - First stage of development

A

Junctional naevus

368
Q

Melanoyctic Lesions: Naevi - Second stage of development

A

Compound Naevus

369
Q

Melanoyctic Lesions: Naevi - Thirs datge of development

A

Intradermal Naevus

370
Q

Melanoyctic Lesions: Naevi - Junctional Naevus

A

Melanocytes proliferate to form clusters of cells at the dermoepidermal junction - nests of melanocytes attach to the epidermis

371
Q

Melanoyctic Lesions: Naevi - Compound Naevus

A

Junctional clusters with groups of cells in the dermis

372
Q

Melanoyctic Lesions: Naevi - Intradermal Naevus

A

All junctional activity is ceased and the naevus becomes entirely dermal

373
Q

Melanoyctic Lesions: Congenital Melanocytic Naevi - Small classification

A

<2cm

374
Q

Melanoyctic Lesions: Congenital Melanocytic Naevi - Medium classification

A

2-20 cm

375
Q

Melanoyctic Lesions: Congenital Melanocytic Naevi - Large classification

A

> 20cm

376
Q

Melanoyctic Lesions: Usual Type Acquired Naevi - Pathophysiology

A

Melanocyte:Keratinocyte Ration breaks down at cutaneous sites to allow the formation of a simple naevi

377
Q

Melanoyctic Lesions: Usual Type Acquired Naevi -Why do immunosuppressed leukaemia patients have more naevi?

A

As naevus induction is immunoregulated

378
Q

Melanoyctic Lesions: Dysplastic Naevi - Presentation

A

Asymmetrical and >6cm in diameter with variegated pigment

379
Q

Melanoyctic Lesions: Dysplastic Naevi -Two types

A

Sporadic
Familial

380
Q

Melanoyctic Lesions: Dysplastic Naevi - Inheritance of familial type

A

Autosomal inheritance

381
Q

Melanoyctic Lesions: Dysplastic Naevi - Familial has a high penetrance of what gene?

A

CDKN2A

382
Q

Melanoyctic Lesions: Dysplastic Naevi - Features

A

Architectural and cellular atypia

383
Q

Melanoyctic Lesions: Dysplastic Naevi - Why does architectural and cellular atypia occur?

A

Host reaction to fibrosis and inflammation

384
Q

Melanoyctic Lesions: Halo Naevi - Presentation

A

Peripheral halo of depigmentation

385
Q

Melanoyctic Lesions: Blue Naevi - Depth

A

Entirely dermal

386
Q

Melanoyctic Lesions: Halo Naevi - Consist of what?

A

Pigment-rich dendritic spindle cells

387
Q

Melanoyctic Lesions: Spitz Naevi - Consist of what cells?

A

Large spindle or epithelioid cells

388
Q

Melanoyctic Lesions: Spitz Naevi - Age

A

<20 years

389
Q

Melanoyctic Lesions: Spitz Naevi - Mimics what disease?

A

Melnaoma

390
Q

Melanoyctic Lesions: Spitz Naevi - Colour

A

Pink

391
Q

Melanoyctic Lesions: Spitz Naevi - Why is it pink?

A

Prominent vasculature

392
Q

Melanoma: Sex incidence

A

More common in females

393
Q

Melanoma: Age incidence

A

Middle age

394
Q

Melanoma: Location

A

Scalp
Face
Neck
Arm
Trunk
Leg

395
Q

Melanoma: How does BRAF cause cell proliferation?

A

Upregulates MEK and ERK

396
Q

Melanoma: What does a suffix b mean?

A

Tumour ulceration

397
Q

Melanoma: How do satellite deposits appear?

A

Local dermal lymphatics

398
Q

Melanoma: Management of melanoma with regional lymph node metastases?

A

Excised by radical lymphadenectomy

399
Q

Melanoma: Where does haematogenous spread metastasise to?

A

Skin
Soft tissue
Heart
Lungs
GIT
Liver
Brain

400
Q

Melanoma: Excision - In situ how much clearance?

A

Clear by circa of 5mm

401
Q

Melanoma: Excision - Invasive but <1mm thick how much clearance?

A

1cm

402
Q

Melanoma: Excision - Invasive but 1-2mm thick how much clearance?

A

2cm

403
Q

Melanoma: Excision - If the sentinel node is positive what is done?

A

Regional lymphadenectomy

404
Q

Examples of pre-cancerous dysplasia

A

Bowen’s Disease
Actinic Keratosis
Viral lesions

405
Q

How is superficial non-melanoma sun damage managed?

A

5% Imiquimod cream

406
Q

Seborrhoeic Keratosis

A

Benign epidermal tumour

407
Q

Seborrhoeic Keratosis: Pathophysiology

A

Benign proliferation of epidermal keratinocytes

408
Q

Seborrhoeic Keratosis: Common in what ages?

A

Elderly

409
Q

Seborrhoeic Keratosis: Leser-Trelat Sign

A

Eruptive appearance of lesions that indicates internal malignancy

410
Q

Seborrhoeic Keratosis: Presentation

A

Has a stuck on appearance - Well-demarcated, raised brown coloured lesion

411
Q

Seborrhoeic Keratosis: Location

A

Face
Trunk

412
Q

Seborrhoeic Keratosis: Surface description

A

Greasy hyperkeratotic surface - may have depressions or small cysts

413
Q

Seborrhoeic Keratosis: Management

A

Most are self-limiting - may need cryotherapy or curettage if requested

414
Q

Bowen’s Disease: Location

A

Legs

415
Q

Bowen’s Disease: What is this?

