1. Skin Tumors
Seyed Morteza Mahmoodi

3. Skin
• Weight - 16% TBW
• Surf. Area - 2sq.m
• Thickness - 0.5-4mm
• Layers -Epidermis
- Basement membrane
-Dermis
- Subcutaneous Layer

4. Composition of skin

6. Epidermis
o Thickness - 0.07-12 mm
o Stratified sq. epithelium
o Different layers
Stratum corneum
(Stratum lucidum)
Stratum granulosum
Stratum spinosum
Stratum basale

8. Cells of the Epidermis
 Melanocytes
 basal layer protect against UV irradiation
 Racial differences are due to variation in
melanin production, not melanocyte numbers
 Merkel cells sensation
 Langerhans’ cells
 Dendritic cells
 Antigen-presenting cells

9. Dermis
 Thickness - 0.6-3mm
 2 layers papillary
reticular
 Skin appendages
 Blood vessels
 Nerve endings
 Cells: Mast cells and Histiocytes

12. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Skin tags
 Syringoma
 Others

14. Seborrheic Keratosis
 One of the most common benign tumors of the skin
 Often confused with malignancies
 Seborrheic keratoses unusual before age 30
 Most people develop at least one seborrheic
keratosis in their lifetime
 Seborrheic keratoses are cosmetically bothersome,
but may also be subject to irritation and
traumatization,

15. Seborrheic Keratosis

16. Clinical Findings
 Typically multiple
 Most often seen on the trunk
 The size and surface appearance of the lesions
vary considerably
 Most are 2 mm to 2.0 cm, although larger lesions
are common
 Lesions may be flat or raised
 The surface may be smooth, velvety, or
verrucous.

17. Color and structure
 The color of lesions is extremely variable,
 Lesions tend to be sharply demarcated,
oval, and often oriented along skin
cleavage lines
 Most have a “stuck-on” appearance and
waxy texture. The surface tends to
crumble when picked.
 Raised or pedunculated seborrheic
keratoses may be indistinguishable from
skin tags and compound melanocytic nevi.

18. Irritated seborrheic keratosis
 When inflamed, SKs become slightly swollen and develop
an irregular, red flare in the surrounding skin.
 Itching and erythema can then appear spontaneously in
other SKs that have not been manipulated and in areas
without SKs.
 With continued inflammation, the SK loses most of its
normal characteristics and becomes a bright red, oozing
mass with a friable surface that itches intensely and
resembles an advanced melanoma or a pyogenic
granuloma.

19. Seborrheic keratosis vs. Melanoma
 SKs can show many of the features of a
malignant melanoma, including an irregular
border and variable pigmentation.
 The key differential diagnostic features are the
surface characteristics.
 Melanomas have a smooth surface that varies in
elevation and in color, density, and shade.
 SKs preserve a uniform appearance over their
entire surface.
 Many SKs occur in sun-exposed areas.

20. Clinical variants
Dermatosis papulosa nigra
Stucco keratoses

21. Treatment
 Cryosurgery is effective for flat to
minimally raised lesions
 Thicker lesions are best removed by
cautery and curettage under local
anesthesia.
 Hypopigmentation or hyperpigmentation
are possible side effects
 Residual scarring is minimal. Applying
gentle pressure to the surrounding skin
often provides enough tension to allow for
easy curettage of lesions.

22. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Coetaneous tags
 Syringoma

23. Moles
 Moles (melanocytic naevi) as they are due to a
proliferation of melanocytes
 Moles may be flat or protruding. They vary in
colour from pink to dark brown or black.
 The number of moles a person has depends on
genetic factors and on sun exposure.
 Melanocytic naevi may be present at birth
(congenital) but more usually begin to grow
during childhood although new ones can appear
at any age, sometimes in crops

27. Variants
 Junctional naevi
 compound naevi
 Intradermal naevi
 Cellular naevi.
 Blue naevi
 Moles may darken following sun exposure
or during pregnancy.
 During adulthood they often lose their
pigmentation, and they may even
disappear in old age.

