Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Head and Neck > Oral Cavity, Oropharynx > Flashcards

Oral Cavity, Oropharynx Flashcards

1
Q

What are the muscles of the tongue?
9

A

Extrinsic muscles: “Good CHoPS”
1. Genioglossus
2. Hyoglossus
3. Chondroglossus (origin - lesser horn of the hyoid)
4. Styloglossus
5. Palatoglossus

Intrinsic muscles: “L TV - think of the superior and inferior borders of the TV”
1. Superior longitudinal muscle
2. Inferior longitudinal muscle
3. Transverse muscle
4. Vertical muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the seven subsites of the oral cavity?

A
  1. Upper and lower lips
  2. Oral tongue
  3. Upper and lower alveolus
  4. Buccal mucosa
  5. Floor of mouth
  6. Retromolar trigone
  7. Hard palate

“Baby Hua FLOUR”
Buccal
Hard palate
Floor of mouth
Lips (upper and lower)
Oral tongue
Upper and lower alveolus
Retromolar trigone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Differential diagnosis of an oral cavity lesion

A
  1. SCC
  2. Minor salivary gland lesions (go through salivary gland differential)
  3. Sarcoma
  4. Lymphomas
  5. Melanomas
  6. HIV related lesions
  7. Inflammatory lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define an adequate margin for mucosal disease of the oral cavity

A
  1. Enough margin to obtain a clear frozen section; OR
  2. 1.5-2.0cm of visible and palpable normal mucosa; OR
  3. 1.5-2.0mm for transoral laryngeal microsurgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the definition of a clear margin for resection of oral cavity cancer?

A

≥5mm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the definition of a close margin for resection of oral cavity cancer?

A

< 5mm

Found to have same prognostic significance for recurrence as positive margins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the definition of a positive margin for resection of oral cavity cancer?

A
  1. Carcinoma at the line of the resection; OR
  2. Carcinoma-in-situ at the line of the resection (However CIN is not an indication for concurrent post-op ChemoRT - suggestion here is to re-resect)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the AJCC T staging of oral cavity cancer (including mucosa of lip, not skin of lip)

A

TX: Primary tumor cannot be assessed

Tis: Carcinoma in situ

T1: Tumor ≤ 2cm AND DOI ≤5mm

T2: Tumor ≤2cm AND DOI >5mm
OR Tumor 2-4 (≤4cm) AND DOI ≤10mm

T3: Tumor 2-4 (≤4cm) AND DOI >10mm
OR Tumor >4cm AND DOI ≤10mm

T4: Moderate advanced or very advanced local disease

T4a: Moderately advanced local disease
- Tumor >4cm AND DOI >10mm; OR
- Invades adjacent structures only (e.g. through cortical bone of the mandible or maxilla, or involves the maxillary sinus or skin of the face) - not superficial erosion of bone/tooth socket (alone) by a gingival primary is not sufficient to classify T4

T4b: Very advanced local disease
- Tumor invades masticator space, pterygoid plates, or skull base and/or encases the internal carotid artery

DOI is not tumor thickness (plumb line - horizon from adjacent normal mucosal basement membrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Identify the Histologic features found in dysplasia of the oral cavity (7)

A

AMPLE BEN
1. A: Abnormal mitotic figures
2. M: Increased Mitoses/mitotic spindling
3. P: Cellular/nuclear Pleomorphism
4. L: Loss of cellular polarity
5. E: Enlarged nucleoli
6. B: Basement membrane not penetrated
7. E: Enlarged number of mitotic figures
8. N: Increased Nuclear:Cytoplasmic ratio

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the common locations of oral cavity SCC? 5

A
  1. Floor of mouth
  2. Glossobuccal sulcus
  3. Retromolar trigone
  4. Lateral tongue
  5. Alveolar ridge

There are all dependent areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the 9 histologic classes of oral cavity/mucosal SCC (~95% of oral mucosal neoplasms)

A
  1. Conventional
  2. Verrucous: Non-metastasizing variant of well-differentiated SCC characterized by an exophytic, warty, slowly-growing with pushing margins rather than infiltrative margins (no BM invasion)
  3. Adenosquamous: Rare, aggressive, characterized by both squamous cell and true adenocarcinoma, most common in larynx
  4. Spindle cell (sarcomatoid): Composed of squamous cell carcinoma and a malignant spindle cell component with a mesenchymal appearance
  5. Cuniculatum: Rare, proliferation of stratified squamous epithelium in broad processes with keratin cores and keratin-filled crypts which burrow into bone tissue
  6. Papillary: Exophytic, papillary growth, good prognosis
  7. Acantholytic: Uncommon, cytological features of malignancy
  8. Basaloid: High-grade variant of SCC composed of both basaloid and squamous components (associated with HPV, ~20%)
  9. Lymphoepithelial (EBV related)

“VASCular PABLo”

Very SAGgy Boobs to Lick A Couple of Penises (vs. cutaneous = Very SAGgy Boobs)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 7 histological features of verrucous carcinoma?

A
  1. Broad-based, exophytic
  2. Well-differentiated epithelium lacking conventional SCC features (no pleomorphism, mitotic activity, etc.)
  3. Church spire acanthosis
  4. No or minimal atypia, confined to basal zone
  5. Invasion with pushing boundaries
  6. Hyperkeratosis (increased thickness)
  7. Parakeratosis

Surgery or consider RT for high grade lesions

ABCDE HIP
Atypia minimal or none, confined to basal zone
Broad based
Church spire acanthosis
Differentiated-well epithelium lacking convenitional SCC features (no pleomorphism, mitotic activity)
Exophytic

Hyperkeratosis (increased thickness)
Invasion with pushing borders
Parakeratosis

Vancouver Pg 111

https://www.pathologyoutlines.com/topic/skintumornonmelanocyticverrucousscc.html

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the AJCC 8th edition clinical and pathological shared nodal staging for oral cavity, HPV negative Oropharynx, salivary gland, unknown primary, non-melanoma skin?

