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Culture Documents
stimulated
by
Secretes
cytokines
Dendritic cell
Constantly
exposed
to
absorbs and
Referred
to
as
neural
dendritic
cell
and defensins
microbial
and
non micro agent
Lymphocyte
protect
against
end
organ
Mediate the dendritic cell
Intraepidermal
UV radiationfor
Responsible
Afferent nerve
microscopic
pattern
Langerhan cell
fiber
physical
sensation:
and
clinical
expression
Sweat glands
pain,
touch , vibration
Adnexal
cutaneous
Hairoffollicles
itchiness,
coldand
and cells
components
Harboring
inflammatory
epithelial
stem
heat.
Maybe
disrupted
by trauma, burns etc.
infectious
disease
1. FRECKLES (ephiles)
Most common pigmented lesion of
childhood and lightly pigmented
individual
1 to several mm in diameter
Tan-red or light brown macules that
appear after sun exposure
2. Lentigo
Refers to a common benign
localized hyperplasia of melanocyte.
occurring at all ages, but often
initiated in infancy and childhood
The pathogenesis is unknown
Pathogenesis
acquired mutations that lead to constitutive
activation of NRAS or the serine/ threonine kinase
BRAF, which lies immediately down- stream of RAS
nevi only rarely give rise to melanomas
oncogene-induced senescence ;
Morphology
Deeper nevus
Superficial cell are:
larger
tend to produce melanin
and grow in nest
are:
smaller
produce little or no
pigment
appears as cord and
Morphological changes
over
consist
of aggregates
or
most junctional
nevi grow
nests
of underlying
round cells that
into
the
time
grow along
the or cords
dermis
as nests
Junctional nevi
Compound
nevi
Intradermal
nevi
dermoepidermal
junction
of cells
Grossly,
lesions
arecombine
small,
compound
nevi
relatively
at, of
symmetric,
the features
and uniform.
junctional
nevi
(intraepidermal nevus cell
nests) with nests and cords
of dermal nevus cells.
In older lesions the
epidermal nests may
be lost entirely
Dysplastic Nevi
May be direct precursors of melanoma
Probability of dysplastic nevus to develop
melanoma
over 50% by age 60
the vast majority of such lesions are clinically
stable and never progress
Pathogenesis
acquired activating mutations in the NRAS and
BRAF genes
inherited loss of function mutations in CDKN2A.
negative regulator of cyclin-dependent kinase 4
(CDK4)
CDKN2A encodes PI6/INK4A
it appears that RAS or BRAF activation and
increased CDK4 activity contributes to the
development of dysplastic nevi.
Morphology
larger than most acquired nevi (often
greater than 5 mm across)
flat macules, slightly raised plaques
with a pebbly surface, or target-like
lesions with a darker raised center and
irregular at periphery
dysplastic nevi occur on both sunexposed and protected body surfaces.
Melanoma
most deadly of all skin cancers and is
strongly linked to acquired mutations caused
by exposure to UV radiation in sunlight
relatively common neoplasm
other sites of origin include the mucosal surfaces
reported incidence of melanoma; more than
76,000 cases and more than 9,700 deaths are
expected in the United States in 2014.
pathogenesis
About 10% to 15% of melanomas are inherited
as an autosomal dominant trait with variable
penetrance
majority of melanoma is sporadic : ultraviolet
radiation (UVR) damage from sun exposure
most commonly arise on sun-exposed surfaces;
the upper back in men and the back and legs in
women
CDKN2a
P15/INK4
b
P16/INk4
a
Inhibits
CDK4 and
CDK6
P14/ARF
Enhance the
activity of p53
tumor supressor
Morphology
melanomas show
striking variations in
color, appearing in shades of black,
brown, red, dark blue, and gray
The borders of melanomas are
irregular and often notched. Unlike the
smooth, round and uniform boarders of
MN
1.Radial growth
.horizontal spread of melanoma within the
epidermis and superficial dermis
.tumor cells seem to lack the capacity to
metastasize
.lentigo maligna- indolent lesion that
remain in the radial phase for several
decades. Usually involving sun-exposed
skin
.Acral/ mucosal lentiginos- melanoma that is
unrelated to sun exposure.
Prognostic factor
Variables thats used in the probability of metastatic
spread:
Clinical feature
ABCDEs of melanoma ( warning signs)
1.
2.
3.
4.
5.
Asymemetry
Irregular Boarders
Variated Color
Increasing Diameter
Evolution or change overtime
Seborrheic Keratoses
occur most frequently in middle-aged or older
individuals.
Arise particularly numerous on the trunk,
although the extremities, head, and neck may
also be involved.
dermatosis papulosa nigra.- multiple small
lesions on the face
pathogenesis
Activating mutations in the fibroblast growth factor
receptor-3
Seborrheic keratoses may suddenly appear in large
numbers as part of a paraneoplastic syndrome- (LeserTrlat sign)
morphology
characteristically appear as round, at,
coinlike, waxy plaques that vary in diameter
from millimeters to several centimeters
uniformly tan to dark brown
velvety to granular surface.
Inspection usually reveals small, round, porelike ostia impacted with keratin
Histologic findings
exophytic and sharply demarcated from the
adjacent epidermis.
Hyperkeratosis occur at the surface
Characteristic feature- small keratin-filled
cysts (horn cysts) and invaginations of keratin
into the main mass (invagination cysts)
Acanthosis Nigricans
Pathogenesis
unifying feature of acanthosis nigricans is a
disturbance that leads to increased growth
factor receptor signaling in the skin
Familial form- germline activation mutation in
tyrosine kinase FGFR3
DM2 , hyperinsulinimia is believe to provoke
increased stimulation of IGFR1
maybe seen together with skeletal deformitiesachondroplasia and thanatropic dysplasia
Morphology
hyperplasia may
be seen, along
with
hyperkeratosis
and slight basal
cell layer
Fibroepithelial Polyp
morphology
Fibroepithelial polyps are soft, fleshcolored, bag-like tumors
attached to the surrounding skin by a
slender stalk
consist of fibrovascular cores covered
by benign squamous epithelium