28. Risk of melanoma
 Malignant melanoma sometimes develops within
congenital melanocytic naevi.
 The risk in a small or medium-sized mole is under
1%
 Melanoma is more likely in the giant naevi
(perhaps about 5% over a lifetime) especially in
those that lie across the spine; the cancer can
start in the skin or within the central nervous
system. It is then very difficult to detect and
treat.

29. Removal of moles
 Although most moles are harmless and can be
safely left alone, moles may be treated under the
following conditions:
 Possible malignancy: a mole that has bled, has
an unusual shape, is growing rapidly or changing
colour.
 Nuisance moles: a mole that is irritated by
clothing, comb or razor.
 Cosmetic reasons: the mole is unsightly.

30. Removal
 Shave biopsy
 scalpel or by electrosurgery. The wound heals to leave a
flat white mark, but sometimes the colour remains the
same as the original mole.
 Excision biopsy
 if the mole is a flat one or melanoma is suspected

31. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Coetaneous tags
 Syringoma

33. Dermatofibroma
 Dermatofibroma is a common, benign,
dermal papule.
 The etiology is unknown.
 Pontaneous benign neoplastic process Vs.
reactive hyperplasia in response to injury
or bite
 These lesions occur more often in women
 Most are asymptomatic, but itching and
tenderness may occur occasionally

34. Clinical findings
 Dermatofibromas discrete firm dermal papules, 3-
7 mm in diameter.
 Most are dome shaped
 Dermatofibromas typically flesh colored to pink
with a poorly defined rim of tan to brown
pigmentation
 Larger ( >3cm) lesions can be worrisome and
may require a biopsy for definitive diagnosis
 Dermatofibromas should be stable in size,
appearance, and color.
 If they are not, they should be biopsied to
confirm their benign nature.

35. Dermatofibroma
Palpation
 The lesion is fixed within the skin, but movable over the
underlying subcutaneous fat. On palpation, the lesion feels
like a firm button. Pinching a dome-shaped dermatofibroma
between two fingers causes the lesion to retract and dimple
below the level of surrounding skin.
Pigmented variant
 Rarely, lesions may be blue to black in color as a result of
hemosiderin deposition, which may resemble melanoma.
The surface may be smooth and shiny to scaly or
excoriated.
Location/Region
 Although dermatofibromas may arise on any cutaneous
surface, most are found randomly distributed on the
extremities. Lesions are usually solitary, however, multiple
lesions are not uncommon. Rarely, dermatofibromas occur
on the palms or the soles. Dermatofibromas should be
stable in size, appearance, and color

39. Treatment
 Dermatofibromas are benign skin tumors
that do not require treatment unless they
are symptomatic, repeatedly traumatized,
or cosmetically bothersome.
 Surgical excision with primary closure is
the treatment of choice for symptomatic
lesions.
 If incompletely excised, the patient
should be warned of possible recurrence.

40. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Pilar cyst
 Keratoacanthoma
 Epidermal cyst
 Coetaneous tags
 Syringoma
 Others

42. Pilar Cyst
 A pilar cyst is a firm, subcutaneous,
keratin-filled cyst originating from the
outer root sheath of the hair follicle.
 Roughly 90% of pilar cysts are found on
the scalp, with the remaining 10%
occurring on the face, neck, back, and
scrotum.
 The epithelium of the outer root sheath
undergoes a different form of
keratinization than cutaneous epithelium.

43. Clinical findings
 The surface is smooth and dome-shaped.
 Pilar cysts may be difficult to distinguish from epidermal
cysts clinically, except by location.
 Both present as a firm, subcutaneous nodules ranging
from 0.5 to 5.0 cm.
 No central punctum is seen over a pilar cyst, as is found
over an epidermal cyst.
 When dissected, a pilar cyst possesses a tough, white-gray
wall that is more resistant to tearing than the wall of an
epidermal cyst.
 The pilar cyst wall separates easily and cleanly from the
surrounding dermis.
 If a pilar cyst ruptures, the area becomes inflamed, red,
and tender and boggy on palpation.

