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Oral Pathology, Test #2 Blake > ch 10 epithelial pathology > Flashcards

ch 10 epithelial pathology Flashcards

1
Q

squamous papilloma

A
  • Benign prolif, thought to be viral induced
  • low infectivity and virulence
  • any age and usually <1/2 cm
  • tx surgical removal, if left may remain the same
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2
Q

Verruca Vulgaris

A
  • virus induced (HPV)
  • frequent in children
  • common on skin and infrequent in oral cavity
  • usually < 5 mm
  • cutaneous horn form extreme accumulation of keratin
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3
Q

what virus is associated with Verruca Vulgaris?

A

HPV

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4
Q

what is the tx for verruca vulgaris?

A
  • skin lesions treated by liquid nitrogen, cryotherapy, surgical or topical keratinolytic agents
  • oral lesions sergical laser, cryotherapy or electrosurgery
  • if untreated 2/3s will disappear in two years
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5
Q
  • viral induced (HPV)
  • considered sexually transmitted
  • teenagers and young adults
  • Koilocytes (pyknotic nuclei surrounded by a clear zone)
A

Condyloma Acuminatum

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6
Q

what different epithelial lesions are assoicated with HPV?

A
  • Verruca Vulgaris
  • Condyloma Acuminatum
  • Verrucous Carcinoma
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7
Q
  • Whites between 40-70 with female predilection
  • Favor gingiva and alveolar mucosa (50%)
  • Most
A

Verruciform Xanthoma

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8
Q
  • Viral induced localized proliferation of squamous cells
  • Usually multiple flat or rounded papules which are usually clustered with normal color (not white)
  • Childhood condition
A

Focal epithelial hyperplasIa

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9
Q
  • considerable acanthosis is hallmark
  • spontaneous regression reported months to years
  • conservative surgical for diagnostic or esthetic
A

focal epithelial hyperplasia

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10
Q

common skin condition in elderly and represents and axquired b9 proliferation of epidermal basal cells

  • chronic sun exposure with hereditary tendency
  • Brown plaque that appears to be “stuck on” skin
A

Seborrheic Keratosis

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11
Q

what disease is associated with the “laser-Trelat sign” (numerous ___with pruritus associated with internal malignancy)

A

Seborrheic Keratosis (SK)

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12
Q

seborrheic keratosis like but in blacks

A

‘Dermatosis papulosa nigra’ occurs in 30% blacks with Autosomal Dominant pattern

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13
Q

what is the histologic finding in Seborrheic Keratosis?

A

horn and pseudo-horn cysts and melanin pigmentation in the basal cell layer

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14
Q

-Skin discoloration is produced by excess of melanin deposition in the epidermis; blond and red hair

A

ephelis (freckle)

-genetic predilection, Autosomal Dominant

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15
Q

-Age spot; liver spot
- Chronic UV light damage; rare
before 40 and 90% whites > 70
-No change in color intensity after exposure to UV light
-Typically multiple; tan/brown
-May reach 1cm; most

A

Actinic Lentigo

-does not undergo malignant transformation

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16
Q

treatment for actinic lentigo (liver spots)

A

-topical retinoic acid can reduce intensity and completely destroyed with Q-switched ruby laser

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17
Q
  • “mask of pregnancy”
  • Symmetric hyperpigmentation of sun exposed skin of face and neck
  • Topical tx with 3% hydroquinone and tretinoin
  • Prevented by minimizing sun exposure
A

Melasma

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18
Q

-Flat brown discoloration caused by focal increase in melanin deposition (maybe increased malanocytes)
-Not related to sun
-May want to separate Labial MM
which probably has sun association
-2:1 female; average age 43 and 33% vermilion zone of lip

A

Oral melanotic macule

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19
Q
  • Racial or physiologic; P-J syndrome; Addison’s disease and Neurofibromatosis
  • Chronic trauma; Chronic AI disease
  • Smokers melanosis
  • Drugs; chloroquine or other quinine derivatives; Phenolphthalein; estrogen; AIDS-related medications
A

