10: Epithelial Pathology Flashcards
papilloma HPV types
6, 11
RRP what is
Recurrent respiratory papillomatosis
6, 11
sinonasal papilloma HPV types
6, 11
focal epithelial hyperplasia aka
Heck disease, HPV 13, 32
heck disease what is
focal epithelial hyperplasia, HPV 13, 32
oropharyngeal SCC HPV type
16
conjunctival papilloma HPV type
6, 11, 16
verruca vulgaris aka
common wart, HPV 2
verruca plana HPV type
3, 10
palmoplantar wart HPV type
1, 4
butchers wart HPV type
2, 7
condyloma acuminatum aka
venereal wart, types 6, 11
veneral wart aka
condyloma acuminatum types 6, 11
cervical SCC HPV types
16, 18
papillomatosis HPV and association
HPV 6 and 11 nevus unius lateris acanthosis nigricans focal dermal hypoplasia (Goltz Gorlin) Down syndrome
RRP what is
reucrrent repiratory papillomatosis
larynx –> hoarsenss
juvenile onset 2/2 maternal genital warts
adult onset
sinonasal papilloma how common, location, variants
10-25% of all sinonasal tumors
1/2 in lateral nasal wall
remainder in maxillary and ethmoid
inverted papilloma most common variant, greatest potential for malignancy
inverted papilloma
most common variant of sinonasal papilloma
greatest potential for malignancy
greatest potential for malignancy in sinonasal papillomas
inverted papilloma
cutaneous horns in which entities
SCC BCC verruca vulgaris Seb K actinic keratosis trichoep
molluscum contagiosum cause, location, histo, prognosis
pox virus
skin of necj, face (particularly eyelid), trunk, genitals
Henderson-Paterson bodies – Molluscum bodies
most cases spontanesous remission
henderson paterson bodies
molluscum bodies
patterson kelly aka
= Plummer Vinson Syndrome
Iron def
Esophageal webbing = fibrous scar
Malignant transformation
plummer vinson syndrome aka
paterson kelly
Iron def
Esophageal webbing = fibrous scar
Malignant transformation
Iron def
Esophageal webbing = fibrous scar
Malignant transformation
plummer vinson
verruciform xanthoma histo and IHC
xanthoma cells: PAS+, diastase resistant granules
CD68+ (KP1), cathepsin
seborrheic keratosis aka
senile wart, basal cell proliferation
Dermatosis papulosa nigra:
Variant of seb k found in blacks above zygoma and eyelids.
Seb k are adenoid and acantholytic type
Variant of seb k found in blacks above zygoma and eyelids
Dermatosis papulosa nigra:
Seb k are adenoid and acantholytic type
Leser-Trelat sign:
Sudden appearance of multiple Seb k indicates malignancy
Sudden appearance of multiple Seb k
Leser-Trelat sign: indicates malignancy
Inverted follicular keratosis of Helwig
= Irritated seb K
= Irritated seb K
Inverted follicular keratosis of Helwig
types of seb k
1- Acanthotic (solid)
2- Hyperkeratotic (papillomatosis)
3- Reticulated ( adenoid)
4- Clonal : intraepidermal nests of basaloid cells resembling Borst-Jadassohn
phenomenon
5- Irritated: heavy inflammatory cell infiltrate and lichenoid features
: intraepidermal nests of basaloid cells resembling Borst-Jadassohn
phenomenon seb k
clonal
heavy inflammatory cell infiltrate and lichenoid features seb k
irritated
mutations in seb k and where else?
= FGFR3 + PIK3CA
also in actinic lentigo
actinic lentigo mutations and where else?
