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Dermatology > Posters- Week 3 derm > Flashcards

Posters- Week 3 derm Flashcards

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Dermatology Board Prep flashcards
1
Q

What is the term for freckles

A

Ephilides

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2
Q

What is the term for liver spots

A

Actinic lentigines

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3
Q

What are ephilides

A

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

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4
Q

What is the genetic defect that codes for freckles

A

One defective copy of MC1R.

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5
Q

What is MC1R?

A

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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6
Q

What codes for hair colour (other than red)?

A

Eumelanin

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7
Q

What codes for red hair?

A

Phaeomelanin

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8
Q

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

A

MC1R converts phaeomelanin to eumelanin.

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9
Q

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

A

You will have both red hair and freckles.

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10
Q

What does MC1R stand for?

A

Melanocortin 1 receptor

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11
Q

How do you acquire actinic lentigines?

A

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

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12
Q

What are melanocytic naevi? How can they be divided?

A

Birthmarks. Can be either congenital or acquired.

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13
Q

Classification of congenital naevus

A

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

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14
Q

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

A

True.

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15
Q

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

A

True

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16
Q

Why do people get acquired melanocytic naevi?

A

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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17
Q

Describe the process of naevus development

A

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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18
Q

What are dysplastic naevi?

A

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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19
Q

Familial dysplastic naevus

A

Strong FH of melanoma

Lifetime risk of melanoma up to 100%

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20
Q

Sporadic dysplastic naevus

A

Not inherited however the risk of melanoma increases slightly.

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21
Q

Name the three rarer naevi

A

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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22
Q

What type of people are more likely to get melanomas?

A

Middle aged
Women
Sun exposed sites

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23
Q

ABCDE of melanoma

A 
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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24
Q

What are the 4 main types of melanoma?

A

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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25
Q

How are melanomas formed?

A

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.

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26
Q

At which stage can a melanoma metastasise?

A

At the vertical growth stage.

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27
Q

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

A

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

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28
Q

What is breslows thickness?

A

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

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29
Q

Prognosis of melanomas

A 
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
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30
Q

How does melanoma spread?

A

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

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31
Q

Treatment of melanomas

A

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.

32
Q

Excision of melanoma guidelines

A

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.

33
Q

What is seborrheic keratoses?

A

Black/brown greasy looking lesion that is often warty.

34
Q

Who is likely to get seborrheoic keratoses?

A

Older Caucasians

35
Q

Treatment of seborrheic keratoses?

A

Reassurance
Curette
Shave

36
Q

Types of skin cancer

A

Melanoma

Non-melanoma- BCC and SCC

37
Q

What do BCC’s arise from?

A

Keratinocytes in the basal layer

38
Q

What do SCC’s arise from?

A

Keratinocytes in supra basal layers

39
Q

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

A

90-95%

40
Q

Describe a basal cell carcinoma

A 
Slow growing lump or non healing ulcer. 
Painless (often ignored)
Pearly or translucent
Visible arborising (branch like) blood vessels
Central ulceration (rodent ulcer)
41
Q

Describe a squamous cell carcinoma

A 
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
42
Q

What is actinic keratoses?

A

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

43
Q

What are the risks of having actinic keratoses?

A

High risk of developing BCC and SCC.

44
Q

Risk factors for developing cancer

A

Sun exposure
Genetic predisposition
Immunosuppression
Environment carcinogens

45
Q

What environmental triggers can cause cancer?

A 
Smoking
Coal tar
Arsenic
Trauma
Ionising radiation
46
Q

What genetic syndromes pre-dispose people to cancer?

A

DNA repair syndromes such as xeroderma pigmentosum.

47
Q

What is xeroderma pigmentosum

A

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

48
Q

Symptoms of xeroderma pigmentosum

A

Photosensitivity
Skin cancers on UV exposed sites
Neurological degeneration

49
Q

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

A

True

50
Q

What is oculocutaneous albinism?

A

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

51
Q

What are patients with O albinism prone too?

A

Sun burn and melanocytic skin cancers

52
Q

What is Gorlins syndrome?

A

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

53
Q

How does cancer come about (general description)

A

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

54
Q

How does UVB affect DNA

A

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

55
Q

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

A

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

56
Q

How are CPD’s and 6-4 PP’s removed?

A

By nucleotide excision repair due to them being relatively stable.

57
Q

What happens to un repaired UV products?

A

They interfere with base pairing during replication.

58
Q

What does UVA do to DNA?

A

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

59
Q

What is oxidative damage to DNA?

A

Oxidation of DNA bases occurs.

60
Q

What does oxidative damage cause?

A

Pair mismatches. Can be repaired by nucleotide excision repair.

61
Q

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

A

SCC

62
Q

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

A

Melanoma and BCC

63
Q

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

A

Melanoma and BCC

64
Q

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

A

BCC
Melanoma
SCC

65
Q

Which skin type is most at risk of developing cancer?

A

type 1

66
Q

What effect does immune suppression have on cancer?

A

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

67
Q

What effect does age have on cancer?

A

Increasing age means increased cancer risk

68
Q

What mutations are common in melanoma?

A

Ras/Raf/MAPK

69
Q

Which drugs target the mutated form of B-raf?

A

Vemurafenib and dabrafenib

70
Q

Name the familial melanoma mutations and what they mean?

A

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

71
Q

How does UV damage induce immunosuppression?

A

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

72
Q

Dasatinib and Imatinib target what?

A

C-Kit. to prevent cell growth

73
Q

Vemurafinib and dabrafenib target what?

A

B-raf to prevent cell growth

74
Q

Trametibib targets what?

A

MEK to prevent cell growth

75
Q

Ipillmumab, Tremelimumab and Pembrolizumab target what?

A

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

Dermatology (21 decks)

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