A

CLINICAL:

NX: Regional LN cannot be assessed

N0: No regional LN metastasis

N1: Single ipsilateral LN, ≤ 3cm in greatest dimension, ENE(-)

N2: Any one of the following, all ENE(-) and none larger than 6cm
- N2a: Single ipsilateral LN >3cm but ≤6cm in greatest dimension, ENE(-)
- N2b: Multiple ipsilateral LN all ≤6cm in greatest dimension, ENE(-)
- N2c: Bilateral or contralateral LN all ≤6cm in greatest dimension, ENE(-)

N3: Any one of the following
- N3a: Any node >6cm in greatest dimension, ENE(-)
- N3b: Any node with ENE(+)

PATHOLOGICAL:

NX: Regional LN cannot be assessed

N0: No regional LN metastasis

N1: Single ipsilateral LN, ≤ 3cm in greatest dimension, ENE(-)

N2: Any one of the following
N2a:
- Single ipsilateral LN ≤3cm, ENE(+)
- Single ipsilateral LN >3cm but ≤6 cm in greatest dimension, ENE(-)
N2b: Multiple ipsilateral LN all ≤6cm in greatest dimension, ENE(-)
N2c: Bilateral or contralateral LN all ≤6cm in greatest dimension, ENE(-)

N3: Any one of the following
N3a: Any node >6cm in greatest dimension, ENE(-)
N3b: ENE+ (except for Single ≤3cm)
- Single ipsilateral LN >3cm in greatest dimension, ENE(+)
- Multiple ipsilateral, contralateral, or bilateral nodes, any with ENE(+)
- Single contralateral node of any size, ENE(+)

“U” or “L” designation may be used for any N category - indicating metastasis above the lower border of the cricoid (U), or below the lower border of the cricoid (L)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does extranodal extension look like clinically? 3 features

A
  • Skin tethering
  • Tethering to underlying structures
  • Nerve involvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are 5 risk factors for lip cancer?

A
  1. Sun exposure
  2. Smoking
  3. Chronic alcoholism (Smoking + EtOH = 2.5x risk)
  4. Poor dental hygiene
  5. Immunosuppression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Outline a differential diagnosis for a lip lesion7

A
  1. SCC (90%) - also 90% lower lip, 90% 5-year OS
  2. BCC (more common on upper lip)
  3. Minor salivary gland lesion (go through MSG differential)
  4. Keratocanthoma
  5. Actinic keratosis
  6. Hyperkeratosis
  7. Melanoma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the AJCC 8th edition T staging for lip cancer?

A

Same as cutaneous non-melanoma SCC

TX: Primary Tumor cannot be assessed
Tis: Carcinoma in situ

T1: ≤2cm in greatest dimension

T2: 2-4cm (>2cm, ≤4cm)

T3: >4cm OR minor bone erosion OR perineural invasion OR deep invasion

T4: Gross cortical bone/marrow invasion, skull base invasion, and/or skull base foramen invasion
- T4a: Gross cortical bone/marrow invasion
- T4b: Skull base invasion and/or skull base foramen involvement

Definitions:
- Deep invasion: Invasion beyond subcutaneous fat or >6mm deep (measured from granular layer of adjacent normal epidermis to the base of tumor)
- Perineural: Tumor cells within the nerve sheath of a nerve lying deeper than the dermis or ≥0.1mm or larger in caliber or presenting with clinical/radiographic involvement of named nerves without skull base invasion or transgression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the resection margins that should be followed for lip excision?

A

T1: 3mm
T2: 5-8mm
T3/4: 1-2cm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are 8 poor prognostic indicators for lip cancer?

A
  1. Cervical metastasis (below are risk factors for occult regional metastasis, thus also criteria for ND I-III ± IV) - drainage pattern upper lip = ipsilateral, lower lip = bilateral
  2. Size > 2cm
  3. Thickness > 4mm
  4. Mandibular invasion
  5. Perineural invasion
  6. Commissure lesion
  7. Recurrent tumors
  8. Poorly differentiated histology
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the indications for elective neck dissection for lip cancer? (5)

A
  1. T3/T4
  2. Commissure involvement
  3. Recurrent disease
  4. PNI
  5. > 4mm depth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are 7 indications for post-op adjuvant radiation therapy (± chemo) for lip cancer?

A

A. RT ALONE:
1. T3 or T4 tumor
2. Perineural invasion
3. Lymphovascular invasion
4. Recurrent tumor
5. Multiple level cervical metastasis

B. CHEMO + RT:
1. Positive margin
2. Extranodal spread

Generally: Early stage single modality (surgery preferred), advanced stage = multimodality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are 3 indications for a vermillionectomy?

A
  1. Carcinoma in situ
  2. Diffuse premalignant disease (Actinic cheilitis)
  3. Multicentric disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are 3 conditions for Moh’s excision of lip cancer?

A
  1. Stage 1 or 2 disease
  2. Thickness ≤ 2.5mm
  3. No muscle involvement

Beyond this, there will likely be regional metastasis or functional impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are 7 histologic features of leukoplakia?

A
  1. Parakeratosis (presence of nuclei in the stratum corneum)
  2. Hyperkeratosis (increased thickness of keratinized layers)
  3. Dyskeratosis (production of keratin prematurely within individual cells below the stratum granulosum)
  4. No pleomorphism (no more than one form of a single cell type)
  5. No anaplasia (therefore no change in a cell or tissue to a less differentiated form)
  6. No desmoplasia (therefore no connective tissue reaction to tumor)
  7. Rare mitotic figures and normal maturation

No MAD Person has 7 PHD’s

No MAD Person = No mitotic figures/rare, no anaplasia, no desmoplasia, no plemorphism
PHD = Parakeratosis, Hyperkeratosis, Dyskeratosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are 5 poor prognostic factors in oral cavity cancer?

A
  1. Increasing stage and size
  2. Increasing tumor thickness (4mm lip, 5mm tongue)
  3. Perineural invasion
  4. Angiolymphatic invasion
  5. p53/p63 overexpression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Outline a differential diagnosis of non-epithelial oral cavity cancer?