= FGFR3 + PIK3CA
also in seb k
bowenoid actinic keratosis histo
Full epithelial thickness of dysplasia
Oral submucous fibrosis presentation
Trismus
Stomatopyrosis: intolerance to spicy food
trismus and intolerance to spicy food
Oral submucous fibrosis
Stomatopyrosis: intolerance to spicy food
ephelis aka and genetics
(freckle): MC1R gene
MC1R mutation
Ephelis (freckle):
FGFR3 + PIK3CA
Seb K and actinic lentigo
ephelis clinical
Increase in melanin deposition
Color changes with sun exposure
ephelis vs melanocytic nevus
ephelis no elevation above skin
ephelis vs lentigo simplex
ephelis not as dark
ephelis vs lentigo simplex
ephelis no elongation of rete ridges
lentigo pigmented hockey sticks/dirty socks
actinic lentigo aka
Lentigo solaris ; Age spot; liver spot; senile lentigo
liver spot aka
Actinic Lentigo; Lentigo solaris ; Age spot; liver spot; senile lentigo
actinic lentigo where, who (age sex), related entities, histo
Occurs on skin not mouth
White older men >70 yrs
Freckles are more prone to develop Actinic Lentigo
Maybe a precursor to Seb K
No change in color intensity with UV light exposure
Elongation of rete ridges
lentigo simplex vs melanocytic nevus
single lesion - identical
lentigo simplex what, where, who and how
Melanocytic hyperplasia Skin not exposed to sunlight Does not darken with the sun Increase in both melanin production and number Elongation of rete ridges Children
multiple lentigo simplex
1-LEOPARD
2-Peutz Jeghers syndrome
3-Lentiginosis profusa
melasma aka and what is
Mask of pregnancy; Chloasma
Acquired, symmetrical hyperpigmentation on sun exposed skin of face and neck
Unknown cause
Proliferation of # and production
melanotic macule aka, what, where
focal melanosis
Increase in deposition of melanin, perhaps melanocytes
Not affected by the sun
Most common site is the lower lip > BM >gingiva > palate
lesions on skin unexposed to sun
lentigo simplex, melanotic macule
melanoacanthoma what is, who, where
Benign, acquired pigmentation of dendritic cells
F> M / Most common site BM but can occur anywhere
congenital nevus where, size(s)
Most common trunk and extremities 15% in H&N Small= <1.5 cm Medium = 1.5-20 cm Large = > 20 cm
developmental nevi
NBCC Nevus Flammeus Epidermal nevus WSN Nevus sebaceous
congenital nevus genetics
NRAS
sutton disease
Major aphthous ulcer
halo nevus aka, where, what, why, prognosis
Leukoedema Acuisitum Centrifugum ; Sutton Nevus
Skin of trunk
Hypopigmentation due to a destruction of the melanocytes by the immune system
Develops from a recent excision of a melanoma
Most regress and require no treatment
Hypopigmentation due to a destruction of the melanocytes by the immune system
halo nevus
from a recent excision of a melanoma
spitz nevus aka, where, who
Benign juvenile melanoma; spindle and epitheliod nevus
Extremities or face
Childhood
spitz nevus genetics and histo
HRAS mutation
Kamino bodies
melanoma aka and genetics
acquired nevus, BRAF
congenital nevus genetics
NRAS
blue nevus genetics
GNAQ
spitz nevus genetics
HRAS
BRAF
melanoma
NRAS
congenital nevus
GNAQ
blue nevus
HRAS
spitz nevus
blue nevus aka and types
Dermal Melanocytoma: Jadasshon-Tieche nevus
1 - common blue nevus
2 - cellular blue nevus
common blue nevus where
2nd most common nevus
Predilection to dorsa of hand and feet, scalp, face
Mucosal lesions on palate
cellular blue nevus where
More than 50% arise in sacrococcygeal or buttock region
tyndal effect
long wavelength (red & yellow) tend to be absorbed more by tissue Short wavelength (blue) tend to be reflected
long wavelength (red & yellow) tend to be absorbed more by tissue
Short wavelength (blue) tend to be reflected tyndal effect
Keratoacanthoma aka and from where
self-healing carcinoma ; Pseudocacinoma ; SCC-KA type
Infundibulum of hair
types of keratoacanthoma
Abortive KA = Involutes 4-6 wks Subungual KA = nail bed Mucosal KA = mucosa Giant KA = >2-3 cm Keratoacanthoma centrifugum marginatum = peripheral growth, central scarring
syndromes with multiple keratoacanthomas
Muir-Torre syndrome: Seb neoplasm + GI malignancy + KA
Xeroderma pigmentosa: AK + SCC + BCC
Muir-Torre syndrome
Seb neoplasm + GI malignancy + KA
Xeroderma pigmentosa
AK + SCC + BCC
Seb neoplasm + GI malignancy + KA
Muir-Torre syndrome
AK + SCC + BCC
Xeroderma pigmentosa
syndromes with early onset of keratoacanthoma
Ferguson-Smith syndrome : nodular lesions / Scottish descents
Witten-Zak syndrome : variable lesion size
scottish descent with multiple nodular keratoacanthomas
Ferguson-Smith syndrome
late onset of keratoacanthoma syndrome
Gryzbowski syndrome : hundreds of papules +GI malignancy
Gryzbowski syndrome
hundreds of papules keratoacanhtoma +GI malignancy
hundreds of papules keratoacanhtoma +GI malignancy
Gryzbowski syndrome
verrucous carcinoma aka
; Snuff Dipper’s pouch ; Ackerman’s Tumor
Oral florid papillomatosis
previous name for verrucous carcinoma
NUT midline carcinoma mutation
Fairly new entity / gene mutation chromosome # 15q14
gene mutation chromosome # 15q14
NUT midline carcinoma
Nasopharyngeal Carcinoma (NPC) : location, who, presentation
Most common site is lateral wall of nasopharynx (fossa of Rosenmὕller)
