H&N: Cancer/Salivary Gland Disease/Endocrine Flashcards
1
Q
In what compartment does the deep lobe of parotid sit?
A
prestyloid.
2
Q
What two veins form the retromandibular vein?
A
internal maxillary vein and superficial temporal vein
3
Q
Stenson’s duct: relationship to the masseter? where does it open into the oral cavity (by what tooth)?
A
lateral to the masseter; opens by the second molar
4
Q
Nerve roots for the greater auricular nerve?
A
C2-C3
5
Q
Parasympathetic innervation to the parotid gland?
A
V3 auriculotemporal by way of otic ganglion (inferior salivary nucleus -> IX ->lesser petrosal nerve -> otic ganglion -> V3
6
Q
Prestyloid tumors vs poststyloid tumors?
A
Prestyloid tumors largely deep lobe of parotid. Poststyloid neurogenic or vascular.
7
Q
Bilateral parotid cysts — suggests what diagnosis?
A
HIV
8
Q
Parotid vs submandibular gland saliva: basal rate vs stimulated? proteinaceous/watery/serous vs high mucin?
A
Parotid: stimulated, proteinaceous/watery/serous. Submandibular: basal rate, high mucin
9
Q
Name 3 etiologies of xerostomia. Name two classes of drugs a/w xerostomia.
A
drug induced, autoimmune, postradiation. Antihistamines, anticholinergics.
10
Q
What is necrotizing sialometaplasia?
A
Lesion of the hard palate - benign but looks like cancer.
11
Q
Name 3-5 potential causes of sialoadenitis.
A
infectious (bacterial, TB), autoimmune (Sjogrens or granulomatous), sialolithiasis, viral (mumps parotitis, HIV)
12
Q
Sjogren’s patients are at increased risk of what type of cancer?
A
non-Hodgkin’s lymphoma/MALT lymphoma in the parotid gland
13
Q
Size “cutoff” for sialolith removal via sialoendoscopy?
A
5mm cutoff.
14
Q
How does lithotripsy work for sialoliths and what percentage will have alleviation of symptoms?
A
Lithotripsy uses sound waves to break up the stones; 75-90% will have alleviation of symptoms, 50% will have resolution of stones
15
Q
Pediatric parotid disorders: a) What is recurrent parotitis of childhood? b) Work type I vs type II branchial cleft cysts?
A
a) young boy keeps having cyclical enlargement of the parotid but otherwise is fine. Treatment is antibiotics with coverage of Staph and dilation of stenson’s duct. b) type I involves EAC, type II does not.
16
Q
Ranula: a) treatment? b) location of plunging ranula relative to mylohyoid?
A
ranula = mucocele associated with a sublingual gland. Resection of ranula and associated gland. b) plunging ranula is deep to mylohyoid
17
Q
Hemangioma vs lymphangioma: a) time of presentation? b) time of involution? c) treatment? d) sclerosing agent for lymphangioma?
A
a) hemangioma at birth, lymphangioma 2-5mo. b) hemangioma involute by 1 year, lymphangioma does not involue. c) hemangioma usually propranolol; lymphangioma sclerosing agent, poss surgery d) OK-432
18
Q
Rate of malignancy in solid parotid tumors for peds vs adult?
A
50% in kids, 20% in adults
19
Q
“Pathology name” (non eponym) for wharthin’s tumor?
A
papillary cystadenoma lymphomatosum
20
Q
Name 2-3 indications for level I-V neck dissection in parotid malignancy.
A
neck dissection: high grade mucoepi, salivary ductal carcinoma, facial nerve invasion, positive lymph node, extraglandular extension.
21
Q
Name 2-3 indications for postop radiation in parotid malignancy.
A
postop radiation: adenoid cystic, residual tumor on facial nerve, positive margins, perineural invasion, positive nodes, high grade tumor, recurrent low grade tumor
22
Q
Most common parotid malignancy in adults? In children?
A
Mucoep most common in adults and kids.
23
Q
Most common malignant tumor for non-parotid salivary glands? What site is most common for that malignancy?
A
Most common non-parotid = adenoid cystic. Palate most common.
24
Q
Name 2-3 risk factors for SCC metastasis to the parotid gland.
A
cutaneous SCC anterior to the imaginary coronal plane through the EAC; SCC or melanoma of the cheek, preauricular skin. depth >4mm, diameter > 2cm
25
Numbering scheme for teeth? (where is 1, where is 32)
teeth get numbered top right to top left, bottom left to bottom right. So #1 is your top right molar and #32 is your bottom right molar
26
4 intrinsic muscles of the tongue?
intrinsic muscles: superior and inferior longitudinal, transverse, vertical.
27
4 extrinsic muscles of the tongue?
Extrinsic muscles: genioglossus, hyoglossus, palatoglossus, styloglossus.
28
4 muscles of mastication?
Mastication: medial and lateral pterygoids, masseter, temporalis
29
Sensory innervation of the tongue?
V3 for sensation and VII for taste anteriorly. IX for sensation and taste posteriorly
30
Motor innervation of the soft palate?