45. Clinical findings
 Pilar cysts almost always develop after puberty.
 The tendency to develop pilar cysts often has an
autosomal dominant inheritance.
 Pilar cysts are multiple in 70% of patients who
have them.
 Pilar cysts persist indefinitely and slowly grow to
a stable size unless they rupture.
 Pilar cysts rupture less frequently than epidermal
cysts, presumably because the pilar cyst
possesses a thicker wall.
 Rupture usually results from an external trauma.
 A brisk foreign body inflammatory reaction
follows and can be quite painful and resembles a
furuncle.

46. Clinical findings pilar cyst
 Large cysts may be cosmetically
objectionable.
 Some cysts are so large and tender, they
may interfere with wearing hats and
helmets.
 Acute inflammation after rupture is often
misdiagnosed as infection.
 Antibiotics are of little value in such cases.
 Incision and drainage under local
anesthesia improve comfort and limit
scarring.
 Elective excision before rupture prevents

47. Treatment
 Pilar cysts are easily removed with excision under local
anesthesia.
 An incision is made over the cyst, exposing the cyst’s
glossy white external surface.
 The cyst wall is freed easily from the surrounding
connective tissue by blunt dissection.
 At this stage, smaller cysts may be expressed intact up
through the incision by steady, firm pressure on each side
of the incision.
 The incised cyst wall is clamped, and through a
combination of gentle traction and pressure on each side of
the incision, the now smaller, partially emptied cyst is
delivered through the incision.
 Larger cysts, which cannot be expressed in this manner,
should be incised and their contents removed by curettage.
 Sutures may be needed to close the incision site.

48. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Pilar cyst
 Keratoacanthoma
 Epidermal cyst
 Cutaneous tags
 Syringoma
 Others

49. Keratoacanthoma
Description
 Keratoacanthoma is a rapidly growing crateriform nodule
with a distinctive clinical appearance that is best regarded
as a low-grade squamous cell carcinoma. The peak
incidence of keratoacanthoma is between ages 50 and 70.
This tumor is rare before 40 years of age. Caucasians with
fair complexions are most often affected.
Epidemiology
 Chemical exposure and human papillomavirus have been
implicated as a cause in animal models, although their role
in humans is controversial. Historically, keratoacanthomas
have been regarded as benign regressing lesions, however,
they should be thought of as variants of squamous cell
carcinoma and treated as s

50. Clinical findings common features
 A keratoacanthoma is a characteristic solitary
flesh-colored to red, crateriform nodule, usually
0.5 to 2.0 cm in diameter.
 The lesion erupts rapidly and is often quite
tender.
 A central keratotic plug or depression conceals a
deep keratinous cavity.
 This plug or depression gives the nodule its
characteristic volcano-like shape.
 The nodule is firm in texture, tender to palpation
and pressure.
 Keratoacanthoma nearly always appears on sun-
damaged skin.
 Typical locations include the face, neck, dorsal
hands and sun exposed extremities.
 It occurs on the legs more often in women.

60. Keratoacanthoma
Clinical
findings :

61. Growth phases ka
 Three growth phases are described:
 1. Proliferative phase: a solitary papule
appears suddenly and then rapidly grows
to its maximum size over 2 to 4 weeks.
 2. Mature phase: the lesion is stable in
size and appearance for weeks to months;
it may appear crateriform if the core has
been partially removed.
 3. Resolving phase: the base becomes
indurated, the central core is expelled, and
the base resorbs, leaving a pitted scar.
This phase may last several months.

62. Treatment
Topical 5-FU
Mechanical debridement
Cryotherapy
Curettege &
Electrodesiccation
Dermabrasion
Surgical excision

63. Ka Treatment
 It is best to presume a diagnosis of
squamous cell carcinoma pending biopsy
results and clinical follow-up.
 An excisional biopsy or shave removal
should be performed.
 It is important to biopsy deep enough to
evaluate the dermis for possible invasion.
 Treatment options include complete
excision with margins and
electrodesiccation and curettage.
 Any of these options are curative in the
vast majority of cases.

64. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Skin tags
 Syringoma
 Others

65. Epidermal Cyst
 Description
 An epidermal cyst is a firm, subcutaneous,
keratin-filled cyst originating from true
epidermis, most often from the hair follicle
infundibulum.
 Epidermal cysts are common, usually
solitary, and arise spontaneously.
 They occur most commonly on the trunk,
postauricular fold and on the posterior
neck.

