11 - Skin Flashcards

1
Q

What is lentigo maligna?

A

Associated with chronic sun exposure

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2
Q

What are the risk factors for malignant melanoma?

A

UV Light (not for acral though)

  • Severe blistering sun burn in childhood
  • Immunosuppression
  • Multiple (>100) or giant (>20 cm) naevi
  • Skin type (Fitzpatrick Skin types I & II)
  • Family history (cyclin-dependent kinase mutations)
  • Genetic mutations (CDK4, xeroderma pigmentosum, melanocortin 1 receptor)
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3
Q

What is the epidemiology of melanoma?

A

5th most common cancer in UK

1.5X more likely in men, with men on trunk and women on legs

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4
Q

Why is there a worse prognosis with melanoma in non-caucasian patients?

A

Often diagnosed late due to:

  • Poor public awareness
  • Lower index of suspicion
  • Detection more challenging (often acral)
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5
Q

What is the progression of melanoma starting from a benign navei?

A

Due to UV light (mostly UVA) causing damage to DNA

  • Benign naevus (typical mole)
  • Dysplastic naevus (atypical mole)
  • Radial growth phase - melanomas tend to extend superficially and outwards initially
  • Vertical growth phase - malignant cells invade the basement membrane and proliferate vertically downwards into the dermis.
  • Metastasis - usually to lymph nodes
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6
Q

What are the features of malignant melanoma?

A

ABCDE

USE DERMATOSCOPE

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7
Q

What are the criteria for a 2 week wait referral for a melanoma?

A

Over 3 points on the 7 point checklist

Major criteria are 2, minor are 1

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8
Q

If dermatoscopy reveals a suspicious mole, what investigation should be done next?

A

Excisional biopsy with 2mm margin and subcutaneous fat

May have punch biopsy if legion is large or close to vital structures

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9
Q

What are the different subtypes of melanoma from most to least common?

A
  1. Superficial spreading (70%)
  2. Nodular (15%)
  3. Lentigo maligna (10%)
  4. Acral lentiginous (<5%)
  5. Desmoplastic melanoma (<1%)
  6. Amelanotic
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10
Q

How do the following melanomas grow:

  • Superficial spreading
  • Nodular
  • Lentigo maligna
A

Superficial Spreading: Initial radial then vertical growth

Nodular: Immediately vertically grow

Lentigo Maligna: long period of intra epithelial growth

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11
Q

What is the histological classification system for melanoma and how does this determine prognosis?

A
  • Breslow thickness: deeper = poor prognosis, from S.Granulosum to epidermis
  • Mitotic index
  • Ulceration: poor prognosis
  • Clark Level I-IV: lost relevance
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12
Q

What is the margin of excision with biopsy for melanoma?

A

Initial 2mm clear margins in excision biopsy then go back after got Breslow thickness

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13
Q

When should you do a sentinel node biopsy in melanoma?

A

When Breslow thickness >0.8mm or if <0.8mm with ulceration

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14
Q

After histological diagnosis of melanoma, what are some further investigations done for staging?

A
  • Lymph node exam: fine needle aspiration (FNA) and cytology if any suspicious
  • Total body CT or PET-CT: only if high-risk for distant metastasis include those with aggressive lesions (pT4, ulcerated, high mitotic index etc.) or the presence of known lymph node spread
  • LDH: useful for risk stratifying
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15
Q

How is melanoma staged?

A

TNM or AJCC

  • Tumour - Breslow thickness (mm) +/- presence of ulceration
  • Node - whether melanoma has spread to lymph nodes and how many
  • Metastases
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16
Q

How is melanoma managed?

A

Always guided by MDT

Wide local excision (WLE)

Removal of the biopsy scar with a surrounding margin of ‘healthy’ skin, with fat, down to muscular fascia

Sentinel Lymph Node Biopsy (SLNB)

Typically, on the morning of surgery, a radio-labeled tracer is injected into the old biopsy scar. A CT scan is then performed which identifies ‘hot spots’

A postitive SLNB usally results in referral for lymphadenectomy. This is stage 3

Electrochemotherapy

Patients with locally advanced melanoma

Uses pulses of electricity together with chemotherapy injected into tumour

Adjuvant therapy

If stage 4

  • Chemotherapy
  • Radiotherapy
  • Immunotherapy
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17
Q

How long after WLE of melanoma are patients followed up for?