A
  1. Lymphoma
  2. Kaposi’s sarcoma
  3. Minor salivary gland cancer

10% occurrence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Outline a differential diagnosis of maxillary and mandibular cysts

A

ODONTOGENIC (Derived from odontogenic epithelium):
1. Periapical/Radicular cyst (80%)
2. Lateral periodontal cyst (variation of periapical cyst) - caused by inflammation; also called inflammatory
3. Dentigerous/follicular cyst (10%)
4. Odontogenic keratocyst (most aggressive)

NON-ODONTOGENIC (5%):
1. Nasopalatine duct cyst
2. Midpalatal cyst of infants
3. Nasolacrimal duct cyst
4. Nasolabial cyst
5. Aneurysmal bone cavity
6. Stafne lingual cortical bone defect (depression secondary to salivary tissue)
7. Giant cell tumors
8. Brown’s tumor
9. Fibrous dysplasia
10. Ossifying fibroma
11. Idiopathic (traumatic bone cyst)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

List the WHO 2017 different diagnosis of odontogenic tumors

A

MALIGNANT ODONTOGENIC TUMORS:
1. Ameloblastic carcinoma
2. Primary intraosseous carcinoma, NOS
3. Sclerosing odontogenic carcinoma
4. Clear cell odontogenic carcinoma
5. Ghost cell odontogenic carcinoma
6. Odontogenic carcinosarcoma
7. Odontogenic sarcomas

BENIGN ODONTOGENIC TUMORS:

A. Epithelial Origin (most common = Ameloblastoma)
1. Ameloblastoma, Conventional
2. Ameloblastoma, Unicystic type
3. Ameloblastoma, extraosseous/peripheral type
4. Metastasizing (malignant) ameloblastoma
5. Squamous odontogenic tumor
6. Calcifying epithelial odontogenic tumor
7. Adenomatoid odontogenic tumor

B. Mixed (Epithelial-Mesenchymal) Origin
1. Ameloblastic fibroma
2. Primordial odontogenic tumor
3. Odontoma (compound vs. complex type)
4. Dentinogenic ghost cell tumor

C. Mesenchymal Origin
1. Odontogenic fibroma
2. Odontogenic myxoma/myxofibroma
3. Cementoblastoma
4. Cemento-ossifying fibroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Outline a differential diagnosis of a multiloculated bone/jaw cyst

A
  1. Myxoma
  2. Ameloblastoma
  3. Aneurysmal bone cyst
  4. Cherubism
  5. Central giant cell granuloma
  6. Hemangioma
  7. Odontogenic keratocyst

MAACCHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Outline a differential diagnosis for a unilocular jaw cyst

A
  1. Metastasis
  2. Multiple myeloma (contains plasma cells)
  3. Plasmacytoma
  4. Brown tumor
  5. Dentigerous cyst
  6. Calcifying odontogenic cyst (Gorlins cyst)
  7. Periapical cyst (rests of Mallessez)
  8. Odontogenic keratocyst
  9. Stafne Cyst (pseudocyst: indent of submandibular gland)
  10. Langerhan cell histiocytosis (including eosinophilic granuloma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Regarding non-odontogenic cysts of the maxilla and mandible, briefly discuss the characteristics of the following:
1. Nasopalatine Duct Cyst (incisive canal cyst)
2. Midpalatal cyst of infants
3. Nasolabial cyst
4. Stafne Bone Cyst (Static bone cavity, latent bone cyst)
5. Aneurysmal bone cyst
6. Idiopathic bone cavity

A
  1. Nasopalatine Duct Cyst (incisive canal cyst)
    - Most common Non-odontogenic cyst
    - Derived from embryologic remnant of the nasopalatine duct
    - Located between the maxillary central incisors (heart-shaped lucency, >10mm)
    - Treatment: EEnucleation and curettage if symptomatic
  2. Midpalatal cyst of infants
    - Arises from epithelium trapped between embryologic palatal shelves (“fissural”), midline palatal mass
    - Tx: Enucleation and curettage
  3. Nasolabial cyst
    - Arise within the labial vestibule, present as a swelling of the upper lip or nasal floor
    - Tx: Excision
  4. Stafne Bone Cyst (Static bone cavity, latent bone cyst)
    - Due to aberrant salivary gland tissue located in the posterior mandible
    - Not actually a cyst
    - Tx: Observation
  5. Aneurysmal bone cyst
    - More common in teenagers with a history of trauma to the mandible
    - Painful
    - Not a true cyst
    - Tx: Rapid enucleation to avoid hemorrhage
  6. Idiopathic bone cavity
    - Not a true cyst, may be secondary to a traumatic intramedullary hemorrhage with degeneration of the clot, resulting in an air-filled bony space
    - Tx: Biopsy to rule out other lesions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the main embyrological structures that form jaw cysts, what do their epithelial residues/remnants become, and what is the resulting odontogenic cyst?

A
  1. DENTAL LAMINA (bulk of the inside part of the tooth)
    - Rests of Serres
    - Becomes: Odontogenic Keratocysts, Lateral periodontal cysts
  2. ENAMEL ORGAN
    - Enamel epithelium
    - Becomes: Dentigerous cysts
  3. EPITHELIAL ROOT SHEATH OF HERTWIG (or Periodontal ligament)
    - Epithelial Rests of Malassez
    - Becomes: Radicular cyst, Periapical cyst, Dental cyst
33
Q

Regarding periapical/radicular cysts, discuss:
1. Location
2. Pathophysiology - 2 (cause and embryologic origin)
3. Clinical signs and symptoms
4. Diagnostic findings - 1
5. Histopathology - 1
6. Complications - 6
7. Treatment

A

LOCATION:
- Most common maxillary/mandibular odontogenic cyst
- Typically located on anterior maxilla and posterior mandible
- Lateral periodonal cyst = less common variant found on lateral aspect of the tooth

PATHOPHYSIOLOGY:
- Nonviable tooth and dental decay causes osteitis of periapical bone from dental canal
- Epithelial CELL RESTS OF MALASSEZ –> proliferate in response to inflammation and cause cyst formation

