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OMS Board Review > 8. Oral Pathology > Flashcards

8. Oral Pathology Flashcards

1
Q

Histologic features of OKC

A

Cyst lined by thin layer of parakeratotic stratified squamous epithelium, which is usually 6-8 layers thick

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2
Q

Nevoid basal cell carcinoma syndrome (Gorlin syndrome)

A

-Multiple basal cell carcinomas
-Multiple OKCs
-Palmar and plantar pits
-Calcified falx cerebri
-Rib anomalies (bifid, missing, partially developed)
-Spina bifida
-Hypertelorism
-Enlarged head circumference due to frontal bossing
-Cleft lip and palate

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3
Q

Odontogenic tumors arising from odontogenic epithelium (6)

A
  • Ameloblastoma
  • Calcifying odontogenic cyst (Gorlin Cyst)
  • Calcifying epithelial odontogenic tumor (CEOT)
  • Adenomatoid odontogenic tumor (AOT)
  • Squamous odontogenic tumor
  • Clear cell odontogenic tumor
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4
Q

Odontogenic tumors arising from odontogenic mesenchyme (4)

A
  • Central odontogenic fibroma
  • Odontogenic myxoma
  • Cementifying fibroma
  • Cementoblastoma
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5
Q

Odontogenic tumors arising from BOTH epithelium and mesenchyme (4)

A
  • Ameloblastic fibroma
  • Ameloblastic fibro-odontoma
  • Ameloblastic fibrosarcoma
  • Odontoma
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6
Q

Ameloblastoma histological subtypes (5)

A
  • Follicular pattern
  • Plexiform pattern
  • Acanthomatous pattern
  • Granular cell type
  • Desmoplastic type
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7
Q

Unicystic ameloblastoma subtypes

A
  • Unicystic
  • Intraluminal type
  • Mural type
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8
Q

Fibro-Osseous Lesions

A

Disease process characterized by normal bone being replaced by fibrous tissue containing a mineralized product.
- Fibrous dysplasia
- Cemento-osseous dysplasia (COD)

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9
Q

MRONJ staging

A

Stage 0: non-exposed bone variant. Non-specific symptoms such as bone pain and unexplainable tooth pain. May have radiographic bone changes not attributable to other source.

Stage 1: exposed and necrotic bone or fistulae that probe to bone in asymptomatic patients with no evidence of infection

Stage 2: Exposed and necrotic bone or fistulae that probe to bone in symptomatic patients with evidence of infection

Stage 3: exposed and necrotic bone or fistulae that probe to bone in symptomatic patients with infection and one or more of the following:
- Exposed necrotic bone extending beyond the alveolus
- Pathologic fracture
- Extra-oral fistula
- Oral antral/oral nasal communication
- Osteolysis extending to the inferior border of the mandible or sinus floor.

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10
Q

Osteoradionecrosis of the jaw risk factors

A
  • Radiation dose >60 Gy
  • Primary tumor in tongue, FOM, alveolar ridge, retromolar triangle, or tonsil
  • Higher stage cancer requiring ostectomy or mandibulectomy
  • Periodontal disease, poor hygiene, dental extractions after radiation, alcohol use, tobacco use, and poor nutrition
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11
Q

Marx “3H theory” for ORN

A

Hypoxic-hypocellular-hypovascular tissue caused by radiation

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12
Q

How does HBO work?

A

Increases tissue oxygenation by stimulating angiogenesis. Also stimulates fibroblast proliferation and collagen formation, which leads to healing. The increased oxygen tension is bactericidal and bacteriostatic.

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13
Q

Marx HBO protocol for treatment of osteoradionecrosis

A

30 HBO dives (100% O2 breathed at 2.4 atmospheres for 90 minutes).

Re-evaluate patient after 30 dives. If improvement (decrease in exposed bone, granulation tissue formation, or re-mucosalization), patient completes full course of up to 60 total dives for full mucosal coverage.

If no improvement after initial 30 dives, patient advanced to stage II. This involves trans-oral debridement or sequestrectomy with primary mucosal repair. If healing progresses, patient completes up to 60 dives. If recurrent bone exposure, patient advanced to stage III.

Stage III, after 30 dives, patient undergoes resection to bleeding bone with primary wound closure and external fixation. Patient then dives until there is complete mucosal closure or a total of 60 accumulated dives.

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14
Q

HBO protocol for prevention of osteoradionecrosis

A

Patients that have received previous tumoricidal head and neck radiation should receive prophylactic HBO therapy prior to oral surgical procedures.

20 dives of HBO followed by 10 dives postoperatively.