Asian M
1
st sign in most cases is an enlarged LN
most common skin cancer
BCC
most common overall cancer
BCC
BCC aka and genetics
rodent ulcer 1- Hedgehog signaling pathway (PTCH = 9q22) 2- SMO 3- TP53 4- BER-EB4 = positive BCC negative in peripheral ameloblastoma
BCC vs ameloblastoma
BER-EB4 = positive BCC
negative in peripheral ameloblastoma
merkel cell tumor cause, origin, IHC, symptoms, who gets it
Polyomavirus Merkel cells are mechanoreceptors CD20 perinuclear dot AEIOU o Asymptomatic o Expanding rapidly o Immunosuppression o Old age
CD20 perinuclear dot
merkel cell tumor
polyomavirus tumor
merkel cell
most common type of BCC
Solid/Nodular (noduloulcerative) 70% cases
sclerosing BCC what is
(Morpheaform): insidious lesion mimics scar tissue / Invasion has occurred
metatypical BCC
mixed features with basaloid and squamous
mixed features with basaloid and squamous
metatypical BCC
morpheaform BCC
insidious lesion mimics scar tissue / Invasion has occurred
aka sclerosing
BCC on skin of trunk with threadlike margins
superficial BCC
most common melanoma
superficial
melanoma with greatest vertical grwowth
nodular
lentigo maligna where, who, aka
(Hutchinson freckle) o Radial growth 15 yrs o Sun exposed areas o Melanoma in situ o Elderly
hutchinson freckle aka
entigo maligna o Radial growth 15 yrs o Sun exposed areas o Melanoma in situ o Elderly
most common oral melanoma
Acral lentiginous melanoma (mucosal lentigenous melanoma)
most common melanoma in black people
Acral lentiginous melanoma (mucosal lentigenous melanoma)
Acral lentiginous melanoma (mucosal lentigenous melanoma) location in mouth
80% in palate and maxillary alveolus
Acral lentiginous melanoma (mucosal lentigenous melanoma) location generally
Feet, subungual area, mucous membrane
sign of melanoma on hands
nail pigmentation
NUT midline Carcinoma genetics
15q19 BRD4-NUT
15q19
NUT midline Carcinoma BRD4-NUT
BRD4-NUT
15q19 NUT midline Carcinoma
9q22
PTCH BCC
PTCH Ca
9q22 BCC
BRAF-MAPK pathway
melanoma
melanoma genetics
BRAF-MAPK pathway
Seb K & Actinic lentigo genetics
FGFR3 and PIK3CA
FGFR3 and PIK3CA
Seb K & Actinic lentigo
papilloma HPV
6 and 11
papillomatosis how presents
extensive coalescing papillary lesions
extensive coalescing papillary lesions
papillomatosis
oral papillomatosis associations
acanthosis nigricans, Goltz-Gorlin, nevus unius lateris
types of laryngeal papillomatosis
juvenile onset (aggressive) and adult onset
verruca vulgaris hpv
2, 4, 6, 40
cutaneous horn present in which entities
verruca vulgaris, seb ker, actinic keratosis, SCC
condyloma acuminatum hpv
2, 6, 11, 53, 54
multifocal epithelial hyperplasia aka and why
heck disease, HPV 13 and 32
HPV 13
heck
HPV 32
Heck
sinonasal papillomas kinds and causes
fungiform (6 and 11), inverted (low HPV), cylindrical (low HPV)
highest malignancy among sinonasal papillomas
inverted, up to 25%
inverted papilloma IHC
CD44+
risk factors for prolonged molluscum contagiosum
HIV, atopic dermatitis, Dariers disease
molluscum bodies aka and what is
henderson paterson, bloated keratinocytes with viral inclusions
henderson paterson aka and what is
molluscum bodies
bloated keratinocytes with viral inclusions
bloated keratinocytes with viral inclusions
molluscum bodies, henderson paterson
verruciform xanthoma seen in association with what
lichen planus, lupus, pemphigus, warty dyskeratoma, GVHD, dysplasia, SCC
VX histo and IHC
granules are PAS+ diastase resistant, CD68+ and cathepsin B+
AD seb ker - who, where, histo type
dermatosis papulosa nigra, black people, zygoma and periorbital; adenoid and acantholytic
seb ker genetics
FGFR3 and PIK3CA
types of seb ker
acanthotic, hyperkeratotic, adenoid
inverted follicular keratosis of helwig what is and special histo
seb ker altered by trauma
whorled epithelium due to metaplasia of lesional cells – squamous eddies
squamous eddies what is
whorled epithelium due to metaplasia of lesional cells
inverted follicular keratosis of helwig (irritated seb ker)
irritated seb ker
inverted follicular keratosis of helwig
whorled epithelium due to metaplasia of lesional cells – squamous eddies
sudden onset of multiple itchy seb kers
leser-trelat
internal malignancy
leser trelat sign
sudden onset of multiple itchy seb kers
indicates internal malignancy
sebaceous hyperplasia association
cyclosporine, corticoids, hemodyalisis, Muir-Torre syndrome
muir torre syndrome what is
visceral malignancies, sebaceous adenomas/carcinomas, keratoacanthomas
ephelis what is and genetics
MC1R mutation, freckle
MC1R mutation
ephelis (freckle)
melasma settings
pregnancy, oral contraceptives, hormonal replacement therapy
very large congenital nevus
bathing trunk nevus aka garment nevus
bathing trunk nevus aka and what is
garment nevus
very large congenital nevus
risks of congenital nevus
increased risk of developing neurocutaneous melanosis (melanotic neoplasms of CNS)
3-15% transformation into melanoma
congenital nevus –> melanoma risk
3-15% transform
most common soft tissue mass of the soft palate
squamous papilloma
goltz gorlin aka
focal dermal hypoplasia – assoc with papillomatosis
when is juvenile onset laryngeal papillomatosis aggresive?
