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Dermatology > Malignant Skin Tumours > Flashcards

Malignant Skin Tumours Flashcards

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Dermatology Board Prep flashcards
1
Q

Basal cell carcinoma subtypes

A

Noduloulcerative (typical)

Pigmented variant

Superficial variant

Sclerosing (morpheaform) variant

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2
Q

Noduloulcerative BCC description

A

skin-coloured papule/nodule with rolled, translucent (“pearly”) telangiectatic border, and depressed/eroded/ulcerated centre

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3
Q

Pigmented variant BCC clinical presentation

A

■ flecks of pigment in translucent lesion with surface telangiectasia

■ may mimic malignant melanoma

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4
Q

Superficial variant BCC clinical presentation

A

■ flat, tan to red-brown plaque, often with scaly, pearly border and fine telangiectasia at margin

■ least aggressive subtype

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5
Q

Sclerosing (morpheaform) variant BCC clinical presentation

A

■ flesh/yellowish-coloured, shiny papule/plaque with indistinct borders, indurated

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6
Q

BCC pathophysiology

A

• malgnant proliferation of basal keratinocytes of the epidermis

■ low grade cutaneous malignancy, locally aggressive (primarily tangential growth), rarely metastatic

■ usually due to UVB light exposure, therefore >80% on face

■ may also occur in previous scars, radiation, trauma, arsenic exposure, or genetic predisposition (Gorlin syndrome)

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7
Q

BCC epidemiology

A
  • most common malignancy in humans
  • 75% of all malignant skin tumours >40 yr, increased prevalence in the elderly
  • M>F, skin phototypes I and II, chronic cumulative sun exposure, ionizing radiation, immunosuppression, arsenic exposure
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8
Q

BCC ddx

A
  • benign: sebaceous hyperplasia, intradermal melanocytic nevus, dermatofibroma
  • malignant: nodular malignant melanoma, SCC
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9
Q

BCC management

A
  • imiquimod 5% cream (Aldara®) or cryotherapy is indicated for superficial BCCs on the trunk
  • fluorouracil and photodynamic therapy can also be used for superficial BCC shave excision + electrodessication and curettage for most types of BCCs, not including morpheaform
  • Mohs surgery: microscopically controlled, minimally invasive, stepwise excision for lesions on the face or in areas that are difficult to reconstruct
  • radiotherapy used in advanced cases of BCC where surgical intervention is not an option
  • vismodegib is approved for metastatic BCC
  • life-long follow-up every 6 mo-1 yr
  • 95% cure rate if lesion <2 cm in diameter or if treated early
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10
Q

Workup/investigations of BCC and other non malignant skin cancers

A
  • History: duration, growth rate, family/ personal Hx of skin cancer, prior therapy to the lesion
  • Physical: location, size, whether circumscribed tethering to deep structures, full skin exam, lymph node exam
  • Biopsy: if shallow lesion, can do shave biopsy; otherwise punch or excisional biopsy may be more appropriate
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11
Q

Surgical margins for non melanoma skin cancers

A
  • Smaller lesions: electrodessication and curettage with 2-3 mm margin of normal skin
  • Deep infiltrative lesions: surgical excision with 3-5 mm margins beyond visible and palpable tumour border which may require skin graft or flap; or Mohs surgery, which conserves tissue and does not require margin control
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12
Q

SCC clinical presentation

A
  • indurated, pink/red/skin-coloured papule/plaque/nodule with surface scale/crust ± ulceration
  • more rapid enlargement than BCC
  • exophytic (grows outward), may present as a cutaneous horn
  • sites: face, ears, scalp, forearms, dorsum of hands
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13
Q

SCC pathophysiology

A
  • malignant neoplasm of keratinocytes (primarily vertical growth)
  • predisposing factors include: UV radiation, PUVA, ionizing radiation therapy/exposure, chemical carcinogens (such as arsenic, tar, and nitrogen mustards), HPV 16, 18, immunosuppression
  • may occur in previous scar (SCC more commonly than BCC)
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14
Q

SCC epidemiology

A
  • second most common type of cutaneous neoplasm
  • primarily on sun-exposed skin in the elderly, M>F, skin phototypes I and II, chronic sun exposure
  • in organ transplant recipients SCC is most common cutaneous malignancy, with increased mortality as compared to non immunocompromised population
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15
Q

SCC differential diagnosis

A
  • benign: nummular eczema, psoriasis, irritated seborrheic keratosis
  • malignant: keratoacanthoma, Bowen’s disease, BCC
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16
Q