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15
Q

4 major types of melanoma

A
  1. superficial spreading (most common, trunk + extremities)
  2. lentigo maligna (face + neck)
  3. nodular (trunk and extremities)
  4. acral lentiginous (rare, palms, soles, mucous membranes, nail beds. African or Asian descent. Most common ORAL form. Worse prognosis).
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16
Q

Breslow depth

A

Measure of prognosis of melanoma (most closely linked to primary tumor thickness vs. subtype).

Breslow depth greater than 1-4mm or with ulceration, sentinel lymph node biopsy is indicated.

For depths greater than 4mm, lymph node dissection should be considered.

Also dictates margin of resection:
Melanoma in-situ 0.5cm
<1mm 1cm
1.01-2.0mm 1-2cm
>2mm 2cm

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17
Q

How is cutaneous melanoma staged?

A

T = THICKNESS (mm)
TX (cannot be assessed)
T0 (no evidence of primary tumor)
Tis (melanoma in situ)
T1 (melanomas 1.0mm or less)
T2 (melanomas >1.0-2.0mm
T3 (melanomas >2.0-4.0mm)
T4 (melanomas >4.0mm)

(a without ulcaration, (b) with ulceration

N = No. OF METASTATIC NODES
NX (cannot be assessed)
N0 (no regional metastases)
N1 (one node)
N2 (two-three nodes)
N3 (four or more tumor-involved nodes)

M = METASTASES
M0 (no distant metastases)
M1a (metastases to skin, muscle or non-regional lymph nodes)
M1b (metastases to lung)
M1c (metastases to CNS)

(0) if LDH normal
(1) if LDH elevated

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18
Q

What are the risk factors for primary mucosal melanoma?

A

Unlike cutaneous counterpart, no association with UV exposure.

Inhaled and ingested carcinogens (smoking, formaldehyde).

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19
Q

Most common form of oral mucosal melanoma

A

Acral lentiginou smelanoma (maxillary alveolar ridge and hard palate)

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20
Q

How is mucosal melanoma staged?

A

TNM

T:
T3 mucosal disease. Limited to mucosa and underlying soft tissue regardless of greatest dimension.
T4a moderately advanced invading deep soft tissue, cartilage, bone or overlying skin
T4b very advanced involving brain, dura, skull base, cranial nerves, masticator space, carotid artery, prevertebral space, mediastinal structures.

N:
NX cannot be assessed
N0 no regional nodes
N1 regional node metastasis

M:
M0 no distant metastases
M1 distant metastases

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21
Q

How is primary mucosal melanoma treated

A

Complete surgical resection, wide dissection of 3cm.

Lymph node dissection on patients with evident regional metastasis. Even in absence of clinically evident nodes, sentinel node biopsy is useful.

Radiation therapy used if patient is poor surgical candidate or margins are inadequate. Ill-defined indications, but usually used only in advanced or recurrent disease.

Chemotherapy offered as palliative care. No increase in 5 year survival.

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22
Q

Basal cell carcinoma 3 subtypes

A
  1. Nodular (most common, shiny or pearlescent papules or nodules with telangiectasias, crusting over central depression or ulceration with rolled border).
  2. Superficial (second most common, scaly pink-red macules on trunk/extremities, least aggressive).
  3. Morpheaform (rarest, indurated plaques, resemble scars, behave more aggressively)
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23
Q

AJCC 8th edition TNM classificaiton of cutaneous squamous cell carcinoma and other cutaneous carcinomas (BCC)

A

T:
TX- primary tumor cannot be assessed
Tis- carcinoma in situ
T1- 2cm or less
T2- 2-4cm
T3- >4cm and/or perineural invasion or deep invasion or minor bone erosion
T4a- gross cortical bone / marrow invasion
T4b- skull base invasion

N:
NX- regional nodes cannot be assessed
N0- no regional lymph node metastases
N1- Single ipsilateral node <3cm
N2a- single ipsilateral node 3-6cm
N2b- multiple ipsilateral nodes none >6cm
N2c- bilateral or contralateral nodes, none >6cm
N3a- lymph node >6cm
N3b- Extranodal invasion

M:
MX- distant metastases cannot be assessed
M0- no distant metastases
M1- distant metastases

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24
Q

Primary lymphatic drainage of the oral cavity.

What are “skip metastases”?

A

Upper cervical lymph nodes including:
Level 1a (submental)
Level 1b (submandibular)
Level 2 (upper jugular)
Level 3 (middle jugular)

Up to 15% of TONGUE carcinomas can have “SKIP METASTASIS” to level 4 (lower jugular) without involving levels 1, 2, 3.

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25
Q

What is a supraomohyoid neck dissection?

A

Removal of lymph node levels 1, 2, 3.

