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derm > Lecture 8: Pigmented, Precancerous lesions (Enochs) > Flashcards

Lecture 8: Pigmented, Precancerous lesions (Enochs) Flashcards

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Dermatology Board Prep flashcards
1
Q

What is Actinic Keratosis?

A

Solar keratosis Neoplastic condition in which precancerous epithelial lesions are found on sun-exposed areas of the body.

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2
Q

What skin type is actinic keratosis MC in?

A

Lighter skin

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3
Q

Where is Actinic Keratosis MC?

A

Any sun exposed skin

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4
Q

What does actinic keratosis look like?

A
  • 2-6 mm plaques
  • Yellowish
  • Hypertrophic
  • Rough
  • Ill-defined border with some scale
  • Underlying red base
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5
Q

Who is MC for actinic keratosis?

A

Immunosuppressed

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6
Q

What cancer can actinic keratosis evolve into?

A

squamous cell carcinoma

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7
Q

What can help and/or resolve actinic keratosis?

A

Protection from UV light

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8
Q

How do you find actinic keratoses?

A

Palpation

“gritty”

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9
Q

How is actinic keratosis dx?

A

Clinically, but refer to derm if unsure.

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10
Q

What is the lower lip involvement version of actinic keratosis called?

A

Actinic cheilitis

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11
Q

If you choose to do dermoscopy, what will show up for actinic keratosis?

A
  • White to yellow surface scale
  • Erythema with pseudo-network around hair follicles
  • linear-wavy vessels
  • follicle openings with yellowish keratotic plugs

Classic gritty feel

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12
Q

What causes actinic keratosis to be pigmented?

A

Collision of solar lentigo and actinic keratosis

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13
Q

When would a biopsy be indicated for actinic keratosis?

A
  • Recurrent, hyperkeratotic
  • Large > 6mm
  • Indurated
  • Painful

R/u invasive carcinoma

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14
Q

What is the MC type of tx for actinic keratosis that is lesion-targeted?

A

Cryosurgery

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15
Q

What meds can treat actinic keratosis?

A
  • 5-FU
  • Imiquimod cream
  • Ingenol mebutate
  • Diclofenac gel
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16
Q

What is the MOA of 5-FU?

A

Blocks DNA synthesis and leading to selective cell death.

you say “FU!” and then you block them and they die of embarassment

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17
Q

How often is 5-FU dosed?

A

BID to affected area for x 2-4w

QD for micronized to face/scalp

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18
Q

What is the main pt education for using 5-FU for actinic keratosis?

A

Success is parallel to pt compliance.

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19
Q

MOA of imiquimod

A

Immunomodulator that stimulates local cytokine induction.

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20
Q

When is imiquimod used?

A

ImmunoCOMPETENT people with non-hypertrophic AK on their face or scalp

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21
Q

How is imiquimod given?

A

Cream nightly, wash after 8 hrs. 2x/wk for 16 wks.

Start at 5%

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22
Q

Main SE of both 5-FU and imiquimod?

A

Local skin rxn

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23
Q

Main pt education for imiquimod

A
  • SE = getting better
  • Wash hands before and after
  • Wash area before
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24
Q

What is the MOA of ingenol mebutate (Picato)?

A
  1. Disruption of the cell membrane and DNA => necrosis
  2. Neutrophil-mediated cytotoxicity that eliminates remaining tumor cells

PLANT DERIVATIVE

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25
Q

When is ingenol mebutate (Picato) used?

A

Actinic Keratosis

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26
Q

How is ingenol mebutate (Picato) administered?

A
  • 0.015% gel for the face/scalp.
  • 0.05% gel for trunk/extremities

Cover affected area for 3d for face, 2d for trunk.

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27
Q

What is the risk of ingenol mebutate (Picato)?

A

Invasive SCC

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28
Q

What is the MOA of diclofenac 3% gel?

A

COX-2 inhibitor

PGE production makes non-melanoma skin CA

Dic(k) = cox

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29
Q

How long do you apply diclofenac 3% gel?

A

BID for 60-90 days

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30
Q

Why might diclofenac 3% gel be preferred over other agents for Actinic Keratosis?

A

Mild skin reaction compared to others.

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31
Q

What are the 5 procedural field therapies for actinic keratosis?

A
  • Cryopeeling
  • Dermabrasion
  • Chemical Peels
  • Laser Resurfacing
  • Photodynamic therapy
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32
Q

A patient is being seen for their first derm visit regarding a few suspicious actinic keratosis. What is the first-line tx?

A

Lesion targeted therapy

  • Cryosurgery
  • Curettage
  • Shave excision
  • Patient education on sunscreen
  • 3 mo f/u
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33
Q

What would be the first two drugs you would choose for a 2nd visit of multiple AKs?

A
  • 5-FU
  • Imiquimod
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34
Q

A patient compliant with topical field therapy and having multiple AKs does not like 5-FU or imiquimod. What can you give them?

A

Diclofenac gel

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35
Q

What is Squamous Cell Carcinoma?

A

Malignant cutaneous epithelial cells, MC on sun-exposed areas.

AK often is a precursor.

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36
Q

What area, if found, is SCC highest risk for metastasis?

A

Oral mucosa and lip

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37
Q

How does differentiated SCC present?

A
  • Hard/firm papule/plaque/nodule
  • Thick, adherent keratotic scale
  • Erythematous, yellow, or skin colored.
  • Found on sun-exposed areas
  • Can cause regional LAN with metastasis
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38
Q

What does undifferentiated SCC look like?

A
  • Soft, fleshy, erosive papule/nodule
  • Papillomatous, like a cauliflower.
  • Bleeds easily
  • Found on less on sun-exposed areas (genitalia, trunk, LE, face)
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39
Q

Top RFs for SCC

A
  • Chronic sun exposure
  • Fair skin, blue eyes
  • FHx
  • Old
  • Scarring
  • HPV
  • Tattoos if traumatic
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40
Q

What is the MC skin cancer in AA?

A

SCC

Even though it is 80x less likely to occur in dark skin.

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41
Q

Why do dark skin ppl rarely get dxd with SCC?

A
  • Doesn’t occur often in darker skinned
  • Occurs in scars and non-sun-exposed areas for darker skin, so its not caught.
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42
Q

What is SCC in situ?

A

Confined to epidermis

Includes Bowen dz and erythroplasia or Queyrat (on testes)

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43
Q

Who is SCC in situ more frequent and aggressive in?

A

Immunosuppressed

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44
Q

What will you often see on the skin of patients with SCC? (besides SCC)

A
  • Solar elastosis
  • AKs
  • Solar lentigines
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45
Q

Most important predisposing factors/locations for SCC

A
  • Old burn scar
  • Chronic cutaneous ulcers
  • Inflammation
  • Irradiation
  • Chronic lymphedema
  • Venous stasis
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46
Q

What is the classic presentation of SCC on dermoscopy?

A

Red vessels as dots, scale/crust, and shiny white structures (Crystalline Structures

SCC - “shiny crusty crystals”

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47
Q

What does pigmented SCC look like?

A

Red vessels + Shiny white structures + brown/gray dots in a linear arrangment.

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48
Q

Besides looking at the actual lesion in SCC, what else is essential to examine?

A

Regional lymph nodes

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49
Q

What is the most effective means of detecting SCC?

A

A thorough H&P

50
Q

What is the characteristic histopathology of SCC biopsy?

A
  • Pleomorphic/hyperchromatic squamous cells with variable nuclear size
  • Loss of full-thickness epidermal maturation
  • Overlying parakeratosis
  • Dyskeratosis
  • Squamous peals
  • Adjacent solar/actinic keratosis
51
Q

What are the subtypes of SCC?

A
  • Bowen dz (SCCIS variant)
  • Acantholytic/adenoid/pseudoglandular
  • Well differentiated
  • Poorly differentiated
52
Q

TOC for SCC

A

Excision with narrow margins (3-5 mm)

Does not apply to oral mucosa, head and neck, or immunocomped pts?

Wider margins are needed if its well-differentiated

53
Q

In high-risk SCC, what is the main TOC?

A

Excision with 6 mm margins if Mohs cannot be done.

54
Q

If we suspect/know SCC with nodal metastases, what secondary procedure is indicated beside excision?

A

Lymph node dissection.

55
Q

For superficial SCCs, whats a less invasive procedure/non surgical option?

A

Electrodessication and curettage x 3 with margins of 3-4 mm

56
Q

For non-surgical candidates with SCC, what can we do? (2nd/3rd line)

A
  • Topical imiquimod
  • Topical/intralesional 5-FU
  • Electrochemo
  • Interferon
  • Photodynamic therapy
57
Q

Pt Ed for SCC

A
  • Check any sus lesions (open sore, pink-reddish growth, irritated or shiny)
  • 30 SPF minimum
  • Seek shade outdoors
  • NO TO TANNING BEDS
58
Q

What characterizes a keratoacanthoma?

A
  • A variant of SCC that grows rapidly
  • Solitary or multiple
  • Involutes over time
59
Q

Histology of keratoacanthoma

A
  • Craterioform
  • Endophytic nodule
  • Well differentiated keratinocytes
  • CENTRAL KERATIN PLUG
60
Q

Tx for keratoacanthoma

A

Mohs or Excision

61
Q

MC skin cancer

A

Basal cell carcinoma

62
Q

MC subtype of basal cell carcinoma?

A

Nodular variant

63
Q

What 3 ethnicities have pigmented BCC as the most common variant?

A
  • African
  • Hispanic
  • Asians
64
Q

What are the 4 types of BCC?

A
  • Nodular (MC overall)
  • Infiltrating
  • Pigmented (MC in african/hispanic/asian)
  • Superficial
65
Q

What happens if BCC is not treated?

A

Local destruction

rarely metastasizes

66
Q

Describe nodular BCC

A
  • Translucent pearly papule/nodule
  • well defined borders
  • Smooth, firm surface with telangiectasias.
  • +/- erosions, sporadic pigmentation
67
Q

Describe ulcerating BCC

A
  • Translucent and pearly
  • Smooth and firm
  • CENTRAL ULCER
  • +/- elevated borders = rodent border
68
Q

Describe sclerosing BCC

A
  • Plaque, scar like lesion
  • Pink/white
  • Telangiectasias
  • ill defined borders
69
Q

Describe superficial multicentric BCC

A
  • Thin plaque/patch
  • Pink/red
  • +/- scaling
70
Q

Describe pigmented BCC

A
  • Firm papule/nodule
  • +/- umbilication
  • Smooth pearly surface
  • Pigmented/stippled globules of pigment
71
Q

Hereditary conditions associated with BCC

A
  • Albinism
  • Xeroderma pigmentosum
  • Nevoid BCC syndrome
  • Rasmussen syndrome
  • Rombo syndrome
  • Darier dz
72
Q

Prognosis for BCC

A

If properly identified and treated, very good! Make sure to keep f/u since 2nd BCC is common.

73
Q

If 2 or more BCC appears in a patient younger than 30, what underlying condition may they have?

A

Nevoid BCC syndrome

Or exposure to ionizing radiation

BCCs will often be bigger

74
Q

Best test for BCC dx

A

Skin biopsy with shave/punch

Biopsy Basal, See Squamous

75
Q

Pt ed for BCC

A

General sun protection

76
Q

What is the tx for BCC?

A
  • Electrodessication and curettage (ED&C)
  • Excision
  • Cryosurgery
  • Radiation
  • Mohs
  • Oral smoothened inhibitors (suppresses hedgehog pathway)

Individualized per pt

77
Q

Mohs criteria for BCC

A
  • Recurrent
  • Aggressive subtype
  • > 2 cm
  • Head/neck location
78
Q

Best tx for BCCs that are recurrent, primary BCCs in the nasolabial folds, or morpheoform histopathology?

A

Mohs

79
Q

What are the pharm options for non-surgical BCC or metastatic BCC patients?

A

Vismodegib (metastatic BCC) or Sonidegib (locally advanced BCC)

(hedgehog pathway inhibitors)

Sonic is a Very fast Hedgehog

80
Q

What is a common melanocytic nevi?

A

Benign overgrowth of skin cells

81
Q

What are the two types of common melanocytic nevi and what is the more sus one?

A
  • Congenital MN (CMN) is a developmental defect in melanoblasts. Big ones = increased risk for melanoma
  • Acquired (MN) = develops in early childhood but regresses after 60
82
Q

What are the clinical features of a common melanocytic nevi? (4)

A
  • Asymptomatic without change
  • Symmetric
  • Sharp borders
  • Uniform color
83
Q

How do you dx a common acquired nevomelanocytic nevi?

A

Dermoscopy

84
Q

Indications for excision of unconfirmed common acquired nevomelanocytic nevi? (5)

Confirmed = no tx

A
  • Located on scalp, anogenital, mucosa
  • Rapid change
  • Irregular borders
  • Erosions
  • Persistent itching/pain/bleeding
85
Q

What is dysplastic melanocytic nevi? (DN)

A

Pigmented lesion resulting from proliferation of Atypical melanocytes

86
Q

When does dysplastic melanocytic nevi (DN) occur?

A

Late onset childhood to middle adulthood

87
Q

Why is dysplastic melanocytic nevi scary? (DN)

A

Precursor to superficial spreading melanoma

Increases risk for melanoma

88
Q

Clinical features of dysplastic melanocytic nevi (DN) (5)

A
  • Asymptomatic
  • Irregular shape
  • Sharp and ill-defined borders
  • Variegated color
  • Maculopapular
89
Q

Dx of dysplastic melanocytic nevi (DN)

A

Clinical

If confirmation needed, via histopatho

90
Q

Tx of dysplastic melanocytic nevi (DN)

A
  • Obs with dermoscopy
  • Excision with biopsy if necessary to r/o melanoma

Indications: changing or can’t closely observe.