with HPV 11
juvenile onset laryngeal papillomatosis presentation and cause
can obstruct airway, related to maternal history of genital warts, hoarseness
risks with laryngeal papillomatosis
in smokers and history of radiation can progress into SCC
prominent granular cell layer, elongated rete ridges converge to center of lesion (cupping effect)
verruca vulgaris
blunter broader epithalial projections
condyloma acuminatum
when does anogenital condyloma acuminatum progress into SCC
with high risk HPV 16, 18, 31
HPV in condyloma acumiatum
2, 6, 11, 53, 54
heck’s disease HLA
DR4
HLA DR4 epithelial condition association
heck disease
mitosoid cell what is and in what
cell with altered nucleus that looks like a mitotic figure; in heck
where are rete ridges in heck
epithelial is acanthotic upward; rete ridges at level of normal epithelium
schneiderian papillomas are what
sinonasal papillomas
aka for fungiform sinonasal papilloma
exophytic, everted, septal
fungiform sinonasal papilloma where, what, malignant potential
HPV 6, 11
nasal septum
no malignant potential
inverted sinonasal papilloma where, what, malignant potential
most common
HPV 6, 11, 16, 18
lateral nasal wall and sinuses (usually maxillary)
MONOCLONAL! Cd44 + (vs papillary SCC)
most aggressive and up to 25% SCC transformation
most common sinonasal papilloma
inverted
most aggressive sinonasal papilloma
inverted
actually monoclonal
25% –> SCC
papilloma on nasal septum
prolly fungiform
papilloma on lateral nasal wall
inverted or cylindrical (oncocytic)
papillary SCC vs inverted sinonasal papilloma
papilloma is CD44+
least common sinonasal papilloma
cylindrical or oncocyti
HPV in cylindrical sinonasal papilloma and aka
aka oncocytic
no HPV
hybrid or mixed sinonasal papilloma
inverted + cylindrical
cylindrical sinonasal papilloma aka, where, what, malignant potential
aka oncocytic
no HPV assoc
lower aggression/malignant potentil
lateral nasal wall and sinuses (usually maxillary)
are sinonasal polyps neoplastic?
no; non-neoplastic proliferations composed of epithelial and stromal elements
multiple inflammatory sinonasal polyps in children concern for
cystic fibrosis
multiple inflammatory sinonasal polyps in adults why
inflammatory: history of rhinitis, allergy, aspirin intolerance, diabetes
inflammatory sinonasal polyps how many and where
multiple, bilateral
antrochoanal sinonasal polyp where, how many
arise in antrum, extend to nasal cavity, 90% single
antrochoanal sinonasal polyp vs inflammatory
antrochoanal pedunculated, less inflamed
inflammatory - sessile, highly inflamed myxoid/gelatinous stroma, can have charcot-leyden crystals
charcot leyden crystals
asthma – in inflammatory sinonasal polyps
single sinonasal polyp likely what kind
antrochoanal
molluscum what kind
pox, DNA
when does molluscum resolve
6-9 months
how common is dermatosis papulosa nigra
30% of black ppl
secretory nature of sebaceous glans
holocrine
sebaceous hyperplasia associations
cyclosporing, corticoids, hemodyalisis, Muir_torre syndrome
sebaceous hyperplasia vs BCC
sebaceous expresses sebum on ceompression
rhinopyma what i, who, histo
hypertrophy of sebaceous glands of nasal dome
pts with long standing acne rosacea
enlarged bumpy nasal dome
facial flushing with drinking hot liquids, alcohol, spicy foods,
histo: hyperplasia of sebaceous glands
hypertrophy of sebaceous glands of nasal dome
rhinopyma
pts with long standing acne rosacea
long standing acne rosacea presentation
rhinopyma
hypertrophy of sebaceous glands of nasal dome
age spots on sun exposed skin of older people
actinic lentigo
actinic lentigo age and where
older people, UV damage, sun exposed skin
more common in people with freckles on face
multiple simple lentigines what to consider
lentiginosis profusa, Peutz Jeghers, and LEOPARD
LEOPARD components
lentigines (multiple), ECG abnormalities, Ocular hypertelorism, Pulmoary stenosis, Abnormal genitalia, Retarded growth, Deafness
lentigo simplex sun or no
skin not exposed to sunlight
melasma associations
pregnancy, oral contraceptives, hormonal replacement therapy
oral melanotic macule mechanism and role of sun
unrelated to sun
focal increase in melanin and possibly # of melanocytes
laugier Hunziker syndrome
pigmentation of lips and buccal mucosa an longitudinal melanonychia (linear pigmentation of nail)