Some surgeons routinely include level 4 for tongue carcinomas due to possibility of “skip metastasis”.

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26
Q

How are level 2 nodes divided?

A

Level 2a includes nodes anterior to spinal accessory nerve CN11.

Level 2b (submuscular recess above splenius capitis and levator scapulae fascia) includes nodes posterior to CN11.

Controversy regarding removal of level 2b for clinically node negative neck in oral cavity SCC due to small percentage of level 2b involvement (6%) and dreaded complication of shoulder dysfunction and pain syndrome from dissection of CN11.

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27
Q

Most common malignancy in oral cavity

A

Squamous cell carcinoma (more than 90% of oral cavity SCC).

Other malignant tumors of the oral cavity = minor salivary gland cancers, sarcomas, mucosal melanomas, lymphoma.

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28
Q

Most common 3 subsites of oral cancer

A
  1. lateral border of tongue
  2. floor of mouth
  3. buccal mucosa
  4. retromolar trigone
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29
Q

Risk factors oral SCC

A

Tobacco (initiator)
Alcohol (promoter)

Tobacco risk 5-9 fold
Alcohol risk 3-9 fold
Combined alcohol and tobacco 100 fold increase

Some studies = poor oral hygiene, chronic mechanical trauma, vitamin A, C, E deficiency, infectious agents like Candida and syphilis.

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30
Q

HPV association with SCC

A

HPV causes >80% of oropharyngeal SCC as opposed to 3-5% of oral cavity cancers.

HPV positive tumors have improved response to radiation and improved survival compared to HPV negative tumors.

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31
Q

Radiographic imaging used in workup for SCC

A

Dental radiography (50% demineralization required for radiolucency to be discernible)

CT: shows central necrosis, extracapsular spread, bony detail. Lymph nodes >1.5 cm at levels I, II and >1cm at level III are considered metastatic. Should be oval shape, if rounded more suspicious.

MRI: better for perineural invasion. Overestimates bony invasion. MRI with contrast in T1 weighted is best for tongue invasion.

PET-CT: deoxy-glucose (FDG) radiolabeled glucose molecules with radiotracer in PET scans. Any tissue with high metabolic rate lights up. Inflammation lowers specificity. Very high uptake suggestive of metastasis. Lymph nodes with standard uptake value (SUV) > 2.5 are pathological.

CXR: initial screening for distant metastasis or second primary.

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32
Q

Most common distant metastatic sites for SCC

A

lungs, liver, bones

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33
Q

How is oral squamous cell carcinoma classified (TNM)?

A

TNM

Tx: primary tumor cannot be assessed
Tis: carcinoma in situ
T1: tumor <2cm with DOI <5mm
T2: tumor <2cm with DOI 5-10mm OR tumor 2-4cm with DOI <10mm
T3: Tumor >4cm or any tumor with DOI 10-20mm
T4a: moderately advanced local disease invades adjacent structures only (cortical bone, maxillary sinus, skin of face), or extensive with bilateral tongue involvement or DOI >20mm
T4b: very advanced local disease, tumor invades masticator space, pterygoid plates, or skull base and/or encases the internal carotid artery.

Nx: regional lymph nodes cannot be assessed
N0: no regional lymph node metastasis
N1: metastasis in a single ipsilateral lymph node, <3cm
N2: a. metastasis in single ipsilateral node 3-6cm; OR b. multiple ipsilateral lymph nodes <6cm, OR c. bilateral or contralateral nodes <6cm
N3: a. metastasis in lymph node larger than 6cm or b. clinically overt extranodal extension.

M0: no distant metastasis
M1: distant metastasis

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34
Q

How is oral squamous cell carcinoma staged based on TNM?

A

Stage 0: Tis N0 M0
Stage 1: T1 N0 M0
Stage 2: T2 N0 M0
Stage 3: T3 N0 M0; T1/2/3 N1 M0
Stage 4a: T4a N0,1 M0; T1/2/3/4a N2, M0
Stage 4b: T4b any N M0
Stage 4c: Any T Any N M1

In general, early stage 1 or 2 disease defines a relatively small primary tumor (T1, T2) without any nodal involvement or distant metastasis.

Advanced stage 3 or 4 cancers include larger primary tumors (T3 or T4) with metastases to regional nodes or distant sites.

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35
Q

How are early stage oral SCC (Stage 1 and 2) treated?

A

surgery or radiation alone (survival rates comparable, but surgery preferred)

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36
Q

How is advanced stage oral cancer (stages 3 and 4) treated?

A

Surgery as initial treatment modality followed by adjuvant radiation therapy +/- chemotherapy

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37
Q

What are some indications for adjuvant radiation for oral SCC?

