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Oral Board Review Textbook > Oral Pathology > Flashcards

Oral Pathology Flashcards

1
Q

What is the recurrence of glandular odontogenic cyst and what is the treatment?

A

-30% recurrence
-Curettage

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2
Q

What gene is OKC associated with?

A

-PTCH tumor suppressor gene

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3
Q

What is the treatment of OKC?

A

-Enucleation and curettage with peripheral ostectomy
-May decompress prior to treatment
-5-FU possibly
-Cryotherapy possibly (penetrates 1.5 mm into bone

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4
Q

What is the recurrence rate of calcifying odontogenic cyst and the treatment?

A

-Low recurrence rate
-Conservative surgical removal

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5
Q

What are the types and subtybes of ameloblastoma?

A

-Unicystic (unicystic, intraluminal, mural)
-Peripheral
-Malignant

Histologic: Follicular, plexiform, acanthomatous, granular cell, desmoplastic

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6
Q

What is the treatment for ameloblastoma (conventional, unicystic with intraluminal confinement, peripheral, malignant, ameloblastic carcinoma)

A

-Conventional: Marginal or en block resection using 1-1.5 cm margins, with one anatomic barrier
-Unicystic with intraluminal confinement: Enucleation with long term follow-up
Peripheral: 2-3 mm margins
-Malignant ameloblastoma: En block possible chemo therapy. Mets to lung most common
-Ameloblastic carcinoma: 2-3 cm margins with neck dissection

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7
Q

What is the treatment and recurrence rate for CEOT?

A

-Resection with 1-1.5 cm margins. Anatomic barrier
-Conservative resection with peripheral ostectomy recurrence of 15%

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8
Q

What is treatment for AOT?

A

-Conservative enucleation (typically has thick fibrous capsule)

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9
Q

What is treatment of an odontogenic myxoma?

A

-Resection with 1-1.5 cm margins and anatomic barrier

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10
Q

What is the treatment for cemento-ossifying fibroma?

A

-Conservative enucleation for small lesions (usually well encapsulated)
-Large lesions require resection with 5 mm borders

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11
Q

What is the recurrence and treatment of cementoblastoma?

A

-Low recurrence rate
-Excision with removal of involved tooth

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12
Q

What is the treatment of ameloblastic fibroma?

A

-Conservative excision with close follow-up
-More aggressive excision for recurrent lesions

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13
Q

What is the treatment for ameloblastic fibrosarcoma?

A

-Radical surgical excision with 1-1.5 cm margins and anatomic barrier
-Metastasis uncommon but locally aggressive

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14
Q

What is the treatment of an ameloblastic fibro-odontoma?

A

-Enucleation and curettage
-It is a developmental stage of an odontoma

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15
Q

What is the treatment of an odontoma?

A

-Complex or compound
-Excision

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16
Q

What gene is associated with fibrous dysplasia?

A

-GNAS gene mutation/deletion

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17
Q

What are the types and characteristics of fibrous dysplasia?

A

-Monostotic: Most common. One bone affected, usually stabilize after skeletal maturation
-Polyostotic: Usually associated with syndromes (Jaffe-Lichtenstein, McCune Albright . Cafe au lait spots)

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18
Q

What is the treatment for fibrous dysplasia?

A

-Conservative
-Surgical contouring or debulking for cosmetic deformity
-Lot of blood loss
-Consider bisphophonates
-Radiation contraindicated (transform to sarcoma)

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19
Q

What are the three variants of cemento-osseous dysplasia?

A

-Focal: Single site
-Periapical: Anterior mandible periapical region
-Florid: Multiple sites

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20
Q

How is cemento-osseous dysplasia diagnosed and managed?

A

-Teeth vital
-Presumptive diagnosis (black female)
-Avoid surgery due to hypovascularity and tendency of osteomyelitis

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21
Q

What is the recurrence rate and treatment of central giant cell tumor?

A

-Enucleation, curettage and peripheral ostectomy
-Recurrence 20%
-Resection with 1 cm margins for recurrent lesions

-For large lesions, consider intralesional corticosteroid injections 1:1 mixture of local anesthesia and triamcinolone 10 mg/mL weekly for 6 weeks. 2 cc for every 1 cc of lesion
-Consider calcitonin, inferferon alpha-2a, imatinib, bisphophonates, denosumab

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22
Q

What is the treatment of peipheral giant cell granuloma?

A

-Excision down to bone

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23
Q

What is the MOA of denosumab?

A

-Xgiva/Prolia
-RANK Ligant inhibitor
-Prevent osteoclast differentiation

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24
Q

What is the MOA of bisphosphonates?

A

-Inhibit osteoclast function and increase osteoclast apoptosis

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25
Q

What are the four types of melanoma?

A

-Superficial spreading (most common)
-Lentigo Maligna (large, flat)
-Nodular
-Acral lentiginous melanoma (rare, mucous membranes, african american descent, worse prognosis)

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26
Q

What is the prognosis of melanoma related to?

A

-Primarily linked to tumor thickness
-Breslow depth in mm

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27
Q

What margins are necessary in melanomas?

A

-2 cm margins
-Possibly lymph node dissection

28
Q

What are the risk factors for mucosal melanomas?

A

-Inhaled/ingested carcinogens

29
Q

What is the treatment of mucosal melanomas?

A

-3 cm margin resection
-Lymph node dissection
-Possible radiation
-Chemo for palliative

30
Q

What are the subtypes of basal cell carcinoma?

A

-Nodular (most common, shiny)
-Superficial (least aggressive)
-Morpheaform (rarest, look like scars)

31
Q

What is ‘skip metastasis’?

A

-Up to 15% of tongue cancers can have a skip metastasis to level 4 without involving levels 1-3 (lymph nodes)

32
Q

What is the most common neck dissection for SCCa?

A

-Supraomohyoid neck dissection with levels 1-3 vs 1-4

33
Q

What are the lymph node levels?

A

-Level 1a: Submental. (Mandible, anterior belly of digastric, hyoid bone, mylohyoid forms floor)

-Level 1b: Submandibular: (Mandible, anterior belly of digastric, stylohyoid, hyoid bone, mylohyoid and hyoglossus are the floor)

-Level 2a/b: Jugular lymphatic. (Skull base, sternohyoid, posterior border of SCM, carotid bifurcation). 2a vs 2b divided by spinal accessory nerve

-Level 3: Middle jugular. (Carotid bifurcation, omohyoid, sternohyoid, posterior border of SCM)

-Level 4: Lower jugular. (Omohyoid to clavicle, sternohyoid, posterior border of SCM)

-Level 5: Posterior triangle of neck (posterior border of SCM, trapezius, clavicle. Rarely involved in oral squamous cell carcinoma

-Level 6: Central compartment. (carotid artery, hyoid, sternal notch). Rarely involved in oral squamous cell

34
Q

What are the most common sites of metastasis for SCCa?

A

-Lungs
-Bones
-Liver

35
Q

What is your management of leukoplakia?

A

-Biopsy
-Complete removal of dysplasia

36
Q

What is PVL?

A

-Proliferative verrucous leukoplakia
-Not associated with smoking
-Will usually develop into SCC or verrucous carcinoma

37
Q

How is oral lichem planus related to SCCa?

A

-Erosive and atrophic subtypes are premalignant and warrant long-term follo-wup and biopsy

38
Q

What is the concept of field cancerization?

A

-If patient has a cancerous lesion, should be on high alert for other lesions
-Entire aerodigestive tract could be affected
-Carcinogens result in cumulative DNA mutations along entire lining of tract

39
Q

What lymph node findings are concerning, what percentage of patient’s present with regional node involvement with SCCa?

A

-30% present with regional node involvement
-Painless, hard, matted, fixed or greater than 1-1.5 cm in size

40
Q

Describe the nomenclature in TMN classification?
aTNM
cTNM
pTNM
rTNM
m suffix (pTmNM)
y prefix ycTNM

A

-aTNM: Autopsy classification
-cTNM: Clinical staging
-pTNM: Pathologic staging
-rTNM: Recurrent tumor
-m suffix: More than one primary tumor
-y prefix: After initial multimodal therapy

41
Q

How is depth of invasion measured?

A

-Distance in mm from horizon of the basement membrane

42
Q

How does nodal status affect survival of SCCa?

A

-Single most important prognastic factor
-Stage I/II: >80% survival
-Having a single positive lymph node reduces prognosis by 50%

43
Q

What is extranodal extension?

A

-Extension of metastatic carcinoma within a lymph node through the capsule into the surrounding connective tissue

44
Q

Describe T1, T2, T3, T4a, T4b classification of SCCa.

A

-T1: Tumor less than 2 cm, DOI <5 mm
-T2: Tumor less than 2 cm, DOI 5-10 mm or Tumor 2-4 cm with DOI <10
T3: Tumor >4 cm or DOI 10-20 mm (any size)
T4a: Through cortical bone of mandible or sinus. DOI >20 mm.
T4b: Advanced. Tumor invades through a space

45
Q

Describe the N classifications Nx, N0, N1, N2abc, N3ab

A

-Nx: Unable to assess lymph node
-N0: No lymph nodes
-N1: Single ipsilateral lymph node 3 cm or smaller
-N2a: Single ipsilateral lymph node 3-6 cm
-N2b: Multiple lymph nodes no larger than 6 cm
-N2c: Bilateral or contralateral node no larger than 6 cm
-N3a: Lymph node larger than 6 cm
-N3b: Clinically overt ENE (extra-nodal extension)

46
Q

Describe the stages of SCCa.

