Epithelial Pathology Flashcards

1
Q

ephildes

A

common, small pigmented macules of skin

freckles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

transmission of ephelides

A

autosomal dominent predlication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

demographics of ephelides

A

blue eyes, fair skin, red or light blond hair

young adutls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

clinical features of ephelides

A
  1. face / arms / back
  2. excess melanin in basal cells of epidermis (no increase in melanocytes)
  3. 3-4mm in diameter, sharply demarcated, light brown
  4. from less than 10 to hundreds
  5. lesions darken on sun exposure and lighten in shade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

prognosis of ephelides

A

do not progress to melanoma
no treatment necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

synonyms of actinic lentigo

A

senile lengigo
age spots
liver spots
solar lentigo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

etiology of actinic lentigo

A

associated with chronic VU light damage (happens in sun exposed areas - face, dorsum of hands, arms)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

demogrpahics of actinic lentigo

A

90% of whites over 70 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

clinical features of actinic lentigo

A
  1. benign brown skin macule, even pigmented
  2. well demarcated, border may be regular or irregular
  3. no darkening on sun exposure (unlike ephelides)
  4. 5mm - 1cm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

prognosis of actinic lentigo

A

no progression ot melanoma
no treatment required unless for esthetic reasons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

actinic chelitis

A

lower lip vermilion counterpart of actinic keratosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

etiology of actinic keratosis

A

cumulative UV radiation induced skin damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

histopathology of actinic keratosis

A

hyperkeratosis with some degree of epithelial dysplasia or even superficially invasive squamous cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

demographics of actinic keratosis

A

50% of white adults with history of significant lifetime sun exposure

uncommon under 40 years of age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

demographics of actinic cheilitis

A

uncommon under 45 years

almost 10:1 male predilection (due to outdoor / sunlight exposure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

clinical features of actinic keratosis

A

common areas: face neck, hands, bald scalp skin

irregular scale like plaques with sandpaper like texture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

clinical features of actinic cheilitis

A

areas of vermillion
obliteraiton of margin between vermilion of lip and skin
chronic scaling
crusting
ulceration
fissuring of lip

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

treatment of actinic keratosis

A

precancer

cryotherapy, electrocautery, topical agents

long term follow up necessary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

treatment of actinic cheilitis

A

lip shave (vermilionectomy)

6-10% cases will progress to lip cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

different types of eptihelial skin cancers

A

basal cell carcinoma
squamous carcinoma
melanoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