A

T3/T4 tumors
Positive or close <5mm margins
2 or more cervical lymph nodes containing metastatic cancer
Perineural or lymphovascular invasion
Extracapsular spread

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38
Q

When should adjuvant radiation be given?

A

within 6 weeks after surgery (poorer outcome with delayed treatment)

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39
Q

What are some indications for adjuvant chemotherapy?

A

Positive resection margins
Extracapsular spread

Improved survival outcome and locoregional control with adjuvant chemoradiation therapy with Cisplatin for these two adverse features. Chemotherapy is used to sensitize cancer cells to the effects of radiation.

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40
Q

Most commonly used chemotherapeutic agent for H&N cancers.

What are its side effects?

What would be used in the case of renal insufficiency?

A

Cisplatin. Given weekly or Q3 weeks.

Side effects include ototoxicity, nephrotoxicity, peripheral neuropathy, gastrointestinal toxicity.

Carboplatin may be used for patients with renal insufficiency.

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41
Q

What is an FDA approved alternative used for patients that cannot tolerate Cisplatin?

A

Cetuximab (monoclonal antibody targeting the endothelial growth factor receptor (EGFR).

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42
Q

When is a neck dissection performed for oral SCC?

A
  • Patients with clinically negative neck with >20% chance of occult regional metastasis: Selective Neck Dissection (only nodal groups determined to be at highest risk for metastasis are removed).
  • Oral tongue SCC with DOI >4mm believed to have >20% chance of regional metastasis, SND.
  • Oral tongue SCC >4mm DOI within 1cm of midline, bilateral neck dissection.

SND often involves “supraomohyoid neck dissection” levels 1-3. Level 4 often included for tongue carcinomas due to skip metastasis.

Nodal positive neck (N+ neck) generally receive comprehensive neck dissection with removal of level 1-5 nodes.

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43
Q

How is comprehensive neck dissection classified?

A

Radical neck dissection (RND)
Modified radical neck dissection (MRND)
Extended neck dissection (END)

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44
Q

Radical neck dissection
vs.
Modified radical neck dissection

A

RND: Radical en bloc lymphadenectomy levels 1-5 along with SCM, IJV, CN11

MRND: same as RND, except preservation of one or more non-lymphatic structures (SCM, IJV, and/or CN11) no invaded by cancer.
- MRND type 1: CN 11 preserved
- MRND type 2: CN 11, IJV preserved
- MRND type 3: CN 11, IJV, and SCM preserved

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45
Q

What is an extended neck dissection?

A

RND or MRND in addition to removal of traditionally preserved anatomic structures such as the carotid artery, hypoglossal nerve, or level 6 or 7 nodes. END is reserved for cancer spread into these extended locations.

46
Q

Describe your technique for a neck dissection

A

Utility incision mastoid process gentle curve over midneck to contralateral submental region.

-Incision skin, subq
-Expose platysma, sharply divide
-Subplatysmal flaps elevated to inferior border of mandible and clavicle
-External jugular vein and greater auricular nerve found over SCM
-MMB encountered with aggregates of level IB nodes
-Nerve should be ID’d with nerve stim or loupes, retract superiorly and protect.
-Fascia over SCM divided, lateral to medial levels 2, 3, 4 exposed
-Spinal accessory nerve is ID’d and dissected from surrounding fascia to level of posterior belly of digastric
-Lymph nodes from levels 2a and 2b can be dissected
-Dissection inferiorly for level III, dissected off IJV, carotid a. Avoid vagus nerve. Dissect nodes from levels 1A and 1B.
-Close with 1-2 suction drains, close platysma, close skin in layers.

47
Q

Describe neurologic dysfunction that can occur as a complication from neck dissection

A

(1) Spinal accessory nerve CN 11: “Shoulder Syndrome” - loss of function of trapezius. Pain, limited arm abduction at shoulder, winging of scapula, loss of contour of the shoulder due to muscle atrophy. Intentional in RND and not a complication. Treatment is PT.

(2) Trunk of facial nerve. Managed best at time of transection with primary repair.

(3) Hypoglossal nerve. Difficulty swallowing and speech. Tongue deviates to affected side.

(4) Phrenic nerve. Ipsilateral elevation of diaphragm. Dyspnea, cardiac irritations, GI symptoms due to displacement of abdominal content.

(5) Vagus nerve: loss of sensatoin to tonsillar region, posterior 1/3 of tongue, pharynx. Diminished movement of soft palate. Deviation of uvula. Difficulty swallowing, aspiration risk.

48
Q

What can be injured primarily during a LEFT neck dissection?

