Pathology of the GI Tract- Oral cavity and salivary glands (part 3 of 4) Flashcards

1
Q

what is the odontogenic tumor we discussed?

A

keratocystic odontogenic tumor

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

the keratocystic odontogenic tumors are most commonly seen in what age group?

A

most often diagnosed in patients between 10 and 40

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

95% of head and neck cancers are what type?

A

squamous cell carcinomas (SCCs)

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

what is the etiology of SCC in the head/neck?

A

it is multifactorial–> 1) HPV 2) tobacco and alcohol 3) Betel quid and Paan (india/asia) 4) actinic radiation and pipe smoking

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

what is now the leading cause of SCC in the head/neck?

A

HPV

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

what variants of HPV are associated with OPSCC?

A

HPV 16 and 18

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

what is at the most risk for HPV related cancers of the head and neck?

A

white, non-smoking males age 35-55

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

in the head and neck, HPV demonstrates tropism for what?

A

lymphoid-associated structure of the oropharynx, including the palatine and lingual tonsils

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

what does infection of the tonsillar epithelium with HPV result in?

A

aberrant basal cell differentiation, dysplasia, carcinoma in situ, and finally invasive carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

the oncogenic potential of HPV can largely be explained by the activity of what?

A

two viral genes encoding E6 and E7

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

what does HPV E7 inhibit/block?

A

p21 and RB pathways

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

what does HPV E6 inactivate/inhibit?

A

p53

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

what happens to the HPV genome and what does this suggest?

A

the HPV genome is integrated into the host genome, suggesting that integration of viral DNA is important for malignant transformation

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

how do patients with HPV-positive SCC compare to patients with HPV-negative tumors?

A

patients with HPV-positive SCC have greater long-term survival than those with HPV negative tumors

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

what are the clinical presentations associated with OPSCC?

A

non specific symptoms such as sore throat, ear ache, pain on swallowing, and weight loss; can present as a metastatic tumor in the lymph node

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

how can you identify if the OPSCC is caused by HPV?

A

if there is overexpression of p16 (a cell cycle inhibitor); or if the brown staining is positive

17
Q

what is the second most common cause of classic oral SCC?

A

smoking/ tobacco

18
Q

the development of classic oral SCC is driven by what?

A

the accumulation of mutations and epigenetic changes that alter the expression and function of oncogenes and tumor suppressor genes

19
Q

several genes have been proposed as playing critical roles in SCC- what are they?

A

TP53, CDKN2A, and PIK3CA

20
Q

a number of novel and potentially targetable genetic alterations have been identified in cases of SCC, what are they?

A

NOTCH1 and FAT1

21
Q

what is the most frequently mutated gene in cases of SCC?

A

TP53

22
Q

where are the common locations for oral SCC to present?

A

ventral tongue, floor of mouth, lower lip, soft palate, gingiva (look under dentures)

23
Q

what are the classic SCCs typically preceded by?

A

the presence of premalignant lesions

24
Q

what are two examples of premalignant lesions associated with classic oral SCC?

A

erythroplakia and leukoplakia

25
Q

how is leukoplakia defined?

A

a white patch or plaque that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease

26
Q

what % of leukoplakias end up to be precancerous?

A

25%

27
Q

how is erythroplakia defined?

A

a red, velvety, possibly eroded area within the oral cavity that usually remains level with or may be slightly depressed in relation to the surrounding mucosa

28
Q

which is worse, leukoplakia or erythroplakia?

A

erythroplakia- this premalignant lesions is almost always associated with severe dysplasia/ carcinoma in situ

29
Q

what are the characteristics of dysplasia?

A

pleomorphism, increased mitotic figures, loss of architectural orientation, and loss in cell uniformity

30
Q

what two histologic terms should point you directly towards SCC?

A

keratin pearls and intercellular bridges

31
Q

what is a marker for SCC?

A

p63 and cyclin D1

32
Q

what is the theory of field cancerization?

A

multiple independent primary tumors develop as the result of years of chronic exposure of the mucosa to carcinogens

33
Q

how do first primary tumors compare to second primary tumors?

A

first primary tumors have a much higher survival rate, whereas second primary tumors are the most common cause of death