A

-Stage 0: Tis (carcinoma in situ), N0, M0
-Stage 1: T1 N0 M0
-Stage 2: T2 N0 M0
-Stage 3: T3 N0 M0 or T1-3 N1 M0
-Stage 4a: T4a N0,1 M0 or T1-4a N2 M0
Stage 4b: T4b Any N M0
Stage 4c: M1

47
Q

What is the clinical and pathologic margin of SCCa?

A

-Clinical: 1-1.5 cm
-Pathologic: 5 mm

48
Q

How are Stage 1-2 SCCa managed compared to stage 3-4

A

-Stage 1-2: Primarily surgery/neck dissection
-Stage 3-4: Surgery with adjuvant radiation +/- chemo

49
Q

Who is on a tumor board?

A

-Surgical oncology
-Radiation oncology
-Medical oncology
-Pathology
-Social Work
-Radiologist
-Dietician

50
Q

What are the guidelines for adjuvant radiation?

A

-T3-4 tumors
-Close <5 mm resection margin
-2 or more lymph nodes with perineural invasion/ENE
-Given within 6 weeks of surgery

51
Q

What is the advantage of IMRT (intensity-modulated radiotherapy)?

A

-Similar success and radiation to tumor cells
-Less effect to adjacent structures

52
Q

What are guidelines for adjuvant chemotherapy?

A

-Positive resection margin
-Extracapsular spread

-Use cisplatin

53
Q

What is the follow-up period for SCCa patients?

A

-q1-3 months for first 2 years
-4-6 months after 2 years

54
Q

What are indications for neck dissection with a tongue lesion?

A

-DOI >4 mm
-If within 1 cm of midline, need bilateral neck dissection
-Levels 1-4

55
Q

What structures are included in a radical neck dissection?

A

-Levels 1-5
-SCM
-IJV
-CN XI

-Used in N3 disease or gross extracapsular spread

56
Q

How are modified neck dissections classfied?

A

-Medina classification
-Type 1: CN 11 preserved
-Type 2: CN 11, IJV preserved
-Type 3: CN 11, IJV, SCM preserved

57
Q

What causes shoulder syndrome s/p neck dissection, what are the symptoms?

A

-Damage to spinal accessory nerve

-Loss of function of trapezius
-Pain, limitation in arm abduction at shoulder, winging of scapula, loss of contour of shoulder

-Treat with PT

58
Q

What is the treatment of facial nerve transection in a neck dissection/parotidectomy?

A

-Best managed with primary repair

-Cross face facial nerve, hypoglossal facial nerve crossover, microneurovascular free tissue transfer

-Static/dynamic slings from temporalis fascia or fascia lata can help with cosmesis but not function

59
Q

What are the symptoms of hypoglossal nerve injury?

A

-Difficulty with swallowing and speech
-Tongue will deviate towards the affected side

60
Q

What are the symptoms of phrenic nerve injury?

A

-Ipsilateral elevation of diaphragm on CXR
-Mediastinal shift, paradoxical movement of lung, cardiac irritation and dyspnea. Nausea/vomiting, abdominal pain

61
Q

What are symptoms of vagus nerve injury?

A

-Loss of sensation to tonsillar region, posterior 1/3 of tongue and pharynx
-Can see diminished movement of soft palate and deviation of uvula
-Difficulty swallowing and aspiration risk

62
Q

What are symptoms and management of thoracic duct injury?

A

-Primarily in left neck dissection
-Try to identify intraop. Have anesthesia valsalva and observe chyle (creamy/milky fluid). Over suture the duct

-Can lab test for triacylglycerol

-If ID post-op, pressure dressings, suction drains and negative wound pressure, diet modification, antibiotics

-Surgical exploration if no resolution within 14 days or 7 days with high output >500 mL/day

63
Q

What is the management for a carotid artery blowout s/p neck dissection?

A

-Secure definitive airway
-Try packings, fluid resuscitation and pressure
-Undergo angiography
-Vascularized tissue coverage if artery exposed

-May need IR embolization, stenting, wound management, occlusion
-May need surgical ligation

64
Q

How does a PET-CT detect cancer cells?

A

-Evaluated uptake of the cells using the marker 18-Fluorodeoxyglucose

65
Q

How long after treatment should a PET-CT be obtained?

A

-12 weeks after radiation

Oral Board Review Textbook (26 decks)

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