Clinical: Melanoma, Non Melanoma and Benign Skin Lesions Flashcards

1
Q

What is the most common non-melanoma skin cancer?

A

Basal Cell Carcinoma

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2
Q

What are the 3 types of basal cell carcinomas?

A

Superficial, Nodular and Infiltrative

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3
Q

How does BCC arise?

A

Derived from immature pluripotent epidermal cells and is composed of cells with similarities to basal cell layer of epidermis and appendages

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4
Q

Who does BCC commonly affect?

A

Middle aged, sun exposed patients

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5
Q

Is BCC slow/fast growing and locally/widely destructive?

A

Slow growing and locally destructive. May ulcerate.

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6
Q

How can BCC kill?

A

By invading the eye and damaging the brain

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7
Q

What is the typical transformation of BCC from an early lesion to a developed one?

A

Early: pale, translucent papules or nodules with overlying superficial telangiectasis.
Late: ulcerated with raised, rolled edge

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8
Q

What does a superficial BCC look like?

A
  • Brown plaques with raised thread like edge

- Tissue needs to be resected

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9
Q

What does an infiltrative BCC look like?

A
  • Morphoeic causes destruction if neglected
  • Ill defined edge and slow growing
  • May infiltrate tissue widely
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10
Q

What does a nodular BCC look like?

A
  • Well defined nodule, looks stuck on

- Shiny and pearly

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11
Q

What is the best management for BCC?

A
  • Early nodular BCC is best excised
  • At difficult lesions around the eyes- Mohs’ micrographic surgery
  • Clearance of more than 90% of tumours should be achieved
  • Cryotherapy for small, localised, low risk lesions
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12
Q

What does squamous cell carcinoma arise from?

A

Epidermal keratinocytes

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13
Q

Where does a patient typically present with SCC?

A

On sun exposed areas such as bald scalp, tops of ears, face and back of hands

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14
Q

When does SCC behave most aggressively?

A
  • In immunocompromised patients

- On the lips and ears

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15
Q

What is the first choice management for SCC?

A

Complete surgical excision

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16
Q

What is the cure rate for most SCC if the excision is cut with a 3-4mm margin?

A

90-95% for most SCC

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17
Q

What can be given to patients with high risk for further SCCs?

A

Systemic retinoids

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18
Q

What is Actinic Keratosis?

A

Hyperkeratotic Erthythematous lesions arising on chronically sun exposed areas

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19
Q

What is the risk of progression Actinic Keratosis to SCC?

A

0.1%

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20
Q

Does SCC always have to arise from Actinic Keratosis?

A

No, it can arise de-novo

21
Q

What may indicate a transformation of Actinic Keratosis to SCC?

A

Increase in size, ulceration, bleeding, pain or tenderness

22
Q

What is the histology of Actinic Keratosis?

A

Moderate squamous cell dysplasia. Not as dysplastic as Bowen’s disease.

23
Q

What is Bowen’s disease?

A

In situ, SCC on lower leg of elderly woman

24
Q

What can Bowen’s disease mimic?

A

Inflammatory diseases

25
What is the presentation of Bowen's disease?
Slow growing, well demarcated, scaly, erythematous plaque
26
What may be difficult to distinguish Bowen's from?
Superficial BCC
27
What does Bowen's disease often co-exists with?
Venous stasis
28
What is the % chance of Bowen's disease developing into SCC?
3%
29
What is the histology of Bowen's disease?
Crowding, hyperkeratosis, parakeratin
30
How is Bowen's disease managed?
Non surgical procedures are often preferred. Incisional biopsy to confirm diagnosis.
31
What is keratoacanthoma?
A benign squamous tumour, difficult to distinguish from SCC as it clinically and histologically similar.
32
How does keratoacanthoma develop?
Rapid growth over weeks-moths then spontaneous resolution
33
What does keratoacanthoma look like?
Isolated dome shaped nodule with central keratin plug
34
What is the most common type of cutanous T cell lymphoma?
Mycosis Fungiodes
35
"scaly rash (like psoriasis) tumour that can on for 20-30 years"
Mycosis Fungiodes (cutaneous lymphoma)
36
What is the defective gene copy in freckles?
MCIR gene
37
Often referred to "age spots" or "liver spots", what are they?
Actinic Lentigines
38
What is Actinic Lentingines?
"Age spots" related to UV exposure -Increased number of melanocytes along the basement membrane but without the formation of nests that occur in melanocytic naevi
39
How does Seborrheoic Keratosis arise?
Benign proliferation of epidermal keratinocytes
40
What do Seborrheoic Keratosis commonly look like and where do they appear?
- Very common in ageing skin, found on face and trunk | - Warty, 'stuck on' appearance with a greasy hyperkeratotic surface with a visible pinpoint keratin plug
41
Are Melanocytic naevi most commonly congential or acquired?
Acquired before the age of 25
42
What is melanocytic naevi?
Localised, benign clonal proliferations of melanocytes
43
What is the % of babies typically born with melanocytic naevi?
1%
44
What are the 3 types of acquired naevi and in what stage of life do they develop?
1) Junctional naevus in childhood 2) Compound naeves in adolescence/ early adulthood 3) Intradermal naevus in adulthood
45
Describe where Junctional, compound and Intradermal Naevi are found
Junctional: clusters of melanocytes found at the DEJ Compound: clusters of melanocytes found at the DEJ and in dermis Intradermal: clusters of melanocytes found entirely in the dermis
46
How does the difference in appearance vary between the junctional, compound and intradermal naevi and how do these differences arise?
Junctional: macular, circular or oval mid-dark brown appearance Compound and Intradermal: both seen as nodules due to dermal content. Intradermal is less pigmented than compound.
47
What are the 2 clinical settings of dysplastic naevi?
- Sporadic: not inherited | - Familial: strong FHx of melanoma, autosomal inheritance, high lifetime risk of developing melanoma
48
Give some examples of rarer naevi
Blue naevi, Halo naevi, Spitz naevi
49
How does a congenital naevus differ from an acquired naevus in how it looks?
Congenital: larger, slightly raised, becomes more rugose and elevated as the child grows older