most common type of epithelial skin cancer

A

basal cell carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

etiology of epithelial skin cancer

A

sun exposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

body surfaces affected by BCC

A

80% of skin on face

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

associations of BCC

A

nevoid basal cell carcinoma syndrome (tumor suppressor gene PTCH1 mutation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
clinical appearance of BCC
firm painless papule enlarges with a central depression and rolled borders umbilication with resultant ulceration - rodent ulcer fine blood vessels over lesion
26
MOHs surgery
moh's micrographic surgery for best esthetic results for BCC excellent aesthetics with this procedure
27
melanomas
-malignancy of melanocytic differentiiation -most are cutaneous; 3rd most common skin cnacer -5% of skin cancers; 65% of deaths due to skin cancer -fair skin patient, 40-70 years
28
etiology of cutaneous melanoma
malignancy of melanocytic differentation
29
predisposing factors fo cutaneous melanoma
-acute sun damage with blistering sunburn early in life -tendency to burn easily -indoor occupation; outdoor recreation -family history -personal history
30
statistics of cutaneous melanoma
93.3% 5-year survival (because people are aware)
31
ABCDE of cutaneous melanoma (clinical description)
asymmetry border irregularity color variation diameter greater than 6mm evolving rapidly in shape / size / color / surface
32
amelanotic melanoma
-lack pigment -challenging to diagnose -will require immunological stains for accurate diagnosis -melanoma with ZERO pigment
33
acral lentiginous melanoma
8% of melanomas -affect palms, soles, oral mucosa (no relation to soalr exposure) -MOST COMMON CLINICOPATHOLOGIC TYPE OF MELANOMA IN PERSONS OF COLOR -begins as darkly pigmented macule with irregular borders
34
cutaneous melanoma treatments
-surgical excision with / without lymph nodes -chemotherapy, radiation therapy with little impact on the disease -biologica agents ot boose immune system
35
breslow's depth of invasion
determines prognosis of melanoma
36
seborrheic keratosis
common skin condition (does not occur on mucosa)
37
transmission of seborrheic keratosis
some cases are hereditary (autosomal dominant)
38
demographics of seborrheic keratosis
onset during the 4th decade of life become more pregalent thereafter
39
clinical features of seborrheic keratosis
-most common on skin of face / trunk / extremities -begins as small pigmented macules and evolve to enlarge and raise with fine fissured, pitted surface -stuck on dirty candle wax
40
dermatosis papulosa nigra
-form of seborrheic keratosis in about 30% of blacks -autosomal dominant trait -multiple small pigmented papules over skin of zygoma
41
treatment of seborrheic keratosis
no treatment required, except for esthetic purposes
42
caution with seborrheic keratosis
melanomas may look like seborrheic keratosis sudden eruptions of multiple seborrheic keratosis with pruritus (leser-trelat sign) associated with internal malignancy
43
squamous papilloma
most common benign intraoral epithelial neoplasm
44
relationship of squamous papilloma with HPV
may / may not show human papilloma virus direct cause / effect is uncertain
45
clinical features of squamous papilloma
solitary lesion, typically found on soft palate / uvula or tongue -finger like fronds, usually pedunculated, may be sessile -range of color (reddish to white)
46
histology of squamous papilloma
-orthokeratinized or parakeratinized surface -papillary proliferation of surface epithelium -finger like projections of fibrous CT that support the epithelial proliferation
47
treatment of squamous papilloma
conservative excision, including base of lesion prognosis is excellent
48
HPV
DNA virus nearly 100 subtypes
49
HPV types
24 types, specifically infect genital and oral mucosa tropism for epithelial cells
50
high risk types of HPV
16, 18, 31 stornlgy associated with cervical, anogenital and some oropharyngeal cancers
51
modes of transmission of HPV
sexually transmitted
52
immunization (vaccine) of HPV
gardasil immunization of girls and boys at ages 11 / 12
53
verruca vulgaris common name
common wart
54
causes of verruca vulgaris
common lesion caused by several strains of HPV HPV 2 / 4 / 6 / 40
55
clinical features of verruca vulgaris
-frequently affects children - hands and facial skin -usually sessile, exophytic, papillary lesion; often multiple
56
transmission of verruca volgaris infection
contagious autoinoculation
57
classic histopathology of verruca vulgaris
-hyperkeratotic epithelium raised into finger-like proections -elongated rete pegs converge towards center of lesion producing a "cupping" effect -prominent granular cell layer with coarse, clumped keratohyalin granules -koilocytes
58
koilocytes
virally infected cells with pyknotic nuclei and clear perinuclear cytoplasm
59
treatment of verruca vulgaris
spontaneous regression common in kids excision, cryotherapy, keratolytic agents may recur
60
HPV types associated with multifocal epithelial hyperplasia
13 and 32