A

Thoracic duct injury. Lead to large loss of plasma, triglycerides, fatty acids, electrolyte disturbances, reduction of immunocompetence due to depletion of circulating lymphocytes and lead to hypoalbuminemia.

Observe for chyle egress (milky, creamy fluid). If identified, oversuture duct. Lab testing of fluid with triacylglycerol level greater than 110 mg/dL or presence of chylomicrons is pathognomonic of chyle leak.

If ID’d postop, conservative management with pressure dressings, suction drains, negative pressure therapy, bed rest, head of bed 30 degrees, fat free diet, broad spectrum antibiotics. No resolution in 14 days, surgical exploration.

49
Q

What is a carotid artery blowout and what is the risk during neck dissection?

A

3-4% of patients who undergo radical neck dissection. Prior radiotherapy increases risk 7 fold. Preceded by heralds or sentinal bleeds. Vessel ligation if frank blow out.

50
Q

How do you perform a carotid artery ligation?

A

Incision through anterior border of SCM, retract posteriorly to expose carotid sheath. Enter carotid sheath, retract IJV laterally, mobilize vagus nerve, and ligate carotid.

51
Q

What is nevoid basal cell carcinoma syndrome?

A

NBCCS is an autosomal dominant inherited condition with features that can include multiple basal cell carcinomas of the skin, multiple OKCs, intracranial calcifications, and rib and vertebral anomalies.

52
Q

Differential diagnosis of multilocular radiolucent lesions

A
  • Ameloblastoma
  • OKC
  • Dentigerous cyst
  • Ameloblastic fibroma
  • Central giant cell tumor
  • Odontogenic myxoma
  • Aneurysmal bone cyst
  • Traumatic bone cyst
  • Calcifying epithelial odontogenic tumor
  • Lateral periodontal cyst
  • Calcifying odontogenic cyst
  • Intraosseous mucoepidermoid carcinoma
  • Hyperparathyroidism (brown tumor)
  • Cherubism
  • Intrabony vascular malformations
53
Q

Histologic features OKC

A

Thin squamous cell epithelial lining (8 cells or fewer)
Lack of rete ridges, epithelial-connective tissue interface is flat
Parakeratinized and corrugated epithelial surface
Hyperchromatic basal cell layer composed of cuboidal cells which show prominent palisading “tombstone” effect

54
Q

If brown tumor of hyperparathyroidism is in the differential diagnosis, what lab value should be obtained?

What must be done for definitive treatment of this lesion?

A

Serum calcium

Tumor is derived from primary hyperparathyroidism, which leads to abundant hemorrhage and hemosiderin deposition within the tumor (giving it a brown color). Removal of hyperplastic parathyroid tissue is necessary in this condition.

55
Q

Differential diagnosis of a unilocular radiolucency

A
  • Dentigerous cyst
  • Calcifying odontogenic cyst
  • OKC
  • Ameloblastoma
  • Odontogenic myxoma
  • Central giant cell granuloma
  • Calcifying epithelial odontogenic tumor (Pindborg tumor)
  • Ameloblastic fibroma
  • Adenomatoid odontogenic tumor
  • Arteriovenous aneurysm of bone and other vascular bone tumors
  • Carcinoma arising in a dentigerous cyst
  • Intraosseous mucoepidermoid carcinoma

BROAD DIFFERENTIAL = lesions of cystic pathogenesis, neoplastic (benign or malignant) lesions, and vascular anomalies (least common)

56
Q

Cyst that shows “ghost cells” on histopath

A

Calcifying odontogenic cyst. Unilocular radiolucency with calcifications in the lining sometimes makes them partially radiopaque. Treatment is by enucleation.

57
Q

Treatment of central giant cell granuloma

A

In addition to aggressive curettage, treatment alternatives include intralesional steroid injection, systemic calcitonin, and treatment with interferon-alpha

58
Q

Uncommon expansile tumor usually seen in younger patients (during first two decades of life)

A

Ameloblastic fibroma: treated with enucleation and curettage, although larger tumors may require resection.

59
Q

Rationale for resection margins of ameloblastoma

A

Average extension into surrounding bone beyond normal tumor margin is 4.5mm (range 2-8mm).

Resection margin should be at least 10mm beyond the bony (radiographic) margin of the tumor for large, multicystic ameloblastomas.

Cure rate for resected tumors 95-98%
High recurrence (70%) with enucleation and curettage alone.