Melanin Pigmentation

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20
Q
  • Benign acquired pigmentation characterized by dendritic macrophages dispersed throughout epithelium
  • Exclusively in Blacks with F predilection
  • BM most common site; 3rd-4th decades
A

oral melanoacanthoma

  • Alarming growth rate; can reach several cm in a few weeks
  • Incisional biopsy to r/o melanoma
  • No treatment indicated
  • Several instances spontaneous resolution after biopsy
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21
Q
  • Alarming growth rate; can reach several cm in a few weeks
  • Incisional biopsy to r/o melanoma
  • No treatment indicated
  • Several instances spontaneous resolution after biopsy
A

oral melanoacanthoma

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22
Q
  • Common mole/nevus
  • Neural crest origin
  • Most present before 35
  • Whites have more nevi than Asians or blacks
  • Intra-oral palate and gingiva
A

acquired melanocytic nevus

-the cells have a “pear” shape(?)

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23
Q

what are the types of acquired melanocytic nevus?

A
  • Junctional
  • compound
  • intramucosal
24
Q

Leukoplakia

A
  • White lesion that does not rub off
  • 20% premalignant or malignant on initial biopsy
  • High risk FOM, VT and SP
  • Risk of malignant transformation is greater than the risk associated with unaltered mucosa
  • 1/3 of oral cancers have leukoplakia in close proximaty
25
Q
  • Most common oral precancer representing 85% of lesions

- Common and may affect 3% of white adults (70% male)

A

Leukoplakia

26
Q

different etiologies for leukoplakia

A
  • Tobacco
  • Alcohol
  • Sanguinaria
  • Ultraviolet radiation
  • Microorganisms
  • Trauma
27
Q

prevalence of Leukoplakia as age increases

A

prev increases, ave age 60 is the same ave age for cancer

28
Q

precancerous changes

A
  • Enlarged hyperchromatic nuclei with prominent nucleoli
  • Increased nuclear-to-cytoplasmic ratio
  • Pleomorphic nuclei and cells
  • Dyskeratosis and increased mitotic activity
  • Abnormal mitotic figures
  • Bulbous or teardrop shaped rete ridges
  • Keratin pearls
  • Loss of epithelial cohesiveness
29
Q

to be classified as cancer, it needs to…

A

breach the basement membrane

30
Q

the technical term for cheek chewing

A

Morsicatio Buccarum

31
Q
  • Red lesion that does not rub off
  • No known cause
  • 80-90% premalignant or malignant
A

Erythroplakia

  • Represents sites in which epithelial cells are so immature or atrophic they no longer produce keratin
  • Pattern that frequently reveals advanced dysplasia upon biopsy
  • Biopsy red in mixed lesions!
32
Q

field cancerizaion

A

once you have cancer, you are more likely to get other cancers

33
Q

smokeless tobacco keratosis is more prevalent in India due to…

A

longer contact and tobacco leaves combined in a quid with betal leaves, area nuts and slaked lime

34
Q

oral submucous fibrosis

A

Chronic, progressive, scarring, high risk precancerous condition related to chronic placement of betal quid (areca nut and slaked lime) or paan and found in .4% indian villagers
-Produces mucosal rigidity
-Trismus and mucosal pain
when eating spicy foods
-Blotchy marblelike pallor and a progressive stiffness of subepithelial tissues
-Tongue immobile if involved

35
Q

submucosal fibrous band on BM, SP and LM

A

Oral submucous fibrosis

36
Q

“betal chewer’s mucosa”

A
  • brownish-red discoloration

- oral submucous fibrosis

37
Q

Premalignant alteration of the LL that results from long-term excessive exposure to uv component of sunlight
! A person with chronic sunlight exposure and compromised immunity has increased risk
! Males 10:1

A

actinic cheilosis
-May report scaly material that can be peeled off with some difficulty, only to reform in a few days
! With further progression, chronic focal ulceration especially in areas of mild trauma from cigarettes or pipe stems
! SCCa 6-10% cases; seldom before 60; preventable cancer

38
Q

if a person does reverse smoking and gets cancer, where in the oral cavity would the cancer most likely be located?

