Posters- Week 3 derm Flashcards by Mhairi Allison

What is the term for freckles

Ephilides

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What is the term for liver spots

Actinic lentigines

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What are ephilides

Patchy increase in melanin pigment which occurs after UV exposure.
Islands/clumps of melanocytes

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What is the genetic defect that codes for freckles

One defective copy of MC1R.

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What is MC1R?

A gene that encodes for the MC1R protein that sits on th cell surface. It determines balance of pigment in the skin and the hair.

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What codes for hair colour (other than red)?

Eumelanin

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What codes for red hair?

Phaeomelanin

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What is the significance of MC1R in relation to eumelanin and phaemelanin?

MC1R converts phaeomelanin to eumelanin.

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What happens if you have two defective copies of MC1R gene?

You will have both red hair and freckles.

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What does MC1R stand for?

Melanocortin 1 receptor

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How do you acquire actinic lentigines?

Related to UV exposure causing an increase in melanin and basal melanocytes. Also get epidermal elongation of rate ridges.

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What are melanocytic naevi? How can they be divided?

Birthmarks. Can be either congenital or acquired.

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Classification of congenital naevus

Small<2cm
Medium >2cm but less than 20cm
Larger lesions >20cm

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If you have a large congenital melanocytic naevi you have a 10-15% greater risk of developing a melanoma. T or F.

True.

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Congenital melanocytes naevi get more rugose and elevated as the child grows T or F.

True

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Why do people get acquired melanocytic naevi?

During infancy the melanocyte to keratinocyte ratio breaks down at a number of cutaneous sites which allows formation of a simple naevus.

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Describe the process of naevus development

Junctional naevus- clusters of melanocytes at the demo-epidermal junction (darker brown)
Compound naevus- junctional clusters plus groups of cells in the dermis. (lighter shade of brown)
Intradermal naevus- all junctional activity has ceased. (light brown colour)

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What are dysplastic naevi?

They have variated pigment and an asymmetrical border. they are generally greater than 6cm. Can be classified as either familial or sporadic.

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Familial dysplastic naevus

Strong FH of melanoma

Lifetime risk of melanoma up to 100%

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Sporadic dysplastic naevus

Not inherited however the risk of melanoma increases slightly.

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Name the three rarer naevi

Halo naevi- peripheral halo of pigmentation. Inflammatory progression and lots of lymphocytes.
Blue naevi- Entirely dermal and consist of pigment rich dendritic spindle cells
Spitz naevi- benign juvenile melanoma. Usually occur in less than 20 year olds. Consist of large spindle/epithelial cells. May mimic melanoma but most are benign.

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What type of people are more likely to get melanomas?

Middle aged
Women
Sun exposed sites

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ABCDE of melanoma

A- Asymmetry
B- border- well defined or ill defined
C- colour- red at all? changes in colour
D- diameter- has it got bigger?
E-evolution- has it changed?

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What are the 4 main types of melanoma?

Superficial spreading - commonest
Acral/mucosal lentiginous- acral (fingers, palms, soles of feet) and mucosal.
Lentigo maligna- sun damaged- face, neck, scalp
Nodular- occurs in varied sites but often on the trunk. Usually in older patients.

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How are melanomas formed?

Grow as mocules either entirely in situ or with dermal micro invasion. Called the rapid growth phase. Eventually the melanoma cells invade the dermis forming an expansile mass with mitoses- vertical growth phase.

At which stage can a melanoma metastasise?

At the vertical growth stage.

Are nodular melanomas more or less aggressive than the other melanomas?

They are more aggressive- no evidence of them going through the rapid growth phase. Just straight into the vertical growth phase.

What is breslows thickness?

Deepest part of the tumour from the granular layer in mm.

Prognosis of melanomas

``` pTis- melanoma in situ- 100% survival pT1- tumour <1mm- 90% survival pT2- tumour 1-2mm- 80% survival pT3- tumour 2-4mm-55% survival pT4- >4mm- 20% survival ```

How does melanoma spread?

Spreads to the local dermal lymphatics then to the regional lymph nodes Or blood spread to the heart, lungs, GI tract

Treatment of melanomas

Primary excision to give clear margins Some also receive a sentinel node biopsy If this is postiive- regional lymphandecntomy Advanced disease- chemo, immuno or genetic therapies.

Excision of melanoma guidelines

In situ- clear by circa of 5mm If invasive and less than 1mm thick- 1cm clearance If invasive and greater than 1mm thick- 2cm clearance.

What is seborrheic keratoses?

Black/brown greasy looking lesion that is often warty.

Who is likely to get seborrheoic keratoses?

Older Caucasians

Treatment of seborrheic keratoses?

Reassurance Curette Shave

Types of skin cancer

Melanoma | Non-melanoma- BCC and SCC

What do BCC's arise from?

Keratinocytes in the basal layer

What do SCC's arise from?

Keratinocytes in supra basal layers

What do non-melanoma skin cancers contribute to the overall percentage of skin cancers?

90-95%

Describe a basal cell carcinoma