71. Potential to rupture
 Cysts frequently develop in areas of
friction.
 Most epidermal cysts arise from the
squamous epithelium of the hair follicle.
 Unlike pilar cysts, the epidermal cyst wall
is fairly delicate and thus prone to rupture.
 Rupture is followed by foreign body
reaction to keratin extruded into the
dermis and acute inflammation.
 Such lesions appear to be infected.
However, cultures are usually sterile.

72. Typical findings/characteristic findings
 Epidermal cysts are firm, dome-shaped,
pale yellow, cystic nodules ranging in size
from 0.5 to 5.0 cm in size.
 Cysts are somewhat mobile but are
tethered to the overlying skin through a
small punctum that often appears as a
comedo.
 This punctum represents the follicle from
which the cyst developed.
 These cysts may be flat or flush to the
surface of the skin or elevated well above
the surface. In either case, they are easily
palpable.

73. Excision
 Epidermal cysts that have not previously ruptured can be
excised easily and completely under local anesthesia.
Epidermal cysts on the face may rupture and lead to
scarring.
 Cosmetic considerations of elective surgical excision must
be weighed against scar formation resulting from rupture.
 Such lesions are far more difficult to remove once they
have ruptured.
 Recurrent epidermal cysts that have previously ruptured
and scarred are best excised along with the surrounding
scar once the inflammation has subsided.
 Asymptomatic epidermal cysts occurring elsewhere do not
require treatment.

74. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Skin tags
 Syringoma
 Others

75. Skin Tags
 Description
 Skin tags or achrocordons, are common, benign,
fleshy papules occurring in the skin folds.
 They are uncommon before age 30 and common
thereafter.
 Skin tags are more common in overweight
persons. Roughly 25% of adults have at least one
skin tag.
 The majority of patients with skin tags have only
a few such lesions.
 There may be a familial tendency toward multiple
skin tags.
 Undisturbed lesions are usually asymptomatic.
 Skin tags may become irritated by friction,
jewelry or clothing.
 They may become tender and may bleed, when
traumatized, twisted, torn, or thrombosed.

76. Clinical findings
 Skin tags are skin-colored or slightly pigmented,
1 to 5 mm pedunculated papules.
 They are typically not difficult to diagnose.
 They may be flat or filiform, although most are
soft, fleshy, and pedunculated on a thin stalk.
 The axillae are the most common location to find
skin tags.
 Skin tags also occur on the neck, eyelids, as well
as in other intertriginous areas such as the
inframammary and inguinal creases.
 The overwhelming majority of skin tags are
benign and have no internal disease association.

81. Treatment
 Asymptomatic skin tags do not require
treatment.
 Patients often request removal for
bleeding, tenderness or for cosmetic
reasons.
 Skin tags are best treated by scissor
excision with or without local anesthesia.
 Electrocautery and cryosurgery can also
be used.
 Many dermatologists feel that histologic
confirmation is usually not necessary, but
submission of all skin tags for histologic
review is a topic of debate

82. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Skin tags
 Syringoma
 Others

83. Syringoma Description
 Syringomas are the most common tumor
of the intraepidermal eccrine sweat
glands.
 These appendage tumors develop after
puberty and increase in number
throughout young adulthood.
 Lesions are asymptomatic, stable in size
and appearance, and persistent.
 The autosomal dominant inheritance of
multiple syringomas is well established.
 Syringomas occur with increased
frequency in individuals with Down
syndrome or trisomy 21.

84. Clinical Findings
 Syringomas are small, skin-colored to yellow, 1-
to 2-mm papules.
 They are most commonly found on the lower
eyelids.
 They also occur on the malar cheeks, axillae,
upper chest, abdomen, umbilicus, and vulva.
 Papules are usually symmetrically distributed
and asymptomatic.
 Syringomas persist indefinitely and remain small.
 They have no potential for malignancy.
 They may resemble flat warts or sebaceous
hyperplasia.
 Facial lesions are of cosmetic concern, and most
patients request removal of larger lesions.
 The patient may be concerned that the lesions
are cancerous.
 Women seeking evaluation of vulvar lesions may

91. Treatment
 Syringomas may be removed for cosmetic
purposes.
 Electrodesiccation and curettage, laser
surgery, and trichloroacetic acid may be
used with variable success.
 Sharp dissection or scissor excision of
lesions is easily performed under local
anesthesia.
 All of these procedures can lead to
scarring, so care and precision are
warranted.
 In some patients, syringomas are too
numerous to remove all lesions
completely.