CLINICAL PRESENTATION:
- Typically asymptomatic
- May illicit pain with percussion or heat

DIAGNOSTIC FINDINGS:
1. Radiographic: Radiolucency at root apex of tooth with associated dental caries or pulp injury

HISTOPATHOLOGY:
- Stratified squamous epithelium lining

COMPLICATIONS:
1. Local cellulitis
2. Fascial plane infections
3. Abscess formation
4. Fistula to oral cavity, skin, nasal cavity
5. Sepsis
6. Jugular vein thrombosis
7. Osteomyelitis
8. Orbital extension
9. Rare malignant transformation

TREATMENT:
1. Antibiotics
2. Drainage of abscess
3. Endodontic therapy, root canal to remove tooth

Vancouver Pg 114

34
Q

Regarding Dentigerous/Follicular cysts, discuss:
1. Epidemiology
2. Pathophysiology
3. Clinical signs and symptoms
4. Diagnostic findings
5. Histopathology
6. Complications
7. Treatment

A

EPIDEMIOLOGY:
- Second most common maxillary/mandibular odontogenic cyst

PATHOPHYSIOLOGY:
- Disruption of late odontogenesis associated with an impacted tooth, especially third molar of mandible/maxilla
- Impacted tooth causes enlargement of follicle/crown (ie. dental sac of mesenchymal cells surrounding the developing tooth)
- Cyst then grows within the normal dental follicle

CLINICAL PRESENTATION:
- Initially asymptomatic
- Often diagnosed late with jaw deformity

RADIOGRAPHIC FINDINGS:
- Radiolucency at crown of an unerupted tooth
- May displace teeth

HISTOPATHOLOGY:
- Outer thin connective tissue wall with a thin stratified squamous epithelium inner layer

COMPLICATIONS:
- Risk of malignant transformation in cyst wall (unicystic ameloblastoma, epidermoid carcinoma)

TREATMENT:
- Enucleation and Curettage

Vancouver pg 114

35
Q

Regarding Odontogenic Keratocyst/Keratocystic Odontogenic Tumor, discuss:
1. Epidemiology/Location
2. Pathophysiology
3. Clinical Presentation
4. Diagnosis
5. Histopathology
6. Treatment
7. Association

A

EPIDEMIOLOGY:
1. 2nd or 3rd decade
2. Common location - Ramus or angle, mandibular third molar
3. More aggressive and difficult to remove than other odontogenic cysts

PATHOPHYSIOLOGY:
- Arises from rests of Serres - remnants of dental lamina
- Causes bone destruction, frequent recurrence
- If multiple - think Gorlin syndrome (basal cell nevus syndrome)
- May be associated with a crown of unerupted tooth (follicular cyst) or tooth root (periapical cyst)

CLINICAL PRESENTATION:
- Typically asymptomatic

DIAGNOSTIC FINDINGS
- Based on histology
- Radiographic finding: Similar to primordial cysts - ovoid, well demarcated lesions

HISTOPATHOLOGY
- FNA: White keratin-containing aspirate
- Thin stratified squamous epithelium, columnar or cuboidal basal cell layer
- Both parakeratin (wavy parakeratin) or orthokeratin may be present
- Lumen may be filled with degenerated keratin or cystic space
- “Picket fence pallisading”

COMPLICATIONS:
1. Local destruction
2. Secondary infection
3. 10-60% recurrence

TREATMENT: Controversial
- Enucleation & curettage with aggressive burring of the cyst (recurrence rate >50% - often multilocular)
- Some advocate segmental resection with 1cm margin (might be too aggressive, given benign nature)

ASSOCIATION: Basal cell nevus syndrome
- Autosomal dominant
- Multiple KCOTs, basal cell carcinoma
- Bifid ribs
- Hypertelorism
- Mandibular prognathism
- Calcification of falx cerebri - 85%
- Palmar pitting - 65%
- Depressed midface
- Frontal and parietal bossing

36
Q

Regarding Primordial cysts, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Complications
5. Treatment

A

PATHOPHYSIOLOGY:
- Degeneration of odontogenesis results in cyst development where a tooth would normally develop

CLINICAL PRESENTATION:
- Typically asymptomatic

RADIOGRAPHIC FINDINGS:
- Ovoid, well-demarcated lesions, may be multiloculated

COMPLICATIONS:
- May become secondarily infected
- 50% considered keratocystic odontogenic tumors

TREEATMENT:
1. Enucleation and curettage
2. Must consider keratocystic odontogenic tumor if recurs

37
Q

Regarding eruption cysts, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Treatment

A

PATHOPHYSIOLOGY:
- Developmental cyst within the soft tissues

CLINICAL PRESENTATION:
- Bluish cyst overlying the alveolar ridge, typically resolves

RADIOGRAPHIC FINDINGS:
- Translucent, dome-shaped cyst

TREATMENT:
- Usually none, excise if symptomatic

38
Q

What are four types of ameloblastoma, according to the WHO 2017 classification?

A
  1. Conventional (solid/multicystic) type
  2. Unicystic: more aggressive, requires excision with 3cm margins
  3. Extraosseous/peripheral type
  4. Metastasizing (malignant)

(This is in order from most frequent to least)

70% mandible, 30% maxilla

  • Not the same as Ameloblastic Carcinoma!!
39
Q

Regarding Ameloblastoma, discuss:
1. What is the tissue origin of ameloblastoma?
2. What is the pathophysiology?
3. Epidemiology?
4. Clinical types?
5. Clinical presentation

A
  • Benign neoplasm, arises from the dental Lamina
  • Locally invasive (thought of as the oral counterpart to basal cell carcinoma)

Epidemiology:
- Occurs 3rd-4th decade
- 80% mandibular (30% maxillary)
- Rare malignant transformation

Clinical types:
1. Central: arises in bone (intraosseous)
2. Plexiform unicystic: more aggressive, occurs in lining of follicular cysts or impacted teeth
3. Peripheral: arises in soft tissue around alveolar bone, much less aggressive, may be treated with local excision

Clinical presentation:
- Slow growing
- Painless
- Intrabony mandibular swelling
- May resorb tooth roots

40
Q

What is the radiologic finding in conventional (solid/multicystic) ameloblastoma?