61
ethnic predilection of multifocal epithelial hyperplasia
isolates of native indians of north and central america and brazil
62
clinical features of multifocal epithelial hyperplasia
1. multiple sessile, pink and white, papules of the gigniva, buccal and labial mucosa 2. asymptomatic 3. mostly found in children, may be foudn in older patients
63
Transmission of multifocal epithelial hyperplasia
HPV virus - contiguous contact of one mucous membrane and another Between people → between objects (ex. Food, fomites)
64
mitosoid bodies
cells with unusual arrangement of nuclear chromatin resembling abnormal mitotic figures (mitosoid bodies) seen n spinous layer associated with multifocal epihtelial hyperplasia
65
Management of multifocal epithelial hyperplasia
Tend to regress spontaneously Topical interferon application
66
Condyloma
gnital warts venereal warts
67
Modes of transmission of condyloma acuminatum
Spread by direct contact
68
HPV types involved with condyloma acuminatum
Caused by any one of several strains of HPV High risk strains (HPV 16 and 18) associated with cervical carcinoma
69
clinical features of condyloma acuminatum
-may affect oral mucosa -usually diagnosed in teenagers and young adults -clinically presented as multiple sesile papules or plaques with cauliflower-like surface -affect the labial mucosa, soft palate, and lingual frenum most common
70
koilocytes
Histopathologically, characterized by parakeratotic papillary proliferation of surface epithelium with blunted fronds, acanthosis, broad rete ridges, and increased mitosis Perinuclear clearing (koilocytosis) is seen in the cells of the spinous layer associated with condyloma
71
Molluscum contagiosum
common cutaneous infection caused by DNA poxvirus
72
Demographics of molluscum contagiosum
Usually seen in children and young adults
73
Clinical appearance of molluscum contagiosum
Multiple pink papules affect the skin of the neck, eyelids, trunk, or genitalia Each papule as a central core or depression
74
Molluscum bodies
-Histopathologically distinctive -Lobular proliferation of surface epithelium -Epithelial cells exhibit basophilic “molluscum (henderson-paterson) bodies” that are filled with viral particles -Move to top of skin and exfoliate → release lots of pox virus (creates divot!)
75
Treatment of molluscum contagiosum
Consists of curettage or liquid nitrogen, although lesions often resolve spontaneously in the immune competent host in six to nine months Very difficult to treat
76
melanotic macule
common, harmless lesion that may be seen either ont he lip or intraorally increased amount of melanin pigment in the basal cell layer of epithelium
77
clinical features of melanotic macule
-tan to dark brown, uniformly pigmented, demarcated margins -no change with sun exposure -could represent post-traumatic melanosis
78
indications for biopsy fo melanic macule
-Lesions on vermilion zone of lip are often excised for cosmetic purposes -Tissues should be submitted for microscopic examination -Intraoral lesions may need to be excised to rule out early melanoma
79
demogrpahics of melanoacanthoma
young, adult african american females
80
Clinical features of melanoacanthoma
Occurs on skin and oral mucosa Dark macule to patch that often arises rapidly Mimics melanoma
81
Histopathology of melanoacanthoma
Long dendrites
82
Treatment of melanoacanthoma
Biopsy to establish diagnosis Spontaneous resolution may be seen following biopsy
83
Prognosis of melanoacanthoma
Subsequent additional lesions may arise in same patient
84
acquired melanocytic nevus
moles -One of the most common lesions -Average 20/person in caucasians -My develop from first year of life through the fourths decade -Oftn involute with aging
85
acquired melanocytic nevi types
functional compound intradermal
86
junctional nevi
first stage, appear flat and usually appear dark -function of epithelium and CT -nevus cells present among basal epithelial cells
87
compoudn nevus
may evolve from jucntioanl nevus as the patient grows older -proliferaiton of nevus occurs with some of the nevus cells dropping off into the superficial CT -may begin to dhow elevation clincially
88
intradermal nevus
with time, nevus cells may proliferate to the extent that they are completley contained within the dermal CT -elevated, with variable degree of pigmentation (many are normal skin color) -no more nevus cells left in epithelium
89
intraoral presentation of acquired melanocytic nevus
infrequently, melanocytic nevi can develop in oral cavity usually located on the hard palate or attached gingiva, but potentially any site an be affected
90
management of acquired melanocytic nevus
no treatment absolutely neceesary
91
risk fo malignant transformation of melanocytic nevus
1 in a million changes in nevus or chronic irritation of a nevus would be reason for excision biopsy
92
congenital melanocytic nevi
type of melanocytic nevus present at birth 1% of newborns
93
small vs large nevi
designated as large or small, with small <15cm being uch more common large congenital nevus is also known as "garment nevus" or "bathing trunk" nevus due to extensive involvement on patient's skin