92. Benign Tumors
 Seborrheic Keratosis
 Melanocytic neavi
 Dermatofibroma
 Keratoacanthoma
 Pilar cyst
 Epidermal cyst
 Coetaneous tags
 Syringoma
 Others

93. Pyogenic granuloma
 Pyogenic granulomas are a benign
overgrowth of blood vessels. They present
as rapidly growing pinkish red nodules
which are friable and readily bleed. They
may follow trauma and are often found on
the fingers and lips. They are best excised
to exclude an amelanotic malignant
melanoma.

95. Cherry angioma
 Campbell de Morgan spots
 These are benign angiokeratomas that
appear as tiny pinpoint red papules,
especially on the trunk, and increase with
age. No treatment is required.

97. Swellings arising from the skin
Benign Tumors
 Benign
Papillomata
 Sebaceous cyst
 Strawberry
nevus
 Histiocytoma

99. Premalignant Lesion
Leukoplakia
Actinic Keratosis
Radiation Keratosis
Tar Keratosis
Arsenical Keratosis
Bowens disease
 Erythroplakia of
Queyrat
Pagets disease

100. Leucoplakia
 Etiology : Smoking, Syphilis, Sepsis,
Sharp edge of the tooth, Spirits, Spices ---
the 6 S
 Incidence: Occurs in 40 – 70 yrs of age
with male dominance

101. Histopathology
 Gross feature: White hyperkeratotic patch
in the mucosa
 Histology : hyperkeratosis over a
thickened acanthotic but orderly mucosal
epithelium.

102. Leukoplakia
 White plaques
 Etiology
* age = 40-70 yrs
* sex = males
* habits = tobacco ,alcohol ,use of chronic
irritants
* inf. = HPV-16
* others = ill fitting dentures

103.  Clinical findings :

104. Actinic or solar keratosis
 Etiology : Sun exposure (U.V) and
hydrocarbons contact
 Incidence : in persons past middle life
 Prognosis : SCC may develop

105. Actinic Keratosis
Etiology
• Synonyms - solar keratosis, senile
keratosis
• Age = >40
• Sex = male
• Occupation = outdoor works
• Race = fair skinned, blue eyes
• Genetics = xeroderma
pigmentosum

106. Histopathology
 Gross feature: White hyperkeratotic patch
in the mucosa
 Histology : hyperkeratosis over a
thickened acanthotic but orderly mucosal
epithelium.

107. Histopathology
 Gross feature: Lesions are less than 1 cm
in diameter; are tan brown, red or skin
colored; and have a rough, sandpaper like
consistency.
 Multiple lesions on the face and the backs
of hands
 Histology : Building up of excess keratin,
cytological atypia and associated basal cell
hyperplasia

108.  Clinical
findings:

116. Prevention
 recreational exposure
 Sunscreen & protective clothing

117. Radio dermatitis
 Early: erythema, which goes onto
desquamation and pigmentation
 Late: atrophy, irregular hyperpigmentation
and telangectasis and hair loss.
 SCC may eventually develop

118. Radiation Keratosis
Etiology :
Exposure to ionizing radiation

119. Clinical
findings

120. Arsenical Keratosis
 Clinical findings:

121. Tar Keratosis
Synonym : Tar wart
Etiology :
exposure to polycyclic aromatic
hydrocarbons

122. Clinical
findings :

123. Bowen Disease
 A.k.a. carcinoma in situ and squamous
intraepidermoid neoplasia.
 Etiology : Involve predominantly skin
unexposed to the sun (i.e., protected).
Role of HPV 16.
 Incidence : Involves the genital region of
both men and women above the age of 35
 Prognosis : May transform into SCC

124. Histopathology
 Gross feature : Solitary, thickened, gray-
white, opaque plaque with shallow
ulceration and crusting
 Histology : the epidermis shows
proliferation with numerous mitoses, some
atypical.