A
  1. Soap bubbles appearance (or “honeycombed”)
  2. Expanding radiolucent multiloculations

Vancouver Pg 115

41
Q

What are 6 histologic patterns of ameloblastoma? What are the classic histologic findings? 2

A
  1. Granular cell
  2. Desmoplastic
  3. Follicular or simple (most common)
  4. Acanthomatous
  5. Plexiform (more aggressive, occurs in lining of follicular cysts or impacted teeth)
  6. Basal cell

“God Damn Fucking Ameloblastoma Pathology Bullshit”

Histologic findings:
- Cystic spaces lined with tall columnar epithelium, filled with stellate reticulum (central mass of loosely arranged cells), surrounded by a dense fibrous collagenous stroma
- Ameloblasts - Reversal with polarization - nuclei are facing away from the basement membrane (Vickers-Gorlin change)

https://www.pathologyoutlines.com/topic/mandiblemaxillaameloblastoma.html

Vancouver Pg 115

42
Q

What is the treatment of ameloblastoma?

A
  1. Wide excision with immediate reconstruction
    - Mandible: 1cm bony margin
    - Maxillary: 1.5cm bony margin
    - 3-5cm margin for unicystic types with plexiform histology
43
Q

What are the 7 risk factors for ameloblastoma recurrence?

A
  1. Large
  2. Multicystic
  3. Follicular subtype (most common)
  4. Plexiform subtype (worst prognosis - need 3cm margins)
  5. Positive margins
  6. Enucleation and curettage instead of excision
  7. Distant metastasis
44
Q

Regarding Malignant Ameloblastoma, discuss:
1. Pathophysiology
2. Clinical presentation - 1
3. Radiographic findings - 1
4. Diagnosis - how does the pathology differ from regular ameloblastoma?
5. Treeatment - 3

A

PATHOPHYSIOLOGY:
- Rare malignant degeneration from ameloblastoma, resulting in metastasis

CLINICAL PRESENTATION:
- Regional or distant metastasis with aggressive local invasion

RADIOGRAPHIC FINDINGS:
- Radiolucency with poorly defined margins

DIAGNOSIS:
1. Biopsy of metastasis reveals similiar histology to primary ameloblastoma with malignant features (atypical mitotic figures, invasion, pleomorphism)

TREATMENT:
1. Aggressive local resection
2. Neck disseection for positive lymphadenopathy
3. Consideer post-operative radiation and/or chemotherapy

45
Q

Regarding Calcifying Epithelial Odontogenic Tumors (Pindborg Tumor), discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology
5. Treatment

A

PATHOPHYSIOLOGY:
- Rare
- Benign infiltrating lesion associated with impacted molars
- Derived from the STRATUM INTERMEDIUM (layer of two or three cells between the inner enamel epithelium and the newly forming cells of the stellate reticulum)

CLINICAL PRESENTATION:
- Slow growing
- Painless
- Intrabony mandibular swelling (similar to ameloblastoma)
- Can be infiltrative and destructive

RADIOGRAPHIC FINDINGS:
- Unilocular radiolucency with calcifications

HISTOPATHOLOGY:
- Sheets or islands of epithelial cells with eosinophilic cytoplasm
- May contain AMYLOID with concentric calcifications or PSAMMOMA-LIKE BODIES (LIESEGANG RINGS)

TREATMENT:
1. Similar to ameloblastoma

https://d45jl3w9libvn.cloudfront.net/jaypee/static/books/9788184487121/Chapters/images/44-2.jpg

46
Q

Regarding Ameloblastic Fibroma, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology
5. Treatment

A

PATHOPHYSIOLOGY:
- True neoplasm with epithelial and mesenchymal elements
- Occurs in younger patients (5-20 years old)

CLINICAL PRESENTATION:
- Similar to ameloblastoma

RADIOGRAPHIC FINDINGS:
- Similar to ameloblastoma

HISTOPATHOLOGY:
- Islands of columnar or cuboidal epithelium with various arrangements (islands, cords, strands)
- Central papilla-like connective tissue

TREATMENT:
1. Enucleation and curettage (does not require 1cm margin like ameloblastoma)

47
Q

Regarding Ameloblastic Odontoma, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology - what is the common histopathologic finding?
5. Treatment

A

PATHOPHYSIOLOGY:
- Hamartomatous (non-neoplastic) lesion derived from epithelial (enamel-secreting) and mesenchymal (dentin-secreting) elements
- Associated with Dentigerous cysts

CLINICAL PRESENTATION:
- Typically asymptomatic
- May prevent tooth eruption

RADIOGRAPHIC FINDINGS:
- Radiopaque mass surrounded by a thin radiolucency (may be associated with an unerupted tooth)

HISTOPATHOLOGY:
- Preseence of dentin and enamel (similar to a dental follicle)
- “GHOST” cells - swollen/enlarged epithelial cell with eosnophilic cytoplasm, but without a nucleus

TREATMENT:
1. Enucleation and curettage (low risk of recurrence)

https://vetclinpathimages.files.wordpress.com/2018/03/ghost-cells-1-equine-1-imha-arrows.png?w=700

48
Q

Regarding Adenomatoid Odontogenic Tumor, discuss:
1. Pathophysiology
2. Clinical presentation - what is the classic presentation in terms of where its located, sex and age predilection
3. Histopathology
4. Treatment

A

PATHOPHYSIOLOGY:
- Hamartomatous growth (benign)

CLINICAL PRESENTATION:
- “TWO-THIRDS TUMOR”: 2/3 occur in the anterior maxilla, 2/3 occur in females, 2/3 associated with an impacted tooth (cuspids), occurs in the 2/3rd decades of life
- Maxillary mass, typically anterior to the molars
- Slow, progressive growth

