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(J2) GI II Test 1 > Oral Cavity and Salivary Glands > Flashcards

Oral Cavity and Salivary Glands Flashcards

1
Q

What are dental caries?

(causes and prevention)

A

Tooth decay

Cause:

-demineralization of of tooth due to acid producing bacteria (Streptococcus mutans)

Prevention:

  • good oral hygine
  • avoid high sugar intake
  • fluoride
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2
Q

What is gingivitis?

(cause)

A

gingival erythema, edema, and bleeding

Cause:

  • biofilm that forms on and between teeth
  • accumulation leads to plaque formation which can calcify (tartar)
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3
Q

What is periodontitis?

(cause)

A

inflammation of support structures of the teeth (ie. periodontal ligament)

Cause:

-shift in oral flora from gram (+), facultative anaerobes to gram (-), anaerobes -> inflammation

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4
Q

What are possible complications of periodontitis?

A
  • tooth loss (periodontal ligament damage)
  • brain abscess
  • infective endocarditis
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5
Q

What are aphthous ulcers?

(cause)

A

shallow, grayish painful ulcerations; thin layer of exudate and narrow rim of erythema

  • resolve spontaneously (7-10 days)
  • likely to recur

Cause:

  • unknown etiology
  • associated with immune disorders
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6
Q

What is an oral traumatic/irritation fibroma?

(description and treatment)

A

benign, fibrous, nodular mass on inner buccal surface along bite line (caused from irritaiton of biting cheek)

-submucosal fibrous proliferation; fairly circumscribed

Treatment:

-complete excision

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7
Q

What is an oral pyogenic granuloma?

(description and treatment)

A

benign, soft, ulcerated red/purple mass along gingiva

-high vascularized (red -> not truly pyogenic) proliferation of granulation tissue

Treatment:

  • complete excision
  • can regress or progress to ossifying fibroma
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8
Q

What condition are pyogenic granulomas classically associated with?

A

pregnancy: they are also called “pregnancy tumors”

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9
Q

What is an oral ossifying fibroma?

(description and treatment)

A

benign, firm, red ulcerated/nodular lesion on gingiva

-fibrous and ossifying -> firm (differentiates from pyogenic granuloma)

Treatment:

  • excision down to periosteum
  • recurrent and originate form periodontal ligament
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10
Q

What are oral tori?

A

bony outgrowth (exostoses) in the oral cavity

  • most commonly of the palate -> torus palatinus
  • typically asymptomatic
    (ddx: adenoid cystic carinoma -> commonly forms mass on palate)
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11
Q

How does HSV infection present in the oral cavity?

A

Acute herpetic gingivostomatitis:

HSV-1 > HSV-2

  • vesicles with clear fluid; rupture to form painful, red-rimmed, shallow ulcers
  • vesicles/ulcers last for ~3-4 weeks
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12
Q

How is an HSV infection diagnosed?

A

Tzanck test:

-vesicular fluid/base sample shows multinucleated giant cells w/ possible viral inclusion bodies

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13
Q

What is a long-term complication of oral HSV infection?

A

Recurrent herpetic stomatitis:

  • original infection migrates to nerve ganglia where it become dormant
  • can later be reactivated (sunlight and stress) to affect area associated with infected ganglia -> cold sores
  • trigeminal ganglia most commonly affected
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14
Q

How does candidia infection present in the oral cavity?

(appearance and risk factors)

A

Thrush:

white/gray membrane that is easily scraped off revealing erythematous base

-pseudohypae on budding yeast (microscopic)

Risk factors:

  • broad spectrum abx -> change in oral flora
  • compromised immune system (HIV/AIDS, pregnancy, DM)
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15
Q

What deep fungal infections present in the oral cavity?

(risk factor and potential complication)

A
  • Aspergillus
  • Cryptococcus
  • Zygomycetes (mucor)

Risk factor:
-immunosupression

Complications:

-brain, sinus, and orbital infections

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16
Q

What is an identifying characteristic of Aspergillus?

A

45° angle, branching pseudohypae w/ septae

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17
Q

How does scarlet fever present in the oral cavity?

A

Strawberry/raspberry tongue (white/red, respectively, tongue with prominent papilae)

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18
Q

How does measles present in the oral cavity?

A

Koplik spots

-ulcerations surrounding opening of parotid duct

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19
Q

How does mononucleosis present in the oral cavity?

A
  • palatal petheciae
  • pharyngitis/tonsilitis
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20
Q

How does diptheria present in the oral cavity?

A

tough pseudomembrane over tonsils/retropharynx -> heavy bleeding if removed

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21
Q

How does HIV present in the oral cavity?

A

Hairy leukoplakia:

-“hairy” thickening that can’t be scraped off of side of tongue

-hyperkeratotis and acanthotic w/ “balloon” cells in stratum spinosum (microscopic)

-caused by EBV infection

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22
Q

How does SJS/TEN present in the oral cavity?