94
risk of malignant transformation for congenital melanocytic nevi
high 1% for small 15% for large
95
treatment of congenital melanocytic nevi
staged excision for large excision for small
96
blue nevi
-may affect any cutaneous mucosal site -appear blush / gray due to depth of the melanin pigment -simpel excision -excellent prognosis
97
nicotine stomatitis
white patch of posteiror hard palate and soft palate
98
Etiology of nicotine stomatitis
Acute onset Secondary to heat of pipe / cigar, cigarette
99
Clinical features of nicotine stomatitis
Numerous pinpoint red areas signify inflamed openings of ducts of minor mucous glands of the palate
100
Management of nicotine stomatitis
Resolves spontaneously
101
Any malignant potential?
no
102
Tobacco pouch keratosis
due to placement of quid containing smokeless tobacco Wrinkled, corrugated hyperkeratosis Does not show clear margin from surrounding mucosa Asymptomatic
103
types of smokeless tobacco that have hgher cancer / precancer rates
loose leaf tobacco dry snuff
104
Leukoplakia (definition)
white patch of oral mucosa that cannot be scraped off and cannot be diagnosed clinically or microscopically as any other condition
105
White lesions that are not leukoplakia
Leukoderma (blend with surroundings, less severe when stretched) cheek chewing (rigid boundary) frictional / ridge keratosis, nicotine stomatitis, smokeless tobacco, keratosis
106
Common sites in the oral cavity for oral precancer and cancer
Lateral tongue Ventral tongue Floor of mouth Anterior pillar of tonsils Lateral soft palate
107
Histology of leukoplakia (dysplasia)
Typically some degree of hyperkeratosis (wet keratin appears white) Pre Cancerous changes may be evident microscopically - epithelial dysplasia Mild (low grade), moderate, severe dysplasia or carcinoma-in-situ (high grade)
108
clinical features of leukoplakia
1. sharply demarcated white plaques with smooth, verrucous or micronodular surface 2. crisp margins 3. cracked mud like appearance (because of movement)
109
speckled leukoplakia
if red component is present
110
low grad dysplasia
not as many changes from normal
111
high grade dysplasia
large change from normal (poorer prognosis) treated just like cancer
112
when to complete excision for leukoplakia
when high grade / cancer
113
how to take incisional biopsy from leukoplakia
from different areas of the lesion different portions of lesion will behave differently
114
management of low grade dysplasia
1. discontinue carcinogenic habits and frequent follow up 2. biopsy if any progressive change (ex increase in size, thickening, ulceration, erosion, pain, mobility of tooth, exophytic growth, atlered sensation)
115
management of high grade dysplasia
remove by the most convenient means available submit tissue for assessment of margins
116
prognosis of leukoplakia
1. prognosis is guarded 2. 33% of dysplastic lesions will transform to squamous cell carcinoma 3. 30% of leukoplakia will recur
117
dysplasia
altered development
118
dysplasia in context of cancer
signifies disorder at cellular and tissue level microscopically identifiable as changes associated with premalingancy / malignancy
119
cellular changes of precancer / cancer related dysplasia
1. abnormal variation in nuclear size and shape 2. abnormal variation in cell size and shape 3. increased nuclear / cytoplasmic ratio 4. hyperchromatic nuclei 5. increased mitotic figures 6. abnormal mitotic fitures
120
arthitectural (tissue) changes of precancer / cancer related dysplasia
1. disordered maturaiton from basal to squamous cells 2. increased cellular density 3. basal cell hyperplasia 4. dyskeratosis 5. bulbous drop shaped rete pegs 6. acantholysis
121
hallmark of squamous carcinoma
compromise of basement membrane
122
clinical features of proliferative verrucous leukoplakia
1. uncommon, high risk presentation 2. extensive and often multiple keratotic plques in older adults 3. hyperkeratosis / hyperplasia with variable dysplasia
123
age impacted by PVL
females (mean age 65 years) males (mean age 49 years)
124
gender impacted by proliferative verrucous leukoplakia (PVL)
female predilection (4:1) with only 1/3 having traditional risk factors
125
risk factors for PVL
no history of alcohol or tobacco use common in post-menopausal women
126
treatment of PVL
1. optimal treatment remains to be determined 2. surgical or ablative therapy, but recurrence common 3. malignant transformation is frequent complication, even in lesion without previous biopsy evidence of dysplasia
127
prognosis of proliferative veracious leukoplakia - high risk presentation
100% will transform to carcinoma 70% of patients developed SCCa within 8 years (40% died as result of carcinoma)
128
erythroplakia
red patch that cannot be diagnosed as any other condition clinically or microscopically more serious than leukoplakia
129
etiology of erythroplakia
pipe smoking
130
management and prognosis of erythroplakia
treatment and prognosis are similar to leukoplakia having a siilar degree of epihtelial can be excised patient education is important!
131
causes of sanguinaria leukoplakia