60
Q

Histologic types of ameloblastomas (7)

A
  • Follicular
  • Plexiform
  • Acanthomatous
  • Granular cell
  • Desmoplastic (ant. maxilla/mandible, more radiopaque due to high amt. of dense connective tissue)
  • Basal cell
  • Unicystic (more commonly in younger patients: luminal, intraluminal, and mural. Luminal and intraluminal can be treated with enucleation and close observation, mural types should be treated more aggressively).
61
Q

Differential diagnosis of periapical radiolucent lesions

A
  • Periapical granuloma
  • Residual cyst
  • Cemento-osseous dysplasia (early)
  • Idiopathic bone cavity (simple bone cyst, traumatic bone cyst)
  • Lingual salivary gland depressions (Stafne defect)
  • Neural lesions (neurilemoma, neurofibroma usually associated with mandibular canal)
  • Lateral periodontal cysts
  • Ameloblastoma
  • OKC
  • Central giant cell tumor
  • Intraosseous mucoepidermoid carcinoma
  • Metastatic disease
62
Q

Differential diagnosis of mixed radiolucent-radiopaque lesions

A
  • Fibrous dysplasia
  • Cemento-osseous dysplasia (periapical, focal, and florid)
  • Paget’s disease of bone (osteitis deformans)
  • Osteomyelitis, osteoradionecrosis, and bisphosphonate-induced osteonecrosis of the jaws
  • Osteoblastomas
  • Calcifying odontogenic cyst (Gorlin cyst)
  • AOT, CEOT, AFO, Odontoma, Cementoblastoma
63
Q

Surgical treatment of ossifying fibroma

A

Small tumors may be treated with enucleation and curettage with 1-2mm margins (as long as they have not lost their encapsulation and margins remain well demarcated from surrounding bone).

Resection with 5mm margins if:
- Tumors have reached a larger size
- Loss of encapsulation (radiographically or clinically)
- Tumor is within 1cm of the inferior border of the mandible
- There is involvement of the maxillary sinus or nasal cavities

64
Q

Categories of infectious pathology

A

Bacterial, viral, fungal

65
Q

Categories of neoplastic pathology

A

Epithelial, connective tissue, glandular, lymphatic, osseous, muscle, and vascular tumors.

Benign or malignant.

66
Q

Is an open biopsy of the parotid gland necessary in pathology?

A

It is not necessary to perform an open biopsy of the parotid gland, because 80% of parotid masses are benign; therefore, a parotidectomy is appropriate as a diagnostic and treatment modality.

67
Q

Differential diagnosis of slow-growing parotid mass

A
  1. Pleomorphic adenoma (most common tumor of major salivary glands, 75% in tail of parotid).
  2. Warthin’s tumor (papillary cystadenoma lymphadenosum). Also benign, slow-growing, elderly males older than 50. 10% can present bilaterally.
  3. Monomorphic adenoma (benign tumor of all major and minor salivary glands). Includes canalicular adenoma (minor glands of lips), and basal cell adenoma (parotid).
  4. Malignant salivary gland neoplasms (mucoepidermoid carcinoma, adenoid cystic carcinoma, acinic cell carcinoma, polymorphous low-grade adenocarcinoma, squamous cell carcinoma).
68
Q

Treatment of choice for pleomorphic adenoma of the parotid gland

A

Enucleation is associated with recurrence rates of up to 40%
Treatment of choice is superficial parotidectomy (recurrence 2-3%)
Remove tumor en bloc while maintaining integrity of the capsule with 5mm cuff of normal tissue. Dissect carefully from facial nerve.

69
Q

Treatment of choice for pleomorphic adenoma of the palate

A

Excise with 5mm margin, including overlying mucosa and underlying periosteum

70
Q

Complications of superficial parotidectomy (list)

A

Facial nerve paralysis, hemorrhage, hematoma, infection, skin flap necrosis, trismus, salivary fistula, sialocele, seroma formation.

Long term = Frey syndrome, hypoesthesia of greater auricular nerve, tumor recurrence, cosmetic defomrity

71
Q

What percentage of parotid tumors are benign?
What percentage of submandibular gland tumors are benign?
What percentage of minor salivary gland tumors are benign?
What percentage of sublingual gland tumors are bengin?

A

Parotid 80%
Submandibular 60%
Minor 50%
Sublingual 10%

72
Q

What is Frey syndrome?

A

Auriculotemporal nerve syndrome or gustatory sweating

Relatively common long-term complication of parotidectomy. Localized sweating and dermal flushing during salivary stimulation.

Caused by aberrant connections between severed secretomotor parasympathetic fibers as they anastamose with severed postganglionic sympathetic fibers that supply sweat glands in the face in the auriculotemporal region.

30-60% of patients after parotidectomy. Only 10% require treatment.

Treatment = surgical disruption of aberrant neural connections or use of botulinum toxin.

73
Q

Do mucoceles have an epithelial lining?