A
  • oral ulcers
  • stomatitis
  • cheilitis
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23
Q

How does leukemia present in the oral cavity?

A

monocytic AML w/ leukemia cutis:

-infiltration of skin and gingiva with monocytes

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24
Q

How does Peutz-Jeghers syndrome present in the oral cavity?

(what is this a risk factor for)

A

polyps and hyperpigmented spots in the mouth

risk factor for cancer (particularly colon cancer)

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25
Q

What drug is particularly associated with gingival hyperplasia?

A

phenytoin (dilantin) anticonvulsant medication

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26
Q

What is Osler-Weber-Rendu disease?

A

Hereditary hemorrhagic telangiectasia

autosomal dominant vasulopathy resulting in telangiectasias in skin and mucosa

-favors face (nasal and oral cavities) -> epistaxis and GI bleeds

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27
Q

What is a multilocular keratocystic odontogenic tumor?

What sets it apart from other odontogenic cysts?

A

epithelium-lined cyst derived from odontogenic epithelium

  • this particualr type is especially aggressive and can recur
  • more common in males between age of 10-40

(epithelium lined cysts are relatively rare in the skeleton aside from the odontogenic type which occurs in the jaw)

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28
Q

What is the most common cancer of the head and neck?

A

Squamous cell carcinoma

29
Q

What are the risk factors for oral squamous cell carcinoma?

A
  • HPV
  • tobacco
  • alcohol
  • betel quid and paan (India/Asia)
  • radiation
30
Q

What are the main types of oral SCC?

A
  • HPV-induced SCC
  • classic oral SCC (tobacco related/HPV negative)
31
Q

What is the clincal presentation of oral SCC?

A
  • dysphagia
  • weight loss
  • sore throat
  • ear ache
  • lymph node mass (cervical)
32
Q

What is the histological appearance of oral SCC?

A

wide variety of appearances based on varying degrees of differentiation

-well differentiated shows more keratinization

level of differentiation has little impact on behavior of lesion

33
Q

Where does HPV-induced oral SCC typcially occur?

A
  • tonsils
  • base of tongue
  • pharynx

HPV has a tropism for lymphoid structures which are largely located in the oropharynx

34
Q

What is the mechanism of EBV-induced oral SCC?

A

EBV proteins E6 and E7 inhibit tumor supressors p53 and RB respectively

35
Q

What molecule acts as a diagnostic marker for HPV-induced oral SCC?

What else is this marker used for?

A

p16; it is upstream of Rb which is inhibited by HPV E7, causing it to accumulate

It is also used as a prognostic factor

36
Q

Where does classic oral SCC typcially occur?

A
  • ventral tongue
  • floor of mouth
  • lower lip
  • soft palate
  • gingiva

(think more oral cavity compared to HPV-induced)

37
Q

What is the mechanism of classic oral SCC?

A

Typically preceded by premalignant lesions (erythroplakia/leukoplakia)

loss of function of p53 -> tobacco related carcinogens cause accumulation of mutations

p63 and NOTCH1 mutations also common

38
Q

What are the premalignant lesions of oral SCC?

A
  • leukoplakia
  • erythroplakia
39
Q

What is leukoplakia?

A

precancerous lesion for SCC

White plaque that cannot be scraped off (not the same as hairy leukoplakia)

40
Q

What is erythroplakia?

A

precancerous lesion for SCC

red, velvety lesion (essentially a more vascularized leukoplakia)

  • possible erosion
  • can be raised or depressed
41
Q

Which oral precancerous lesion is more concerning?

A

erythroplakia: almost always has severe dysplasia

42
Q

What is the treatment for leukoplakia and erythroplakia?

A

biopsy, both have high enough risk of becoming malignant

43
Q

What is a common epidemiological feature of oral SCCs and precancerous lesions?

A

they all have male predominance

44
Q

What is the prognosis of HPV-induced oral SCC?

A

better than classic oral SCC, responds better to therapy

-p16 used as prognostic factor

45
Q

What is the prognosis of classic oral SCC?

A

worse than HPV-induced

  • classic is typically caught in later stages
  • screening for precancerous lesions improves survivability
  • has a propensity to form multiple, independent primary tumors -> field cancerization (tobacco induced carcinogenesis occurs in multiple places due to prolonged, diffuse exposure of oral cavity)
  • secondary tumors are most common cause of death
46
Q

What is xerostomia?

(causes)

A

dry mouth due to lack of saliva production from salivary glands

Cause:

  • medications (anticholinergic, antidepressant/psychotic, antihypertensive, antihistamine, diuretics, muscles relaxants, sedatives, analgesics)
  • Sjögren syndrome (autoimmune)
  • radiation
47
Q

What is sialadenitits?