pigmentation of lips and buccal mucosa and longitudinal melanonychia (linear pigmentation of nail)
laugier Hunziker syndrome
longitudinal melanonychia
(linear pigmentation of nail) laugier Hunziker syndrome
(linear pigmentation of nail)
longitudinal melanonychia
laugier Hunziker syndrome
oral melanoacanthoma race gender cause
almost exclusively in black ppl, F predilection
reactive
progression of acquired melanocytic nevus
junctional (pigmented macule), compount (less pigmented papule), intradermal/intramucosal (papillary, hair, no pigment)
can acquired nevus go away
yes
cells in acquired nevus by depth
type A - superficial, epithelioid
B - middle, lymphocyte like
C - deeper, spindle
risks of congenital nevus
3-15% –> melanoma
halo nevus cause
hypopigmented halo bc melanocytes destroyed by immune system, seen in pts with recent melanoma excision
kamino bodies where what
eosinophilic globoid in spitz nevus
histo spitz nevus
epithelioid and spindle cells, similar to melanoma but young age and small size
spitz nevus IHC
S100+, NSE+
color reflection effect in blue nevi
Tyndall
combined nevus
blue nevus + overlying melanocytic nevus
blue nevus + overlying melanocytic nevus
combined nevus
LAMB syndrome
lentigines, atrial and mucocutaneous myxomas, blue nevi (subset of Carney complex)
balloon cell nevus histo
large, pale, polyhedral balloon cells (clear cells)
oculodermal melanocytosis aka, cause, look, distribution
aka nevus of Ota
diffuse distribution of proliferating melanocytes
unilateral facial and/or ocular slate-blue pigmentation
follow trigeminal V1/V2
unilateral facial and/or ocular slate-blue pigmentation
follow trigeminal V1/V2
oculodermal melanocytosis aka nevus of Ota
nevus of Ota aka, cause, look, distribution
oculodermal melanocytosis
diffuse distribution of proliferating melanocytes
unilateral facial and/or ocular slate-blue pigmentation
follow trigeminal V1/V2
dysplastic nevus where, histo
light-exposed areas, premalignant, melanocytes show nuclear atypia, may be syndrome associated
dysplasia in leukoplakia %
5-25%
sanguinaria associated keratosis where
mx vestibulr or alveolar mucosa
leukoplakia ffrom microorganisms
syphilis - dorsal tongue leukoplakia; candida, hpv
dorsal tongue leukoplakia
syphilis
leukoplakia progression
thin (mild) –> thick (homogeneous) –> nodule/granular –> verrucous
PVL look, starting point, demographic, risks and how soon
multiple lesions, starts in gingiva and spreads to other areas, non smoking females (4:1)
clinically can become similar to verrucous carcinoma, transforms into SCC withint 8 y
erythrileukoplakia why red
read areas atrophic and can’t make keratin
dysplasias –> SCC risks by grade and how soon
2-4y: mild 4% mod 10% sev 35% erythroleuko 47%
erythroplakia locations
most are FOM, tongue, soft palate
smokeless tobacco keratosis progression
painless gingival recession, possible with bone destruction
smokeless tobacco keratosis mucosa look
thin gray white plaque with blending borders on the area where tobacco is placed
parakeratin pointed projections above epithelial layers name and in what
what else under basement membrane
chevroning in smokeless tobacco keratosis
can have amyloid like areas around BMs and blood vessels
which smokeless tobacco/snugg higher risk of SCC
dry (vs moist)
when would smokeless tobacco keratosis resolve after cessation
2 week s
oral submucosal fibrosis demographic and look
pale and marble like stuff mucosa – betel quid users
betel quid other name
areca nut
oral submucosal fibrosis chief complaint
trismus and pain when eating spicy foods
more in BM, SP and retromolar are
trismus and pain when eating spicy foods indicator of
oral submucosal fibrosis
betel chweres mucosa look and risk
brown red but not precanceorus
nicotine stomatitis resolves how soon
within 1 month after discontinuation
actinic keratosis risk factors
sun damage in light skinned persons
immunosuppresion, albinism, xeroderma pigemtosum, Cockayne sundrome, Bloom syndrome, Rothmund-Thompson syndrome
full thickness dysplasia in actinic keratosis name
bowenoid actinic keratosis
bowenoid actinic keratosis
full thickness dysplasia
risks with actiniv keratosis
10% progress to SCC
dysplasia in oral submucous fibrosis how often and what other risks/how often
dysplasia in 10-15% of cases