128. Bowen’s disease
Clinical findings:

130. Erythroplasia of Queyrat
 Etiology : Role of HPV 16
 Incidence : Men, usually above age of
25yrs
 Prognosis : Has a potential to develop into
invasive carcinoma

131. Histopathology
 Gross feature : Appears on the glans penis
and prepuce as single or multiple shiny
red, velvety plaques.
 It may at times produce a discharge and
become painful.

132. Erythroplasia of Queyrat
 Bowen’s disease of the penis
 Clinical features :

133. Management
 Excision biopsy
 Curettage
 Electrodessicatio
n
 Cryotherapy
 Protection
 5 fluorouracil
cream
 Dermabrasion
 CO2 laser
vaporization.
 Photodynamic
therapy (for
Bowen Disease)

134. Cutaneous Horn
Synonym – cornu cutaneum
Clinical finding :

135. Paget’s Disease
Clinical findings:

137. Carcinomas
 Basal cell
carcinoma
 SCC
 Malignant
melanoma
(nodular)

138. BASAL CELL CARCINOMA BCC
 Definition and etiology:
 Basal cell carcinoma is a malignant
neoplasm arising from the basal cells of
the epidermis
 Most basal cell carcinomas are caused by
sunlight-induced damage to the skin.

139. BCC

150. Clinical features:BCC
 Basal cell carcinoma is the most frequent
malignancy in the United States,
 with more than 750,000 new cases
reported annually. Although basal cell
carcinoma
almost never metastasizes, its malignant
nature is emphasized by the local
destruction
that it can cause.
As with other sun-induced neoplasms of
the skin, fair-complected
 individuals and those with a lot of sunlight
exposure are most likely to develop
basal cell carcinoma.

151. Clinical features BCC
 Clinically, there are four major types of basal cell carcinomas:
nodular,
 superficial, morpheaform, and pigmented.
 Rarer types include cystic and keratotic carcinoma and
fibroepithelioma of Pinkus.
 They are, of course, found most commonly on sun-exposed skin.
 Nodular basal cell carcinomas, the most common type, appears
 as a pearly semitranslucent papule or nodule that has a depressed
center,
 telangiectasia, and rolled waxy border. Crusting and ulceration
frequently occur.
 The most common location is on the face, particularly the nose.
Superficial basal cell carcinomas look quite different.
 They are red, slightly scaling, slightly crusted, well-demarcated
 eczematous-appearing patches that most commonly occur on the
trunk.
 Infiltrative or morpheaform basal cell carcinoma appears as an
atrophic, whitish, scarlike eroded or crusted plaque.
 Pigmented basal cell carcinoma is a shiny brown, blue, or black
papule or nodule.

152. DD BCC
The differential diagnosis
 of basal cell carcinoma depends on the
type.
 For nodular basal cell carcinoma, the
differential diagnosis includes ;
 Sebaceous hyperplasia, fibrous papule of
the nose, nonpigmented nevus, and
squamous cell
 carcinoma. Dermatitis, psoriasis, and
Bowen’s disease (squamous cell carcinoma
in
 situ) appear similar to superficial basal cell

153. DD BCC
 Seborrhoeic keratosis,pigmented nevus, and,
most important, malignant melanoma must be
ruled out in
the case of pigmented basal cell carcinoma.
 For crusted nonhealing scarlike lesions,
the differential diagnosis is mainly between
basal cell and squamous cell carcinoma.
 A skin biopsy, either shave, punch, or excision,
should be accomplished to confirm the diagnosis
of basal cell carcinoma.
 The tumor is composed of a thickened
epidermis with invasive buds and lobules of
basaloid cells.