HISTOPATHOLOGY:
- Spheres of cuboidal and spindle cells
- Amyloid and dystrophic calcifications

TREATMENT:
1. Enucleation and curettage (low risk of recurrence since often degenerates)

49
Q

Regarding Calcifying Odontogenic Cyst (Gorlin’s cyst), discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology
5. Treatment

A

PATHOPHYSIOLOGY:
- Dervied from PROLIFERATING EPITHELIUM, necrotic degeneration forms cysts

CLINICAL PRESENTATION:
- Anterior mandibular asymptomatic swelling

RADIOGRAPHIC FINDINGS:
- Well circumscribed radiolucency with central calcifications

HISTOPATHOLOGY:
- Cyst with solid forms
- Lined by eosinophilic cells and “ghost” cells (swollen/enlarged epithelial cell with eosnophilic cytoplasm, but without a nucleus)
- May cause giant-cell reaction

TREATMENT:
1. Enucleation and curettage (enbloc resection for rare neoplastic variants)

https://vetclinpathimages.files.wordpress.com/2018/03/ghost-cells-1-equine-1-imha-arrows.png?w=700

50
Q

Regarding Cementomas, discuss:
1. What are they?
2. What are the 3 main types?
3. Clinical presentation?
4. Treatment?

A

CEMENTOMAS: Class of benign tumors that secrete cementum (calcified connective tissue covering the outer surface of the root of the tooth and provides a medium for insertion of periodontal ligament fibers)

TYPES:
1. Periapical Cemental Dysplasia
- More common in black females
- Multiple lesions
- Develops through varying stages (osteolytic, cementoblastoma, maturation)

  1. Cementoblastoma
    - True benign tumor of cementoblasts of the tooth root
    - Usually from first mandibular tooth
  2. Cementifying Fibroma
    - Similar to an ossifying fibroma

CLINICAL PRESENTATION:
- Asymptomatic mandibular bony mass

TREATMENT:
- Observation for periapical cemental dysplasia
- Curettage with extraction for cementoblastomas

51
Q

Regarding Odontogenic Fibroma and Myxomas, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology
5. Treatment

A

PATHOPHYSIOLOGY:
- Arise from the PERIODONTAL LIGAMENT, DENTAL PAPILLA, OR DENTAL FOLLICLE

CLINICAL PRESENTATION:
- Slow growing, asymptomatic mandibular mass

RADIOGRAPHIC FINDINGS:
- Smooth bordered radiolucency
- May occur around the crown of an unerupted tooth

HISTOPATHOLOGY:
- Fibromas contain an abundance of collagen-producing fibroblasts
- Myxomas have fewer cells with a mucoid intraceellular matrix

TREATMENT:
1. Fibromas require simple enucleation
2. Myxomas are more difficult to excise - 25% recurrence rate

52
Q

Regarding Osseous dysplasia, discuss:
1. Pathophysiology
2. Clinical presentation
3. Diagnosis
4. Treatment

A

PATHOPHYSIOLOGY:
- Reactive disorder

CLINICAL PRESENTATION:
- More common in young african americans
- Alveolar bone mass
- Typically asymptomatic

DIAGNOSIS:
1. Biopsy
2. Panorex or plain x-rays: Multiple radiolucent/radiopaque intraosseous lesions, “cotton wool” appearance

TREATMENT:
1. Observation
2. Excision if symptomatic

53
Q

Regarding Ossifying Fibromas, discuss:
1. Pathophysiology
2. Clinical presentation
3. Radiographic findings
4. Histopathology
5. Treatment

A

PATHOPHYSIOLOGY:
- Benign
- Non-odontogenic tumor of the mandible or maxilla

CLINICAL PRESENTATION:
- More common in females
- Painless
- Slow growing mandibular mass
- May displace teeth

RADIOGRAPHIC FINDINGS:
- Well-demarcated, cannonball-like, homogeneous opacity

HISTOPATHOLOGY:
- Abundant collagen with varying calcification

TREATMENT:
1. Enucleation with curettage
2. May consider en bloc resection for aggressive or recurrent lesions

54
Q

Regarding Fibrous Dysplasia, discuss:
1. Pathophysiology
2. Clinical presentation
3. Types
4. Diagnosis
5. Treatment

A

PATHOPHYSIOLOGY:
- Genetically based, hamartomatous lesion of maxilla or mandible
- Medullary bone replaced by fibro-osseous tissue

TYPES:
1. Mono-ostotic: One bone involved, most common form
2. Poly-ostotic: More than one bone involved (e.g. McCune-Albright SYndrome - polyostotic fibrous dysplasia, precocious puberty, abnormal skin pigmented lesions)
3. Juvenile: Rapidly destructive, aggressive, destroys teeth, refractory to treatment

CLINICAL PRESENTATION:
- More common in middle aged women or young patients
- Slow growing, painless, well-circumscribed marble-like mass
- Destroys bone
- Unilateral facial deformity (mass does not cross midline; developmental plates)

DIAGNOSIS:
1. Biopsy
2. CT, Panorex, and X-rays (Ground glass, “Chinese writing”, irregular, multiloculated, diffuse margins, eggshell-thin cortex from destruction of cortical bone, may obliterate the sphenoid and frontal sinuses)

TREATMENT:
1. Excision and curettage of lesions if disfiguring, cosmetic shaping

55
Q

Regarding Torus Mandibularis and Palatinus, discuss:
1. Pathophysiology / what is it
2. Clinical presentation
3. Diagnosis
4. Treatment

A

PATHOPHYSIOLOGY:
- Developmental anomaly
- ENLARGEMENT of bone of the lingual surface of the mandible or the hard palate

CLINICAL PRESENTATION:
- Typically asymptomatic

DIAGNOSIS: Clinical exam

TREATMENT:
- Observation, excision if symptomatic

56
Q

Regarding Cherubism, discuss:
1. Pathophysiology and inheritance
2. Clinical presentation
3. Radiographic findings
4. Treatment