(causes)

A

inflammation of the salivary glands

Causes:

  • trauma (mucocele and ranula)
  • autoimmune (Sjögren)
  • viral (mumps)
  • bacterial (sialolithaiasis -> Staph aureus/Strep viridians)
48
Q

What is the most common lesion of the salivary glands?

A

mucocele

49
Q

What is a mucocele?

(cause and appearance)

A

blueish fluctuant, fluid-filld lesion

-granulation tissue lined cyst (microscopic)

-most commonly on the lower lip

caused by trauma resulting in damage/obstruction to salivary gland ducts -> secretions spill out into surrounding tissue

most prominent in tolders and elderly (due to increased fall risk)

50
Q

What is a ranula?

(cause and appearance)

A

fluid-filled lesion of the sublingual gland duct

  • epithelial-lined cyst (microscopic)
  • under the tongue

caused by trauma resulting in damage/obstruction to sublingual gland duct -> secretions spill out into surrounding tissue

-can worsen to disect down through mylohyoid -> plunging ranula

51
Q

What is the most common tumor of the salivary glands?

(benign or malignant)

A

pleomorphic adenoma/mixed tumor (benign)

52
Q

What is the most common malignant tumor of the salivary glands?

A

mucoepidermoid cacinoma

53
Q

What is the general trend of tumor location in salivary glands?

What is the general trend of a tumor being malignant vs. benign salivary gland tumors?

A

Larger glands have an increased tumor risk

tumor prevalence:

parotid > submandibular > sublingual

Smaller glands have an increased risk of metastatic tumors

metastatic prevalence

sublingual > submandibular > parotid

54
Q

What is the epidemiology of salivary gland neoplasms?

A
  • female predominance
  • 50-70 for benign
  • 70+ for malignant
55
Q

What is a pleomorphic adenoma/mixed tumor?

(description)

A

benign, mixed epithelial and mesnchymal (divergent differentiation) salivary gland tumor

-well demaracted, partially encapsulated, rounded mass -> protrusions into surrounding tissue

-very heterogenous appearing (microscopic)

56
Q

Where are salivary pleomorphic ademona/mixed tumors seen?

A
  • predominately parotid glands (60% of all parotid tumors)
  • less common in submandibular glands
  • rare in minor salivary glands
  • almost never multifocal or bilateral
57
Q

What is the prognosis for pleomorphic adenoma/mixed tumor?

A
  • incompletely encapsulation -> protrusions that are missed upon enucleation -> recurrence
  • parotidectomy -> greatly reduced recurrence
  • can transform to an aggressive malignant cancer
  • transformation risk increases with age
58
Q

What gene rearrangement is associated with pleomorphic adenoma/mixed tumor?

A

PLAG1 (PLeomomorphic Adenoma)

59
Q

What is a Warthin tumor (papillary cystadenoma lymphomastosum)?

(description)

A

benign salivary gland tumor

  • well encapsulated, rounded mass
  • cystic spaces lined by a double layer of epithelium cells
  • “oncocytic” appearance of epithelial cells
  • lymphocytic infiltrate of the stroma
60
Q

What is associated with development of a Warthin tumor?

What characteristic of Warthin tumor is partially explained by this?

A

Smoking -> 8x increased risk

(it can occur bilaterally, that is likely attributed to smoking and field cancerizatin or some similar mechanism)

61
Q

Where are Warthin tumors seen?

A
  • only parotid gland
  • can be bilateral (unlike pelomorphic adenoma)
62
Q

What is odd about the epidemiology of Warthin tumors?

A

they are male predominant, unlike most other salivary gland tumors which are female predominant

63
Q

What is mucoepidermoid carcinoma?

(description)

A

malignant tumor of salivary glands

-cyst-like spaces filled with mucus

64
Q

Where are mucoepidermoid carcinomas seen?

A

-primarily parotid gland

65
Q

What gene rearrangement is associated with mucoepidermoid carcinoma?

A

MECT1-MAML2

(MucoEpidermoid Carcinoma)

66
Q

What is adenoid cystic carcinoma?

(description)

A

malignant salivary gland tumor

  • cribiform pattern
  • perineural spread
67
Q

Where are adenoid cystic carcinomas seen?

A

mostly minor salivary glands

-palatal mass (ddx torus palatinus)

68
Q

What is the prognosis of adenoid cystic carcinoma?

A
  • good short term prognosis, it is slow growing
  • it tends to spread along nerves so it can recur years later with a greatly poorer prognosis
69
Q

What part of the clinical presentation of adenoid cystic carcinoma seperates it from most of the other salivary gland tumors?

A
  • it has perinerual growth -> pain
  • more predominant in minor salivary glands than other tumors

(J2) GI II Test 1 (14 decks)

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