Cutaneous Onoclogy Flashcards

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1
Q

Name two genetic conditions that may pre-dispose youth cutaneous cancer.

A

basal cell nevus syndrome (loss of tumor suppression)

xeroderma pigmentosum (impaired DNA repair)

note the immune system plays a major role in promoting/ controlling cancer

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2
Q

Describe conditions on the spectrum of malnocytic lesions.

A
common nevi (junctional, compound, dermal), small and medium congenital nevi and dysplastic nevi, 
melanoma
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3
Q

What are the clinical features of benign melanocytic nevi?

A

groups of melanocytes in the skin,
distribution and number related to genetics
number of nevi associated with melanoma risk
3 types junctional, compound and dermal
born with few, gain more from late childhood to mid 30’s; should be oval to round and well-circumscribed

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4
Q

Compare and contrast junctional, compound and dermal nevi.

A

junctional: flat dark mark (1st/2nd decade)
compound: occur at the junction at the dermis, appear lighter and raised
dermal are within the dermis and are domed pink papules

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5
Q

What are the treatments for common nevi?

A

reassurance that it is not cancerous, discuss photo protection, excise (if changing or atypical, repeatedly traumatized or cosmetic)

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6
Q

What are the clinical presentation of congenital nevi?

A

present at birth
small, medium or large
frequently cobbled and develop coarse hair
giant congenital nevi have an increased risk of melanoma

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7
Q

What is the clinical presentation of dysplastic nevi?

A

nevi with atypical cells and abnormal nevus architecture, variegated tan, brown or pink, irregular shape, indistinct borders and frequently >5mm that continue to develop throughout life not normally apparent until puberty, common on trunk; excision is warranted in giant nevi or with serverely displastic nevi

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8
Q

Describe the prevalence and risk factors of melanoma.

A

malignant proliferation of melanocytes accounts for 75% of cancer deaths although it it not the most common kind
risk factors include:
numerous, large, dysplastic nevi, history of melanoma, tanning, sunburn, higher SE, genie DNA repair defects and immunosuppression

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9
Q

Describe the development of melanoma.

A

⅓ arise from nevi, ⅔ arise de novo, melanocytes lose their normal growth regulation and grow out radially then grow enter a vertical growth phase (most important marker is Breslow depth

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10
Q

What doe the ABCDE of melanoma stand for?

A

asymmetry, borders, color, diameter and evolving

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11
Q

What are the 4 subtypes of melanoma?

A

superficial spreading(60-70%, long radial growth phase), nodular (15-30%, shortest radial growth phase, fastest growing), lentigo maligna (5-15%), older adults, longest radial growth phase, flat asymmetric color variation, common on the face) a and acral lentiginous (5-10% common with darker skin types, palmar, plantar or subugual location)

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12
Q

What is a Hutchinson sign?

A

blacken patch that spreads to the proximal nail fold

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13
Q

What is the standard treatment for melanoma?

A

wide excision with appropriate margins, setinal lymph node biopsy for melanomas (1-4 mm depth), close follow-up with skin exams and lymph node surveillance

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14
Q

What is the single greatest predictor of survival of melanoma prognosis?

A

Breslow depth, lymph node or distant metastases make the disease more difficult to treat

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15
Q

What are often difficult to differentiate from melanoma?

A

dysplatic nevi

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16
Q

What is an epidermoid cyst?

A

trapped epidermal cells caused by injury to the skin or blocked hair follicle which becomes a pocket of macerated keratin.

17
Q

What is the clinical presentation of an epidermoid cyst?

A

domed nodule (compressible and mobile subcutaneous mass attached to epidermis), foul-smelling, ricotta cheese like keratin may be expressed, rupture may lead to inflammation but true infection is rare

18
Q

What is the treatment for a epidermoid cyst?

A

intralesional steroids or oral antibiotics if inflamed, if excised, must excise entire cyst if recurrently inflamed (do not excise when actively inflamed)

19
Q

What is a seborrheic keratosis/ clinical presentation?

A

benign overgrowth of the epidermis which is common is 40s or 50s which can be flesh-colored, tan, brown or black most common to appear no the trunk (grow on top of skin)

note: pseudohorn cysts grow with pearls of keratin

20
Q

How are seborrheic keratosis treated?

A

inflamed lesions can be scrapped up (curettage) or frozen off cyrotherapy and reassurance

21
Q

What is actinic keratosis/ clinical presentation?

A

sun-induced, pre-cancerous lesions of the epidermis where DNA damage causes dysregulation of the cell cycle and differentiation. presents as pink to red sandpapery papules (better felt than seen) on sun-exposed areas

22
Q

Are actinic keratosis dangerous?

A

only 1-2% convert to squamous cell carcinoma, but be suspicious is lesion: persists after treatment, rapidly grows, becomes indurated or ulcerated/mucosal

23
Q

Squamous cell carcinoma is the second most common skin cancer and is 3x more likely than BCC to affect people who are _____. SCC affects which areas?

A

immunocompromised; affects sites lined with squamous epithelium (skin, mouth, esophagus, penis, anal mucosa with high risk for metastasis with lips, ears, perianal/genital regions and hand)

24
Q

What might cause pathogenesis of SCC?

A

DNA disruption (UV or HPV, chemical carcinogens), chronic inflammation (ulcers or burns) or may progress from actinic keratosis

25
Q

What is the clinical presentation of SCC?

A

well demarcated, thin plaque, resembling a superficial BCC, AK, eczema or psoriasis

26
Q

What is Bowen’s carcinoma?

A

in- situ SCC

27
Q

What differentiates a squamous cell carcinoma?

A

invasive SCC is an erythematous plaque or nodule, that is scaly, has an indurated base and may become ulcerated

28
Q

What is the treatment for SCC?

A

low risk sites can be treated with excision, high risk or large tumor should be treated with Mohs (prognosis with metals is very poor)

29
Q

Where is basal cell carcinoma most common?

A

malignant tumor of the basal keratinocyte, it is the most common cancer in the US, 90% is found on the head and neck (nose being most common and is more likely with immunocompetent patients

30
Q

What are the 3 subtypes of basal cell carcinoma?

A

nodular (50-80%), superficial (15%) and morpheaform (5%)

31
Q

Describe the clinical presentation of basal cell carcinoma.

A

nodules of basaloid cells in the dermis, appears pearly or translucent, often with talangectasias, rolled border and friable (may have a central erosion or ulceration

32
Q

Describe the clinical presentation of superficial basal cell carcinoma.

A

erythmatous thin plaque with an overlying scale which is slow glowing which favors the trunk, caused by a basaloid tumor cells budding directly into the epidermis (subtlies- translucency, friability/crusting, rolled border)

33
Q

Describe the clinical presentation of basal cell carcinoma morfeaform.

A

most aggressive subtype, presents with depressed, atrophic, scar-like hypo pigmented papules with indistinct margins (occurs with infiltration of surrounding skin)

34
Q

What is the prognosis for BCC?

A

very rarely metastasizes, untreated can lead to significant local tissue destruction; higher risk if in the mask area of the face

35
Q

Define Mohs micrographic surgery. What type of cancer is it used for?

A

systematic and methodical way of removing skin cancers and sectioning the tissue which achieves a smaller margin of normal skin with greater assurance of a cure; for high-risk non-melaonma skin cancers in critical sites

allows for examination of all margins that were in contact with the patient

36
Q

What are the disadvantages of Mohs micrographic surgery?

A

time consuming and expensive (controversial for some tumors ie. melanoma)