A

No (in contrast to salivary duct cysts), the extravasation of mucus produces a wall of inflamed fibrous tissue.

74
Q

Describe the approach to submandibular gland excision

A

Incision 1.5-2.0 cm below inferior border of mandible, dissection through platysma. Investing layer of deep cervical fascia incised at inferior-most extent of the dissection. Facial artery and vein ligated. Gland removed with capsule (which is an extension of the fascia that surrounds the gland).

Submandibular duct identified and ligated. Lingual nerve identified as it courses lateral to medial (passing inferior to Wharton’s duct) in the area of the 1st-2nd molars (lateral to the hypoglossal nerve).

75
Q

Complications of surgical excision of submandibular gland

A

Nerve injury (lingual and hypoglossal, MMB of facial).

Xerostomia (submandibular glands produce 70% of saliva)

76
Q

Sialoliths most common within which gland and which duct?

A

submandibular gland, Wharton’s duct (80-90%). This is because of the thicker, mucoid secretions of the gland and the long, convoluted, and superiorly directed path of the duct.

5-10% in parotid gland/duct

0-5% sublingual or minor glands

77
Q

Management of acute suppurative parotitis

A

Primarily medical: rehydration, empiric antibiotic therapy (S. aureus = beta-lactamase resistant penicillins, first generation cephalosporins, clindamycin), nutritional support, stimulation of salivary flow (sialogogues)

Surgical intervention if areas of loculation within the gland.

78
Q

Risk factors for parotitis

A

Comorbid states with decreased salivary flow or immunosuppression.

Diabetes, alcoholism, autoimmune disorders (Sjogren’s), medications (TCAs, anticholinergics, diuretics), dehydration, malnutrition, neoplasm, ductal obstruction.

79
Q

Classifications of parotitis

A

Acute (bacterial) suppurative parotitis
Nonsuppurative parotitis
Chronic recurrent parotitis

80
Q

Four broad categories of differential diagnoses for neck mass

A
  1. Anatomic (transverse process of C1, hyoid bone, thyroid/cricoid cartilage, prominent or atherosclerotic carotid bulbs)
  2. Inflammatory and/or infectious (bacterial, viral, parasitic, and fungal; sialadenitits, sialolithiasis)
  3. Congenital (ID’d at early age but may be seen later: thyroglossal duct cyst, branchial cleft cyst, dermoid cyst, lymphangioma, ranula)
  4. Neoplastic (fixed; metastatic disease from SCC, lung, thyroid, and salivary gland malignancies; melanoma; primary neck tumors from salivary gland lesions, lymphoma, or thyroid masses; benign masses such as lipomas, neural tumors, vascular lesions, sebaceous cysts, fibromas)
81
Q

Midline masses of the neck

A

Thyroglossal duct cyst: midline, anterior neck. Appear post URI. Moves with swallowing.

Dermoid cyst: midline, deep to cervical fascia, slow growing, do not move with tongue.

82
Q

Lateral mass of neck

A

Branchial cleft cyst
- First branchial cleft cyst (Type I preauricular/postauricular, Type II near mandibular angle)
- Second branchial cleft cyst (most common, anterior edge of SCM)
- Third branchial cleft cyst (very rare)
- Fourth branchial cleft cyst (extensive)

83
Q

What is the difference between mild, moderate, and severe dysplasia histologically?

A

Mild dysplasia: cellular atypia limited to the basilar and parabasilar epithelial layers.

Moderate dysplasia: involves the basal layer up to the midportion of the spinous layer.

Severe dysplasia: extends more than halfway through the epithelium but does not involve full-thickness.

Carcinoma in situ: dysplasia of the entire epithelial layer without invasion of the basement membrane into underlying tissue.

84
Q

Absolute contraindications to hyperbaric oxygen

A

Untreated pneumothorax
Optic neuritis
Fulminant viral infections
Congenital spherocytosis

85
Q

Complications of hyperbaric oxygen

A

Seizures
Decompression sickness
Ear barotrauma

86
Q

“Golden window” after radiation

A

4 month period after radiation that allows for definitive care, including extractions (effects of radiation are time dependent and take several months to affect wound healing).

87
Q

Smoking and risk of SCC
Alcohol and risk of SCC

A

Smoking 5-9x
Alcohol 3-9x
Together 100 fold increased risk

88
Q

Indicators of nodal metastasis on CT

A

Nodes greater than 1.5 cm
Central necrosis
Ovoid shape
Fat stranding

89
Q

Indications for postoperative radiation therapy oral SCC

A

Positive or near margins
Significant perineural or perivascular invasion
Bone involvement
Multiple nodal involvement
Extracapsular spread
Stage III or IV disease

Typically 6,000 cGy in divided doses initiated soon after healing from initial surgery is complete

90
Q

Metastasis of SCCa involves what?