SCC management

A
  • surgical excision with primary closure, skin flaps or grafting
  • Mohs surgery
  • lifelong follow-up (more aggressive treatment than BCC)
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17
Q

SCC prognosis

A
  • good prognostic factors: early treatment, negative margins, and small size of lesion
  • SCCs that arise from AK metastasize less frequently (~1%) than other SCCs arising de novo in old burns (2-5% of cases)
  • overall control is 75% over 5 yr, 5-10% metastasize
  • metastasis rates are higher if diameter >2 cm, depth >4 mm, recurrent, involvement of bone/muscle/ nerve, location on scalp/ears/nose/lips, immunosuppressed, caused by arsenic ingestion, or tumour arose from scar/chronic ulcer/burn/genital tract/sinus tract
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18
Q

Bowen’s disease (SCC in situ) clinical presentation

A
  • sharply demarcated erythematous patch/thin plaque with scale and/or crusting
  • often 1-3 cm in diameter and found on the skin and mucous membranes
  • evolves to SCC in 10-20% of cutaneous lesions and >20% of mucosal lesions
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19
Q

Bowen’s disease (SCC in situ) management

A
  • same as for BCC
  • biopsy required for diagnosis
  • topical 5-fluorouracil (Efudex®) or imiquimod (Aldara®) used if extensive and as a tool to identify margins of poorly defined tumours
  • cryosurgery
  • shave excision with electrodessication and curettage
20
Q

Keratocanthoma clinical presentation

A
  • rapidly growing, firm, dome-shaped, erythematous or skin-coloured nodule with central keratin-filled crater, resembling an erupting volcano
  • may spontaneously regress within a year, leaving a scar
  • sites: sun-exposed skin
21
Q

Keratocanthoma pathophysiology

A
  • epithelial neoplasm with atypical keratinocytes in epidermis
  • low grade variant of SCC
22
Q

Keratocanthoma etiology

A

• HPV, UV radiation, chemical carcinogens (tar, mineral oil)

23
Q

Keratocanthoma epidemiology

A

• >50 yr, rare <20 yr

24
Q

Keratocanthoma differential diagnosis

A
  • treat as SCC until proven otherwise

* hypertrophic solar keratosis, verruca vulgaris

25
Q

Keratocanthoma management

A

• surgical excision or saucerization (shave biopsy) followed by electrodesiccation of the base, treated similarly to SCC

26
Q

Malignant melanoma clinical presentation

A
  • malignant characteristics of a mole: “ABCDE” mnemonic

* sites: skin, mucous membranes, eyes, CNS

27
Q

Malignant melanoma clinical subtypes of malignant melanoma

A
  • lentigo maligna
  • lentigo maligna melanoma (15% of all melanomas)
  • superficial spreading melanoma (60-70% of all melanomas)
  • nodular melanoma (30% of all melanomas)
  • acral lentiginous melanoma (5% of all melanomas)
28
Q

Malignant melanoma pathophysiology

A

• malignant neoplasm of pigment-forming cells (melanocytes and nevus cells)

29
Q

Malignant melanoma epidemiology

A
  • incidence: 1/75 (Canada) 1/50 (US)
  • risk factors: numerous moles, fair skin, red hair, positive personal/family history, 1 large congenital nevus (>20 cm), familial dysplastic nevus syndrome, any dysplastic nevi, immunosuppression, > 50 common nevi, and sun exposure with sunburns, tanning beds
  • most common sites: back (M), calves (F)
  • worse prognosis if: male, on scalp, hands, feet, late lesion, no pre-existing nevus present
30
Q

Malignant melanoma ddx

A
  • benign: nevi, solar lentigo, seborrheic keratosis

* malignant: pigmented BCC

31
Q

Malignant melanoma management

A
  • excisional biopsy preferable, otherwise incisional biopsy
  • remove full depth of dermis and extend beyond edges of lesion only after histologic diagnosis beware of lesions that regress – tumour is usually deeper than anticipated
  • high dose IFN for stage II (regional), chemotherapy (cis-platinum, BCG) and high dose IFN for stage III (distant) disease
  • newer chemotherapeutic, gene therapies, and vaccines starting to be used in metastatic melanoma
  • radiotherapy may be used as adjunctive treatment
32
Q

Does this patient have a mole or melanoma? abcde checklist

A

ABCDE checklist

Asymmetry

Border (irregula and/or indistinct)

Colour (varied)

Diameter (increasing or >6 mm)

Enlargement, elevation, evolution (i.e. change n colour, size, or shape)

Sensitivity 92% (CI 82-96%)

