Brainscape's Knowledge GenomeTM

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


See full index

ENT Boards > Head and Neck > Flashcards

Head and Neck Flashcards

1
Q

Describe the 5 phases of the cell cycle

A
  • G0 = resting phase
  • G1 = Growth phase 1 in preparation for DNA synthesis
  • S = DNA synthesis
  • G2 = Growth phase 2 in preparation for division
  • M = Mitosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

During which stages of the cell cycle are cells most and least susceptible to damage from Chemo/XRT?

A
  • S = DNA synthesis (most resistant phase)
  • G2 = Growth phase 2 in preparation for division (2nd most sensitive phase)
  • M = Mitosis (most susceptible phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Describe 5 methods for targeting a Vector to a specific cell type

A
  1. Tumor-specific promoter
    • Activate promoter gene expression specifically in tumor cells (ex CEA, AFP)
  2. Non-specific promoter
    • Drive replication in all susceptible cell types, higher risk for toxicity (ex CMV)
  3. Direct, receptor-targeting
    • Create ligand for specific receptor characteristic of tumor cells
  4. Indirect, inverse-targeting
    • DEtarget healthy, non-tumor cells to improve vector selectivity for cancer cells
  5. Indirect, protease-targeting
    • Selective infection of cells w/ specific surface protease (which activate the viral receptor and allow viral entry)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

List different viral vectors currently in use in H&N cancer

A
  • Adenovirus
  • Reovirus
  • Rhabdovirus
  • Measles
  • Mumps
  • HSV
  • Vaccinia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are two gene types involved in cell growth in cancer?

A
  • Tumor Suppressor Genes (limit cell growth through negative feedback)
  • ProtoOncogenes > Mutated Oncogenes (induce cell growth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which Tumor Suppressor Genes are involved in H&N Cancer?

A

p53 - Regulates cell cycle & apoptosis
- Involved in > 50% of HNSCC
- Bad prognosis
p16 (protein from CDKN2A gene) - Suppresses cyclin-dependent pathways
- Involved in > 70% of HNSCC
- Surrogate marker for HPV
- Good prognosis
RB - Inhibits transcription factor E2F
- Involved in > 60% HNSCC

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

Which Oncogenes are involved in H&N Cancer?

A

EGFR - Mutation promotes epidermal overgrowth
- Involved in > 90% HNSCC
- Poor prognosis
Cyclin D1 - Phosphorylates Rb, accelerates cell cycle
- Associated with increased recurrence, nodal mets, death
RET Translocation - Receptor TK involved in cell growth
- Associated with MEN2
RAS - Signal transducer for surface growth factor receptors
BRAF - Protein kinase activated by oncogenic RAS to increase growth factor signaling
- Associated with PTC
C-MYC - Transcription regulator
- Common in HNSCC
- Associated with Burkitt’s Lymphoma
- Poor prognosis
BCL-2 - Counteracts p53 & inhibits apoptosis
- Good prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

In what situation does HPV+ status NOT improve prognosis

A

History of smoking > 10 years

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

Discuss possible mechanisms of immunocompromise in HNSCC

A

HOST-related:
- Comorbid condition (ex. HPV, SLE, DM2, etc)
- Circulating immune complexes
- Suppressor T-cells
- Ig-blocking Antibodies
- TGF-B
TUMOUR-related:
- Tumor production of immunosuppressant agents (ex. VEGF, IL-1, IL-10)
- Tumor suppression of innate immunity
- Tumor antigenic modulation
EXOGENOUS:
- Chemo/XRT
- Immunosuppressant medications (ex. steroids, IFN, methotrexate, cyclophosphamide, etc)

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

Methods to assess adequate cerebral perfusion prior to carotid ligation

A
  • Balloon occlusion test
  • 4-vessel angiography (carotids & vertebrals)
  • SPECT
  • Xenon-133 flow scan
  • CTA/MRA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the incidence of CVA/stroke following carotid occlusion at different speeds?

A

Acute occlusion (ex. ligation in OR w/o pre-op measures) = 50%
Gradual occlusion over <7d (ex. intraluminal tumor invasion) = 30%
Gradual occlusion over >7d (ex. vessel compression by tumor, or pre-op tx) = 5%

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

What intervention can be done pre-op to reduce the likelihood of CVA post surgical ICA ligation

A

Pre-op embolization (aka permanent balloon occlusion):
- Embolization of ICA just proximal to ophthalmic artery takeoff
- Reduces stump emboli
- 2 weeks pre-op
- Monitor for 72h post-procedure

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

List the segments of the ICA

A

C1 = Cervical
C2 = Petrous TB
C3 = Foramen Lacerum
C4 = Cavernous Sinus
C5 = Clinoid
C6 = Ophthalmic
C7 = Communicating

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

Define Simultaneous Tumors

A

Separate primary tumors diagnosed at same time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Define Synchronous Tumors

A

Separate primary tumors diagnosed within 6 months of each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define Metachronous Tumors

A

Separate primary tumors diagnosed > 6 months of each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Define 2nd Primary

A

Separate primary tumor, based on:
- Different cell type
- Different location
- Different metastatic nodal group

**10% risk 2nd primary in non-smokers
**Risk increases to 50% in smokers
**50% develop within 2 years of 1st primary

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

How does continued smoking & ETOH use affect risk of recurrence and 2nd primary?

A

Up to 50% risk recurrence and/or 2nd primary

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

Describe the phases of clinical trials

A

PHASE 1 = Safety trial (dose determination, side effects)
PHASE 2 = Efficacy trial (does it work?)
PHASE 3 = Comparative trial (how does it compare to standard therapies?)
PHASE 4 = Post-marketing assessment of long-term complications

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is RECIST?

A

Response Evaluation Criteria in Solid Tumours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

According to RECIST, what qualifies as a measurable lesion?

A

10mm in long axis on clinical or CT exam

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

According to RECIST, what qualifies as a pathological LN?

A

15mm in short axis on CT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

According to RECIST, what is a target (or index) lesion?

A

Largest, most representative lesion (max 5 total, or 2/organ
- Used to track and assess treatment response
- More does not yield more accurate assessment and just wastes time & resources)

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

Define Objective Response (OR) according to WHO and RECIST

A

RECIST = Change in sum of longest dimensions of target lesions (max 2 lesion/organ, max 5 lesions overall)
WHO = change in sum of [longest dimension x cross dimension]s of all lesions

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

Define Complete Response (CR) according to WHO and RECIST

A

RECIST = Disappearance of all lesions/disease (AND reduction in LNs to <10mm) by 4+wks
WHO = (same)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Define Partial Response (PR) according to WHO and RECIST

A

RECIST = >30% decrease by 4+wks
WHO = >50% decrease by 4+wks

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

Define Stable Disease (SD) according to WHO and RECIST

A

RECIST = no Partial Response or Progressive Disease (no change)
WHO = same

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

Define Progressive Disease (PD) according to WHO and RECIST

A

RECIST = >20% (min 5mm) increase over smallest sum, or new lesion(s)
WHO = >25% increase in any lesion, or new lesion(s)

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

Seven roles for chemo in HNSCC

A
  • Neo adjuvant
  • Adjuvant (+margins, +ECS)
  • Non-surgical candidate
  • Palliation
  • Investigative
  • Primary treatment in NPC
  • Organ-preservation in T3-4 larynx
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What factors determine the success of chemo?

A
  • Tumor burden (# cells)
  • Inherent/acquired resistivity to chemo
  • % cells in M-phase of cell cycle (responsive phase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

How many cells must a tumor have before it’s palpable?

A

> 100,000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Indications for chemo

A

Primary
- In combination with radiation therapy for certain malignancies (nasopharyngeal, oropharyngeal, hypopharyngeal, and laryngeal)
- Lymphoma
- Not a surgical candidate

Adjuvant
- Positive margins
- Extracapsular spread
- Investigative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the max age for consideration of chemo?

A

70y - above this too toxic??

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What classes of chemotherapy are available?

A

AAAATTBB

Alkylating Agents (Cisplatin, Carboplatin)
Alkaloids (Vincristine, Vinblastine)
Antibiotics (Bleomycin, Mitomycin, Hydroxydaunomycin)
Antimetabolites (Methotrexate, 5-FU)
Taxanes (Paclitaxel, Docitaxel)
Topoisomerases (Etoposide, Topotecan)
Biologics - Targeted (Cetuximab, Ipilimumab)
Biologics - Nonspecific (Gefitinib, Sunitinib)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Aklylating Agents: MOE, Dosing, side effects

A

MOA: Interferes w/ DNA synthesis & replication
Dosing: Cisplatin 100mg/m2, up to 3 doses, q3wks
Side Effects: Oto/neuro/nephro-toxicity, myelosuppression, mucositis, dermatitis

Cisplatin = Most effective single-agent chemo
Carboplatin has less oto/neuro/nephro effects, but +++myelosuppression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Akaloids: MOE, Dosing, side effects

A

Vincristine, Vinblastine

MOA: Interferes w/ microtubule formation
Side Effects: peripheral neuropathy, alopecia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Antibiotics (Chemotherapy): MOE, Dosing, side effects

A

Bleomycin, Mitomycin, Hydroxydaunomycin

MOA: Interferes w/ DNA synthesis & replication
Side Effects: pulmonary fibrosis, myelosuppression

38
Q

Antimetabolites: MOE, Dosing, side effects

A

Methotrexate: interferes w/ DNA synthesis via impaired Folate metabolism
5FU: interferes w/ DNA synthesis via defective Uracil analog

Side Effects: mucositis, dermatitis, myelosuppression

39
Q

Taxanes: MOE, Dosing, side effects

A

Paclitaxel, Docitaxel

MOA: disrupt microtubule function = impaired cell division in M phase
Side Effects: neuropathy, alopecia

40
Q

Topoisomerases: MOE, Dosing, side effects

A

Etoposide, Topotecan

MOA: prevent DNA unwinding for replication
Side Effects: mucositis, dermatitis

41
Q

Biologics (Targeted): MOE, Dosing, side effects

A

Cetuximab, Ipilimumab

MOA: monoclonal antibodies against EGFR
Side Effects: cardiotoxicity, dermatitis

42
Q

Biologics (Nonspecific): MOE, Dosing, side effects

A

Gefitinib, Sunitinib

MOA: tyrosine kinase inhibitors that inhibit EGF/VEGF
Side Effects: dermatitis

43
Q

In general, is combination chemo any more effective than single agent?

A
  • No change in overall survival
  • More side effects
  • However higher response rates seen w/ some combos (Cis-5FU; Carbo-Taxol)
  • Carbo-5FU used sometimes instead of Cisplatin when Cis contraindicated due to renal failure
44
Q

In general, is induction chemo any more effective than concurrent?

A
  • No change in overall survival
  • Some studies suggest concurrent better, but can do either (centre-specific)
  • BUT can’t do BOTH induction and concurrent -> far too toxic for anyone to handle
    (rare exception: NPC)
  • Best induction combo: Docitaxel-5FU-Cisplatin
45
Q

Describe the broad categories of radiation therapy

A

External Beam (Photon, electron)
Brachytherapy
Ingested (RAI)
Proton, Neutron

46
Q

Describe the types of External Beam Radiation

A

Conventional 3D-Conformational
- Manual, multi-beam, uniform intensity
Intensity Modulated RT (IMRT)
- Computerized, multi-beam, variable intensity
Image-guided RT
- Repeat imaging throughout treatment course to modify target/volumes
Stereotactic
- Uses external frame [ex. face mask] for minimal movement, high precision
Gamma knife (“Radiosurgery”)
- Stereotactic single large dose/small volume

47
Q

Compare Mega-Volt (Photon) vs Electron Beam RT

A

MEGAVOLT = photons, deep tissue penetration, surface-sparing
EB = electrons, superficial penetration, spares deep tissues

48
Q

Discuss IMRT

A

Intensity-Modulated Radiation Therapy
- Uses photons
- Multi-beam
- Intensity varies -> moderates dose across field to contour target volume to lesion

49
Q

Possible methods of deliverying brachytherapy

A
  • Interstitial (rods)
  • Intercavitary (seeds)
  • Surface Mould
50
Q

Advantages of brachytherapy

A
  • Direct application of radiotherapy
  • Minimizes effects on surrounding tissues
  • Continuous dose
51
Q

Disadvantages of brachytherapy

A
  • Local tissue necrosis
  • May miss some areas of tumor
  • Inconsistent dose delivery to cells at different proximities
  • Pt is radioactive throughout treatment duration (must remain isolated, away from kids & pregnant women, etc)
52
Q

Describe the different methods of cell injury by XRT

A

Direct injury
- Direct DNA damage
Indirect injury
- Creates oxygen free radicals which further damage DNA

53
Q

4 Rs of Radiotherapy Damage

A

REPAIR
- Inhibits ability of tumor cells with sublethal injuries to repair between doses (normal cells heal faster, tf can repair before next dose)
REDISTRIBUTION
- Allows more cells to shift into into M-phase (the most radio-sensitive)
REOXYGENATION
- Allows reaccumulation of oxygen in tissues (tumor cells only radiosensitive when oxygenated)
REPOPULATION
- Delivers higher/faster doses to tissues to ensure maximum dose is reached prior to onset of tumor repopulation (which usually occurs ~5wks)

54
Q

Define Gray and Rad

A

RAD - Radiation Absorbed Dose
GRAY - Dose of radiation required to have 1J of energy absorbed by 1 kg of matter
1Gy = 1 J/kg = 100 rad

**Rad has largely been replaced by Gy in modern measurement/lingo

55
Q

Most common acute and late XRT-related toxicities

A

ACUTE = mucositis
LATE = tissue fibrosis

56
Q

WHO Mucositis Grading

A

Grade 1: edema & erythema
Grade 2: erythema +/- patchy ulceration, solid diet tolerated
Grade 3: diffuse ulceration (liquid diet only)
Grade 4: severe ulceration and pain (PO diet impossible, enteral support/intubation necessary)
(NCI adds -Grade 5: death)

57
Q

Typical XRT Indications

A

Neoadjuvant (to shrink)
T3-4
N2b+ (multiple +nodes)
ECS
Perineural/lymphovascular invasion
Positive margins
Unable to undergo surgery
Palliation

58
Q

Typical Head and Neck Radiation Dose

A

DEFINITIVE = 70 Gy (in 35f over 7wks)
ADJUVANT = 60-66 Gy (in 30-33f over 6-6.5wks)

59
Q

Traditional Head and Neck Radiation Regimen

A

2 Gy daily, 5/wk, x7wks (Total 70 Gy)

60
Q

Hyperfractionated Head and Neck Radiation Regimen

A

1.2 Gy BID, 5/wk, x7wks (Total 81 Gy)
- Higher overall dose
- More inconvenient than once daily
- Worse acute toxicities, better late toxicities
- Better Reoxygenation & Redistribution
- No OS improvement

61
Q

Accelerated Head and Neck Radiation Regimen

A

1.6 Gy BID, 5/wk, x6wks (Total 67 Gy)
- Same overall dose, faster application
- More inconvenient than once daily
- Worse acute toxicities, better late toxicities
- Better Reoxygenation & Redistribution, prevents Repopulation
- No OS improvement

62
Q

Accelerated + Boost Head and Neck Radiation Regimen

A

1.8 Gy daily to large field, 5/wks, 6wks

PLUS 1.6 Gy to small field in 2nd dose on last 12d (Total 72 Gy)

63
Q

Split Course Head and Neck Radiation Regimen

A

Accelerated course interrupted by 2wk break in the middle
- Allow repair of normal tissue

64
Q

Hypofractionated Head and Neck Radiation Regimen

A

50 Gy in 3-5 sessions over 2-4wks
- Palliative

65
Q

Radiation Regimen to Nodal Basins

A

Primary XRT:
- N0 = 44-64 Gy
- N+ = 66-74 Gy (same as primary site)
Adjuvant XRT:
- N0 = 44-64 Gy
- N+ = 60-66 Gy (same as primary site)

66
Q

Early complications of XRT

A

Mucositis (most common)
Xerostomia (50% reduction after 20 Gy, 75% reduction after 50 Gy)

67
Q

Late complications of XRT

A

Skin necrosis
Tissue fibrosis
Myelopathy
Hypothyroidism
ORN (50 Gy)
Dental caries
Trismus
Xerostomia
ETD
SNHL
Cataracts (6 Gy)
Retinopathy, Optic Nerve injury (50 Gy)
Cranial neuropathies
Carotid artery stenosis
Transverse myelitis -> L’Hermitte’s Sign (50 Gy)
Spinal necrosis (50 Gy)
Brain necrosis (70 Gy)
2e malignancy

68
Q

What is L’Hermitte’s Sign?

A

Electric-shock sensation down arms from cervical spine transverse myelitis (also seen in MS)

69
Q

Advantages of Neoadjuvant XRT

A
  • Shrinks tumor load
  • Pre-op tissues are more radio-sensitive than post-op (better blood supply)
  • Tumor seeding (local & distant via LV showering of mets) during surgery may be reduced due to reduced viability
70
Q

Disadvantages of Neoadjuvant XRT

A
  • Obscures margins
  • Resection/recon more difficult due to fibrosis, scar, poor blood supply
  • Poor wound-healing >40 Gy
  • Lowers overall XRT dose that can be given
  • Harder to stage clinically/pathologically during/after surgery
71
Q

Advantages of Adjuvant XRT

A
  • Addresses bad histologic features (+margins, ECS, PNI, LVI, high T/N)
  • Treat subclinical disease
  • Treat disease inaccessible w/ surgery
72
Q

Disadvantages of Adjuvant XRT

A
  • Complications of XRT
  • More susceptible to wound breakdown & complications
  • Higher risks as # modalities increases
73
Q

Best time to start post-op XRT for maximum effect

A

< 6wks (ideally 3wks, but realistically usually ends up closer to 6wks)

74
Q

General anti-cancer mechanisms of concurrent chemo-XRT

A
  • Recruits cells from G0 to M phases
  • Synchronizes cells into same phase, increasing effectiveness of both chemo + XRT
  • Radiosensitizes, prevents radiation resistance
  • Inhibits tumor cell repair from sublethal XRT injury
  • Causes tumor shrinkage -> allows increased drug & O2 delivery
  • Can act on different subsets of tumor cells (ex. those that may be radioresistant)
75
Q

What are Marx’s Stages of ORN, and how are they treated?

A

STAGE 1 = exposed bone
- Local topical care, debride, biopsy, culture & IV antibiotics, nutritional support, Pentoxifylline
- 30-40 HBO dives
STAGE 2 = does not respond to HBO
- Partial resection, local flap closure, and complete total 40 HBO dives
STAGE 3 = full-thickness ORN, pathologic #, orocutaneous fistula
- Resect & free flap or plate; 10 extra post-op HBO dives

76
Q

What is the class and MOA of Pentoxifylline?

A

Xanthine Derivative
- Increases circulation & blood flow (ie. for ORN, claudication, PVD, etc)
- Prevent bronchoconstriction (asthma, etc)

MOA:
- Inhibit phosphodiesterases:
- Lowers blood viscosity: increases blood cell deformability -> allows increased circulation
- Vasodilation
- Decrease platelet aggregation

77
Q

What findings on CT suggest ORN

A
  • Radiolucency
  • Cortical thinning
  • Moth-eaten appearance
  • Loss of trabecular structure
  • Pathologic #
  • Sequestrum (island of dead bone)
78
Q

Mechanism of Action of Hyperbaric Oxygen

A
  • Increases amount of O2 dissolved in solution
  • Increases diffusion distance from capillaries
  • Increases neovascularization
  • Increases fibroblast proliferation
  • Improves leukocyte oxidative killing
  • Synergy w. certain abx (Fluoroquinolones, Aminoglycosides, Ampho B)
79
Q

Phases of Hyperbaric Oxygen Treatment

A

LAG PHASE (tx 1-8):
- Increased capillary budding & collagen synthesis
- Little detectable clinical change
- Little change in O2-tension
LOG PHASE (tx 8-22):
- Angiogenesis, increased
- Fibroblasts/collagen/cellularity
- Rapid response phase
- Log increase in O2-tension
PLATEAU PHASE (22+):
- O2-tension plateaus @ 85% even w. more txs
- Plateau of clinical response

80
Q

Indications for Hyperbaric Oxygen Treatment

A
  • ORN
  • SSNHL
  • Decompression sickness (incl. inner ear decompression sickness)
  • Certain infections: Osteomyelitis, Nec Fasc, malignant OE
  • Poor wound healing
  • Flap failure
  • Pre and post dental work (especially extractions) in radiated pt
81
Q

Contraindications to Hyperbaric Oxygen Treatment

A

ABSOLUTE:
- Untreated pneumothroax
- Active cancer

RELATIVE:
- Airway disease (asthma, COPD, bullous emphysema)
- History of seizures (seizures from O2 toxicity are a potential complication of HBOT))
- Claustrophobia
- Pregnancy
- Uncontrolled fever higher risk of seizures)
- Meds: Doxorubicin

82
Q

Definition of a close margin

A

≤ 5mm

83
Q

When can a biopsy be considered reliable post XRT?

A

3 months
- Lethally injured cells & normal cells are identical; injured cells must be allowed to die off (lyse), which requires 4-5 cycles of mitosis

84
Q

Describe the ECOG scoring system and its significance

A

Eastern Cooperative Oncology Group
- Predicts ability to undergo/continue treatment

0 = Fully active (~Karnovsky 90-100)
1 = Symptomatic but ambulatory, can do light work (~K 70-80)
2 = Symptomatic, in bed <50% of day, can do self care (~K 60-50)
3 = Very symptomatic, in bed >50% of day, limited self-care (~K 30-40)
4 = Bedbound (~K 10-20)
5 = Dead

Usually only patients ECOG 1-2 or better are fit enough to undergo chemo-XRT

85
Q

Describe the Karnovsky Index and its significance

A

Another performance scale to measure patient functional status & fitness for treatment

0 = Perfectly well
…
100 = Dead

Parallels ECOG

86
Q

When must you treat the N0 Neck (Regardless of T Stage)?

A

Nasopharynx - Bilateral Levels II - V
Oropharynx - Unilateral Levels II - IV
- Tonsil - Unilateral up to T3N2b, above this do bilateral
- Palate - Bilateral
- BOT - Bilateral
Hypopharynx - Unilateral Levels II - IV +/- VI
Supraglottis - Bilateral Levels II - IV +/- VI
Subglottis - Bilateral Level VI +/- VII

87
Q

When must you treat the N0 Neck with an Oral Cavity Primary?

A

T2+ OR tongue depth ≥4mm
- Unilateral levels I - III/IV
- Bilateral if crosses midline

88
Q

When must you treat the N0 Neck with a Glottic Primary?

A

T3+
- Unilateral levels II - IV +/- VI
- Bilateral if bilateral disease

89
Q

When must you treat the N0 Neck with a Salivary Gland Primary?

A

T3+
- Unless one of the low-grade tumors (acinic, low grade mucoepidermoid, PLGA)
- Decision to prophylactically treat neck for N0 in adenoid cystic is controversial

90
Q

When should you never treat the N0 neck?

A

N0 nasal cavity, sinuses, non-melanoma skin, thyroid (except medullary)
- Exception = maxillary sinus (gets adjuvant XRT to the neck for ≥T3 disease but no neck dissection unless N+

91
Q

Layers of the Epidermis

A

Stratum Corneum
Stratum Lucidum
Stratum Granulosum
Stratum Spinosum
Stratum Basale

ENT Boards (1 decks)

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