17 - Benign and Malignant Skin Tumours Flashcards

1
Q

How can skin cancers for classified?

A
  • Melanotic (malignant melanoma)
  • Non-melanotic (BCC and SCC)
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2
Q

What is an Actinic Keratosis and what does it look like?

A

Premalignant scaly spot found on sundamaged skin e.g face, hands, back, arms

Can regress or can progress to SSC

Often looks crumbly with yellow-white crust (keratotic) if solitary or erythematous if multiple

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3
Q

What are some differential diagnoses for Acitinic Keratoses?

A
  • BCC
  • Bowen’s
  • Psoriasis
  • Seborrhoeic keratosis

IF IN DOUBT BIOPSY!

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4
Q

What is the epidemiology of Actinic Keratoses?

A
  • Fair skin with history of sunburn
  • History of long hours spent outdoors for work or recreation (e.g lived abroad)
  • Immunocompromised
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5
Q

What is the simple way to tell the difference between an acitinic keratoses and seborrheic keratoses?

A

AK usually are flat or slightly raised that cannot be moved but SK can move and look like they are stuck on like a sticker

Also SK can be tan coloured

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6
Q

AK is a precursor for SSC. What advice can you give to patients if they have AKs to prevent the progression?

A
  • Avoid sun/wear sunscreen
  • Wear hats and clothes that cover the skin
  • Advise patient to monitor skin and educate them that it can predispose to skin cancer.
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7
Q

How are actinic keratoses treated?

A

Solitary/Keratotic/Thick Crust Lesions:

- Cryotherapy

  • Shaving/Curettage

- Surgical excision, pathology and stitches

Field/Flat Red Lesions:

- 5-Fluorouracil cream

- Imiquimod cream is an immune response modifier

  • Diclofenac cream

- Photodynamic therapy

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8
Q

How does photodynamic therapy work?

A

Light sensitive medicine is applied then light is applied to the area and this produces free radicals and causes cell death

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9
Q

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

A

SCC in-situ

Pink scaly plaques

Flat edges NOT rolled like BCC

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10
Q

What are some risk factors for developing Bowen’s disease?

A
  • Sun exposure
  • Immunosuppressants
  • Immunosuppression e.g lymphoma
  • Radiation
  • Arsenic
  • HPV
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11
Q

How is Bowen’s disease diagnosed?

A

- Dermascopy: will show red irregular scaly plaque with crops of rounded and coiled blood vessels

- Biopsy: will show full thickness dysplasia

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12
Q

How is Bowen’s disease treated?

A

It can turn to SCC but unlikely. If it does go to SCC then likely to metastasise

  • Observe
  • Cryotherapy with liquid nitrogen
  • Curretage
  • 5Fluorouracil
  • Imiquimod (off-licence)
  • Photodynamic therapy
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13
Q

HOW CAN YOU TELL THE DIFFERENCE BETWEEN AK, BOWEN’S AND SCC?

A

will come back to

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14
Q

What is the prevalence of different skin cancers?

A

Most common to least:

  • BCC
  • SCC
  • MM
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15
Q

How does an SCC (cancer of keratinocytes) present?

A
  • Firm irregularly defined nodule that may persistently ulcerate and crust
  • Usually on sun-exposed areas
  • Often grow quickly and tender to touch
  • Invasive and has the potential to metastasise
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16
Q

What are the risk factors for developing an SCC?

A

- Excessive UV exposure e.g occupation, lived abroad

- Pre-malignant skin e.g AK

- Chronic inflammation e.g leg ulcer, cutaneous lupus, HPV

- Immunosuppresion

- FHx

- Skin type 1

- Xeroderma pigmentosa

17
Q

Which types of SCC are more likely to metastasise?

A
  • Lip
  • Ear
  • Non sun-exposed site
  • >2cm diameter or >2mm thick
  • Host immunosuppression
18
Q

How is SCC investigated and diagnosed?

A
  • Dermascopy
  • Biopsy or excision then biopsy
  • Consider lymph node biopsy and MRI if think it has metastasised
19
Q

How is SCC treated?

A

- Complete surgical excision with margins of normal tissue around the outside. May need flap to close

- Moh’s micrographic surgery for ill-defined, large, or recurrent tumours

- Radiotherapy if large and non resectable tumour

20
Q

What is the pathophysiology of SCC?

A

- UV light causes mutation in p53 tumour suppressor gene

  • Ageing, smoking, immunosuppressants (e.g Azathioprine), HPV also induce mutations in tumour suppressor genes
  • Allows keratinocytes to mutate and reproduce without being killed
21
Q

What is the prognosis of BCC? (Rodent Ulcer)

A
  • Most common skin cancer
  • Very slow growing
  • Rarely metastasises
  • Often recurrent
  • Increased risk of developing other skin cancers
22
Q

What are some risk factors for BCC?