Specificity 100% (CI 54-100%)

33
Q

Risk factors for melanoma

A

no SPF is a SIN

Sun exposure
Pigment traits (blue eyes, fair/red hair, pale complexion)
Freckling

Skin reaction to sunlight (increased incidence of sunburn)
Immunosuppressive states (e.g. renal transplantation)
Nevi (dysplastic nevi; increased number of benign melanocytic nevi)

34
Q

When to conduct node dissection for lesions in melanoma

A

> 1 mm thick
OR <1 mm and ulcerated
OR >1 mitoses/mm2 (Stage IB or higher melanoma patients should be offered a sentinel lymph node biopsy)

• Assess sentinel node at time of wide excision

35
Q

Melanoma staging

A

T1 < 1 mm
Stage I T1a (a = no ulceration)-T2a
5 year survival 90%

T2 1.01-2mm
Stage II T2b-T4b (b= ulceration)
5 year survival 70%

T3 2.01-4mm
Stage III any nodes
5 year survival 45%

T4 > 4 mm
Stage IV any mets
5 year survival 10%

36
Q

Lentigo maligna clinical description

A

■ malignant melanoma in situ (normal and malignant melanocytes confined to the epidermis)

■ 2-6 cm, tan brown/black uniformly flat macule or patch with irregular borders

■ lesion grows radially and produces complex colours

■ often seen in the elderly

■ 10% evolve to lentigo maligna melanoma

37
Q

Lentigo maligna melanoma clinical description

A

■ malignant melanocytes invading into the dermis

■ associated with pre-existing solar lentigo, not pre-existing nevi

■ flat, brown, stain-like, gradually enlarging with loss of skin surface markings

■ with time, colour changes from uniform brown to dark brown with black and blue

■ found on all skin surfaces, especially those often exposed to sun, such as the face and hands

38
Q

Superficial spreading melanoma clinical description

A

■ atypical melanocytes initially spread laterally in epidermis then invade the dermis

■ irregular, indurated, enlarging plaques with red/white/blue discolouration, focal papules or nodules

■ ulcerate and bleed with growth

39
Q

Nodular melanoma clinical description

A

■ atypical melanocytes that initially grow vertically with little lateral spread

■ uniformly ulcerated, blue black, and sharply delineated plaque or nodule

■ rapidly fatal

■ may be pink or have no colour at all, this is called an amelanotic melanoma

■ “EFG” elevated, firm, growing

40
Q

Acral lentiginous melanoma clinical description

A

■ ill-defined dark brown, blue-black macule

■ palmar, plantar, subungual skin

■ melanomas on mucous membranes have poor prognosis

41
Q

Cutaneous T-Cell Lymphoma clinical presentation

A

• Mycosis fungoides (limited superficial type)
■ characterized by erythematous patches/plaques/nodules/tumours, which may be pruritic and poikilodermic (atrophy telangiectasia, hyperpigmentation, hypopigmentation)
■ common sites include: trunk, buttocks, proximal limbs
■ mildly symptomatic, usually excellent prognosis for early disease

• Sézary syndrome (widespread systemic type)
■ rare variant characterized by erythroderma, lymphadenopathy, WBC >20 x 109/L with Sézary cells
■ associated with intense pruritus, alopecia, palmoplantar hyperkeratosis, and systemic symptoms (fatgue, fever)
■ often fatal

42
Q

Cutaneous T-Cell Lymphoma pathophysiology

A

• clonal proliferation of skin-homing CD4 T-cells

43
Q

Cutaneous T-Cell Lymphoma epidemiology

A

• >50 yr old, M:F 2:1

44
Q

Cutaneous T-Cell Lymphoma ddx

A

• tinea corporis, nummular dermatitis, psoriasis DLE, Bowen’s disease

45
Q

Cutaneous T-Cell Lymphoma investigations

A
  • skin biopsy (histology, “lymphocyte antigen cell” markers, TcR gene arrangement)
  • blood smear looking for Sézary cells or flow cytometry (e.g. CD4:CD8 >10 is Sézary)
  • imaging (for systemic involvement)
46
Q

Cutaneous T-Cell Lymphoma management

A

• Mycosis fungoides
■ depends on stage of disease
■ topical steroids and/or PUVA, narrow band UVB (NBUVB, 311-313mm)

• Sézary syndrome  
■ oral retinoids and IFN 
■ extra-corporeal photopheresis  
■ may need radiotherapy for total skin electron beam radiation  
■ may maintain on UV therapy 
■ other chemotherapy agents

Dermatology (11 decks)

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