near 8% progress into SCC
actinic cheilitis occupation
outdoor – farmers, sailors
actinic cheilitis risks
6-10% SCC progression
keratoacanthoma causes
UV(95% on sun exposed skin), HPV (26 or 37), tar, immunosuppression, trauma
HPV in keratoacanthoma
26 or 37
keratoacanthoma phases and when
growth 6 wks
stationary 6 wks
involution 6-2 months
how soon does keratoacanthoma involute
6-12 months
ferguson smith
multiple non involutin keratoacanthomas, earli life, hereditary (AD 9q22-31)
multiple non involutin keratoacanthomas, earli life, hereditary
ferguson smith
9q22-31
ferguson smith
multiple non involutin keratoacanthomas, earli life, hereditary
eruptive grzybowski
100s of small keratoacanthomas in skin and upper digestive tract; sign of internal malignancy
100s of small keratoacanthomas in skin and upper digestive tract
eruptive grzybowski
sign of internal malignancy
keratoacanthoma histo
center of lesion is crater like and keratin filled; surrounding epithelium constricts neck of the lesion. downward proliferation isehs adjacent tissues and its extent is regular (inverted cup)
center of lesion is crater like and keratin filled; surrounding epithelium constricts neck of the lesion. downward proliferation isehs adjacent tissues and its extent is regular (inverted cup
keratoacanthoma
plummer vinson aka
paterson kelly – increased risk of SCC of esophagus, oropharynx, and posterior mouth
SCC gender , deaths per year, new cases per year, % of all cancers in US
8th M/15th F
5300 deaths
35k new cases
3% of all cancers
esophageal webs are
intertwining fibrous bands of scar in esophagus, higher malignancy rate
increased risk dorsal tongue scc which infection
tertiary syphilis
HPV SCC of oropharynx types
16, 18, 31, 33
locations for SCC in mouth
tongue, FOM, soft palate, gingiva, cheek, labial mucosa, hard palate
gingival SCC where and who
posterior md, similar to PG or IFH, least associated with tobacco,, most common in F
SCC distant met sites
lung, liver, bones
desmoplasia aka and what is
scirrhous change; dense fibrosis in CT induced by SCC cells
dense fibrosis in CT induced by SCC cells
desmoplasia
orall SCC risks for what else
synchronous (33%) or metachronous (66%, within 3years) cancers of upper aerodigestive tract, esophagis, stomacj, lunh
verrucous carcinoma aka
ackermans tumor
verrucous carcinoma associations and from what
smokeless tobacco, may arise from PVL
verrucous carcinoma survival
90% with surgery without neck dissection
papillary SCC location and look
oropharynx, hypopharynx, larynx, sinonasal tract-worst prognosis
exophytic, looks like papilloma with fibrovascular cores
DYSPLASTIC epithelium
papillary SCC histo and causes
looks like CIS, not hyperkeratotic, not highly invasive
HPV 6, 11, 16, 18
spindle cell carcinoma aka
pseudosarcoma, sarcomatoid SCC
ackermans tumor aka
verrucous carcinoma
spindle cell ca which component is invasive
spindle
spindle cell ca location
oral cavity and larynx
spindle cell ca reason
dysfunctional cadherin-catenin complex
1/3 develop as recurrence after RT for well-diff SCC (dedifferentiation)
spindle cell ca IHC
CK+ (AE1/AE3, CAM 5.2)
spindle cell ca predictor of prognosis
depth of invasion, not size
adenosquamous ca location
posteriorly
adenoid squamous cell carcinoma why the look and where
acantholysis – not true glandular structures
mostly on lip
basaloid SCC where
larynx, pyriform sinus, base of tongue
basaloid SCC histo look
superficial SCC (well diff or in situ) + basaloid epithelium comedonecrosis common
comedonecrosis which SCC, which Ca
basaloid SCC, SNUC (sinonasal undifferentiated carcinoma)
wood dusts exposure which ca
sinonasal adenoca, intestinal type
more in men
sporadic more in women
second most common glandular sinonasal malignancy
sinonasal adenoca intestiinal type
after adenoid cystic ca
most common glandular sinonasal malignancy
adenoid cystic ca
sinonasal adenoca intestinal type location
ethmoid sinus in menm
nasal cavity and mx sinus in women
sinonasal adenoca intestinal type histo
glands lined with pleomorphic columnar cells in back to back pattern
histo types of sinonasal adenoca intestinal type
papillary, colonic, solid, mucinous, mixed
sinonasal adenoca intestinal type IHC
CD20, CDX2
CK variable
glands lined with pleomorphic columnar cells in back to back pattern
sinonasal adenoca intestinal type
sinonasal adenoca non intestinal type grades and features
high hrade: Males, mx sinus, markedly atypical and pleomorphic
low grade - no sex predilection, nasal cavity
sinonasal adenoca non intestinal type histo
small glands lined with a single layer of uniform cells (seromucinous carcinoma), back to back
small glands lined with a single layer of uniform cells but malignant
sinonasal adenoca non intestinal type histo
sinonasal undifferentiated carcinoma origin, causative associations
schneiderian membrane or olfactory epithelium
some cases associated with smoing, EBV, and radiation (weak)
sinonasal undifferentiated carcinoma histo
nests, trabeculae, ribbons of medium sized polygonal cells with organoid appearance
comedonecrosis common
nests, trabeculae, ribbons of medium sized polygonal cells with organoid appearance
comedonecrosis common
sinonasal undifferentiated carcinoma histo (SNUC)
SNUC IHC
sinonasal undifferentiated carcinoma
CD (7, 8, 19)
negative for synapto/chromo
olfactory neuroblastoma aka, what age
esthesioneuroblastoma
rare <10yo (unlike usual neuroblastoma)
bimodal peaks (15 and 50)
most in adults
olfactory neuroblastoma histo
nests of round cells separated by fibrovascular septa, may have neurofibrillary stroma
true rosettes (Flexner-Wintersteiner) and pseudorosettes (Homer Wright)
Flexner-Wintersteiner
true rosettes in olfactory neuroblastoma
Homer Wright
pseudorosettes in olfactory neuroblastoma
olfactory neuroblastoma types
A - nasal cavity
B - external to paranasal sinus
C - beyond nose and paranasal sinuses
olfactory neuroblastoma IHC
CD56, NSE, synapto, chromo
neuroendocrine ca aka on location
oat cell ca in lung
carcinoid tumor in HI
most common non squamous tumor of the larynx and risk factor
tobacco related
MDNEC (atypical carcinoid tumor) – Mills scheme
Mills scheme types of carcinoids
WDNEC - carcinoid tumor
MDNEC 0 atypical carcinoid tymor
PDNEC small cell (small cell undiff)
PDNEC large cell (large cell undiff)
salt and pepper nuclei, nuclear moldingm, crush artifact
neuroendocrine
neuroendocrine IHC
NSE+, chromo, synapto
nasopharyngeal carcinoma origin, geography
from lining epithelium of lymphoid ricj nasopharynx
high incidence in China, intermediate in SE asia, low in US
nasopharyngeal carcinoma associated factors
EBV, vit C def, salt fish diet (nitrosamines
nitrosamines malignancy
nasopharyngeal carcinoma
middle aged person with recurrent persistent otitis media consider
nasopharyngeal carcinoma
location for nasopharyngeal carcinoma
lateral wall at rosenmullers fossa
first sign of nasopharyngeal carcinoma
in 60%, first sign is an enlarged metastatic lymph node
nasopharyngeal carcinoma types
1 - keratinizing, SCC
2 - differentiated, nonkeratinizing
3 - undifferentiated, nonkeratinizing (lymphoepithelioma, lymphoepithelial carcinoma)
worst prognosis among nasopharyngeal carcinoma types and why
type 1 worse, prolly 2/2 response to radiation
lymphoepithelioma what is and types
type 3 of nasopharyngeal carcinoma (undifferentiated, nonkeratinizing)
Regaud type: clusters, nests, or aggregates of neoplastic epithelial cells with lymphocytes
Schminke type: dispersed tumor cells forming a syncytial net
: dispersed tumor cells forming a syncytial net
lymphoepithelioma Schminke type
clusters, nests, or aggregates of neoplastic epithelial cells with lymphocytes
lymphoepithelioma Regaud type
most common cancer
basal cell carcinoma
why does BCC pop up
mainly due to UV
also arsenic ingestion, immunosuppression, PUVA for psoriasis
syndromic associations for BCC (6x)
Gorlin syndrome, xeroderma pigmentosum, albinism, Rasmussen, Rombo, and Bazex-Christol-Dupre
BCC genetics
PTCH (9q22) + p53 + SMO
PTCH gene location and disease
9q22 – BCC
clinical patterns of BCC
noduloulcerative (most common: telangiectatic vessels, aka rodent ulcer)
pigmented (nodular with melanocytes)
sclerosing (morpheaform – mimics scar)
superficial (multifocal, mimics psoriasis)
syndromic (sun exposed AND non exposed areas)
collision tumor of BCC and SCC
basosquamous carcinoma
merkel cells where and what
epidermis; primarily associated with nerve endings
risk factors for merkel cell carcinoma
UV light and immunisuppression (transplant, HIV, lymphocytic leukemia)
may be caused by the merkel cell polyoma virus
which virus in merkel cell carcinoma
merkel cell polyoma virus
merkel cell carcinoma location and look
75% facial skin
dome shaped nodule with smooth surface and telangiectasis (rarely ulcerates)
vowel mnemonic for merkel cell carcinoma
AEIOU: asymptomatic expands rapidly immunosuppressed older people UV exposed areas
merkel cell carcinoma IHC and special stains
CK20+ (perinuclear dot-like)
synapto chromo NSE
TTF1 to exclude lung met
Grimelius stain shows granules
Grimelius stain
merkel cell carcinoma shows granules
risks with merkel cell carcinoma
25% of patietns develop additional malignancies (SCC skin, hemato, breast/ovary adenoca)
microcystic adnexal carcinoma aka
sclerosing sweat duct carcinoma
sclerosing sweat duct carcinoma aka
microcystic adnexal carcinoma
microcystic adnexal carcinoma behavior, location
cytologically bland but locally aggressive
plaque-like indurated lesion of upper lip
microcystic adnexal carcinoma histo
squamous/basaloid cells horn cysts in superficial portion ductal structures in deeper portions neural/vascular invasion desmoplastic stroma
squamous/basaloid cells horn cysts in superficial portion ductal structures in deeper portions neural/vascular invasion desmoplastic stroma
microcystic adnexal carcinoma
melanoma genetics
50-70% BRAF mutation (Ras-Raf-Erk pathway)
BRAF mutation what and pathway
melanoma!
Ras-Raf-Erk pathway
(Ras-Raf-Erk pathway)
BRAF - melanoma
most common melanoma
superficial spreading
which melanoma can be amelanotic
nodular
which melanoma is in situ and from what
lentigo maligna – from hutchinson’s freckle
most common melanoma in oral cavity
acral lentiginous melanoma
most common melanoma in black people
acral lentiginous melanoma
types of melanoma
superficial spreading, lentigo maligna, nodular, acral lentiginous
superficial spreading melanoma location
intercapsular area in males, back of leg in female
melanoma IHC
HMB45, Melan A, Mart -1 , Fontana-Masson, S100
how is melanoma prognosis graded
Breslow classification: depth of invasion associated with poorer prognosis for skin lesions
Breslow classification
for melanoma
prognosis ~ depth of invasion
which labs/ presentation associated with poorer melanoma of skin prognosis
elevated serum lactic dehydrogenase (LDH) and ulceration
which locations associated with poorer prognosis for skin melanoma
interscapular Back
posterior and lateral Neck
posterior upper Arm
Scalp
BNAS
which demographic etter prognosis for melanoms
women and pts <50yo
survival for oral melanoma
which is better, which is worse
13-22% survival
better for younger
worse for amelanotic
how to ddx spitz nevus from melanoma
spitz more in childhood, pink, and small size
spitz nevus IHC
S100+ and NSE+
combined nevus
blue nevus + melanocytic nevus
blue nevus + melanocytic nevus
combined nevus
pale and marble-like stiff mucosa
oral submucosal fibrosis
betel chewers mucosa
brown red, not pre-cancerous; and lichenoid lesions
risk factors for actiic keratosis
immunosuppression, albinism, xeroderma pigmentosum, Cockayne syndrome, Bloom syndrome, Rothmund Thompson syndrome
bowenoid actinic keratosis
actinic keratosis + CIS
actinic keratosis + CIS
bowenoid actinic keratosis
origin of keratoacanthoma
from hair follicle infundibulum
what arises from hair follicle infundibulum
keratoacanthoma
multiple keratoacanthomas that don’t involute
Ferguson Smith
hundrend of keratoacanthomas in skin and upper digestive tract
Eruptive Grzybowski; sign of internal malignancy
wood and leather exposure predisposes to what and where
sinonasal intestinal type adenocarcinoma (maxillary sinus)
nasopharyngeal carcinoma arises from
lining epithelium of lymphoid-ricj nasopharynx
lining epithelium of lymphoid-ricj nasopharynx gives rise to
nasopharyngeal carcinoma
factors associated with nasopharyngeal carcinoma
EBV, vitamin def, salt fish diet (nitrosamines)
which BCC is multifocal
superficial
which BCC is sclerosing
morpheaform
which BCC is on sun exposed and nonexposed skin
syndromic
which BCC has melanocytes
pigmented
which BCC is telangiectatic and ulcerated
nodular aka rodent ulcer
mohs micrographic surgery
uses frozen sections to ensure complete removal of BCC/SCC
which surgery uses frozen sections to ensure complete removal of BCC/SCC
mohs micrographic surgery
which melanoma has no radial phase
nodular