A

Squamous cell carcinoma in-situ

416
Q

Bowen’s Disease: Common in what sex

A

Females

417
Q

Bowen’s Disease: Presentation

A

Scaly patch or plaque with an irregular border and no dermal invasion

418
Q

Bowen’s Disease: Presentation

A

Scaly patch or plaque with an irregular border and no dermal invasion

419
Q

Acitinic Keratosis: Presentation

A

Atypical Bowenoid lesions with variable epidermal dysplasia

420
Q

Acitinic Keratosis: Common precursor to what?

A

Invasive SCC

421
Q

Acitinic Keratosis: Location

A

Scalp
Face
Hands

422
Q

Acitinic Keratosis: Management

A

Topical Cytotoxic - 5-Flurouracil

423
Q

Viral Lesions: Erythroplasia of Queryat-Penile Bowen’s are associated with what virus?

A

HPV

424
Q

Viral Lesions: HPV-16 is associated with what?

A

Penile dysplasia

425
Q

Squamous Cell Carcinoma: Factors that increase risk? (5)

A

Thickness - >4mm
Poor differentiation
Lymphatic and vascular space invasion
Perineural spread
Sites of Poor Prognosis - Scalp, Ear or Nose

426
Q

Xeroderma Pigmentosum: Aetiology

A

Defect in one nucleotide excision repair gene - XPA-G

427
Q

Xeroderma Pigmentosum: Presentation

A

Skin cancer on UV-exposed site with neurological degeneration

428
Q

Xeroderma Pigmentosum: Most individuals develop what by the age of 2?

A

Solar lentigins

429
Q

Oculocutaneous Albinism

A

Rare inherited disorders characterised by a reduction or complete lack of melanin pigment in the skin, hair and eyes

430
Q

Oculocutaneous Albinism: Inheritance pattern

A

Autosomal recessive

431
Q

Oculocutaneous Albinism: Absence or defective what?

A

Tyrosinase

432
Q

Oculocutaneous Albinism: Clinical presentation (5)

A

Sun sensitivity - increases the risk of skin cancer
Photophobia
Nystagmus - involuntary eye movement
Amblyopia - Lazy eye
Lack of pigment in the retina

433
Q

Naevoid Basal Cell Carcinoma: Alternate name

A

Gorlin’s Syndrome

434
Q

Naevoid Basal Cell Carcinoma: Aetiology

A

Autosomal dominant familial cancer syndrome

435
Q

Naevoid Basal Cell Carcinoma: Major features of clinical presentation (4)

A

Early onset with multiple BCC
Palmar pits
Jaw cysts
Ectopic calcification falx

436
Q

Naevoid Basal Cell Carcinoma: Minor features of Clinical presentation (3)

A

Skeletal abnormality
Cardiac or Ovarian fibroma
Medulloblastoma

437
Q

Photoageing: Age normal ageing starts

A

35

438
Q

Photoageing: Fat in normal ageing

A

Subcutaneous fat is lost

439
Q

Photoageing: Why does the skin become dry in normal ageing?

A

Due to less hair follicles, sweat and sebaceous glands

440
Q

Photoageing

A

Ageing of the skin in addition to normal ageing on sun exposed sites

441
Q

Photoageing: Solar Elastosis

A

Skin coarse and yellow with a loss of elastic quality

442
Q

Photoageing: What irregular pigmentation occurs?

A

Freckling
Lentigo

443
Q

Photoageing: Presentation

A

Easy bruising
Telangiectasia
Atrophy
Roughness and Dryness
Deep wrinkling

444
Q

Ersipelas

A

Superficial form of cellulitis localised to the dermis and lymphatic system

445
Q

Ersipelas: Causative organism

A

Streptococcus pyogenes

446
Q

Ersipelas: Clinical presentation

A

Well demarcated erythematous plaque

447
Q

Ersipelas: Location

A

Face

448
Q

Ersipelas: Associated symptoms

A

Fever
Systemic upset

449
Q

Ersipelas: Management

A

Oral Flucloxacillin

450
Q

Photosensitivity

A

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

451
Q

Photosensitivity: What classfication is used for skin types?

A

Fitzpatrick skin types

452
Q

Photosensitivity: Type 1 Skin type

A

Very fair skin that always burns and never tans

453
Q

Photosensitivity: Type 2 Skin Type

A

Fair that usually burns and sometimes tans

454
Q

Photosensitivity: Type 3 Skin Type

A

Medium that sometimes burns and usually tans

455
Q

Photosensitivity: Type 4 Skin Type

A

Olive that rarely burns and always tans

456
Q

Photosensitivity: Type 5 Skin Type

A

Brown that never burns and always tans

457
Q

Photosensitivity: Type 6 Skin Type

A

Black that never burns and always tans

458
Q

Keratoacathoma

A

Rapidly growing epidermal tumours

459
Q

Keratoacathoma: Presentation

A

Red papule with a central crater-like crusty keratinous plug

460
Q

Keratoacathoma: Location

A

Sun-exposed sites

461
Q

Keratoacathoma: Diameter

A

2-3cm

Dermatology (5 decks)

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