Premalignant and Malignant Skin Tumors 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
2
Q
most common epithelial precancerous lesion
A
actinic keratosis
3
Q
actinic keratosis aka
A
solar keratosis
4
Q
actinic keratosis
____% develop malignancy
A
20 to 25% develop to malignancy especially on forearm of white males
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
6
Q
six histologic types of
actinic keratosis:
A
Hypertrophic
Atrophic
Bowenoid
Acantholytic
Pigmented
Lichenoid
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
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
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
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
11
Q
tx actinic keratosis
for extensive, broad, or numerous lesions
A
topical 0.5% 5-FU or imiquimod 5% cream
12
Q
is an interferon (IFN) inducer and apparently eradicates actinic keratoses by producing a local immunologic reaction against the lesion
A
Imiquimod
13
Q
treatment of choice for severe actinic chelitis
A
CO2 laser
14
Q
prevent further solar damage
A
Low fat diet and daily use of sunscreen
15
Q
Cornu cutaneum
A
cutaneous horn
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
17
Q
cutaneous horn tx
A
Excision biopsy with histologic examination of the base
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%
19
Q
_______% cutaneous horn may overlie premalignant keratoses
A
20–30%
20
Q
20% m utaneous horn ay overlie
A
SCCs or BCCs
21
Q
1/3 of_______ associated with CA
A
penile horns
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
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
24
Q
Leukoplakia is found chiefly in
A
men >40 y/o
25
LEUKOPLAKIA
| May transform to CA in
1-20 years
26
leukoplakia
| if ulceration, red areas, or erosions are scattered throughout, the lesion is most likely
precancerous
27
leukoplakia
if ulceration, red areas, or erosions are scattered throughout, the lesion is most likely precancerous.
this is indicated
biopsy
28
leukoplakia -> CA
| rapid course of transformation in
immunosuppressed transplant patients
29
leukoplakia
| Lesion on the Lip: related to
chronic actinic chelitis
30
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
chronic actinic chelitis
31
term used to describe white, corrugated plaques that occur primarily on the sides of the tongue of patients with AIDS
a virally induced lesion
Oral Hairy Leukoplakia
32
occur in obese women after menopause as grayish white, thickened prurity patches that may become fissured and edematous from constant rubbing and scratching
Leukoplakia of the Vulva
33
Leukoplakia of the Vulva
| differentiated from lichen planus by
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
34
Leukoplakia of the Vulva
| most frequently confused with
lichen sclerosus et atrophicus and other vulval atrophies
35
LEUKOPLAKIA
| etiology
Excessive use of poorly fitting dentures
Sharp and chipped teeth
Poor oral hygiene
Tobacco smoking, reverse smoking
Betel nut chewing
Alcohol
36
______% transformation rate of intraoral leukoplakia into SCC with the red lesions having a higher risk
6-10%
37
Predictors of a higher risk of SC carcinoma development (from leukoplakia) include
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
38
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.
Aneuploid leukoplakia
39
leukoplakia
| tx
Complete removal: fulguration, simple excision, crytherapy and CO2 laser
Stop use of tobacco
Isotretinoin 1-2 mg/kg/day for 3 months
5- FU
40
Squamous Cell Carcinoma in situ
BOWEN’S DISEASE
41
An intraepidermal SCC, may become invasive
BOWEN’S DISEASE
42
Lesion looks like an eczema
scaling erythematous
When intraepithelial growth becomes invasive, nodular infiltration forms, which becomes ulcerated and fungating
BOWEN’S DISEASE
43
Sites
| BOWEN’S DISEASE
anywhere on the body, mucous membranes
44
Possible agents that can induce BD:
HPV of certain types arsenic exposure sun exposure
45
The squamous carcinoma that evolves from BD tends to be
more aggressive than SCC arising in actinic keratosis.
46
the lesions are multicentric and behave like genital warts
Differential Diagnosis
BOWEN’S DISEASE
Bowenoid Papulosis
47
BOWEN’S DISEASE
| Treatment:
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
48
Imiquimod 5% cream, applied once a day for up to 16 weeks
BOWEN’S DISEASE
response rate
90% response rates
49
could be added to this treatment for hyperkeratotic lesions or to enhance penetration.
BOWEN’S DISEASE
Tazarotene
50
indications for Mohs microsurgery
Large, ill-defined lesions, or lesions in which preservation of normal tissue is critical
51
SCC in situ on the glans penis or prepuce
ERYTHROPLASIA OF QUEYRAT
52
ERYTHROPLASIA OF QUEYRAT
| Caused by
HPV types (16, 18, 31, 35).
53
Single or multiple well-circumscribed, erythematous, moist, velvety or smooth, red-surfaced plaques on the glans penis
ERYTHROPLASIA OF QUEYRAT
54
ERYTHROPLASIA OF QUEYRAT
| Most commonly affects
uncircumcised men, usually over 40 y/o
55
resulving scc whihch is more aggressive
erythroplasia of queyrat
vs BOWEN’S DISEASE
ERYTHROPLASIA OF QUEYRAT
56
ERYTHROPLASIA OF QUEYRAT
| Factors suggest that a biopsy is indicated:
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
57
Once the diagnosis of SCC in situ of the penis is made, the patient’s sex partner(s) should be referred for evaluation because
Sexual partners of men with SCC of the penis are more likely to develop preinvasive and invasive cancer of the cervix or anus
58
ERYTHROPLASIA OF QUEYRAT
| tx
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
59
zoon’s balanitis
balanitis plasmacellularis
60
a benign inflammatory lesion of the glans penis, which histologically demonstrates a plasma cell-rich infiltrate
balanitis plasmacellularis
61
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
balanitis plasmacellularis
62
most often affected
| balanitis plasmacellularis
Uncircumcised men from ages 24 to 85 are most often affected
63
counterpart of balanitis in women.
Vulvitis chronica plasmacellularis
64
The vulva shows a striking lacquer-like luster.
Erosions, punctate hemorrhage, synechiae, and a slate to ochre pigmentation may supervene
Vulvitis chronica plasmacellularis
65
same disease on the oral mucosa, lips, cheeks, and tongue (Vulvitis chronica plasmacellularis)
Plasmacytosis circumorificialis
66
tx
| plasmacellularis
Potent topical steroids, pimecrolimus cream 1%, tacrolimus ointment 0.1%, and imiquimod cream 5%
Circumcision
Laser ablation
67
unilateral, sharply defined eczema caused by epidermal metastases from underlying ductal adenocarcinoma of the breast
Paget’s disease
68
Begins as an erythematous crusted or keratotic, circumscribed pruritic patches
Later become infiltrated and ulcerated
Nipple may or may not be retracted
Paget’s disease
69
large, round, clear-staining cells with large nuclei, appearing singly or in small nests between the squamous cells
Paget cells
70
paget cells
| mitoses
Paget’s disease
71
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.
PD
72
how to differentiate atopic dermatitis from PD
Presence of bilateral lesion, suggesting a benign process
73
tx PD
Surgical excision with margins and radiotherapy
Mastectomy
74
EXTRAMAMMARY PAGET’S DISEASE
| affects adults, usually between
65 and 70 years of age
75
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
EXTRAMAMMARY PAGET’S DISEASE
76
tx EMPD
Mohs’ microsurgery
CO2 laser
Monitor CEA levels for disease response
77
PRIMARY CUTANEOUS T- CELL LYMPHOMAS
Mycosis fungiodes
Pagetoid Reticulosis
Sezary Syndrome
Granulomatous Slack Skin
Lymphomatoid Papulosis
78
in order to be called PRIMARY
the skin lesion should appear first before lymphadenopathy
79
A malignant neoplasm of T- lymphocyte origin, almost always a memory T-helper cell
M>F
MYCOSIS FUNGIODES
80
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
EARLY PATCH/ PLAQUE STAGE
81
Lesions are more infiltrated and may resemble psoriasis or a subacute dermatitis
Palms and soles may be involved with hyperkarotic, psoriasiform, and fissuring plaques
PLAQUE STAGE
82
Infiltration becomes more marked and leads to discoid patches or extensive plaques, which may eventually coalesce but with normal skin interspersed
PLAQUE STAGE
83
More advanced, painful superficial ulcerations may occur with enlarged, nontender, firm and freely movable lymph nodes
PLAQUE STAGE
84
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
TUMOR STAGE
85
Generalized
exfoliative
process
with
universal redness
Hair is scanty, nails dystrophic, palms and soles hyperkeratotic and at times, may have generalized hypermigmentation
erythrodermic type
86
Over time, the lesions may become infiltrated plaques
plaque stage
87
Tumors masy eventually appear
tumor stage
88
tx mycosis fungoides
Topical corticosteroids
Topical nitrogen mustard
Topical carrmustine
Ultraviolet therapy
Radiation treatment - usual
Biologic response modifiers: interferon
Retinoids
Systemic chemotherapy – usual
89
leukemic phase of mycosis fungoides
SEZARY SYNDROME
90
Leukocytosis >30,000/mm3
Sezary cells
SEZARY SYNDROME
91
helper T cells with deeply convoluted nuclei) in the peripheral blood, skin and lymph nodes
sezary cells
92
tx
| sezary syndrome
Methrotrexate
Photophoresis
Interferon alfa
Retinoids
Chlorambucil and prednisone
Fludarabine
93
SQUAMOUS CELL CARCINOMA
| face hands
Face: BCC > SCC
Hands: SCC > BCC
94
The lesion may be superficial, discrete and hard, asnd arises from an indurated, rounded, elevated base: dull red and contains telangiectases
SQUAMOUS CELL CARCINOMA
95
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
SQUAMOUS CELL CARCINOMA
96
On the lower lip, SCC often develops on
actinic cheilitis
97
SCC important hx
History of smoking in lips
98
lower lip upper lip
| scc
Lower lip SCC > upper lip
99
gender
| SCC
M>F
100
SCC etiology
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
most cells are well-diffrentiated
| SCC
Grade 1
102
undifferentiated or anaplastic
| SCC
Grade IV
103
SCC
| metastases
0.5-5.2%
104
SCC
| Risk of metastasis rises for lesions
larger than 2 cm, thicker than 4mm and lip lesions thicker than 8 mm
105
tx scc
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
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
BASAL CELL CARCINOMA
107
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%)
BASAL CELL CARCINOMA
108
Dry, psoriasiform, scaly lesions on the trunk and limbs that have little tendency to invade or ulcerate, and enlarge only very slowly
Superficial BCC
109
May grow to 10-15cm without ulceration
Erythematous plaques with a threadlike raised border, telangiectasia and atrophy
Superficial BCC
110
hx Superficial BCC
History of arsenic ingestion over a long period
111
9-11% of BCCs
Superficial BCC
112
6% of BCCs
Pigmented BCC
113
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
Pigmented BCC
114
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
FIBROEPITHELIOMA OF PINKUS
115
Superficial and resembles a fibroma or papilloma
May overlie breast carcinomas
FIBROEPITHELIOMA OF PINKUS
116
dome shaped, blue-gray cystic nodules clinically similar to eccrine and apocrine hidrocystoma
4-8% of all BCCs
CYSTIC BASAL CELL EPITHELIOMA
117
Waxy sclerotic plaques in the head and neck with absence of a rolled edge, ulceration and crsting
Telangiectasia is prominent
MORPHEA-LIKE EPITHELIOMA
118
Resistant to radiation and electrocautery
2% of all BCCs
MORPHEA-LIKE EPITHELIOMA
119
Resembles localized scleroderma that presents a cictricial surface with nests of active lesions that are usually ulcerated
Resistant to radiation and electrocautery
2% of all BCCs
120
Fine waxy border or threadlike raised edge and telangiectasia present
Occurs amost exclusively on the cheeks
May be seen on the forehead
CICATRICIAL BCC / “FIELD FIRE EPITHELIOMA”
121
CICATRICIAL BCC / “FIELD FIRE EPITHELIOMA”
| tx
Excision: Moh’s icrosurgery or ionizing radiation therapy
122
Deep ulcer that burrows into the subcutaneous tissue, cartilage and bone with the floor of the ulcer covered by viscid necrotic material
RODENT ULCER/ JACOB’S ULCER
123
A neglected BCC which has formed an ulceration
RODENT ULCER/ JACOB’S ULCER
124
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
RODENT ULCER/ JACOB’S ULCER
125
RODENT ULCER/ JACOB’S ULCER
| tx
Excision – lesions > 5-7mm
Moh’s microsurgery
Electrosurgery
Curettage
Ionizing radiation therapy
Topcial 5-FU
Cryosurgery
Laser therapy
126
RODENT ULCER/ JACOB’S ULCER
| prophylaxis
Sun avoidance
Sunscreens
127
Originate from melanocyte at the dermo-epidermal junction
Half develop in preexisting nevi: other ½ appear spontaneously
MELANOMA
128
ABCD criteria for recognizing early melanoma
A- Asymmetry
B – Border irregularity
C – Color variegation
D – Large Diameter >6mm
129
etiology
| melanoma
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
4 Melanoma Types
Lentigo Maligna
Superficially spreading melanoma
Acral-lentigious melanoma
Nodular melanoma
131
melanoma in Situ, Noninvasive Melanoma
LENTIGO MALIGNA
132
Begins as a tan macule that extends peripherally, with gradual uneven darkening irregular edge and color variegation, due to areas of regression
Gradually enlarges
LENTIGO MALIGNA
133
After a radial growth period 5-20 years, downwards vertically growing melanoma usually develops within it
LENTIGO MALIGNA
134
best evidence of malignant transformation
| LENTIGO MALIGNA
Palpable nodule within the original macule
135
5% of all melanomas
LENTIGO MALIGNA
136
70% of all melanomas
Most common type
No preference for sun-damaged skin
Can occur in covered areas
SUPERFICIALLY SPEADING MELANOMA
137
common site
| SUPERFICIALLY SPEADING MELANOMA
Upper back for both sexes
Shin for women are the commonest sites
138
Tendency to multicoloration with a notched border
SUPERFICIALLY SPEADING MELANOMA
139
Horizontal or lateral growth into the adjoining epidermis continues for 1-5 years, before invasion into the dermis –shorter radial growth
SUPERFICIALLY SPEADING MELANOMA
140
faster growth than the Lentigo Melanoma
SUPERFICIALLY SPEADING MELANOMA
141
10% of all melanomas
Most common type among Hispanics and Native Americans
Japanese,
black,
ACRAL-LENTIGINOUS MELANOMA
142
ACRAL-LENTIGINOUS MELANOMA
Most common site in blacks:
foot ( 60% with subungual or plantar lesions)
143
An irregular enlarging black macule on the palms or sole, digit, tip or nail fold or bed
ACRAL-LENTIGINOUS MELANOMA
144
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
Hutchinson’s sign
145
Dark macule/patch in subungual area
Ask for hx of trauma – possible hematoma
Do nail biopsy – punch biopsy of the nail beds
Partial ungiectomy
146
Pigmented papule or nodule of varying size
Arise without an apparent radial growth phase
No radial growth, only vertical growth
15% of all melanomas
NODULAR MELANOMA
147
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
NODULAR MELANOMA
148
is the most common cause of death
melanoma
CNS metastasis
149
staging melanioma
clark
150
melanoma in situ
Clark level I (pTis)
151
tumors 0.75 mm or < in Thickness
but invades the papillary dermis
Clark level II (pTI)
152
>0.75 mm thick but not >1.5mm thick
tumors that invade to the papillary reticular dermal interface
Clark level III (pT2)
153
>1.5mm thick but <4mm thick and/or
tumors that invade the reticular dermis
Clark level IV (pT3)
154
There is involvement of subcutaneous tissue
Clark level IV (pT3):
155
> 4mm thick and /or
tumors that invade the subQ tissue and or
satellites within 2 cm of the primary tumor
Clark level V (pT4):
156
melanoma
| Overall survival rate is___% for early diagnosis
80
157
melanoma
(+) regional LN disease
survival
30-35%
158
melanoma
| Distant metastases: 5- year survival rate is
10%
159
3 Most common skin CA
BCC (basal cell carcinoma)
o
Least rate of mets
SCC (squamous cell carcinoma)
Melanoma
o
Fastest rate of metastasis
160
regression melanoma
poorer prognosis
161
Presence of leukoderma at distal sites
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
CNS metastasis
| melanoma tx
Radiation therapy
