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Dermatology > Premalignant and Malignant Skin Tumors > Flashcards

Premalignant and Malignant Skin Tumors Flashcards

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Dermatology Board Prep flashcards
1
Q

Signs and symptoms of solar damage on face back of hands, solar lentigenes – freckles, facial telangiectasia, poikiloderma of the neck

A

actinic keratosis

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2
Q

most common epithelial precancerous lesion

A

actinic keratosis

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3
Q

actinic keratosis aka

A

solar keratosis

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4
Q

actinic keratosis

____% develop malignancy

A

20 to 25% develop to malignancy especially on forearm of white males

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5
Q

this type of actinic keratosis

may lead to cutaneous horn formation, is most frequently present on the dorsal forearms and hands

A

hypertrophic type

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6
Q

six histologic types of

actinic keratosis:

A

Hypertrophic

Atrophic

Bowenoid

Acantholytic

Pigmented

Lichenoid

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7
Q

factors affecting development of actinic keratosis

A

UV exposure

X-ray

Aromatic hydrocarbon

Arsenic

Third degree burn

Large scar

Previous exposure to HPV

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8
Q

indications biopsy

actinic keratosis

A

If there is a palpable dermal component, or if on stretching the lesion there is a pearly quality

Any lesion larger than 6 mm

any lesion that has failed to resolve with appropriate therapy for actinic keratosis

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9
Q

tx

actinic keratosis

A 
tx like SCC
cryotherapy with liquid nitrogen
topical 0.5% 5-FU or imiquimod 5% cream
dermabrasion
CO2 laser
Low fat diet and daily use of sunscreen
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10
Q

tx actinic keratosis
most effective and
practical when there are a limited number of lesions

When correctly performed, healing usually occurs within a week on the face, but may require up to 4 weeks on the arms and legs

A

cryotherapy with liquid nitrogen

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11
Q

tx actinic keratosis

for extensive, broad, or numerous lesions

A

topical 0.5% 5-FU or imiquimod 5% cream

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12
Q

is an interferon (IFN) inducer and apparently eradicates actinic keratoses by producing a local immunologic reaction against the lesion

A

Imiquimod

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13
Q

treatment of choice for severe actinic chelitis

A

CO2 laser

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14
Q

prevent further solar damage

A

Low fat diet and daily use of sunscreen

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15
Q

Cornu cutaneum

A

cutaneous horn

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16
Q

Skin colored horny, excrescences, 2-60 mm long, sometimes divided into several antler-like projections, with a red base and slighty thicker than its extremity

A

CUTANEOUS HORN

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17
Q

cutaneous horn tx

A

Excision biopsy with histologic examination of the base

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18
Q

cutaneous horn

Most often benign, with the hyperkeratosis being superimposed on an underlying seborrheic keratosis, verruca vulgaris, angiokeratoma, molluscum contagiosum, or trichilemmoma about _____% of the time

A

60%

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19
Q

_______% cutaneous horn may overlie premalignant keratoses

A

20–30%

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20
Q

20% m utaneous horn ay overlie

A

SCCs or BCCs

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21
Q

1/3 of_______ associated with CA

A

penile horns

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22
Q

Whitish thickening of the epithelium of the mucous membranes, occurring as lactescent superficial patches of various sizes and shapes, that may coalesce to form diffuse sheets

A

LEUKOPLAKIA

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23
Q

The surface is glistening and opalescent, often reticulated, and somewhat pigmented

The white pellicle is adherent to the underlying mucosa

At times it is a thick, rough, elevated plaque

A

LEUKOPLAKIA

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24
Q

Leukoplakia is found chiefly in

A

men >40 y/o

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25
Q

LEUKOPLAKIA

May transform to CA in

A

1-20 years

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26
Q

leukoplakia

if ulceration, red areas, or erosions are scattered throughout, the lesion is most likely

A

precancerous

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27
Q

leukoplakia
if ulceration, red areas, or erosions are scattered throughout, the lesion is most likely precancerous.
this is indicated

A

biopsy

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28
Q

leukoplakia -> CA

rapid course of transformation in

A

immunosuppressed transplant patients

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29
Q

leukoplakia

Lesion on the Lip: related to

A

chronic actinic chelitis

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30
Q

consists of a circumscribed or diffuse keratosis, almost invariably on the lower lip

Preceded by an abnormal dryness of the lip and may be caused by biting the lips, smoking or chronic sun exposure

A

chronic actinic chelitis

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31
Q

term used to describe white, corrugated plaques that occur primarily on the sides of the tongue of patients with AIDS

a virally induced lesion

A

Oral Hairy Leukoplakia

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32
Q

occur in obese women after menopause as grayish white, thickened prurity patches that may become fissured and edematous from constant rubbing and scratching

A

Leukoplakia of the Vulva

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33
Q

Leukoplakia of the Vulva

differentiated from lichen planus by

A

the absence of discrete, rectangular, or annular flat papules of violaceous hue in the mucosa outside the thickened patches, about the anus, on the buccal mucosa, or on the skin

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34
Q

Leukoplakia of the Vulva

most frequently confused with

A

lichen sclerosus et atrophicus and other vulval atrophies

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35
Q

LEUKOPLAKIA

etiology

A

Excessive use of poorly fitting dentures

Sharp and chipped teeth

Poor oral hygiene

Tobacco smoking, reverse smoking

Betel nut chewing

Alcohol

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36
Q

______% transformation rate of intraoral leukoplakia into SCC with the red lesions having a higher risk

A

6-10%

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37
Q

Predictors of a higher risk of SC carcinoma development (from leukoplakia) include

A

older age

female sex

nonsmokers

large size

presence on the lateral or ventral tongue
floor of the mouth, or retromolar/soft palate complex

erythroleukoplakia

nonhomogeneous morphology

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38
Q

type of leukoplakia that

has a high rate of transformation into aggressive squamous cell carcinoma

the cancers derived from it are more likely to be lethal.

A

Aneuploid leukoplakia

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39
Q

leukoplakia

tx

A

Complete removal: fulguration, simple excision, crytherapy and CO2 laser
Stop use of tobacco
Isotretinoin 1-2 mg/kg/day for 3 months
5- FU

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40
Q

Squamous Cell Carcinoma in situ

A

BOWEN’S DISEASE

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41
Q

An intraepidermal SCC, may become invasive

A

BOWEN’S DISEASE

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42
Q

Lesion looks like an eczema

scaling erythematous
When intraepithelial growth becomes invasive, nodular infiltration forms, which becomes ulcerated and fungating

A

BOWEN’S DISEASE

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43
Q

Sites

BOWEN’S DISEASE

A

anywhere on the body, mucous membranes

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44
Q

Possible agents that can induce BD:

A

HPV of certain types arsenic exposure sun exposure

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45
Q

The squamous carcinoma that evolves from BD tends to be

A

more aggressive than SCC arising in actinic keratosis.

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46
Q

the lesions are multicentric and behave like genital warts

Differential Diagnosis
BOWEN’S DISEASE

A

Bowenoid Papulosis

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47
Q

BOWEN’S DISEASE

Treatment:

A

Imiquimod 5% cream, applied once a day for up to 16 weeks
Combination treatment with imiquimod 5% cream, three times a week, and 5% 5-FU, twice a day (except at the times of the imiquimod application

Tazarotene
Photodynamic therapy
Mohs microsurgery

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48
Q

Imiquimod 5% cream, applied once a day for up to 16 weeks
BOWEN’S DISEASE
response rate

A

90% response rates

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49
Q

could be added to this treatment for hyperkeratotic lesions or to enhance penetration.
BOWEN’S DISEASE

A

Tazarotene

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50
Q

indications for Mohs microsurgery

A

Large, ill-defined lesions, or lesions in which preservation of normal tissue is critical

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51
Q

SCC in situ on the glans penis or prepuce

A

ERYTHROPLASIA OF QUEYRAT

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52
Q

ERYTHROPLASIA OF QUEYRAT

Caused by

A

HPV types (16, 18, 31, 35).

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53
Q

Single or multiple well-circumscribed, erythematous, moist, velvety or smooth, red-surfaced plaques on the glans penis

A

ERYTHROPLASIA OF QUEYRAT

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54
Q

ERYTHROPLASIA OF QUEYRAT

Most commonly affects

A

uncircumcised men, usually over 40 y/o

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55
Q

resulving scc whihch is more aggressive

erythroplasia of queyrat
vs BOWEN’S DISEASE

A

ERYTHROPLASIA OF QUEYRAT

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56
Q

ERYTHROPLASIA OF QUEYRAT

Factors suggest that a biopsy is indicated:

A

The lesion is fixed (does not move or resolve).

The patient lacks other stigmata of psoriasis or another skin disease that could affect the glans penis

The patient’s sexual partner has cervical dysplasia.

The lesion does not resolve with effective topical therapy for irritant balanitis, candidiasis, and psoriasis

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57
Q

Once the diagnosis of SCC in situ of the penis is made, the patient’s sex partner(s) should be referred for evaluation because

A

Sexual partners of men with SCC of the penis are more likely to develop preinvasive and invasive cancer of the cervix or anus

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58
Q

ERYTHROPLASIA OF QUEYRAT

tx

A

Topical 5% 5-FU cream applied once a day under occlusion (with the foreskin or a condom)

Imiquimod cream 5%, applied between once a day and three times a week

excision, laser treatments

photodynamic therapy

Radiation therapy

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59
Q

zoon’s balanitis

A

balanitis plasmacellularis

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60
Q

a benign inflammatory lesion of the glans penis, which histologically demonstrates a plasma cell-rich infiltrate

A

balanitis plasmacellularis

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61
Q

red patch, which is usually sharply demarcated and usually on the inner surface of the prepuce or on the glans penis

lesion is erythematous, moist, and shiny.

It occurs as a single lesion, but may consist of several confluent macules

asymptomatic adenopathy

A

balanitis plasmacellularis

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62
Q

most often affected

balanitis plasmacellularis

A

Uncircumcised men from ages 24 to 85 are most often affected

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63
Q

counterpart of balanitis in women.

A

Vulvitis chronica plasmacellularis

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64
Q

The vulva shows a striking lacquer-like luster.

Erosions, punctate hemorrhage, synechiae, and a slate to ochre pigmentation may supervene

A

Vulvitis chronica plasmacellularis

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65
Q

same disease on the oral mucosa, lips, cheeks, and tongue (Vulvitis chronica plasmacellularis)

A

Plasmacytosis circumorificialis

66
Q

tx

plasmacellularis

A

Potent topical steroids, pimecrolimus cream 1%, tacrolimus ointment 0.1%, and imiquimod cream 5%

Circumcision

Laser ablation

67
Q

unilateral, sharply defined eczema caused by epidermal metastases from underlying ductal adenocarcinoma of the breast

A

Paget’s disease

68
Q

Begins as an erythematous crusted or keratotic, circumscribed pruritic patches

Later become infiltrated and ulcerated

Nipple may or may not be retracted

A

Paget’s disease

69
Q

large, round, clear-staining cells with large nuclei, appearing singly or in small nests between the squamous cells

A

Paget cells

70
Q

paget cells

mitoses

A

Paget’s disease

71
Q

acanthosis is present, the granular layer is preserved, and there is no parakeratosis, but atypical cells may be “spat out” into the stratum corneum

a layer of basal cells separates the Paget cells from the basement membrane and is seen crushed beneath the nests of Paget cells.

A

PD

72
Q

how to differentiate atopic dermatitis from PD

A

Presence of bilateral lesion, suggesting a benign process

73
Q

tx PD

A

Surgical excision with margins and radiotherapy

Mastectomy

74
Q

EXTRAMAMMARY PAGET’S DISEASE

affects adults, usually between

A

65 and 70 years of age

75
Q

Lesions are similar to those of the nipple but may go undiagnosed longer and thus become more extensive

A nonhealing eczematous patch that persists for years

Intense pruritus and sometimes pain

Bleeding is a late sign

A

EXTRAMAMMARY PAGET’S DISEASE

76
Q

tx EMPD

A

Mohs’ microsurgery

CO2 laser

Monitor CEA levels for disease response

77
Q

PRIMARY CUTANEOUS T- CELL LYMPHOMAS

A

Mycosis fungiodes

Pagetoid Reticulosis

Sezary Syndrome

Granulomatous Slack Skin

Lymphomatoid Papulosis

78
Q

in order to be called PRIMARY

A

the skin lesion should appear first before lymphadenopathy

79
Q

A malignant neoplasm of T- lymphocyte origin, almost always a memory T-helper cell
M>F

A

MYCOSIS FUNGIODES

80
Q

Macules or slightly infiltrated patches or plaques 1-5 cm in diameter

May be generalized or begin localized to one area, then spread

Sites: lower, abdomen, buttocks and upper thighs and breast

Lesions may have an atrophic surface or mottled dyspigmentation and telangiectasis

A

EARLY PATCH/ PLAQUE STAGE

81
Q

Lesions are more infiltrated and may resemble psoriasis or a subacute dermatitis

Palms and soles may be involved with hyperkarotic, psoriasiform, and fissuring plaques

A

PLAQUE STAGE

82
Q

Infiltration becomes more marked and leads to discoid patches or extensive plaques, which may eventually coalesce but with normal skin interspersed

A

PLAQUE STAGE

83
Q

More advanced, painful superficial ulcerations may occur with enlarged, nontender, firm and freely movable lymph nodes

A

PLAQUE STAGE

84
Q

Large nodules on infiltrated apparently healthy skin

plaques

and

on

Nodules break down and form deep oval ulcers with bases covered with a necrotic grayish substance and rolled edges

Sites: trunk, anywhere on the skin, mouth and upper respiratory tract

A

TUMOR STAGE

85
Q

Generalized
exfoliative

process

with

universal redness

Hair is scanty, nails dystrophic, palms and soles hyperkeratotic and at times, may have generalized hypermigmentation

A

erythrodermic type

86
Q

Over time, the lesions may become infiltrated plaques

A

plaque stage

87
Q

Tumors masy eventually appear

A

tumor stage

88
Q

tx mycosis fungoides

A

Topical corticosteroids

Topical nitrogen mustard

Topical carrmustine

Ultraviolet therapy

Radiation treatment - usual

Biologic response modifiers: interferon

Retinoids

Systemic chemotherapy – usual

89
Q

leukemic phase of mycosis fungoides

A

SEZARY SYNDROME

90
Q

Leukocytosis >30,000/mm3

Sezary cells

A

SEZARY SYNDROME

91
Q

helper T cells with deeply convoluted nuclei) in the peripheral blood, skin and lymph nodes

A

sezary cells

92
Q

tx

sezary syndrome

A

Methrotrexate

Photophoresis

Interferon alfa

Retinoids

Chlorambucil and prednisone

Fludarabine

93
Q

SQUAMOUS CELL CARCINOMA

face hands

A

Face: BCC > SCC

Hands: SCC > BCC

94
Q

The lesion may be superficial, discrete and hard, asnd arises from an indurated, rounded, elevated base: dull red and contains telangiectases

A

SQUAMOUS CELL CARCINOMA

95
Q

On early stage, tumor is localized, elevated and freely movable

Later it gradually becomes more diffuse, depressed and fixed -> invades underlying tissue

Advanced lesions, the surface may be cauliflower-like, composed of densely packed, filamentous projections, between which are clefts filled with viscid, purulent, malodorous exudate

A

SQUAMOUS CELL CARCINOMA

96
Q

On the lower lip, SCC often develops on

A

actinic cheilitis

97
Q

SCC important hx

A

History of smoking in lips

98
Q

lower lip upper lip

scc

A

Lower lip SCC > upper lip

99
Q

gender

SCC

A

M>F

100
Q

SCC etiology

A

Ultraviolet light

Thermal injury to the skin

Chemicals such as polycyclic aromatic hydrocarbons, arsenic, paraffin, creosote, anthracene, tobacco smoke tars and chromates

Chronic radiation dermatitis from x-radiation or radium

HPV esp. types 16, 18, 30, 33

Marjolin’s ulcer

Certain dermatoses, such as porokeratosis of Mibelli, nevus sebaceous, and lichen sclerosus et atrophicus

101
Q

most cells are well-diffrentiated

SCC

A

Grade 1

102
Q

undifferentiated or anaplastic

SCC

A

Grade IV

103
Q

SCC

metastases

A

0.5-5.2%

104
Q

SCC

Risk of metastasis rises for lesions

A

larger than 2 cm, thicker than 4mm and lip lesions thicker than 8 mm

105
Q

tx scc

A

Moh’s surgical technique

Radiation therapy

Retinoids, electrochemotherapy, photodynamic therapy, beta carotene, interferons and intratumoral chemotherapy

Metastatic disease: cisplatin and doxorubicin or bleomycin

PREVENTION: sunscreens

106
Q

A tumor composed of one or few small, waxy, semitransluscent nodules forming around a central depression that may or may not be ulcerated. Crusted and bleeding

A

BASAL CELL CARCINOMA

107
Q

edge of the larger lesions has a characteristic rolled border

Telangiectases course through the lesion

Bleeding on slight injury is common

Rarely metastasize

Most frequently found on the face (85% are found in the head and neck) and esp. on the nose (25-30%)

A

BASAL CELL CARCINOMA

108
Q

Dry, psoriasiform, scaly lesions on the trunk and limbs that have little tendency to invade or ulcerate, and enlarge only very slowly

A

Superficial BCC

109
Q

May grow to 10-15cm without ulceration

Erythematous plaques with a threadlike raised border, telangiectasia and atrophy

A

Superficial BCC

110
Q

hx Superficial BCC

A

History of arsenic ingestion over a long period

111
Q

9-11% of BCCs

A

Superficial BCC

112
Q

6% of BCCs

A

Pigmented BCC

113
Q

Has all features of the basal type, with brown or black pigmentation, usually on the trunk

More frequent in dark-complected persons

Caused by arsenic ingestion

A

Pigmented BCC

114
Q

Premalignant fibroepithelial tumor

Elevated, skin-colored, sessile lesion on the lower trunk, lumbosacral area, groin and thigh and may be as large as 7 cm

A

FIBROEPITHELIOMA OF PINKUS

115
Q

Superficial and resembles a fibroma or papilloma

May overlie breast carcinomas

A

FIBROEPITHELIOMA OF PINKUS

116
Q

dome shaped, blue-gray cystic nodules clinically similar to eccrine and apocrine hidrocystoma

4-8% of all BCCs

A

CYSTIC BASAL CELL EPITHELIOMA

117
Q

Waxy sclerotic plaques in the head and neck with absence of a rolled edge, ulceration and crsting

Telangiectasia is prominent

A

MORPHEA-LIKE EPITHELIOMA

118
Q

Resistant to radiation and electrocautery

2% of all BCCs

A

MORPHEA-LIKE EPITHELIOMA

119
Q

Resembles localized scleroderma that presents a cictricial surface with nests of active lesions that are usually ulcerated

A

Resistant to radiation and electrocautery

2% of all BCCs

120
Q

Fine waxy border or threadlike raised edge and telangiectasia present

Occurs amost exclusively on the cheeks

May be seen on the forehead

A

CICATRICIAL BCC / “FIELD FIRE EPITHELIOMA”

121
Q

CICATRICIAL BCC / “FIELD FIRE EPITHELIOMA”

tx

A

Excision: Moh’s icrosurgery or ionizing radiation therapy

122
Q

Deep ulcer that burrows into the subcutaneous tissue, cartilage and bone with the floor of the ulcer covered by viscid necrotic material

A

RODENT ULCER/ JACOB’S ULCER

123
Q

A neglected BCC which has formed an ulceration

A

RODENT ULCER/ JACOB’S ULCER

124
Q

BCC runs a chronic course, during which new nodules develop, crusts form and fall off, and the ulceration enlarges

As a rule, there is a tendency for the lesions to bleed without pain or other symptoms

A

RODENT ULCER/ JACOB’S ULCER

125
Q

RODENT ULCER/ JACOB’S ULCER

tx

A

Excision – lesions > 5-7mm

Moh’s microsurgery

Electrosurgery

Curettage

Ionizing radiation therapy

Topcial 5-FU

Cryosurgery

Laser therapy

126
Q

RODENT ULCER/ JACOB’S ULCER

prophylaxis

A

Sun avoidance

Sunscreens

127
Q

Originate from melanocyte at the dermo-epidermal junction

Half develop in preexisting nevi: other ½ appear spontaneously

A

MELANOMA

128
Q

ABCD criteria for recognizing early melanoma

A

A- Asymmetry

B – Border irregularity

C – Color variegation

D – Large Diameter >6mm

129
Q

etiology

melanoma

A

Light complexion

Light eyes (e. blue-eyed)

Blond or red hair

Occurrence of blistering sunburns in childhood

Heavy freckling

Tendency to tan poorly and sunburn easily

Chronically sun-exposed

130
Q

4 Melanoma Types

A

Lentigo Maligna

Superficially spreading melanoma

Acral-lentigious melanoma

Nodular melanoma

131
Q

melanoma in Situ, Noninvasive Melanoma

A

LENTIGO MALIGNA

132
Q

Begins as a tan macule that extends peripherally, with gradual uneven darkening irregular edge and color variegation, due to areas of regression

Gradually enlarges

A

LENTIGO MALIGNA

133
Q

After a radial growth period 5-20 years, downwards vertically growing melanoma usually develops within it

A

LENTIGO MALIGNA

134
Q

best evidence of malignant transformation

LENTIGO MALIGNA

A

Palpable nodule within the original macule

135
Q

5% of all melanomas

A

LENTIGO MALIGNA

136
Q

70% of all melanomas

Most common type

No preference for sun-damaged skin

Can occur in covered areas

A

SUPERFICIALLY SPEADING MELANOMA

137
Q

common site

SUPERFICIALLY SPEADING MELANOMA

A

Upper back for both sexes

Shin for women are the commonest sites

138
Q

Tendency to multicoloration with a notched border

A

SUPERFICIALLY SPEADING MELANOMA

139
Q

Horizontal or lateral growth into the adjoining epidermis continues for 1-5 years, before invasion into the dermis –shorter radial growth

A

SUPERFICIALLY SPEADING MELANOMA

140
Q

faster growth than the Lentigo Melanoma

A

SUPERFICIALLY SPEADING MELANOMA

141
Q

10% of all melanomas

Most common type among Hispanics and Native Americans

Japanese,

black,

A

ACRAL-LENTIGINOUS MELANOMA

142
Q

ACRAL-LENTIGINOUS MELANOMA

Most common site in blacks:

A

foot ( 60% with subungual or plantar lesions)

143
Q

An irregular enlarging black macule on the palms or sole, digit, tip or nail fold or bed

A

ACRAL-LENTIGINOUS MELANOMA

144
Q

black discoloration of the proximal nail fold at the end of a pigmented streak (melanonycjoa striata) may signal inv. Of nail matrix

Sign of malignancy in nail matrix

A

Hutchinson’s sign

145
Q

Dark macule/patch in subungual area

A

Ask for hx of trauma – possible hematoma

Do nail biopsy – punch biopsy of the nail beds

Partial ungiectomy

146
Q

Pigmented papule or nodule of varying size

Arise without an apparent radial growth phase

No radial growth, only vertical growth

15% of all melanomas

A

NODULAR MELANOMA

147
Q

Sun-exposed areas of the head, neck and trunk

May grow much larger and become papillary fungoid or ulcerated

Bleeding is usually a late sign

A

NODULAR MELANOMA

148
Q

is the most common cause of death

melanoma

A

CNS metastasis

149
Q

staging melanioma

A

clark

150
Q

melanoma in situ

A

Clark level I (pTis)

151
Q

tumors 0.75 mm or < in Thickness

but invades the papillary dermis

A

Clark level II (pTI)

152
Q

> 0.75 mm thick but not >1.5mm thick

tumors that invade to the papillary reticular dermal interface

A

Clark level III (pT2)

153
Q

> 1.5mm thick but <4mm thick and/or

tumors that invade the reticular dermis

A

Clark level IV (pT3)

154
Q

There is involvement of subcutaneous tissue

A

Clark level IV (pT3):

155
Q

> 4mm thick and /or

tumors that invade the subQ tissue and or

satellites within 2 cm of the primary tumor

A

Clark level V (pT4):

156
Q

melanoma

Overall survival rate is___% for early diagnosis

A

80

157
Q

melanoma
(+) regional LN disease
survival

A

30-35%

158
Q

melanoma

Distant metastases: 5- year survival rate is

A

10%

159
Q

3 Most common skin CA

A

BCC (basal cell carcinoma)

o

Least rate of mets

SCC (squamous cell carcinoma)

Melanoma

o

Fastest rate of metastasis

160
Q

regression melanoma

A

poorer prognosis

161
Q

Presence of leukoderma at distal sites

A

Leukoderma is (+) immunologically mediated response to melanin

Paradoxical effect: can indicate metastasis but it has better prognosis because the immune system is already attacking malignant cells

162
Q

CNS metastasis

melanoma tx

A

Radiation therapy

Dermatology (6 decks)

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