associated with use of extract of native indian bloodroot
132
what is sanguinaria found in
herbal oral health care products
133
clinical features of sanguinaria leukoplakia
1. homogenous white patch 2. slight "cracked mud" like appearance 3. distinct margin 4. cannot scratch away (not a pseudomembrane)
134
common sites of sanguinaria leukoplakia
maxillary gingiva canine premolar region
135
sanguinaria vs leukoplakia
1. sites differ 2. clinically identical to leukoplakia 3. to be managed like leukoplakia 4. complete excision with clear margins 5. close follow up for recurrence or new lesions
136
SCC
most common oral malignancy and second most common cutaneous malignancy
137
SCC arises from ____
surface epithelial cells
138
etiology of SCC
arises from pre-existing actinic keratosis in many instances due to chronic sun (UV light) exposure
139
common sites of SCC
face helix of ear dorsum of hands and arms are common sites
140
management of SCC
1. treatment consists of surgical excision 2. actinically induced SCC generally are well differentiated and grow slowly 3. prognosis is generally very good if lesion is identified early in course
141
intraoral SCC is known as
oral cancer
142
statistics of SCC
1. intraoral squamous cell CAs are usually (75-80%) associated with tobacco cigarettes, with or without alcohol 2. significant percentage (25-30%) are not associated with any identifiable risk factors - usually lateral tongue of younger people or gingiva of older women
143
etiology of intraoral SCC
tobacco reverse smoking pipe moking UV
144
associations of SCC with systemic conditions
plummer vinson syndrome graft vs host disease syphilitic glossitis submucous fibrosis preivous radiation chronic inflammation, poor oral hygiene
145
demographics of oral SCC
1. oral SCC accounts for 2-4% of all cancers in the US 2. most occur in older adults 3. men outnumber women by 2:1 ratio
146
clinical features of carcinoma of oral SCC
1. irregular shape, mixture of red and white clinically 2. often ulcerated 3. exophytic (Growing out) or endophytic (growing in) growth pattern 4. often much firmer than surrounding tissues 5. early lesions are asymptomatic
147
differential diagnosis of oral SCC
1. nonspecific ulcer 2. specific indications (TB, histoplasmosis, syphilis) 3. immune mediated conditions (wegen'ers, crohn's) 4. carcinoma should be #1 in differential! (take biopsy!)
148
radiographic features of SCC bone involvement
1. ragged radiolucency is characteristic of bone involvement 2. due to direct invasion of bone (usually late phenomenon)
149
histopathology of carcinoma
1. microscopically, invades cords and nests of malignant squamous epithelial cells arise from dysplastic surface epithelium 2. tumor cells show an increase nuclear / cytoplasmic ratio, cellular and nuclear pleomorphism, and mitotic activity 3. varying degrees of keratin seen 4. intravascular, lymphatic, and perineural invasion may be seen
150
SCC of lip
1. one of more common sites of involvement 2. secondary to ultraviolet light exposure 3. arises in the setting of actinic cheilitis 4. slow growing, well differentiated lesion
151
SCC of tongue
1. majroity of patients have history of cigarette smoking and alcohol abuse 2. when oral SCCa is seen in younger (<40) people, almost always develops at tongue
152
SCC of floor of mouth
1. almost equal to lateral tongue as common site fo oral SCCa 2. most patients have history of cigarette smoking and alcohol abuse
153
SCC of gingiva / alveolar mucosa
1. unusual site epidemiologically for oral SCCa 2. more common in women at this site 3. more common in patients with no identifiable risk factors for oral SCCa
154
SCC of buccal mucosa
not very common site
155
SCC of palate
1. most SCCa's affecting the palate arise on the lateral soft palate 2. rather rare to find this malignancy on the hard palate 3. may be different to determine whether lesion developed in maxillary sinus and invaded the floor
156
staging helps
to dsicern extent of cancer
157
how to stage cancer
1. size of tumor (T) 2. involvement of regional lymph nodes (N) 3. whether the cancer has spread to different parts of body (M) 4. depth of invasion
158
parameters for depth of invasion
if less than 5mm, fine! (stay at current staging) more than 5mm, T value goes up by 1
159
neck level 1a
submental
160
neck level 1b
submandibular
161
neck level IIa
upper jugular (anterior)
162
neck level IIb
upper jugular (posterior)
163
neck level III
mid jugular
164
neck level IVA
lower jugular
165
neck level IVB
medial supraclavicular
166
neck level VA
upper posterior triangle
167
neck level VB
lower posterior triangle
168
neck level VC
lateral supraclavicular
169
neck level VI
anterior cervical
170
nek level VIIA
retro-pharyngeal
171
neck level VIIB
retrostyloid
172
nek level VIII
parotid
173
neck level IX
bucco-facial
174
neck level XA
retro-auricular
175
neck level XB
occipital
176
treatment of oral carcinoma
wide surgical excision / radiation therapy neck node dissection is based on staging chemotherapy not much impact
177
prognosis of oral cancer
one of the worse cancer prognosis 67% 5-year survival rate