A
  • UV exposure
  • History of severe/frequent sunburn in childhood
  • Skin type 1
  • Increasing age
  • Male
  • Immunosuppressed
  • Previous history of skin cancer
  • FHx (Genetic Predisposition)
23
Q

What is the pathophysiology of BCC?

A
  • Mutations in the PCTH tumour suppressor gene, can be triggered by UV radiation
  • Can also inherit gene defects e.g P53, RAS
24
Q

What are the different presentations of BCC?

A

Nodular (most common)

  • Small skin coloured or pink nodule with surface telangiectasia and pearly rolled edge.
  • May have necrotic or ulcerated centre (rodent ulcer)

- TURP

Superficial

- Scaly irregular plaque with microerosions on younger patients

- Morphoeic

- Basosquamous

25
Q

How do you describe a nodular BCC?

A

Small skin coloured papule/nodule with surface telengactasia and a pearly rolled edge

Can have a ulcerated or necrotic centre (rodent ulcer)

26
Q

How is a BCC treated?

A

- Surgical excision with 3-5mm borders of normal tissue and histopathology (non-urgent referral)

- Mohs Micrographic surgery if high risk, recurrent tumours

- Shave, Curettage, Cryotherapy, Topical PDA, Topical Imiquimod if small and well-defined low risk tumour

27
Q

What defines a BCC as being high risk?

A
28
Q

What is malignant melanoma and what are the risk factors for developing this?

A

Invasive malignant tumour of melanocytes with the potential to metastasise

  • UV exposure
  • Sunburn
  • Skin type 1
  • >50 melanocytic or atypical moles
  • Family history
  • Previous melanoma
  • Old age
29
Q

What is the epidemiology of malignant melanoma?

A

5th most common cancer in the UK

More common in men and fair skinned people

30
Q

What are some pre-cursor lesions for malignant melanoma?

A
  • Benign melanocytic naevus (normal mole)
  • Atypical or dysplastic naevus (funny-looking mole)
  • Atypical lentiginous junctional naevus (flat naevus in heavily sun damaged skin) or atypical solar lentigo
  • Large congenital melanocytic naevus (brown birthmark)

75% OF MELANOMAS ARISE FROM NORMAL SKIN

31
Q

What are the stages of growth for melanoma?

A
  • Benign naevus
  • Dysplastic naevus
  • Radial growth phase
  • Vertical growth phase
  • Metastases
32
Q

How do melanomas tend to present?

A

ABCD Superficial, EFG Nodular

A - Asymmetrical shape

B - Border irregularity

C - Colour irregularity

D - Diameter > 6 mm

E - Evolution (change in size or shape)

Symptoms - Itchy, Bleeding, Crusting

E - Elevated

F - Firm to touch

G - Growing

Usually on legs in women and trunk in men

33
Q

What is the 7 point checklist?

A

2 for each major, 1 for each minor

Anything 3 or more needs urgent 2ww referral

34
Q

What are the different types of melanoma (most to least common) and how do they present differently?

A

Superficial Spreading ABCDE:

  • Most common. Grows on lower limbs. UV exposure
  • Radial growth phase then vertical

Nodular EFG:

  • Second most common
  • Aggressive
  • Grow vertically first so more advanced at presentation

Lentigo Maligna:

  • Common on the face of elderly
  • Chronic sun exposure
  • Long period of intraepithelial growth so slow

Acral Lentigous

  • Usually on palms, soles of feet, nails
  • Hutchinson’s sign (2ww)
  • Not linked to UV exposure

Desmoplastic

  • Often amelanocytic!!!
35
Q

How is a suspected melanoma diagnosed and managed generally?

A

Surgical excision under local anaesthetic and send for histopathology is the investigation and treatment. Take 2mm margin of ‘normal’ skin and cuff of subcutaneous fat around the mole

Wide local excision may then be needed after results if malignant

NEVER SAMPLE, NEED TO EXCISE WHOLE THING!

36
Q

How does the histology of a melanoma determine the prognosis?

A

- Breslow thickness (strongest prognostic indicator): measures from S.Granulosum to deepest part of infiltration

- Ulceration: more aggressive so worst prognosis

- Mitotic Index

- Stage of Melanoma (AJCC)

- FNA and Cytology of lymph nodes

37
Q

How is malignant melanoma staged?

A

American Joint Committee on Cancer (AJCC) system

Based on Breslow thickness of primary tumour, lymph node involvement and evidence of metastases

Stage 1 to 4

38
Q

How is a melanoma treated after it has been surgically excised and proven histologically to be malignant?

A

Non-metastatic:

- WLE: removal of the biopsy scar with a surrounding margin of ‘healthy’ skin, with fat, down to muscular fascia. Margin depends on Breslow thickness

- Sentinel node biopsy and clearance if positive

  • ?Radiotherapy

Metastatic:

  • Chemotherapy
  • Immunotherapy
39
Q

If somebody has a dysplastic mole what should you advise them?

A
  • Monitor with photos and check other moles too
  • SKIN PROTECTION FROM SUN!!!!! Avoid sunbeds, wear SPF