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2.1 Elizabeth DSA cards GI 2 Exam 1 COPY > Path: Oral Cavity, Salivary glands > Flashcards

Path: Oral Cavity, Salivary glands Flashcards

1
Q

focal demineralization of tooth structure (enamel and dentin) by acidic metabolites of fermenting sugars that are produced by bacteria

A

dental caries (tooth decay)

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2
Q

what is incorporated into crystalline structure of enamel, contributing to the resistance to degradation by bacterial acids?

A

fluoride -> forms fluoroapatite

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3
Q

rate of dental carries in US vs. developed nations?

A
  • decreasing in US d/t improved dental hygiene

- increasing in developing nations d/t increased consumption of processed foods

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4
Q

inflammation of the oral mucosa surrounding the teeth

  • result of poor oral hygiene
  • leads to accumulation of dental plaque and calculus
A

gingivitis

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5
Q

sticky, colorless biofilm that collects between and on the surface of teeth
- mixture of bacteria, salivary proteins, and desquamated epithelial cells

A

dental plaque

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6
Q

bateria in plaque release acids from sugar and rich foods, thereby eroding the enamel surface and contributing to the development of?

A

caries

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7
Q

inflammatory process that affects the supporting structures of the teeth (periodontal ligaments), alveolar bone, and cementum

A

periodontitis

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8
Q

periodontitis can lead to what?
- including complete destruction of the periodontal ligament, which is responsible for the attachment of the teeth to alveolar bone, leading to loosening and eventual loss of teeth

A

serious squelae

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9
Q

adult periodontitis is associated primarily with what 3 organisms?

A
  • A. actinomycetemcomitans
  • Porphyromonas gingivalis
  • Prevotella intermedia
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10
Q

periodontal disease can be a component of systemic diseases such as?

A
  • AIDS
  • leukemia
  • Crohn disease
  • DM
  • Down symdrome
  • sarcoidosis
  • syndromes assoc with defects in neutrophils
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11
Q

periodontal infections can be the origin of important systemic diseases, including:

A

infective endocarditis, and pulmonary or brain abscesses

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12
Q

common, often recurrent, exceedingly painful, superficial oral mucosal ulcerations of unknown etiology

A

aphthous ulcers (canker sores)

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13
Q

tend to be prevalent within certain families and may also be associated with immunologic disorders including celiac disease, inflammatory bowel disease, and Behcet disease

A

aphthous ulcers

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14
Q

submucosal nodular mass of fibrous connective tissue stroma, that occurs primarily on the buccal mucosa long the bite line or gingiva

A

traumatic fibroma (irritation fibroma, focal fibrous hyperplasia)

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15
Q

inflammatory lesion typically found on the gingiva of children, young adults and pregnant women (pregnancy tumor)
- highly vascular proliferation of organizing granulation tissue

A

pyogenic granuloma

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16
Q

common gingival growth that is most likely reactive in nature rather than neoplastic

  • some may arise from long-standing pyogenic granuloma, while others develop denovo from cells of the periodontal ligament
  • peak incidence is young females
A

peripheral ossifying fibroma

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17
Q

uncommon lesion of oral cavity

  • reactive/inflammatory growth that is covered by intact gingival mucosa, but it may be ulcerated
  • lesions are well delimited and easily excised
A

peripheral giant cell granuloma

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18
Q

most orofacial herpetic infections are caused by which Herpes type?

A

HSV-1

- but oral HSV-2 (genital herpes) infections do occur

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19
Q

abrupt onset of vesicles and ulcerations of the oral mucosa, particularly the gingiva
- accompanied by lymphadenopathy, fever, anorexia, and irritability

A

acute herpetic gingivostomatitis

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20
Q

what occurs at the site of primary inoculation or in adjacent mucosa associated with the same ganglion?

A

recurrent herpetic stomatitis

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21
Q

what other viral infections can involve the oral cavity as well as head and neck region?

A

herpes zoster (chicken pox/shingles), EBV, cytomegalovirus, enterovirus (hand-foot-mouth dz), and rubeola (measles)

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22
Q

normal component of the oral flora in approx 50% of the population, the most common fungal infection of the oral cavity

A

candida albicans

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23
Q

what are the three major clinical forms of oral candidiasis?

A

pseudomembranous (most common = thrush), erythematous, and hyperplastic

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24
Q

superficial gray to white inflammatory membrane composed of matted organisms enmeshed in a fibrinosuppurative exudate that can be readily scraped off to reveal underlying erythematous inflammatory base

A

thrush (pseudomembranous candidiasis)

NOTE: infection typically remains superficial except in the setting of immunosuppression, or those on broad-spectrum antibiotics

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25
Q

fiery red tongue with prominent papillae (raspberry tongue); white coated tongue through which hyperemic papillae project (strawberry tongue)

A

scarlet fever

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26
Q

spotty erythema in the oral cavity often precedes the skin rash; ulcerations on the buccal mucosa about Stensen (parotid) duct produce Koplik spots