A

PATHOPHYSIOLOGY:
- Autosomal dominant mutation
- Results in symmetric enlargement of mandibular body and ramus (rarely involves maxilla) as bone is replaced with painless, cyst-like growths

CLINICAL PRESENTATION:
- Painless
- Round “cherub” face (broad cheeks, enlarged jaw)
- Regresses at puberty

RADIOGRAPHIC FINDINGS:
- Multilocular cystic changes in the mandible and maxilla
- Often in the anterior ends of the ribs as well

TREATMENT:
1. Observation
2. May consider surgical options after puberty if persistent

57
Q

Regarding Paget’s disease (Osteitis Deformans), discuss:
1. Pathophysiology and genetics
2. Phases of disease - 3
3. Clinical presentation - 6
4. Diagnosis - 3 investigations to be done. What are some lab findings?
5. Radiographic findings
6. Complications - 7
7. Treatment

A

PATHOPHYSIOLOGY:
- Autosomal dominant - SQSTM1 gene
- Increased bone resorption and formation resulting in dense, but fragile, bone
- Involves the lumbosacral regions and skull

PHASES:
1. Lytic: Replacement of bone with vascularized stroma, “destructive phase”
2. Mixed: Increased osteoclastic and osteoblastic activity, formation of Paget bone
3. Sclerotic: Decreased osteoclastic activity, increased hard, dense bone formation

CLINICAL PRESENTATION:
- More common in >40 years old (compared to fibrous dysplasia which affects younger patients)
- Bone pain
- Enlarged skull
- Dorsal kyphosis
- Bowed legs
- Nonunion fractures
- Hearing loss (CHL and SNHL)
- Neurologic sequelae from compressive effects

DIAGNOSIS:
- Panorex and plain x-rays: polyostotic, mosaic pattern of bone
- Bone scan (evaluate extent of disease)
- Elevated serum alkaline phosphatase ALP (marker to monitor therapy), calcium, and urine hydroxyproline from increased bone turnover

RADIOGRAPHIC FINDINGS:
1. Multiple, multiloculated, well-defined radiolucencies (lytic lesions)
2. Thin cortex
3. Sclerotic lesions in later phases

COMPLICATIONS:
1. Hypercalcemia
2. Polycythemia (increase in RBC)
3. Cardiac failure
4. Malignant transformation (giant cell tumor, osteosarcoma)
5. Neurologic compression
6. Normal pressure hydrocephalus
7. Pathologic fractures

TREATMENT:
1. Consider physical therapy to increase muscle support if asymptomatic and localized
2. Medical management for symptomatic or complications (e.g. calcitonin, cytotoxic agents, etidronate, analgesics)

58
Q

What are ways to reduce fracture risk for a marginal vs. segmental mandibulectomy?

A

1.5cm inferior strut

59
Q

What are the 4 subsites of the oropharynx?

A
  1. Anterior wall (glossoepiglottic area) - includes base of tongue (posterior to the vallate papillare) and vallecula
  2. Lateral wall (tonsil, tonsillar fossa and tonsillar faucial pillars, and glossotonsillar sulci
  3. Posterior wall
  4. Superior wall (inferior surface of the soft palate, uvula)
60
Q

What are the two main types of oropharyngeal cancer according to the NCCN?

A

HPV + and HPV -

61
Q

What is the likelihood of malignancy for a cystic neck mass in > 40 years old? What is the top 3 differential for a cystic neck mass?

What about for patients under 40 years old?

A

Likelihood of malignancy = 80%

  1. Cancer in Waldeyer’s ring (oropharynx or nasopharynx) - p16+ oropharyngeal cancer most common
  2. Papillary thyroid cancer
  3. Branchiogenic cancer or cyst (carcinoma arising from a branchial cyst)

Note: 50% of tonsil masses will have nodal metastasis at presentation, 72% if base of tongue is involved

For patients under 40, the most likely diagnosis is branchial cleft cyst, but the differential here is broad

62
Q

What are the surgical approaches for management of oropharyngeal carcinoma? 5

A
  1. Trans-oral
    - Trans-oral laser surgery
    - Trans-oral-robotic surgery
  2. Suprahyoid/transhyoid approach
  3. Lip-split mandibulotomy
  4. Mdnaibular swing
  5. Pull-through technique (mandibular lingual release)
    - Apron flap
    - Visor flap (lower lip paresthesia)
  6. Lateral Pharyngotomy ??

Vancouver Pg 125 photos

63
Q

What are the advantages of transoral robotic surgery over standard transoral approaches? (5)

A
  1. 3-D endoscopic visualization
  2. Potentially shorter operative time
  3. Reduces blood loss, infection, and other complications
  4. Less morbidity, pain, shortened hospital stay
  5. Improved cosmetic and functional outcome
64
Q

What are 7 benefits of transoral robotic surgery?

A
  1. Avoidance of disfiguring mandibulotomy
  2. Minimization or elimination of need for chemoradiation therapy
  3. Avoidance of tracheostomy
  4. Quicker return to normal speech and swallowing
  5. Significantly less pain
  6. Decreased blood loss
  7. Shorter recovery time and hospital stay
65
Q

What are the disadvantages of transoral robotic surgery over standard transoral approaches? (4)

A
  1. Limited surgical field of view
  2. Steep learning curve
  3. Potential for difficult hemostatic control
  4. Cost / not every centre has a robot
  5. Loss of tactile feel of tumor
66
Q

What are the main anatomical areas for which transoral robotic surgery can be applied? 6

A
  1. Oropharynx: tonsil, BOT, palate, pharyngeal wall
  2. Skull base
  3. Parapharyngeal space
  4. Larynx (usually requires translaser microsurgery)
  5. Hypopharynx (usually requires translater microsurgery TLM)
  6. Supraglottis
67
Q

What are 6 risks of transoral robotic surgery?