A

on the palate

39
Q

if a person gets oral cancer and they are a non-smoker, what is a general characteristic of that patient?

A

Female, young and have mutations of p53 and other suppressor genes

40
Q

effect of alcohol on cancer contraction

A

Significant potentiator or promoter
! 15 fold increase in oral Ca if combined with smoking
! Cirrhosis of liver found in 20% of male patients with oral cancer

41
Q

effect of Phenols in oral cancer contraction

A

Increased Ca in wood products industry (exposed to certain chemicals especially phenoxyacetic acid)
! Also wood workers at increased risk for nasal and nasopharyngeal carcinoma

42
Q

Plummer-Vinson Syndrome associated with > risk of SCCa of esophagus, oropharynx and posterior mouth
! Malignancies develop at earlier age with (this)

A

iron deficiency

43
Q

iron deficiency

A

Impaired cell mediated immunity and iron is essential for normal functioning of epithelial cells of upper digestive tract
! Esophageal webs susceptible to malignant transformation (fibrous bands of scar tissue)

44
Q

Vitamin A deficiency

A

Produces excessive keratinization
! Vitamin A may play a preventative role in precancer and cancer
! Betacarotene and retinoic acid therapy associated with regression in severity of dysplasia

45
Q

Leutic glossitis

A

syphilis

46
Q

when ‘staging’ oral cancer, what are the different letters used and what do they classify?

A

T=size of primary tumor
N=involvement of lymph nodes
M=distant metastasis

47
Q

Carcinoma of the tongue is more likely to have metastasized when located on which portion of the tongue?

A

Posterior 1/3 (80% metastasized and 20% local0

anterior 2/3 (80% local and 20% metastasized)

48
Q

cancer of maxillary sinus

A

Elderly and 80% cases advanced
! Symptoms include unilateral stuffiness, ulceration or mass of hard palate or alveolar bone
! If 2nd division of trigeminal involved, intense pain of midface or maxilla
! Teeth in area loosened and “motheaten” appearance on X-ray
! Superior displacement protrusion of eyeball

49
Q

Skin Melanoma are more likely if you have what physical characteristics?

A
  • Redder your hair
  • Fairer your skin
  • Bluer your eyes
  • Sun exposure
50
Q

what are the four clinicopathologic types of melanoma?

A
  1. superficial spreading melanoma
  2. nodular melanoma
  3. Lentigo malignant melanoma
  4. Acral lentiginous melanoma
51
Q

Most common form of melanoma
! 70% cutaneous lesions
! Interscapular region of males and back of legs in females
! Invasion indicated by appearance of surface nodues or induration; usually 1 year after precursor macule
! Satellite macules or nodules around primary lesion

A

superficil spreading melanoma

52
Q
  • 15% of cutaneous melanomas
  • Begins almost immediately in vertical growth phase and appears as nodular elevation and rapidly invades connective tissue
  • Number of cases so undifferentiated to lack pigment (amelanotic)
A

nodular melanoma

53
Q
  • 5-10% cutaneous melanomas
  • Develop’s from precursor lesion called lentigo maligna (Hutchinson’s freckle)
  • Sun-exposed skin of elderly in midface;melanoma-in-situ in purely radial growth phase
  • 15 year radial growth phase
A

lentigo malignant melanoma

54
Q

-Most common form of melanoma in blacks and most common form of oral melanoma
! Palms of hands, soles of feet, sublingual area and mucous membranes
! Oral melanoma is often nodular at time of diagnosis; 6-7th decades; 2/3 male; 4/5 HP or maxillary alveolus

A

Acral Lentigerous melanoma

55
Q

when looking at a melanoma, what are the four things to analyze?

A
  • Asymmetry
  • Border irregularity
  • color variation
  • Diameter (> 6 mm)
56
Q

what areas of the skin have a worse prognosis for melanomas?

A

“BANS”, Back, posterior upper Arm, posterior and lateral Neck, and Scalp

Oral Pathology, Test #2 Blake (7 decks)

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