A

Depends on staging

Patient education for all: self-examination, sun protection, avoiding vitamin D depletion

Discharge if stage 0

Follow-up for up to 5 years (every 3 months initially), depending on stage

Personalised follow-up for Stage IV

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18
Q

What are some examples of immunotherapy used in stage ¾ melanoma?

A
  • ipilimumab
  • nivolumab
  • pembrolizumab
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19
Q

What is some targeted therapy in melanoma and what gene does this target?

A

BRAF gene mutation

Used for aggressive melanomas

  • Vemurafenib
  • Dabrafenib
  • Trametinib
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20
Q

What determines the prognosis with melanoma?

A
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21
Q

What is the 5 year survival with melanoma?

A
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22
Q

How can brain metastases in melanoma be managed?

A
  • Steroids
  • Surgical resection
  • Stereotactic or whole brain radiotherapy
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23
Q

How may brain metastases present?

A
  • Headache
  • Nausea and vomiting
  • Fatigue
  • Weakness
  • Seizures
  • Cranial nerve palsies
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24
Q

How is stage 0-II melanoma managed?

A
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25
Q

How is stage III melanoma managed?

A
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26
Q

How is stage IV melanoma managed?

A
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27
Q

What is the commonest type of skin cancer and the risk factors for this?

A

BCC (from keratinocytes)

  • UV light exposure
  • Family history
  • Fitzpatrick skin types I & II (light skin, tans poorly)
  • Male sex
  • Genetics:
    • Mutations in PTCH, p53, ras, fos
    • Albinism
    • Gorlin’s syndrome
    • Xeroderma pigmentosum
  • Increasing age
  • Previous skin cancers
  • Immunosuppression (e.g. AIDS / transplantation)
  • Carcinogens: Ionizing radiation, arsenic, hydrocarbons
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28
Q

What is Gorlin-Goltz syndrome?

A
  • Genetic condition increases the risk of developing BCCs
  • Autosomal dominant mutation to PTCH1 gene so BCCs develop in adolescence
29
Q

How does a typical nodular BCC present?

A

TURP

  • Telangiectasia
  • Ulceration
  • Rolled edges
  • Pearly edge
30
Q

What are the different subtypes of BCC (most to least common) and how do they appear differently?

A

Nodular (60%)

  • Often on face
  • Flesh-coloured well defined borders with pearly rolled edge, surface telengectasia and central ulceration

Superficial (10%)

  • Erythematous plaque usually on trunk

Morphoeic

  • Deeply invasive and look like scar

Pigmented

  • Often mistook for melanoma

Basosquamous

  • BCC with SCC differentiation, high recurrence and metastases
31
Q

How is a BCC diagnosed?

A
  • Dermatoscopy
  • Biopsy unsure
  • CT if think invasive
32
Q

BCC are stratified based on low-risk or high risk and this determines prognosis and management. What are lesions that are classed as high risk meaning they are likely to recur?

A
33
Q

Apart from defining a BCC as high risk or low risk, how else can we decide the management plan?

A
  • Performance status of patient
  • Co-morbidities
  • Use of antiplatelets or anticoagulants
34
Q

What are the principles of treatment in BCC?

A
35
Q

How is high risk BCC managed?

A

Surgery and radiotherapy

  • Standard surgical excision margins: 4-5mm (may increase for morphaeic and larger BCCs)
  • Radiotherapy good if pt is unsuitable candidate for surgery (contraindicated if for recurred BCC post RT of previous BCC)
36
Q

What type of surgery is done in high risk BCCs?

A

‘Excisional’

  • Wide-local excision (common treatment modality) or
  • Moh’s Micrographic Surgery (typically reserved for high-risk lesions)
37
Q

How are low-risk BCCs managed?

A
  • Surgical excision: ‘Destructive’ surgery via curettage +/- cautery or cryotherapy. Only done in low risk as no histology
  • For superficial BCC: Topical immunotherapy (5-Fluorouracil or Imiquimoid) or Photodynamic therapy
38
Q

What margin is used for excision of BCC?

A

Excised down to subcutaneous fat

  • Low-risk (small <2 cm, well-defined): 4-5 mm provides 95% clearance
  • High-risk (large >2cm, poorly-defined): 5 mm margin provides 82% clearance; consider referral for Moh’s Surgery
  • Recurrent lesions: referral to Skin MDT; re-excision of scar (5-10 mm margins) or Moh’s Surgery +/- Radiotherapy.
39
Q

Most BCCs do not require follow up. When do BCCs need to be followed up?