A
  1. Bleeding (can be severe and life-threatening, POD10 most common) –> Tunica media injury –> aneurysm –> rupture
  2. Dysphagia (requiring initial feeding tube supplementation)
  3. Dysgeusia
  4. Fistula (highest risk when performed in conjunction with neck dissection)
  5. Nasopharyngeal reflux
  6. Velopharyngeal insufficiency

Think: similar risks to doing a tonsil (ie. bleeding, similar timeframe as tonsil POD7-10)

68
Q

What are 9 contraindications to transoral robotic surgery overall?

A

Standard contraindications for head and neck surgery:
1. Medical conditions contraindicating general anesthesia or transoral surgical approaches
2. Inability to adequately visualize anatomy to perform the diagnostic or therapeutic surgical approach transorally
3. Unresectability of involved neck nodes

Specific contraindications for TORS procedures regardless of region/procedure:
1. Mandibular invasion
2. Tongue base involvement requiring resection of >50% of tongue base
3. Pharyngeal wall involvement requiring resection of more than 50% of the posterior pharyngeal wall
4. Radiologic confirmation of carotid artery involvement
5. Fixation of tumor to the prevertebral fascia
6. Medialized carotid artery lying adjacent to tonsil (contraindication for radical tonsillectomy, but not for tongue base resection)

69
Q

What are 4 vascular contraindications to transoral robotic surgery for oropharyngeal cancer?

A
  1. Tonsillar cancer with a retropharyngeal carotid artery
  2. Epicentre of the tumor is in the midline of the tongue base or vallecula, which would put both lingual arteries at risk
  3. Tumor adjacent to carotid bulb or internal carotid artery, which will result in intraoperative exposure of the vessel
  4. Encasement of the carotid artery byt he primary tumor (T4b) or by a metastatic neck node
70
Q

What are the indications for radiation therapy for HPV+ oropharyngeal cancer?

A

Primary modality for p16+ T1 & T2 lesions
- Equal cure rate as surgery

71
Q

What are the indications for chemoRT for p16- oropharyngeal cancer? 3

A
  • T1-2, N0-1: Single modality: RT (66-70Gy) or primary surgery
  • T3-4: CRT or surgery + adjuvant RT
  • Any T, N2-3: CRT or surgery + adjuvant RT
  • Post-op CRT: if extranodal extension or + margins
72
Q

What is the survival of HPV + vs. HPV- oropharyngeal carcinoma?
In what situation does HPV+ disease behave like HPV- disease?

A

HPV+ first, HPV- second:
1. Stage 1: 88% vs. 70%
2. Stage 2: 78% vs. 58%
3. Stage 3: 71% vs. 50%
4. Stage 4: 70% vs. 30%

Overall HPV+ has better survival, unless ≥ 10 pack year smoking history, where the survival behaves like HPV- disease

73
Q

What is the gold standard for HPV testing in an oropharyngeal tumor?

A
  1. HPV E6/E7 mRNA expression (inactivates p53/pRb)
  2. p16 is widely used as a surrogate
74
Q

How do you counsel someone on HPV-related oropharyngeal cancer, regarding transmission?

A
  • HPV is a sexually transmitted virus; most sexually active people will get HPV in their lifetimes. “It is impossible to known with certainty from whom or when you acquired HPV because most people do not know they have it”
  • “Lifetime mutual monogamy or abstinence are the best ways to prevent transmission”
  • The virus is suppressed by a healthy immune system in most people
  • There is currently no test for early detection of oropharyngeal cancer that would be similar to the pap test for cervical cancer
  • HPV is a common virus that does not imply infidelity or promiscuity
  • Most infected people with HPV do not develop signs of symptoms
  • In a subset of people, this virus will go on to cause symptoms / malignancy (but cannot predict who)

Overall prevalence of HPV in American all sites 42.5%

Prevalence of HPV 16 & 18 in American Oral Cavity - 4%, any HPV 7%

75
Q

What are 4 main strategies for de-escalation therapy in the treatment of HPV+ Oropharyngeal SCC?

A
  1. Radiation combined with Cetuximab instead of cisplatin
  2. Induction chemotherapy followed by decreasing radiation doses and/or volumes for good responders
  3. Radiation alone instead of chemoradiation
  4. Transoral surgery followed or not by postoperative radiotherapy
76
Q

What is the workup and management of an unknown primary SCC that is identified in the neck?

A

INITIAL WORKUP:
1. Complete H&N exam including endoscopy
2. FNA of node stain with: HPV (p16), EBV (EBER), Thyroglobulin (Tg), Calcitonin, Melanoma stains, and neuroendocrine stains
3. If repeat FNA is repeatedly negative, take to the OR for open biopsy (historically thought to compromise survival, but this has been disproven)

ONCE DIAGNOSIS OF SCC IN THE NODE ESTABLISHED:
1. CT Neck & Chest (10% detection)
2. PET scan (37% detection)
3. EUA Quadroscopy under anesthesia ± directed biopsy ± tonsillectomy ± tongue base mucosectomy (very center specific) - (35% detection)

IF STILL UNABLE TO FIND PRIMARY, GO TO TREATMENT:
1. Neck dissection followed by adjuvant RT/CRT as dictated by pathology and suspected site of origin (N1 - RT only if high risk features, N2/3 - CRT)
2. Consider radiating the putative mucosal sites (60Gy) of origin based on HPV/EBV status
3. Treatment protocols are highly centre specific
4. 5-year survival 40-60%

77
Q

What are 3 limitations of a PET scan?

A
  1. Size < 5mm
  2. Other conditions that increase FDG uptake, such as:
    - Inflammatory conditions
    - Autoimmune conditions
78
Q

What are the contraindications for marginal mandibulectomy? 4

A
  1. Osteoporosis or osteopenia or use of bisphosphonates
  2. Tumor erosion into mandible
  3. Edentulous (tooth roots eventually degrade and eventually height of mandible is not enough to sustain marginal mandibulectomy)
  4. Previous history of radiation
79
Q

When you consider a patient for TORS for oropharynx?

A
  1. No obvious ENE (centre dependent - cuz you might need chemo and therefore triple therapy after)
  2. Good plane between carotid and tumor, no medialization of carotid

Head and Neck (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions