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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
What are the four types of melanoma?
-Superficial spreading (most common) -Lentigo Maligna (large, flat) -Nodular -Acral lentiginous melanoma (rare, mucous membranes, african american descent, worse prognosis)
26
What is the prognosis of melanoma related to?
-Primarily linked to tumor thickness -Breslow depth in mm
27
What margins are necessary in melanomas?
-2 cm margins -Possibly lymph node dissection
28
What are the risk factors for mucosal melanomas?
-Inhaled/ingested carcinogens
29
What is the treatment of mucosal melanomas?
-3 cm margin resection -Lymph node dissection -Possible radiation -Chemo for palliative
30
What are the subtypes of basal cell carcinoma?
-Nodular (most common, shiny) -Superficial (least aggressive) -Morpheaform (rarest, look like scars)
31
What is 'skip metastasis'?
-Up to 15% of tongue cancers can have a skip metastasis to level 4 without involving levels 1-3 (lymph nodes)
32
What is the most common neck dissection for SCCa?
-Supraomohyoid neck dissection with levels 1-3 vs 1-4
33
What are the lymph node levels?
-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
What are the most common sites of metastasis for SCCa?
-Lungs -Bones -Liver
35
What is your management of leukoplakia?
-Biopsy -Complete removal of dysplasia
36
What is PVL?
-Proliferative verrucous leukoplakia -Not associated with smoking -Will usually develop into SCC or verrucous carcinoma
37
How is oral lichem planus related to SCCa?
-Erosive and atrophic subtypes are premalignant and warrant long-term follo-wup and biopsy
38
What is the concept of field cancerization?
-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
What lymph node findings are concerning, what percentage of patient's present with regional node involvement with SCCa?
-30% present with regional node involvement -Painless, hard, matted, fixed or greater than 1-1.5 cm in size
40
Describe the nomenclature in TMN classification? aTNM cTNM pTNM rTNM m suffix (pTmNM) y prefix ycTNM
-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
How is depth of invasion measured?
-Distance in mm from horizon of the basement membrane
42
How does nodal status affect survival of SCCa?
-Single most important prognastic factor -Stage I/II: >80% survival -Having a single positive lymph node reduces prognosis by 50%
43
What is extranodal extension?
-Extension of metastatic carcinoma within a lymph node through the capsule into the surrounding connective tissue
44
Describe T1, T2, T3, T4a, T4b classification of SCCa.
-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
Describe the N classifications Nx, N0, N1, N2abc, N3ab
-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
Describe the stages of SCCa.
-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
What is the clinical and pathologic margin of SCCa?
-Clinical: 1-1.5 cm -Pathologic: 5 mm
48
How are Stage 1-2 SCCa managed compared to stage 3-4
-Stage 1-2: Primarily surgery/neck dissection -Stage 3-4: Surgery with adjuvant radiation +/- chemo
49
Who is on a tumor board?
-Surgical oncology -Radiation oncology -Medical oncology -Pathology -Social Work -Radiologist -Dietician
50
What are the guidelines for adjuvant radiation?
-T3-4 tumors -Close <5 mm resection margin -2 or more lymph nodes with perineural invasion/ENE -Given within 6 weeks of surgery
51
What is the advantage of IMRT (intensity-modulated radiotherapy)?
-Similar success and radiation to tumor cells -Less effect to adjacent structures
52
What are guidelines for adjuvant chemotherapy?
-Positive resection margin -Extracapsular spread -Use cisplatin
53
What is the follow-up period for SCCa patients?
-q1-3 months for first 2 years -4-6 months after 2 years
54
What are indications for neck dissection with a tongue lesion?
-DOI >4 mm -If within 1 cm of midline, need bilateral neck dissection -Levels 1-4
55
What structures are included in a radical neck dissection?
-Levels 1-5 -SCM -IJV -CN XI -Used in N3 disease or gross extracapsular spread
56
How are modified neck dissections classfied?
-Medina classification -Type 1: CN 11 preserved -Type 2: CN 11, IJV preserved -Type 3: CN 11, IJV, SCM preserved
57
What causes shoulder syndrome s/p neck dissection, what are the symptoms?
-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
What is the treatment of facial nerve transection in a neck dissection/parotidectomy?
-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
What are the symptoms of hypoglossal nerve injury?
-Difficulty with swallowing and speech -Tongue will deviate towards the affected side
60
What are the symptoms of phrenic nerve injury?
-Ipsilateral elevation of diaphragm on CXR -Mediastinal shift, paradoxical movement of lung, cardiac irritation and dyspnea. Nausea/vomiting, abdominal pain
61
What are symptoms of vagus nerve injury?
-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
What are symptoms and management of thoracic duct injury?
-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
What is the management for a carotid artery blowout s/p neck dissection?
-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
How does a PET-CT detect cancer cells?
-Evaluated uptake of the cells using the marker 18-Fluorodeoxyglucose
65
How long after treatment should a PET-CT be obtained?
-12 weeks after radiation

Oral Board Review Textbook (26 decks)

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