A

measles

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27
Q

acute pharyngitis and tonsillitis that may cause coating with a gray-white exudative membrane; enlargement of lymph nodes in the neck, palatal petechiae

A

infectious mononucleosis

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28
Q

characteristic dirty white, fibrinosuppurative, tough, inflammatory membrane over the tonsils and retropharynx

A

diphtheria

29
Q

predisposition to opportunistic oral infections, particularly herpes virus, Candida, and other fungi; oral lesions of Kaposi sarcoma and hairy leukoplakia

A

HIV

30
Q

severe oral infections in the form of gingivitis, pharyngitis, tonsillitis; may extend to produce cellulitis of the neck

A

pancytopenia (agranulocytosis, aplastic anemia)

31
Q

leukemic infiltration and enlargement of the gingiva, often with accompanying periodontitis

A

monocytic leukemia

32
Q

distinctive oral lesion on the lateral border of the tongue that is usually seen in immunocompromised patients and is caused by EBV

  • white, confluent patches of fluffy “hairy” hyperkeratotic thickenings
  • microscopic appearance of hyperparakeratosis and acanthosis with “balloon cells” in the upper spinous layer
A

hairy leukoplakia

33
Q

white patch or plaque (buccal mucosa, floor of mouth, ventral surface of tongue, palate, gingiva) that cannot be scraped off and cannot be characterized clinically or pathologically as any other disease
- age 40-70, 2:1 M:F

A

leukoplakia

  • approx 3% of the worlds population have these lesions -> 5-25% of those are premalignant
  • until proven otherwise by histologic evaluation, all leukoplakias must be considered precancerous
34
Q

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

  • much less common than laukoplakias, but much more ominous*
  • age 40-70, 2:1 M:F
A

erythroplakia

  • epithelium is atypical, and the risk of malignant transformation is much higher
  • 90% disclose severe dysplasia, carcinoma in situ, or minimally invasive carcinoma
35
Q

approx 95% of cancers of the head and neck

  • 6th most common neoplasm in the world
  • multifactoral pathogenesis
A

SCC

- with the remainder largely consisting of adenocarcinomas of salivary gland origin

36
Q

within North America and Europe, classically a disease of middle-aged smokers and drinkers
- in India and Asia, chewing of betel quid and paan is predisposing factor

A

SCC

37
Q

actinic radiation (sunlight) and pipe smoking are predisposing influence for?

A

cancer of the lower lip

38
Q

what HPV strain is associated with 70% of SCC’s of the oropharynx, particularly those involving the tonsils, the base of the tongue, and the pharynx?
- is relatively uncommon

A

HPV-16

NOTE: HPV-assoc SCC incidence has doubled over the last 20 years

39
Q

concept that multiple individual primary tumors develop independently in the upper aerodigestive tract as a result of years of chronic exposure of the mucosa to carcinogens

A

field cancerization
- individual that survives 5 years after initial detection has 35% chance of developing at least 1 new primary tumor within that period of time

40
Q

large number of genetic alterations that bear a molecular signature consistent with tobacco carcinogen induced caners, frequently involve what pathway, as well as what proteins?

A

p53, as well as p63 and NOTCH1 (proteins responsible for the regulation of squamous differentiation)

41
Q

what genetic alterations are responsible for HPV-associated SCC?

A
  • overexpression of p16

- HPV oncoproteins E6 and E7 lead to inactivation of p53 and RB pathways, similar to cervical cancer

42
Q

what do the early stages of oral cavity cancers look like?

A

either as raised, firm, pearly plaques, or as irregular, roughened, or verrucous areas of mucosal thickening, possible mistaken for leukoplakia
NOTE: either pattern may be superimposed on a background of apparent leukoplakia or erythroplakia

43
Q

what happens are oral cavity lesions enlarge?

A

they typically create ulcerated and protruding masses that have irregular and indurated (rolled) borders

44
Q

how does oral cavity SCC progression differ from cervical cancer?

A

oral cavity SCC begins as dysplastic lesions, which may or may not progress to full-thickness dysplasia (CIS) before invading the underlying tissue stroma
- in cervical cancer, full-thickness dysplasia (CIS) develops BEFORE invasion

45
Q

range from well-differentiated keratinizing neoplasms to anaplastic, sometimes sarcomatoid tumors, and from slowly to rapidly growing lesions

A

oral cavity SCC

46
Q

what are the favored sites of local and distant metastasis for oral cavity SCC?

A
  • local: cervical lymph nodes

- distal: mediastinal lymph nodes, lungs, liver, bones

47
Q

an important lesion that must be differentiated from other odontogenic cysts because of it’s aggressive behavior

  • most often diagnosed in pt aged 10-40
  • more commonly in males
  • within the posterior mandible
A

odontogenic keratocyst (OKC), aka keratocystic odontogenic tumor

48
Q
  • radiographically: well-defined unilocular or multilocular radiolucencies
  • histologically: cyst lining consists of a thin layer of keratinized stratified squamous epithelium with a prominent basal cell layer and corrugated epithelial surface
A

OKC

- 80% are solitary lesions, 20% are multiple OKCs

49
Q

what is the tx for OKC?

A

complete removal! because they are locally aggressive

- recurrent rates for inadequately removed lesions can reach 60%

50
Q

dry mouth, resulting from a decrease in the production of saliva

  • major feature in Sjogren syndrome
  • may present as dry mucosa and/or atrophy of the papilae of the tongue, with fissuring and ulcerations
A

xerostomia

51
Q

what is xerostomia most frequently a side effect of?

A

many commonly prescribed classes of medications, including anticholinergic, antidepressant/antipsychotic, diuretic, antihypertensive, sedative, muscle relaxant, analgesic and antihistamine drugs

52
Q

what might also be observed in conditions such as Sjogrens (along with xerostomia)?

A

concominant inflammatory enlargement of the salivary glands

53
Q

what are complications of xerostomia?

A

increased rates of dental caries, candidiasis, as well as difficulty swallowing and speaking

54
Q

lesions of the salivary glands induced by trauma, viral or bacterial infection, or autoimmune disease

A

sialadenitis

55
Q

what are the most common type of inflammatory salivary gland lesion?

  • results from either blockage of rupture of a salivary gland duct, with consequent leakage of saliva into the surrounding connective tissue stroma
  • most common in toddlers, young adults and elderly (more prone to falling)
A

mucoceles

56
Q

what are the most common viral form of sialadenitis?

A

mumps, in which mainly the parotid glands are affected

57
Q

pseudocysts with cyst-like spaced lined by inflammatory granulation tissue or by fibrous connective tissue- cyst spaces filled with mucin and inflammatory cells, particularly macrophages

A

mucoceles

58
Q

epithelial-lined cyst that arises when the duct of the sublingual gland has been damaged

A

ranula

59
Q

common condition, usually secondary to ductal obstruction produced by stones, most often involving the major salivary glands (submandibular)

A

sialolithiasis, nonspecific bacterial sialadenitis

- sometimes occurs in patients receiving long-term phenothiazines that suppress salivary secretion

60
Q

what are the most common offenders of sialolithiasis?

A

S. aureus and Strep vidrians

61
Q

BENIGN tumors that consist of a mixture of ductal (epithelial) and myoepithelial cells, and therefore show both epithelial and mesenchymal differentiation

  • represent about 60% of tumors in the parotid, are less common in the submandibular glands, relatively rare in the minor salivary glands
  • present as painless, slow-growing, mobile, discrete masses within the parotid or submandibular areas or in the buccal cavity
A

pleomorphic adenoma, aka mixed tumors (d/t their diversity)

62
Q

epithelial elements dispersed throughout the matrix, along with varying degrees of myxoid, hyaline, chondroid (cartilage) and even osseous tissue

A

pleomorphic adenoma

63
Q

a high fraction of pleomorphic adenoma are associated with chromosomal rearrangements involving what?

A

PLAG1

- overexpression leads to increased cell growth

64
Q

BENIGN tumor that arises almost exclusively in the parotid gland (only tumor virtually restricted to the parotid*)

  • occurs more commonly in males than females in their 50-60’s
  • smokers have 8x higher risk
A

Warthrin tumor, aka papillary cystadenoma lymphomatosum

65
Q

round to oval encapsulated masses, 2-5cm in diameter, usually arising in superficial parotid gland (where they are readily palpable)

  • transection reveals pale gray surface punctuated by narrow cystic or cleft-like spaces filled with mucinous or serous secretions
  • distinct double layer of lining cells: upper layer of palisading columnar cells with eosinophilic cytoplasm, lower layer of cuboidal to polygonal cells
A

Warthin tumor

66
Q

variable mixture of squamous cells, mucus-secreting cells, and intermediate cells

  • occur mainly in parotids (60-70%), but also account for a large fraction of salivary gland neoplasms (particularly the minor salivary glands)
  • can grow as large as 8cm, lack well-defined capsules and are often infiltrative at the margins
  • most common form of primary malignant tumor of the salivary glands
A

mucoepidermoid carcinoma

67
Q

what salivary gland cancer is assoc with a balanced (11;19)(q21;p13) translocation, creating a fusion gene composed of portions of MECT1 and MAML2 genes?

A

mucoepidermoid carcinoma
- the MET1-MAML2 fusion gene is believed to play a role in the genesis of this tumor, possibly perturbing the NOTCH and cAMP signaling pathways

68
Q

relatively uncommon tumor, which in approx 50% of cases is found in the minor (palatine) salivary glands, but also in the parotid and submandibular glands

  • generally small, poorly encapsulated, infiltrative, gray-pink lesions
  • histo: small cells with dark, compact nuclei and scant cytoplasm, and spaces between cells filled with hyaline material
A

adenoid cystic carcinoma

69
Q

although they are slow growing, they are unpredictable tumors with a tendency to invade perineural spaces
- neoplasms arising in the minor salivary glands have a poorer prognosis than those that arise in the parotid glands

A

adenoid cystic carcinoma

2.1 Elizabeth DSA cards GI 2 Exam 1 COPY (22 decks)

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