154. BCC Treatment:
 Curettage and electrodesiccation of the lesion or
excision are the most common surgical modalities
used to treat basal cell carcinoma.
 Because of the locally destructive nature and
potential for recurrence of the disease, treatment
should be done by an experienced clinician who
can individualize the therapeutic modality
 based on location of the lesion, histopathologic
type, size of the basal cell carcinoma, and its
primary or recurrent status.
 Less commonly used treatments are radiation
therapy, cryosurgery, and topical chemotherapy.
 A specialized surgical technique, Mohs’ surgery,
is indicated for recurrent basal cell carcinoma and
for primary tumors with a high risk of recurrence.

155. Basal cell carcinoma
 Synonyms: basal cell epithelioma,
basalioma,rodent ulcer
 A malignancy arising from the epidermal
basal cells.

156. Etiology and Pathogenesis
 Genetics:
chromosome 9q22.3
(PTCH)
 Sunlight
 Ionizing radiation: 10
Gy
 Carcinogens: tar, oils
and arsenic
 Chronic skin damage:
scars of trauma and
vaccination
 Other factors :
immunosuppression

157. Epidemiology
 Incidence 40-
80/10000. U.S
500,000/ year
 Age =>60 years
 Gender = > men
 Race= less in dark
skinned
 Occupation= outdoor
exposure
 Geography = high
altitudes,equator

158. Clinical findings
 Majority in the face
 Line connecting the corners of the mouth
to the bottom of the ears
 Lower part of the face, scalp and upper
part of the trunk

159. Initial basal cell carcinoma
 Tiny ,indurated
pearly area
 crusted or scabbed
area
 Rolled edge
 Cheek and nose

160. Nodular basal cell carcinoma
 Nodular
 Pearly or waxy
border
 Prominent
telangiectases
 Central dell or
ulceration
D.D: intradermal
melanocytic nevus,
squamous cell
carcinoma, giant

162. Ulcerated basal cell carcinoma
 Synonyms:Ulcus
rodens,rodent ulcer
 Large ,destructive
 Ragged border
 Nasolabial fold,medial canthus
and about the ear
 Crusts and granulation tissues
D.D: factitial ulcers

164. Pigemented basal cell carcinoma
 Blacks,Hispanics,
Native Americans,
Orientals
 Papular or nodular
 Slate-blue to black
D.D:melanocytic
nevus, blue nevus,
malignant
melanoma,
vascular
lesions(angiokerato

165. Cicatricial basal cell carcinoma
 Synonym;
morpheaform basal
cell carcinoma
 Yellow and white
waxy plaques
 Ill defined edge
 Enlarging scar
 Nose, forehead
 Mimic keloid
 Clinically
aggressive

166. Cystic basal cell carcinoma
 Soft translucent papule
 Marked telangiectasia
 eyes
D.D hidrocystoma, adnexal tumors

167. Superficial basal cell carcinoma
 Synonyms:
multicentric,
pagetoid,
eczematoid

Superficial,multiple
 Pink or brown scaly
plaque
 Whip cord edge
 >10cm
 Tumor buds

169. Fibroepithelioma,Metatypical,
BCC in scars
 Fibroepithelioma= soft pink flesh coloured
or pale coloured nodules on the trunk
 Metatypical= cannot differentiate b/w BCC
and SCC under the microscope
 BCC in scars= ulcer not a telangiectatic
nodule. Recurrent BCC and a scar

170. Metastatic BCC
 0.0028 to 0.1%
 Metatypical BCC
 Large ulcerated basal cell carcinomas in
the mid face
 Elderly
 immunocompromised

171. histopathology

172. Histopathology

173. Therapy
 size
 Location
 Subtype

174.  Excision
 Micrographic surgery
 Cyrotherapy
 Curettage and electrodesiccation
 Radiation therapy

175. Course and prognosis
 Slow relentless
growth destroys
tissue locally
 Untreated invades
bone, cartilage
 Usually 95% cure
rate

182. SQUAMOUS CELL CARCINOMA
 Definition and etiology:
 Squamous cell carcinoma is a malignant
neoplasm of keratinocytes that is locally
 invasive and has the potential to
metastasize.
 Ultraviolet radiation, x-rays,
papillomavirus infection, and chemical
carcinogens such as soot and arsenic
cause squamous cell carcinoma.

183. Clinical features SCC
 Squamous cell carcinoma is the second most
common skin cancer in the United States, with
more than 100,000 new cases diagnosed
annually.
 As with other sunlight-induced skin cancers, the
frequency of squamous cell carcinoma is
increased in those who are fair complected or
engage in many outdoor activities.
 The history of a bleeding growth or ulcer should
arouse suspicion of squamous cell carcinoma.
 Squamous cell carcinoma most often arises in
sun-damaged skin.
 It also develops on the mucous membranes and
in areas of chronic injury such as burn scars,
chronic radiodermatitic lesions, chronic draining
sinuses, and areas of erosive discoid lupus
erythematosus.

194. SCC
 The examination reveals a hard papule or
nodule that is erythematous to flesh-
colored, smooth, scaling, and crusted.
 Squamous cell carcinoma in situ(Bowen’s
disease) has a different appearance,
being a well-demarcated, slightly scaling,
slightly crusted, eczematous-appearing
patch.

195. DD SCC
 The differential diagnosis of squamous cell
carcinoma includes
 keratoacanthoma, hypertrophic actinic
keratosis, wart, basal cell carcinoma, and
seborrheic keratosis. Any lesion that is
crusted or ulcerated should be suspected
of being squamous cell carcinoma, and
biopsy must be done.
 This reveals a hyperkeratotic thickened
epidermis containing atypical
keratinocytes that invade the dermis.

196. Treatment SCC Squamous cell carcinoma should be totally
excised.
 Follow-up to monitor for local recurrence as well
as metastases is required.
 The squamous cell carcinomas most likely to
metastasize are those that are large or
histologically poorly differentiated, have deep
invasion, or occur in damaged skin or the mucous
membranes of the lips, glans penis, and vulva.
 Metastasis is generally to the regional lymph
nodes, and careful attention should be given to
examining them for
lymphadenopathy.

197. Squamous cell carcinoma
 Primary cutaneous SCC is a malignant
neoplasm of keratinising epidermal cells

198. Epidemiology
 30-60/100000
 Basal: squamous =5:1 to 10:1
 Age=>40 years
 Sex= men
 Occupation= outdoor workers
 Genetics = xeroderma
pigmentosum
 Geography= equator or high
altitudes

199. Etiology and pathogenesis
 Irradiation: UV,PUVA,Heat
 Chronic degenerative and inflammatory
process
 Chemical carcinogenesis:petroleum,
tobacco
 Oncogenic Viruses: HPV
 Genetic disorders: xeroderma
pigmentosum, Ferguson-Smith
 Immunosuppression
 Personal habits: alcohol and tobacco

200. Clinical findings
 indistinct clinical picture
 Hard exophytic,inflamed nodule
 vermiottes
 Ulcerated and necrotic
 more destructive
 Metastases
Unfavourable signs: rapid growth,induration,
bleeding

202. Histopathology

203. Histopathology

205. Differential Dx:
 Adnexal tumors
 Amelanotic malignant melanoma
 Seborrheic keratosis
 Nodular,indurated, ulcerated lesion

206. Course
 Sun exposed and actinic keratoses =less
metastases
 >2cm
 >4mm depth
 Poorly differentiated
 immunosuppresed
}}More likely toMore likely to
metastasizemetastasize

207. Prognosis
 Location
 Size
 Thickness
 Degree of differentiation
 5 year survival <20-25% if regional nodes
are involved

208. Therapy
 Excision
 Cyrotherapy
 Curettage and
electrodesiccation
 Radiation Therapy
 Sentinal lymph
node dissection

211. Marjolin’s ulcer
 A squamous cell carcinoma which develops
in a chronic scar such as along standing
ulcer or osteomyelitis sinus.
 Slow growth – relatively avascular
 Painless
 Absence of secondary deposits in regional
lymph nodes

216. Extent of the tumor
Prognosis
Management
Malignant Melanoma

217. Level I
Clark
Level V
Level IV
Level III
Level II

218. Breslow
0.75 mm
0.76-1.5 mm
1.51-3.0 mm
>3.0 mm

219. Skin grafts
STSG
epidermis + part of dermis
FTSG
whole thickness of the skin
excised

220. SGT