``` Slow growing lump or non healing ulcer. Painless (often ignored) Pearly or translucent Visible arborising (branch like) blood vessels Central ulceration (rodent ulcer) ```

Describe a squamous cell carcinoma

``` Hyperkeratotic (crusted) lump or ulcer Arises from sun damaged skin Fast growing May be painful and bleed Could have a precursor lesion such as 'actinic keratoses' and Bowens disease ```

What is actinic keratoses?

Dry scaly skin caused by sun exposure (areas exposed to the sun are involved e.g. face) Multiple lesions

What are the risks of having actinic keratoses?

High risk of developing BCC and SCC.

Risk factors for developing cancer

Sun exposure Genetic predisposition Immunosuppression Environment carcinogens

What environmental triggers can cause cancer?

``` Smoking Coal tar Arsenic Trauma Ionising radiation ```

What genetic syndromes pre-dispose people to cancer?

DNA repair syndromes such as xeroderma pigmentosum.

What is xeroderma pigmentosum

A defect in one of the seven nucleotide excision repair (NER) genes (XPA-G). The skin needs these to repair sun damaged skin.

Symptoms of xeroderma pigmentosum

Photosensitivity Skin cancers on UV exposed sites Neurological degeneration

Patients with xeroderma pigmentosum have an increased risk of developing other cancers. T or F

True

What is oculocutaneous albinism?

Lack of melanocytes or melanocytes that don't produce pigment.

What are patients with O albinism prone too?

Sun burn and melanocytic skin cancers

What is Gorlins syndrome?

Also known as neavoid basal cell carcinoma. Syndrome with skin features such as cancers, cysts and skeletal abnormality.

How does cancer come about (general description)

Genetic mutations occur A series of mutations accumulate in a process known as clonal evolution Eventually it accumulates to become cancerous.

How does UVB affect DNA

Causes direct DNA damage (290-320nm) Two types- cyclobutane pyrimidinedimers and pyrimidine pyrimidone photo products

How are the cyclobutane pyrimidinedimers and pyrimidine pyrimidone photo products made?

Both formed by covalent bonding between adjacent pyrimidines on the same DNA strand.

How are CPD's and 6-4 PP's removed?

By nucleotide excision repair due to them being relatively stable.

What happens to un repaired UV products?

They interfere with base pairing during replication.

What does UVA do to DNA?

Causes indirect damage by oxidative damage (320-340nm)

What is oxidative damage to DNA?

Oxidation of DNA bases occurs.

What does oxidative damage cause?

Pair mismatches. Can be repaired by nucleotide excision repair.

A long term outdoors worker is at risk of developing which cancer?

SCC

Someone who has intense/intermittent sun exposure (e.g. recreational like tanning) is at risk of developing which cancer?

Melanoma and BCC

If you burn you are at risk of developing which cancer?

Melanoma and BCC

Artificial UV radiation makes you at risk of developing which cancer?

BCC Melanoma SCC

Which skin type is most at risk of developing cancer?

type 1

What effect does immune suppression have on cancer?

More likely to develop in patients who have UC or crohns (more likely to develop melanoma)

What effect does age have on cancer?

Increasing age means increased cancer risk

What mutations are common in melanoma?

Ras/Raf/MAPK

Which drugs target the mutated form of B-raf?

Vemurafenib and dabrafenib

Name the familial melanoma mutations and what they mean?

CDKN2A- prevents cells from replicating when they contain damaged DNA CDK4- permits cell cycle progression. Mutations in this accelerate cell cycle.

How does UV damage induce immunosuppression?

Depletes langerhan cells Generates UV induced regulatory T cells with immune suppressive activity Secretes anti-inflammatory cytokines by macrophages and keratinocytes.

Dasatinib and Imatinib target what?

C-Kit. to prevent cell growth

Vemurafinib and dabrafenib target what?

B-raf to prevent cell growth

Trametibib targets what?

MEK to prevent cell growth

Ipillmumab, Tremelimumab and Pembrolizumab target what?

CTLA-4 on T cells and PD1 on T cells to activate them to enable tumour killing

Posters- Week 3 derm Flashcards

(75 cards)