Shave, laser, cryo, and electro are all contraindicated.

91
Q

How do you f/u or monitor dysplastic melanocytic nevi? (DN)

A
  • Routine skin exams every 3 months if FHx of DN or melanoma
  • Otherwise 6-12 months.

Tell family members to check too

92
Q

Table of MN vs DN

A
  • MN = several or many
  • MN = symmetrical
  • MN = smaller, around < 5 mm
  • MN = stops in adolescence
93
Q

4 subtypes of melanoma

A
  1. Superficial Spreading Melanoma (SSM) MC
  2. Nodular Melanoma
  3. Lentigo maligna melanoma
  4. Acral lentiginous melanoma (LEAST COMMON)
94
Q

Top 2 RFs for Melanoma

A
  • Genetics
  • Exposure to UVA/UVB with light skin
95
Q

MC cancer in young women 25-29

A

Melanoma

96
Q

Most deadly skin cancer

A

Melanoma

80% of skin cancer deaths

97
Q

How many nevi is a RF for melanoma?

A

more than 25

98
Q

What are the two clinical classifications of melanoma development?

A
  • De novo melanoma = brand new (MC 70%)
  • Precursor melanoma = developed from DN or CMN
99
Q

What do radial/thin and vertical melanoma mean?

A
  • Radial/thin = epidermis only
  • Vertical = extending down leading to metastasis
100
Q

What is the primary prognostic feature of melanoma?

A

Depth of invasion, measured as the Breslow thickness

measured in mm

101
Q

Who dies more from melanoma: men or women?

A

Men

102
Q

MC melanoma metastases sites

A
  • Skin/SC
  • Lymph nodes
  • Lungs
  • Liver
  • Brain

It can go anywhere tho

103
Q

Common features of melanoma

A
  • Asymmetry
  • Border irregularity
  • Color change/variegation
  • Diameter > 6 mm
  • Evolution

Ulceration/bleeding = late signs

104
Q

What is a lightly pigmented melanoma called?

A

Amelanotic

105
Q

Where is SSM MC in men and women?

A
  • Men: trunk
  • Women: LE

Men go shirtless and women wear shorts

106
Q

Which two melanoma subtypes are slow growing?

A
  • Lentigo maligna
  • Acral lentiginous
107
Q

Which melanoma subtype is most likely to ulcerate/bleed?

A

Nodular melanoma

2nd MC after SSM

108
Q

What is an ugly duckling lesion?

A

The weirdest looking pigmented lesion out of many

109
Q

Best test for melanoma

A

Excision biopsy (shave/punch)

110
Q

What are the 5 levels of Clark staging for melanoma?

A
  1. in situ
  2. Invade papillary dermis
  3. Invade papillary dermis and reaches reticular dermis
  4. Invade reticular dermis
  5. Invade SQ fat

I,P,Pr, R, S

111
Q

What are the 3 ways to stage melanoma?

A
  • Clark
  • TNM
  • Breslow
112
Q

When do you need a sentinel lymph node biopsy for Melanoma per breslow thickness?

A

> 0.76 mm on breslow

113
Q

TOC for melanoma

A

Surgical excision

114
Q

What are the guidelines regarding margins for melanoma excision?

A
  • in situ = 0.5 cm (large for lentigo maligna)
  • Less than 1 mm = 1 cm margins
  • 1-2 mm = 1-2 cm margins
  • 2-4 mm = 2 cm margins
  • 4 mm = 2 cm magins

Melanoma uses LARGE margins

115
Q

How often should someone with a FHx of BCC or SCC get a skin exam? Melanoma?

A
  • BCC/SCC = Q6months
  • Melanoma = Q3months
116
Q

In general, what cancers can Mohs be done for?

A

BCC and SCC

Not for melanoma!

High cure rate, low recurrence, minimal tissue loss

117
Q

Indications for simple excision with 5 mm margins

A
  1. Well-defined nodular BCC
  2. Low risk SCC in anatomical appropriate site
118
Q

When is wide local excision with 2-5 cm margins indicated?

A
  1. Well-differentiated SCC
  2. Well-defined large nodular-ulcerative BCC
119
Q

CIs to suturing after punch biopsy

A
  • Active infection
  • Poorly healing skin
120
Q

What do you stabilize skin perpendicular to in punch biopsies?

A

Langer lines

121
Q

Longest wavelength UV

A

UVA

122
Q

What kind of sunscreen do you need?

A

Broad spectrum (ZINC OXIDE)

Covers UVA and UVB

derm (16 decks)

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