A
  • Recurrent
  • Multiple BCCs at once
40
Q

When is Moh’s surgery used for BCC?

A
41
Q

What are risk factors for squamous cell carcinoma?

A
  • Excessive exposure to sunlight / psoralen UVA therapy
  • Immunosuppression e.g. following renal transplant, HIV
  • Smoking
  • Long-standing leg ulcers (Marjolin’s ulcer)
  • Genetic conditions e.g. xeroderma pigmentosum
  • Type I or II skin (fair skin which always burns and never or rarely tans)
  • History of frequent or severe previous sun burn
  • Personal or family history of skin cancer
  • Increasing age
  • Male sex
42
Q

How may SCC present?

A

Irregular, ill-defined red nodule with scale and ulceration

43
Q

How is SCC diagnosed?

A

Biopsy!!!!!!

44
Q

How do you decide if an SCC is high risk or low risk?

A
  • Site
  • Diameter
  • Tumour depth and invasion
  • Histological features and subtype
  • Host immune status
45
Q

How is SCC treated?

A
  • Surgical excision: usually Moh’s micrographic in high risk
  • If local metastases use wide surgical excision radiotherapy
  • Sentinel lymph node biopsy and if positive lymphadenopathy
46
Q

What are the margins for surgical excision of SCC?

A
  • Low-risk tumour (<20mm): 4mm excision margin
  • High-risk tumour (>20mm): 6mm excision margin
47
Q

What are indicators of a good and bad prognosis with SCC?

A

99% 5 YEAR SURVIVAL

48
Q

How is SCC followed up?

A
  • Only follow up the high risk SCC for 2-5 years
  • Patient education on recurrence of disease e.g self-examination of surgical scar site, local skin and lymph nodes and information sheets
49
Q

What is Bowen’s disease and what does it look like?

A

SCC in situ

5-10% chance of turning into SCC

Red scaly patches on sun exposed areas

50
Q

How is Bowen’s disease managed?

A

Topical 5-fluorouracil

  • BD for 4 weeks
  • Often results in significant inflammation/erythema. Topical steroids are often given to control this

Cryotherapy or Excision

51
Q

What are some differentials for actinic keratoses?

A
  • Bowen’s disease
  • Invasive SCC
  • Superficial BCC
  • Amelanotic melanoa
  • Seborrhoeic keratosis
52
Q

What are the different management options of AK depending on the risk of malignant transformation to SCC?

A

Conservative: remove risk factors (UV exposure), emollients, sun cream

Medical: Topicals like Fluorouracil 5%, Diclofenac, Imiquimod 5% cream

Surgical: Cryotherapy, PDT

53
Q

Do AKs need following up?

A

Only if high risk like organ transplant/immunosuppressed

54
Q

What is important to ask a patient about their skin when they have a suspicious lesion?

A
  • Any previous lesions like this?
  • Any other moles/lesions like this?
  • Skin type
55
Q

What does C mean in ABCDE?

A

UNIFORMITY of colour

56
Q

How deep do the following biopsies go?

  • Shave
  • Punch
  • Excision
A
  • Shave: epidermis
  • Punch: dermis
  • Excision: down to subcut fat
57
Q

What skin cancer can you not get on the lips?

A

BCC as arises from hair follicles

58
Q

What immunotherapy can you use in melanoma and when are they used?

A

BRAF inhibitors

Used for T3 and above

59
Q

What is the cause of the different colours in melanoma e.g black, blue, grey, brown?

A
60
Q

What are some melanoma mimics?

A
  • Multicomponenet haemangioma
  • Intracorneal haemorraghe
  • Subungal haematoma
  • Benign longitudinal melanonychia
  • Pigmented Seborrhoeic keratosis
61
Q

How can you differentiate between Bowen’s and BCC?

A

Dermatoscopyy

62
Q

What is this?

A
63
Q

How can you differentiate between a dermatofibroma and a BCC?

A
64
Q

Where are the classic locations for a SCC?

A
65
Q

What are some SCC mimics?

A
  • Traumatised SK
  • Inflammed viral wat
  • Large SK
  • Giant comedone
  • Lymoedema nodule
66
Q

How are secondary skin cancers referred to secondary care?

A
67
Q

How much suncream should you put on and how often?

A
68
Q

How do you use 5FU for AKs?

A
69
Q

What are the excision margins for skin cancer?

A