A

Lung, bones, liver, brain

91
Q

HPV types that have been shown to increase risk of SCCa

A

HPV 16 and 18 (3-5fold)
50% of tonsillar SCCa are HPV positive (treated with chemoradiation)

92
Q

5-year survival oral SCCa

A

50%

93
Q

Differential diagnosis submucosal mass of the posterior hard palate

A
  • Benign salivary (pleomorphic adenoma, monomorphic adenoma, canalicular adenoma)
  • Malignant minor salivary gland tumors (mucoepidermoid carcinoma, adenoid cystic carcinoma, adenocarcinoma).
  • Infectious etiology considered
  • Sarcomas can occur on palate and should be considered.
94
Q

Mucoepidermoid carcinoma grading

A

Scale of I to III
(low, intermediate, high grade)
High grade tumors with nuclear atypia, necrosis, perineural spread, mitoses, bony invasion, lymphatic and vascular invasion, intracystic component, tumor front invading in small nests and islands.
High grade tumors have higher proportion of epidermoid cells and few mucus producing cells.

95
Q

3 major forms of adenoid cystic carcinoma

A

Cribriform, tubular, and solid variants
Cribriform = most common
Solid = worst prognosis

96
Q

Management of low grade vs. high grade mucoepidermoid carcinoma

A

Low grade: has low risk of locoregional recurrence. Surgical extirpation is typically all that is required, along with long-term follow-up. 1cm margins without adjunctive treatment. Do not necessarily need bony resection if no evidence of bony invasion on imaging.

High grade: aggressive malignancy with affinity for regional lymphatic spread and potential for distant metastasis (lungs). More extensive resection with additional management of the neck. Radiation if surgical margins are positive.

97
Q

Adenoid cystic carcinoma considerations

A

Salivary gland malignancy of myoepithelial and ductal cells. Indolent course and propensity for perineural invasion, distant metastasis, locoregional recurrence, “skip lesions” along nerve fibers. Nerves typically sacrificed as proximally as possible (skull base).

98
Q

In a patient with a known primary SCCa, what are the chances there is a synchronous tumor in the upper aerodigestive tract?

A

3-7% (nasopharyngoscopic exam is indicated to eval subepiglottic and supraepiglottic regions, posterior oropharynx, and nasopharynx).

99
Q

How does a PET scan work?

A

Positron emission tomography uses 18F-fluorodeoxyglucose marker to examine sites of increased glucose uptake that are seen with metabolically active cancer cells.

PET can help rule out distant disease and aid in clinical staging of the cancer.

100
Q

What is SUV as it relates to PET scans?

A

Standardized Uptake Values >3 have been shown to correlate with increased metabolic activity associated with some pathologic conditions.

A higher SUV may be correlated with more aggressive tumors.

101
Q

Describe the levels of the neck

A

Level I: submental and submandibular
Level II: upper jugular
Level III: midjugular
Level IV: lower jugular
Level V: posterior triangle
Level VI: prelaryngeal (delphian), pretracheal, and paratracheal
Level VII: upper mediastinal

102
Q

Radical neck dissection

A

Removal of entire cervical lymphatic chain from unilateral neck encompassing levels I-V, spinal accessory nerve, internal jugular vein, and sternocleidomastoid muscle

103
Q

Modified radical neck dissection

A

Levels I-V with preservation of one or more non-lymphatic structures that are included in radical neck dissection (spinal accessory nerve, IJV, SCM)

104
Q

Selective neck dissection

A

Umbrella term to describe when neck nodes of certain “selected” levels are removed and other areas are preserved.

105
Q

Supraomohyoid neck dissection

A

Selective removal of levels I through III.
- Indicated for the N0 neck in oral cavity SCCa with a 20% or greater chance of occult neck disease (aggressive, high-grade tumor with invasion greater than 3mm and perineural invasion).
- Performed on ipsilateral side (except when tumors arise from midline structures such as FOM)

106
Q

Anterior compartment neck dissection

A

Selective removal of level VI (tumors of thyroid, hypopharynx, cervical trachea, cervical esophagus, and subglottic larynx).

107
Q

Posterolateral neck dissection

A

Removal of levels II thru V. Indicated for scalp and auricular tumors.

108
Q

Lateral neck dissection

A

Levels II thru IV. Cancer of the oropharynx, hypopharynx, and larynx.

109
Q

Extended neck dissection

A

Includes removal of structures not routinely involved with radical neck dissection

110
Q
A

OMS Board Review (29 decks)

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