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MBBS - Year 2 > Dermatology - Skin Cancer, Acne, Hair and Nails > Flashcards

Dermatology - Skin Cancer, Acne, Hair and Nails Flashcards

1
Q

Classification of neoplasia

A

Benign and malignant
Melanoma and non-melanoma
According to origin

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2
Q

Where do melanocytes arise from

A

Neuro-ectoderm

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3
Q

Mitotic rate of melanocytes

A

Low mitotic rate

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4
Q

Where can melanocytes in embryonal life be found

A

Diffusely in the dermis

Migration to final location is key

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5
Q

By the end of gestation, dermal melanocytes disappear except for

A

Head and neck
Dorsal aspects of distal extremities - typical sites for dermal melanocytosis and melanocytomas (blue naevi)
Pre sacral

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6
Q

What do ventral neural crest cells form (trunk NCCs)

A

Melanocytes
Neurons, glia of ganglia
Adrenal medulla
Schwann cells

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7
Q

What do cranial neural crest cells

A 
Melanocytes 
Neurons, glia of ganglia 
Dermis of head 
Smooth muscles 
Chondrocyte osteocyte
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8
Q

Proportion of melanosomes in membrane bound packets in different races

A

11% for Africans
37% for Asians
85% for caucasians

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9
Q

Melanocyte/ keratocyte unit

A

Melanocytes present in epithelium 1: 20-40 keratocytes

Melanin stays above the nucleus of basal keratocytes, like an umbrella

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10
Q

How is melanin transferred

A

Transferred to epithelial cells via dendritic processes

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11
Q

What is melanin proaction driven by

A

UV exposure through POMC and alpha-MSH

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12
Q

Natural hx of nave

A

Simple lentigo –> junctional nevus –> compound naves –> intradermal naevus —> regressed naevus

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13
Q

Lentigo

A

Pigmented, flat or slightly raised lesion, not caused by sun exposure

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14
Q

Frequency of melanomas

A

3rd most frequent skin tumour

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15
Q

ABCD of histology of melanomas

A

Asymmetry
Border irregularity
Conspicuous junctional activity
Dermal mitoses

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16
Q

Major types of melanomas

A

Lentigo maligna (LMM)
Superficial spreading
Nodular
Acral-lentiginous

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17
Q

Acral

A

Affecting peripheral parts of body e.g. limbs, ears etc

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18
Q

What are melanoma lesions composed of

A

Melanocytes

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19
Q

Growth phases of melanomas

A

Radial (horizontal)
(Micro) invasive radial
Vertical

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20
Q

Sun damage/ area of LMM

A

Prominent

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21
Q

Sun damage/ area of superficial spreading melanoma

A

Intermittent sun exposure areas

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22
Q

Sun damage/ area of nodular melanoma

A

Anywhere, mainly intermittent

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23
Q

Sun damage/ area of acral lentiginous melanoma

A

Variable

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24
Q

Prognostic factors of melanoma

A 
Breslow thickness 
Ulceration 
Mitotic rate 
Perineural/ Vascular invasion 
TILs
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25
Q

Dysplastic naevus

A

Abnormal but non-cancerous moles on the skin

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26
Q

How does UV rays act as a carcinogen

A

Inhibits DNA repair, apoptosis and cell signalling pathways that prevents skin cancers

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27
Q

Carcinogensis cycle in skin

A

UV

DNA lesion –> mutation —> gene —> cell phenotype —> clonal expansion —-> precancerous or carcinoma

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28
Q

How does UV trigger exposure differ between skin cancer

A

SCC –> flash fry (blistering burns)

BCC –> intermittent simmer (frequently tanning/ burns)

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29
Q

What proportion of BCCs are found on busy sites w. intermittent sun exposure

A

1/3 e.g. trunk and legs

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30
Q

Does the incidence of SCCs or BCCs increase more quickly w/ UV dose

A

SCC

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31
Q

Do SCCs or BCCs occur later in life

A

SCCs

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32
Q

How is vitamin D acquired

A

From UV skin exposure and diet

Calcitriol increases Ca levels

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33
Q

Risk factors for skin cancer

A 
Skin types (Fitzpatrick I)
Sunburns (esp childhood)
Outdoor exposure - occupation (e..g builder)
Living in sunny location 
Immunosuppressed 
Sunbeds & sunbathing
Fhx 
PMH of skin cancers
Genetic disorders e.g. albinism
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34
Q

Transplant pts and skin cancers

A

AK and SCC 10-20x increase in sun-exposed skin
Cancer develops due to imunosupression
SCCs are usually unaggressive

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35
Q

Relevant drugs given to transplant pts that have a relation w/ skin cancer

A

Cyclophosphamide, ciclosporin and azathioprine are mutagens when followed by UVA

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36
Q

Types of albinism

A

Occulocutaneous albinism

Occular albinism

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37
Q

Types of occulocutaneous albinism

A

Type 1: more severe - no melanin

Type 2: some melanin

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38
Q

Occular albinism

A

Normal, or slightly paler than normal for their ethnicity, skin and hair

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39
Q

Common cutaneous precancerous lesions that are UV induced

A

Actinic (solar) keratoses (AKs)
Bowen’s disease (carcinoma in situ)
Lentigo maligna
PUVA keratoses

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40
Q

Common cutaneous precancerous lesions that are viral induced

A

Vulval intraepithelial neoplasms (VIN)
PIN (incl Bowenoid Papulosis)
AIN

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41
Q

Actinic keratoses

A

Solar keratoses

Proliferations of cytologically aberrant epidermal keratinocytes

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42
Q

AK’s and risk of skin cancer

A

Approx 1:100 to 1:1,000 risk of SCC per AK

Strong predictor of development of melanoma or non-melanoma skin cancers

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43
Q

Risk factors for AKs

A 
Individual - older age, M, Fair skin, blonde hair
Cumulative UV radiation exposure 
Immunosuppresion 
Prior hx of AKs of other skin cancers 
V rare genetic disorders
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44
Q

Genetic disorders that are risk factors for AKs

A

Xeroderma pigmentosum
Bloom syndrome
Rothmund-Thomson syndrome

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45
Q

Clinical findings of AKs

A

Sun exposure body sites
Pruritus, brining orb stinging pain, bleeding and crusting
2-6mm erythematous, flat, rough or scaly papule

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46
Q

Arsenical keratoses (ArKs)

A

Associated w. c/c arsenicism

From medicinal, occupational and environmental exposures

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47
Q

Common occupations for ArKs

A 
Miners 
Smelters 
Agricultural 
Computer microchip
Electroplating 
Glassmkainhg
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48
Q

What are ArK’s associated w/

A

Bowen’s disease
BCC
SCC
Internal malignancies

Potential to develop into invasive SCC

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49
Q

Latent period of ArKs

A

40yrs

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50
Q

Aetiology and pathogenesis of ArKs

A

Arsenic reacts w/ -SH (sulfhydrl groups) in tissue proteins

Chromosomal mutations and breaks occur in p53

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51
Q

Clinical findings of ArKs

A

2-10mm, punctuate, yellow, keratitis papules
Seen in palms and soles - thenar and lateral borders of the hands, side of fingers
Areas of constant pressure or repeated trauma

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52
Q

SCC in situ

A

Bowen’s disease
Potential to progress to invasive SCC
Can be seen in genital mms (papilloma virus)

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53
Q

Epidemiology of SCC in situs

A

Rare in individuals younger than 30 years except on genitals

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54
Q

Bowen’s aetiology and pathogenesis

A

UV exposure (sunlight and therapeutic)
Immunosuppression
Infection w/ HPV
C/c arsenicism

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55
Q

Clinical findings of Bowen’s disease

A 
Discrete, slowly enlarging 
Pink to erythematous, thin plaque 
Well-dermacated, irregular borders 
Overlying scale or crust 
Sun-exposed areas
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56
Q

Lentigo maligna

A

Subtype of melanoma in situ
Seen in chronically sun-expsoed areas e.g. cheeks, nose, neck, scalp and ears
Common in 7th and 8th decades

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57
Q

Pathogenesis of lentigo maligna

A

Cumulative sun exposure

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58
Q

LM vs LMM

A

Lentigo maligna may progress to Lentigo Maligna Melanoma w/ time

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59
Q

LM clinical findings

A

Flat, slowly enlarging brown, freckle-like macule
Irregular shape and offering shades of brown and tan
Ill-defined borders

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60
Q

What are BCCs derived from

A

Non-kertainising cells originating in the basal layer of the epidermis

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61
Q

Epidemiology of BCCs aka rodent ulcer

A

Most common cancer in humans

Almost s common as all other others combined

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62
Q

Natural pathway of BCC

A

Untreates, will invade locally and compromised function and cosmoses

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63
Q

Metastasis in BCCs

A

Extremely rare

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64
Q

Risk factors for BCCs

A 
UV exposure 
Light/ red hair 
Blue eyes
Northern European ancestry 
Type 1 or 2 skin 
Freckles 
Fhx
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65
Q

Genetic causes of BCC

A 
Gorlins syndrome (dental cysts and palm pits) - pITCH mutation 
Xeroderma pigmentosum
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66
Q

Clinical px of BCCs

A

Intermittent bleeding
May appear to heal
Pearly, translucent, ulceration, telangiectasis
Rolled edge

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67
Q

BCC subtypes

A 
Nodular BCCs 
Pigmneted BCCs
Superficial BCCs
Morpheaform (sclerosing) BCCs
Fibroepithelium of Pinkus
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68
Q

Features of nodular BCC - most common

A

Translucent papule or nodule seen in sun-exposed areas
Usually, telangiectasia and rolled border
Large lesions have central necrosis (rodent ulcer)

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69
Q

Features of pigmented BCC

A

Subtype of nodular BCC
increased melaninisation –> hyperpigmented, translucent papule/ nodule
May be eroded

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70
Q

Features of superficial BCCs

A

Commonly on trunk
Erythematous patch
May resume eczema

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71
Q

When to suspect superficial BCC

A

Isolated patch of ‘eczema’ that doesn’t respond to treatment

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72
Q

Features of morpheaform (scleroisng) BCC

A

Aggressive variant
Ivory-white appearance
May resemble a scar or morphea

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73
Q

When to suspect morpheaform BCC

A

Unexplained scars

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74
Q

Features of fibroepithelioma od pinkus

A

Pink plywood lesion, commonly on lower back
May be difficult to distinguish from a skin tag
V rare

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75
Q

What is a SCC

A

Malignant neoplasm derived fron suprabasal epidermal keratinocytes
Usually evolves from AKs or Bowen’s disease
Clinical px variable

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76
Q

Predisposing factors for SCC

A 
Precursor lesions, UV, immunosupression 
Burns or long term heat exposure - Marjolin's syndrome
C/c scarring 
Smoking
Some c/c infl dermatoses 
Papillomavirus infection
Geno dermatoses
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77
Q

Geno dermatoses

A

Albinism
Xeroderma pigmentosum
Prokeratosis
Epidermolysis bulls

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78
Q

Clinical findings of SCC

A

Flesh-colour or erythematous
Hyperkertatotic, bleeding, oozing, crusting
Papule, nodule or plaque

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79
Q

What may SCC look like

A

May be pigmented or ulcerate (wet beefy appearnce)
May be cutaneous iron
May be verruccous (wart-like)
Rarely, like an abscess, particularly if in perifungal location

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80
Q

Commonest locations of cutaneous melanoma

A

Men - back

Women - legs, then trunk

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81
Q

Risk factors for cutaneous melanoma

A 
UV radiation exposure 
Phenotypic characteristics 
Hx of prior melanoma 
Fhx of melanomas 
Mutation in p16, BRAF or MCR1R
Xeroderma pigmentosum
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82
Q

Phenotypic characteristics as risk factors

A

Fair skin, tendency to sunburn or freckles
Blue/ green eyes
Red/ blonde hair
Numerous typical Nervi and/ or more than one typical naevus
Large congenital naevus

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83
Q

Subtypes of melanoma

A

Superficial spreading malignant melanoma (SSMM)
Nodular melanoma
LMM
Acral lentiginous melanoma

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84
Q

Features of SSMM

A

Most common sub-type
Most frequently the lower legs of women and upper back of men
Wide range of aprerance
Associated w/ pre-existing naevi

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85
Q

Epidemiology of SSMM

A

Most commonly 4th to 5 th decade on intermittently sun-exposed areas
Most common subtype of melanoma

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86
Q

Most common site of nodular melanoma

A

Trunk

Typically, uniformly dark blue-black or bluish-red raised lesion

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87
Q

Common areas for LMM

A

Face

Many have sub-clinical lateral growth so higher recurrence rates

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88
Q

Epidemiology of Acral Lentiginous Melanoma

A

2% of melanoma in Caucasian
Most common form in darker pigmented
Common in elderly

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89
Q

Most common site of acral lentiginous melanoma

A

Sole, then palm, then subungual

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90
Q

Does hx of trauma exclude dx of acral lentiginous melanoma

A

No

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91
Q

Hutchinson’s sign

A

Pigment on nail fold

Seen in acral lentiginous melanoma

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92
Q

Features of sebborrheic keratosis

A

Well-demarcated, ‘stuck-on’ appearance*

Usually, rough surface

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93
Q

Breslow thickness

A

Predicts melanoma survival

Top of granular layer of the epidermis yo the greatest depth of the tumour in mm

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94
Q

Should a bx be done for melanomas

A

No

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95
Q

Diagnostic methods of skin cancer

A

Hx
Physical examination
Dermascopy
Histopathology

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96
Q

Dermoscopy

A

Simple non-invasive technique to dx skin cancer
Looks at pigment network
Improves sensitivity and specificity for clinical dx

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97
Q

Histopathology for making a dx of skin cancer

A

Gold standard for diagnosing pigmented skin lesion
Based on architectural and cytologic features
Immunohistochemistry may be useful in melanoma dx

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98
Q

Sentinel lymph node bx

A

Staging and prognostic tool for skin cancers
Detects micrometastases in regional LNs
Blue dye + technetium-99 labelled radio colloid solution are injected intradermally at the primary site

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99
Q

When should cutaneous lymphoma be considered

A 
In eczema which hasn't respond to topical steroids 
Usually, scaly red rash 
Less itchy than eczema 
Not as thick as psoriasis 
Slowly progressive over decades
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100
Q

Features of dermis

A

Supportive connective tissue matrix
Loss of collagen and elastic
Highly vascularised

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101
Q

What is the s/c layer of skin made up of

A

Loose connective tissue & adipose tissue

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102
Q

What is a wound

A

Loss of integrity of skin tissue

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103
Q

What its considered a c/c wound

A

Disruption in normal healing process (systemic/ local factors)
Slowed/ incomplete healing (usually at infl of proliferative phases)

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104
Q

Stages of wound healing

A

Haemostasis
Infl phase
Proliferative phase
Maturation & remodelling phase

These phases may overlap

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105
Q

How long does the infl phase of wound healing last

A

0-3 days

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106
Q

Clinical signs seen in infl stage of wound healing

A

Rubor
Calor
Tumour
Dolor

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107
Q

Haemostasis in wound healing

A

Aggregation and degranulation of platelets

Blood clotting and formation of a fibrin plug (eschar) initially fills wound

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108
Q

Role of immune cells in infl opals of wound healing

A

Polymorphonuclear leukocytes, monocytes, macrophages and lymphocytes invade fibrin plug space and secrete growth factors and cytokines to help modulate response

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109
Q

Role of fibroblasts in infl phase of wound healing

A

Help blood vessels from deep fascia and surrounding dermis lay down temp matrix of granulation tissue —> serve as guide for migrating and proliferating cells

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110
Q

How long does the proliferative phase in wound healing last

A

3-21 days

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111
Q

Clinical signs of proliferative phase of wound healing stage

A

No infl signs
Reduced swelling
Reduced wound size (contraction)
Itch

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112
Q

Features of proliferative phase of wound healing

A

Net collagen synthesis
Increased wound tensile strength
Scar formation

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113
Q

Net collagen synthesis in proliferative phase of wound healing

A

Mediated by growth factors, ECM molecule and their receptors
Extensive cell-cell interactions to control cellular behaviour

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114
Q

Increased wound tensile strength in proliferative phase of wound healing

A

Epidermal cells proliferative and move to wound edge to granulation tissue - closes wound
Wound contcraction via forces within myofibroblast

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115
Q

Scar formation in proliferative phase of wound healing

A

Apoptosis of immune cells, fibroblasts, endothelial cells

Remaining fibroblasts continue to lay down collagen (I and III)

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116
Q

How long does the maturation & remodelling phase last in wound healing

A

21 days to 2 years

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117
Q

Why is the duration of maturation & remodelling phase variable in wound healing

A 
Depends on:
Age 
Wound type 
Body location
Duration of infl phase
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118
Q

What occurs in the maturation and remodelling phase

A

Reorganisation of collagen - Type 3 replaced by Tye 1

Temsile strength improves

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119
Q

What can affect speed of wound healing?

A 
Size of wound 
Blood supply to area 
Presence of origin bodies or micro-organisms 
Age and health of pt 
Nutritional status 
Drugs
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120
Q

Types of wound healing

A

Primary intention
Secondary intention
Tertiary intention

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121
Q

Primary intention e.g. surgical incision

A

Immediate closure of wound edges when no loss of tissue has occurred

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122
Q

Features of primary intention wound healing

A

Rapid epithelial cover,
Fast healing
Better cosmetic

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123
Q

Secondary intention of wound healing

A

Examples incl excessive trauma, difficult wound closure, tissue loss
Spontaneous healing of wound direct closure (intentionally left open)

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124
Q

Tertiary intention of wound healing

A

Examples incl traumatic injury, dirty surgery, delayed primary intervention or surgical wounds
Initially left open after removal of non-viable tissue
Wound edges brought together after few dats when wound is clean

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125
Q

Examples of -pre-cancerous lesions

A

AK
Dysplastic naevus/ atypical naevus
Bowens disease
Lentigo maligns

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126
Q

Examples of benign skin lesions

A 
Keratoacanthoma 
Seborrheic wart 
Cutaneous horn 
Viral wart 
Epidermoid cyst
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127
Q

Cryotherapy

A

Sin lesions frozen w/ cryogen - usually liquid N

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128
Q

How does cryotherapy cause cells etch

A

Ice crystal formation
Osmotic differences –> cell disruption
Iscahemic damage

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129
Q

Admins of cryotherapy

A

~1-2 cm from skin on centre of area

Form a circular icefield

130
Q

Indications for cryotherapy

A 
AK 
Viral warts 
Seborrheic warts 
Bowens disease e
Superficial BCC
131
Q

Contraindications of cryotherapy

A

Pigmented lesion
Malignant lesion
Cold urticaria

132
Q

Efudix (5-Flurouracil)

A

Antimetabollte cream inhibiting DNA synthesis

133
Q

Admin of efudix cream

A

OD-BD for 4/52

134
Q

indications of Efudix cream

A

sBCCs
Multiple AKs
Bowen’s disease

135
Q

Indications for imiquimod cream

A

Warts
sBCCs
AK

Immune response modulator

136
Q

Photodynamic therapy

A

Activation of topical porphyrin cream to destroy cancer/ pre cancer
Uses red light

137
Q

Indications of photodynamic therapy

A

AK
Bowen’s
sBCC
Multiple or large lesions

138
Q

Admin of curettage and cautery

A

Inject local anaesthetic
Scrape off lesions
Haemostais by cautery

139
Q

Indications of curettage and cautery

A

Pyogenic granuloma
Cutaneous horn/ AK
Small nodular BCC
Seborrheic wart

140
Q

Contraindications of curettage and cautery

A

Pigmented lesions
Most SCCs
Morpheic BCCs
Poor cosmetic reasons e.g. vermillion border, alar rim, nose tip

141
Q

Admin of shave excision

A

Local anaesthetic
Shave off marked lesion to be removed
Inject w/ blade
Homeostasis by cautery

142
Q

Indications for shave excision

A

Benign naevi

143
Q

Contraindications for shave excisions

144
Q

How is an excision bx carried out

A

Mark lesion to be removed
Local anaesthetic
Excise lesion w/ appropriante margin
Side to side closure if possible

145
Q

Indications for excision bx

A

Suspected tumours

Pigmented lesions

146
Q

Contraindications for excision bx

A

INR too high
Pacemaker fitted
Under treatment w/ antiplatelets/anticoag

147
Q

Factors to consider for RT for skin cancers

A

Type - radiosensitive lesions, morphology of cancer
Site - where surgery may be difficult (e.g. eyelids)
Previous RT
Suitability of other treatments
Pts preferences

148
Q

Moh’s surgery - micrographic surgery

A

Microscopic examination of horizontal section cut from periphery of an excision specimen.
Excellent cure rate but time consuming and expensive

149
Q

Moh’s surgery vs other surgeries for skin lesions

A

Done for recurrent lesions
High risk areas
Aggressive growth

150
Q

Common medico-legal pitfalls w/ removal of skin lesions

A

Communication about risk and side effects - adequate consents
Size of scars from surgery often bigger than pts expect
Cryotherpya produces a fierce burn like reaction

151
Q

Dx and staging of skin cancer

A 
Bx - not from pigmented lesions 
Analysis of thickness/ ulceration of excision sample 
Sentinel LN bx (SLNB)
CT scans/ MRI
PET scan
152
Q

Chemo for skin cancers

A

Given for metastatic malignant melanoma - usually localised and advanced - isolated limb perfusion, may given dacarbazine
Bleomycin for SCC

153
Q

Targeted therapy for skin cancers looking at BRAF and CKIT

A

BRAF inhibitors - vermurafenib

C-KIT - seen in some melanomas, give imatinib

154
Q

Interferon-alpha as adjuvant therapy for skin cancer

A

Used after removal of melanoma by surgery

Used to help reduce recurrent of lesion

155
Q

Signs of SCC

A

Firm, red nodule
Flat sore w/ scanty crust
Fast growing
Irregular border

156
Q

Typical treatments for Aks

A

Cryo
Topical treatments: 5 fluororacil, disclofenac gel, imiquimod
Curettage and cautery
Photodynamic therapy

157
Q

Signs that an AK is developing into a SCC

A

Lesions persisting in spite of treatment
Hyperkertaotic lesions
Lesions becoming nodular

158
Q

What does it mean if a cancer is ‘in situ’

A

It is in the epidermis (above basement membrane)

159
Q

What does it mean if a skin cancer is ‘invasive’

A

Cancer is below basement membrane (invaded dermis)

Increased potential for metastasis due to presence of blood vessels

160
Q

Is seborrheic keratosis benign or malignant

A

V common benign lesion - no increased risk of malignancy

Increase in number w/ age

161
Q

When is seborrheic keratosis removed

A

Cosmetic/ practical reasons

Can use excision, curettage & cautery, laser, cryosurgery

162
Q

Marjolin ulcer

A

Invasive SCC formed in site of scar or ulcer

163
Q

Pathogenesis of SCC

A

Keratinocytes from stratum basale that have replicated and grown up towards surface and down beyond basement membrane

164
Q

SCC on dermatoscope

A

Central keratinisation or ulceration

Chaotic vascular pattern

165
Q

Mainstay of SCC treatment

A

Excision w/ 4-6mm margin

166
Q

Features to look for w/ BCC

A 
Rolled pearly border 
Telangiectasia
Central ulceration 
Bleeding spontaneously 
Slow growing
167
Q

Features of BCC on dermatoscope

A

Telangiectasia
Ulceration
Blue/ grey globules

168
Q

Possible evolution of melanoma

A 
Bleeding 
Itching 
Crusting 
Oozing 
Sensation change
169
Q

Melanoma through a dermatoscope

A

Atypical pigment network
Blue-white veil
Irregular black/ brown globules

170
Q

High risk areas for complications of BCCs

A

Around the eyes
Nasolabial folds
Around ear canal
Posterior auricular sulcus

171
Q

After examining a suspected melanoma, what additional examinations should be done

A

Examine remainder of skin - look for more lesions

Cervical lymph nodes - possible metastasis

172
Q

Definitive treatment of melanoma

A

Wide surgical excision w/ melanoma

173
Q

Relevant prognostic factors for SCC

A

Size of the lesion

Cervical lymph node involvement

174
Q

How can we differentiate hair loss

A

Diffuse vs patchy

Scarring or non-scarring

175
Q

Types of excessive hair growth

A

Hirsutism

Hypertrichosis

176
Q

Stages of hair growth

A

Anagen
Catagen
Telogen

177
Q

Anagen phase of hair growth

A

Long growing phase

178
Q

Catagen phase of hair growth

A

Short regressing phase

179
Q

Telogen phase of hair growth

A

Resting/ shedding phase

180
Q

Main types of hair

A

Languo - fine long hair in foetus
Vellus - fine short hair on all body surfaces
Terminal - coarse long hair

181
Q

Where is terminal hair found

A

Scalp
Eyebrows
Eyelashes
Pubic areas

182
Q

Structure of nails

A

Nail is made up of nail plate (hard keratin), which arises from nail matrix at posterior nail fold
Rests on nail bed

183
Q

Examples of nail matrix abnormalities

A

Nail pitting and ridges

184
Q

Examples of nail bed abnormalities

A

Splinter haemorrhage

185
Q

Examples of nail plate abnormalities

A

Discoloured nails

Thickening of nails

186
Q

What are exclamation mark hairs a pathogonomic sign of

A

Alopecia areata

187
Q

What is associated w/ an isolated patch of alopecia

A

Organ-spp autoimmune disease

Vitiligo

188
Q

Patterns of alopecia areata

A

Ophiasis

Patch type

189
Q

Ophiasis

A

Band of hair loss - usually at circumference of scalp

190
Q

Alopecia areata vs trichotillomania

A

Regrowth of AA shouldn’t have broken hairs, but trichotillomania will

191
Q

Alopecia totalis vs universalis

A

Totalis - loss of skull hair

Universalis - loss of all BODY hair

192
Q

Treatment of alopecia areata

A 
Consider none 
Steroids - top, intralesional, po
Local PUVA 
Minoxidil (topical)
Systemic immunosuppression
193
Q

Causes of non-scarring hair loss (localised)

A

Telogen effluvium
Traction alopecia
Skin condns - psoriasis, tinea capitis

194
Q

Trichotillomania

A

Pt pulls out hair –> broken hair

Associated w/ psychological disorders in adult pts (OCD spectrum)

195
Q

Features of Telogen effluvium

A

Diffuse hair shedding following triggering event
No clear demarcation
Hair pull test is +ve

196
Q

Causes of Telogen effluvium

A 
Significant infection 
Post partum 
Stress 
Wt loss 
Drugs 
Excessive sun exposure 
Discontinuing OCP
197
Q

Examples of drugs causing telogen effluvium

A

Warfarin
HIgh dose PPIs
MTX

198
Q

What are Beau’s line w/ hair shedding pathogonomic for

A

Telogen Effluvium

199
Q

Causes of non-scarring hair loss (diffuse)

A

Androgenic - male pattern baldness
Anagen effluvium - chemo
IDA
Trichotillomania

200
Q

Why is it important to differentiate between non-scarring and scarring alopecia

A

Hair can’t grow back in scarring alopecia

Difference in treatment

201
Q

Ix to perform in scarring alopecia

A

None
FBC, B12, ferritin
TFTs, fasting glucose, organ-spp antibodies

202
Q

Immunological causes of scarring alopecia

A

Lichen planopilaris/ frontal bossing

Lupus

203
Q

Causes of scarring alopecia

A 
Immunological 
Bacterial/ fungal infection (kerion)
Trauma (burns)/ iatrogenic (RT)
Skin cancers and treatment of 
Blistering diseases
204
Q

Poor prognostic factors of alopecia areata

A

Nail signs (pitting or ridging)
Alopecia universalis
Younger age of onset
Hx of atopy

205
Q

Skin condition associated w/ hirsutism

A

Acne vulgaris

206
Q

Hirsutism

A

Androgen-dependent pattern of excessive hair growth

207
Q

Common associated condns with hirsutism

A

Obesity

PCOS

208
Q

Cases of hirsutism

A 
Idiopathic 
Postmenopausal 
PCOS 
Drugs - anabolic steroids 
Cushing' syndrome 
Neoplastic - ovarian tumours secreting androgens, congenital adrenal hyperplasia
209
Q

Ix for hirsutism

A

Fasting blood glucose
Ovrain ultrasound
Cortisol
Sex hormones

210
Q

Tx of hirsutism

A 
Treat underlying cause first 
Hair removal (temp) or permanent (laser)
Finasteride
Spiro 
COCP e.g. Dianette, Yasmin
211
Q

Treatment of androgenic alopecia

A

Minoxidil topically - up to 6/12 to take effect
Finasteride 1mg od po
Hair transplant

212
Q

Localised causes of hypertrichosis

A

Naevus-related (e.g. Becker’s)
Spina bifida
C/c rubbing
Porphyria cutanea tarda

213
Q

Generalised causes of hypertrichosis

A 
Generalised hypertrichosis - X-linked and autosomal dominant 
Hypertrichosis languinose 
Foetal alcohol syndrome 
Paraneoplastic effects 
Drugs 
Porphyria cutaneous tarda
214
Q

Ix for isolated hypertrichosis

A 
FBC. U&Es, LFTS, fasting glucose 
Serum Fe and ferritin 
Hep A-B serology
Serum porphyrins 
US liver - refer to gastroenterology if indicated
215
Q

Potential causes of nail pitting

A 
Psoriasis 
Atopic czema 
Reiter's disease 
Alopecia areata
Pityriasis rosea
Syphilis
216
Q

Most likely dx of nail pitting in a younger person associated w/ a rash

A

Psoriasis

Atopic eczema

217
Q

Features to help differentiate psoriasis from atopic eczema in the hx

A

P - uncommonly presents in childhood vs commonly
P - small amount w/ associated sx (arthritis) vs frequently px w/ atopy
P - less strong familial association w/ rash and other sx
P - no allergic triggers

218
Q

Examination features to help differentiate psoriasis from atopic eczema

A 
P - sclay appearance vs excoriated
P - extensors affected vs flexures 
P - scalp commonly affected vs sometimes 
P - behind ears common vs uncommon 
P - nail disease more severe 
P - plantar involvement common
219
Q

Ix for nail pitting

A 
Not necessarily needed
Total IgE 
Spp RAST 
Patch testing if hand or eyelid rash 
Skin bx if diagnostic doubt
220
Q

Commonest cause of nail pigmentation

221
Q

Ddx of pigmented nail streak

A 
Physiological (e.g. Africans)
Traumatic 
Benign naevus 
Addison's 
Malignant melanoma 
Drugs
222
Q

Ways to grade acne

A

Leed Acne Grading system (1-12)
Mild/ moderate/ severe
Infl/ non-infl

223
Q

Attacking different factors in pathogenesis for acne treatment

A

Target 1 - microcomedone phase - reduce hyper cornification and follicular occlusion
Target 2 - bacteria & infl
Target 3 - hormonal (+/- topical) - women

224
Q

How do we target microcomedone phase in acne tx

A

Topical retinoids e.g. isotret, adapalene
Combined w/ top abx –> anti-infl benefits
Top salicylic 2% wash or 20% azalelaic acid wash if intolerant (skin types V esp)

225
Q

Side effects of retinoids

A 
Initial flare-up 
Teratogenic - must be on 2 forms of contraception 
Depression and suicidal ideations 
Raised lipids and deranged LFTs
Dry skin, lips, mucosa etc 
Skin fragility
226
Q

Why might a pt repeat courses of retinoids

A

Can release months-years later

227
Q

How do we target bacteria and inlet in acne tx

A

Abx

Abx w/ BP

228
Q

Topical abx given for acne

A

Erythromycin and clindamycin

229
Q

Systemic abx given for acne

A

Lymecycline (OD, not inhibited by food in stomach)
Erythromycin (pregnancy safest)
Minocycline, oxytetracycline, doxycyline, trimethoprim - drug resistance?

230
Q

Main side effect of tetracyclines

A

Increases sunburn risk

Cannot be used in pregnancy - yellow teeth in infants

231
Q

How do abx w/ BP work for acne mx

A

Kills anaerobes by oxygen release in follicular environment

232
Q

How do we target hormones in acne mx

A

OCP - Dianette (oestrogen and anti-androgen)

Spiro (anti-androgen)

233
Q

When is is best to use Spiro in acne mx

A

In older women

Coeexisting hirsutism or androgenic alopecia

234
Q

Side effects of Spiro for acne mx

A

Deranges U&E’s
Irregular menstrual cycle
Risk of feminising male foetus

235
Q

What constitutes mild acne

A

Mainly comedomal/ non-infl

236
Q

Open comedones

A

Blackheads - oxidation of plug in sebaceous filament

Usually no erythema

237
Q

Closed comedones

A

Whiteheads

238
Q

Seborrhoea

239
Q

Tx of mild acne

A

Topical retinoids - adapalene (differin), tretinoin, isotret
Azelaic acid
General advice
If infl - topical BP

240
Q

Tx of moderate acne

A

Oral treatment +/- topical: abx, hormones

NB avoid use of different oral and topical abx combin

241
Q

Oral abx for moderate acne

A 
Erythromycin - in pregnant, breastfeeding 
Tetracyline (1g/day)
Doxy - 100mg/day
Lymecycline - od 408mg/day
Minocycline - 2nd line (costly)
Trimethoprim - 3rd line (400-600mg/ day)

Given for 4-6/12

242
Q

Mx of sever acne

A

Oral isotret (Roaccutane)

243
Q

How does Roaccutane work

A

Reduces sebum, comedogenesis, P.acnes and anti-infl actions

244
Q

Causes of failure to respond to acne tx

A

Compliance
P. acne resistance
Gram-ve folliculitis
Incorrect dx

245
Q

NICE Guidelines on referring acne to dermatologist

A 
Acne fulminant or gram-ve folliculitis 
Severe acne requiring isotret 
Dysmorphophobia 
Risk fo severe scarring e.g. keloid
Moderate acne unresponsive to 2 courses abx 3/12 long each 
Endocrine cause e.g. PCOS
Uncertain dx
246
Q

Ddx for acne

A

Rosacea
Perioral eczema
Milia
Gram-ve follicullitis

247
Q

Acne rosacea as a ddx for acne ddx

A 
Occurs in older pts
No nodules, comedones, cysts or scarring 
Truncal involvement rare 
May see rhinophyma 
Associated w/ flushing
248
Q

Perioral eczema as a ddx for acne

A

Pts experience pruirits and dry skin
No comedones
Spares vermillion border

249
Q

Millia as a ddx for acne

A

May be confused w/ closed comedones
Seen in infraorbital locations
May be seen alongside acne

250
Q

Gram-ve folliculitis as a ddx for acne

A

Complication of long-term abx therapy for acne

Hair follicles infected w/ Gram-ve organisms

251
Q

Acne variants

A

Infantile acne
Acne conglobata
Acne exocoriee

252
Q

Features of infantile acne

A

Seen in pts <1 year of age
Likely genetic
Not thought to be androgen related
Usually settles within months

253
Q

Features of acne conglobate

A

Severe nodulocystic acne
Interconnected accesses w. sinuses in between
Scars badly

254
Q

Features of Acne excoriee

A

Mild/ moderate cane exacerbated by picking (psychological disorder)
Causes secondary infection and scarring - cycle

255
Q

Usual course length of isotret

256
Q

Why should oral and topical abx not be combined in acne mx

A

Risk of bacterial resistance

257
Q

What type of contraceptive pill should be avoided in acne mx

A

Progesterone only

258
Q

Minecycline side effects

A

Irreversible slate-grey pigmentation of skin
Abnormal LFTs
Induce SLE phenomenon

259
Q

Things to ask in acne hx

A

Psych effects - what does it stop them from doing, changes they’ve made
What they advice tried
Products currently in use
Areas - face, back, arms, upper chest
Associated sx
Anythings that makes it worse - cyclical, drugs (steroids)
Fhx

260
Q

Acne nodule

A

Solid lesion > 5mm raised above skin

Inflamed and extends to deep layers —> scarring

261
Q

Acne cyst

A

Epithelial lined cavity w/ liquid/ semi-solid material

Heals w/ scarring

262
Q

What is isotret contraindicated in for acne mx

A

Soya allergies

Severe peanut allergy

263
Q

What must you test for before commencing isotret for acne

A

Fasting blood glucose

Lipids

264
Q

What type of skin cancer does wart virus predispose you to

265
Q

What types of hereditary factors cause skin cancers

A

Germ line - e.g. familial melanoma
Acquired mutation e.g. BRAF V600E
Epigenetic - e.g. arsenic toxicity

266
Q

Molecular factors protecting us from skin cancer

A 
Constitutional pigmentation 
Immune system 
DNA repair 
Accurate control of cell division
Behaviour - avoiding UVR > covering up > SPF
267
Q

Gene mutations seen in BCC

A

MC1R
PTCH1
PTCH2
RASA1

268
Q

Mutation in Gorlin’s syndrome

269
Q

Gorli’s syndrome and skin cancer

A

90% of pts develop multiple BCCs

270
Q

Main symptoms of Gorlin’s syndrome

A

Toothy cysts that develop in teenage years
Bones grow longer and larger
Pits of palms and soles

271
Q

Gene mutations in SCC

A

MC1R
OCA1/OCA2
XP mutations
RASA1

272
Q

UV damage and diffenrt types of melanoma

A

Intermittent sunburn - SSMM and nodular
C/c UVR - lentigo MM (and SCC)
UVR-independent - ALM, mucosal and uveal

273
Q

Gene mutations in melanoma

A

MC1R
BRCA2
P53
BRAF V600E

274
Q

How does vemurafenib treat melanoma

A

Monoclonal antibody which stops cell from producing BRAF

BRAF V600E mutation causes too much BRAF –> cells grow and divide

275
Q

What types of melanoma does vemurafenib treat

A

Metastatic SSMM/ nodular MM

276
Q

What type of melanoma can imatinib treat

A

Cancers w/ cKIT mutations

ALM and mucosal melanoma

277
Q

ALM

A

Acral Lentiginous Melanoma

278
Q

Relationship between skin and psyche

A

Psychological consequences of skin disease
Skin manifestations of psychiatric disease
Skin condns caused by drug treatment of psychiatric disease

279
Q

Psychological consequences of skin disease

A

Skin disease have impacts on the person’s mental health

The degree of impact varies depending on many factors (pt and illness related factors)

280
Q

Psychological interventions to help pts w/ skin condns

A

CBT
Self-help material
Group material

281
Q

Measuring psychosocial stress in skin disease

A 
Psoriasis disability index 
DLQI
Acne disability questionnaire 
Genera health questionnaire (GHQ)
Hamilton scale for anxiety and depression
282
Q

How do pts cope w/ and adapt to skin diseases

A

Adjust to change in appearance
Learning to live w/ uncertainty
Coping w/ reactions from others
Maladpating

283
Q

Features of maladapting to skin disease

A

Hiding away (long hair, clothing)
Structuring line around disease
Thinking that other (in addn to themselves) are preoccupied with the disease

284
Q

Skin manifestations of psychiatric illness/ psychological distress

A 
Deliberate self harm 
Dermatitis artefacts 
Parasitosis 
Dysmorphophobia
Trichotillomania 
Excessive handwashing, neurotic excoriations 
Signs of alcohol and substance abuse
Sun sensitivity 
Nicotine-stained fingers
285
Q

Artefactual lesion in skin disease - hypochondriasis

A

In responses to delusional beliefs

286
Q

Artefactual lesion in skin disease - OCD

A

Relief of anxiety from repetitive scratching etc

287
Q

Artefactual lesion in skin disease - dermatitis artefacts by proxy

A

Lesions on another to satisfy psychological need of perpetrators (Munchausen’s syndrome by proxy)

288
Q

Epidemiology of dermatitis artefacts

A

Highest incidence in late teens, early twenties
Often close connection w/ healthcare field
Past hx of serious illness, sexual abuse or loss in childhood not uncommon

289
Q

Clinical picture of D artefacta

A

Dramatic lesions produced secretly and mysteriously
Not characteristic of known dermatoses
Found in reach of pt’s hands

290
Q

Hx and examination of D. artefacta

A

Complicitly strenuously denied

‘Hollow hx’ - inability to elicit evidence of evolutionary changes

291
Q

Why does the pt cause lesions - DA

A

Physical expression of emotional problems
Inability to feel cared for unless something being ‘done’ e..g ointments, ix
‘Learnt’ such behaviour is rewarding
They have a goal

292
Q

Pts goal in DA

A

To satisfy an (unconscious) emotional need to be nurtured

293
Q

What is parasitises

A

Delusion that their bodies are infested w/ some type of organisms
A symptom, not a disease

294
Q

Signs seen in parasitises

A

‘Matchbox’ sign - pieces of debris brought as ‘proof’

295
Q

What may parasitises be secondary to

A

Somatic hallucinations

296
Q

Exbom syndrome

A

Delusional parasitosis

Treated w/ psychotherapy and antipsychotics

297
Q

Dysmorphobia

A

Primary complaint of some external physical defect thought to be noticeable yo others, but objectively, appearance lying within normal limits

298
Q

Trichomalacia

A

Hair roots undergo pathological change in trichotillomania

299
Q

Skin conditions caused by drug treatments of psychiatric disease

A

Lithium, anticonvulsants (acne-like rash)
Chlorpromazine (photosensitivity)
Steroids
Lamotrigiine

300
Q

What constitutes as a legal inability to use and weigh up information (“process”)

A

Compulsive disorder or phobia may erode capacity

Temp factors such as shock, fatigue, pain, drugs

301
Q

What is an Advance Decision

A

A statement of a pt’s wish to refuse a particular type of medical treatment or care of they become unable to make/ communicate decisions for themselves

302
Q

What is an Advance Decision limited to

A

Nothing
Does not have to be just life sustaining treatment
But demands FOR treatment not legally binding

303
Q

When can a pt make an AD

A

Section 24-26 MCA 2005

Can apply to physical and mental health

304
Q

When can an AD be overruled

A

If the pt is sectioned hunted the MHA

305
Q

What needs to be included in an AD

A

Precisely that tx is to be refused
Circumstances when refusal should apply
Pts can use medical or everyday lang
Details of 3rd party present during discussion

306
Q

Who needs to be informed after a pt has made a AD

A

Local hospitals just incase pt is admitted unwell

307
Q

What counts as life sustaining tx

A

To which Dr providing care regards as necessary to sustain life

308
Q

An AD must be

A

In writing (someone else can write the AD on their behalf)
Signed
Witnessed
Incl a statemnet that the AD decision is to apply even iff life is at risk

309
Q

Limitation of an AD

A

Cannot refuse action to keep pt comfortable
Connat stop staff offering food and drink
Cannot use it to request euthanasia
Some people go to extreme lengths to make their wishes known

310
Q

How do you decide if AD is valid looking at MCA

A

Has pt withdrawn the decision?
Has pt made an LPA since then?
Has pt acted inconsistently w/ AD?
Does AD apply to current circumstances and situation?

311
Q

What should be considered when looking at AD validity

A

How long ago decision was mad e
Change sin personal life
Developments in medical tx
Speaking to family/ friends

312
Q

Wha=y are DNAR order necessary

A

Resus is commenced without delay - no time for preliminary discussion
Amount to intervention that may be outcome defining

313
Q

Who can make DNAR orders

A

Most senior clinician in charge of the pt’s care

314
Q

What type of skin cancer should be suspected if a central, keratinised plug is seen

315
Q

Natural hx of SCC

A

Fungated wound

316
Q

Complications of cryo

A 
Hypertrophy scarring 
Post-infl pigmentary changes 
Nerve damage 
Pain 
Blistering 
Recurrent carcinoma
317
Q

Treatment of metastatic non-melanoma skin cancer

A

Aggressive local surgery, LN dissection and post-op RT and chemo

318
Q

When is radiation therapy a primary option for treating skin cancer

A

If surgery contraindicated in BCC or SCC

Pts over 60 are preferred candidates

319
Q

Disadvantages of RT

A

Lack of margin control
Poor cosmoses in some pts
Prolonged course of therapy
Increased risk for reoccurnace

319
Q

Disadvantages of RT

A 
Lack of margin control 
Poor cosmoses in some pts 
Prolonged course of therapy 
Increased risk for reoccurrence
Poor healing on lower leg
Cartilage damage on ear
320
Q

Mx of rosacea

A 
Identify triggers
Sunscreen 
Lymecycline 
Topical metronidazole 
Topical azelaic acid
Laser
321
Q

What is the significance of Breslow’s thickness being > 1mm

A

Sentinel LN bx is indicated to look for evidence of mets

MBBS - Year 2 (20 decks)

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