V3 for tensor veli palatini; X for everything else (levator, palatoglossus, palatopharyngeus, musculus uvulae)
31
What muscle is deep to the palatine tonsils? (Eg what muscle are you separating your tonsillar capsule from)
superior constrictor
32
5 arteries supplying the tonsil?
ascending pharyngeal, tonsillar branch of facial, tonsillar branch of dorsal lingual, lesser palatine, tonsillar branch of ascending palatine
33
What is passavant’s ridge?
mucosal horizontal line that occurs during elevation of the soft palate -- represents superior border of the superior constrictor
34
What do each of the constrictor muscles originate from?
superior constrictor: pterygoid plate, mandible, base of tongue; middle constrictor: hyoid/stylohyoid; inferior constrictor: thyroid cartilage.
35
Function of the medial and lateral pterygoid muscles?
Medial pterygoid elevates/deviation away from midline, lateral pterygoid depresses/deviation towards midline/protrusion
36
Location and significance of a Killian’s dehiscence with respect to cricopharyngeus? Location of a Killian-Jamieson dehiscence? What artery passes through this space? What nerve is at risk with a Killian-Jamieson diverticulum resection?
Killian’s is above cricopharyngeus, Killian-Jamieson is inferior to the cricopharyngeus and the inferior thyroid artery branches passes through that space. RLN is at risk during K-J resection.
37
Auerbach vs Meissner’s plexus?
Auerbach is implicated in achalasia; myenteric/between muscle + mucosa. Meissner’s is submucosal.
38
Descriptions, malignant potential, and treatment for: a) Lichen planus b) Leukoplakia c) erythroplakia
a) lichen planus = reticular/lacy. low malignant potential. topical steroids. b) leukoplakia = hyperkeratotic white lesion, ~10-15% malignant potential. c) erythroplakia 50% malignant potential
39
Most common head and neck site for Ewing’s sarcoma?
mandible
40
Origin of ameloblastoma?
enamel of tooth
41
Potential therapy for each of the following etiologies for dysphagia: a) tongue base weakness b) oral dysfunction c) pharyngeal sensory loss d) vocal cord paresis e) vocal cord paralysis f) failure of UES opening
a) pharyngeal/swallow exercises b) tongue exercises c) texture/thickness/consistency adjustments d) injection e) medialization f) cricopharyngeal myotomy
42
What is plummer vinson syndrome? What hypopharyngeal subsite cancer are they at increased risk for?
iron deficiency anemia, glossitis, esophageal webs. post cricoid space SCC
43
Most common type of TEF?
blind sac in the esophagus with distal fistulous connection to the trachea
44
Where does the subclavian arise from in dysphagia lusoria? Where should it arise from?
arises from descending aorta. Should arise from the innominate
45
Distance to stomach/LES from incisors? Distance to cricopharyngeus?
40cm; 16cm
46
When is the esophagus weakest following an esophageal burn?
4-7 days
47
When do fibroblasts arrive in a healing wound?
2-5 days
48
When does collagen appear in the wound bed of a healing wound?
8-12 days
49
Embryologic origin for parafollicular C cells? For thyroid lobes?
neural crest cells for C cells. ultimobranchial body for thyroid lobes.
50
SLN internal vs external branch functions and course?
internal SLN - sensation to pharynx/supraglottis. external branch - cricothyroid, inferior constrictor
51
RLN functions: motor, sensory, and parasympathetic?
RLN - motor all intrinsic muscles except cricothyroid, also inferior constrictor. Parasympathetic to upper esophagus. Sensory to TVF
52
T3 vs T4: a) which one is active form? b) where does conversion to active form occur? c) half life of each / timing of reassessment for levels after dose change in exogenous form? d) which one is produced in higher amounts by thyroid gland?
a) T3 is active. b) peripheral tissues. c) half-life of T3 is 1-2 days, needs 1-2 weeks to clear before checking levels. half-life of T4 is 5-6 days, needs 4-5 weeks to clear. d) T4 is produced in higher amounts
53
TFTs, pattern of TSH/T3/T4 for: a) subclinical hypothyroidism b) subclinical hyperthyroidism c) hyperthyroidism d) hypothyroidism e) states of high thyroglobulin (eg pregnancy)? f) states of low thyroglobulin (eg anabolic steroids, hypoproteinemia)
a) TSH high but T3/T4 normal. b) TSH low but T3/T4 normal. c) TSH low, T3/T4 high. d) TSH high, T3/T4 low. e) TSH normal, T4 high, T3 low. f) TSH normal, T4 low, T3 high.
54
MOA for PTU and methimazole?
PTU and methimazole decrease organification of iodine.
55
Black box warning for PTU for what devastating side effect? What notable toxicities are associated with methimazole?
PTU a/w liver failure, methimazole with birth defects and agranulocytosis.
56
How to manage PTU/methimazole administration in pregnancy?
Plan for PTU in first trimester, switch to methimazole after.
57
What is Lugol’s solution and why do people give it?
super saturated iodine, though to decrease vascularity of the thyroid prior to surgery for grave’s disease
58
Graves: pathophysiology and management?
anti-TPO/autoantibodies activating TSH receptors. antithyroid meds vs total thyroidectomy vs RAI.
59
toxic multinodular goiter: pathophysiology and management?
iodine uptake scan, will have hot areas diffusely throughout. Treatment is RAI vs antithyroid medications vs surgery.
60
Uninodular toxic goiter: pathophysiology and management?
single hyperactive nodule. iodine uptake scan identifying hot nodule. Thyroid lobectomy vs RAI, meds usually don’t work except for reducing hyperactivity prior to surgery.
61
Hashimoto’s vs deQuervain’s /subacute granulomatous: a) symptoms? b) management?
Hashimoto’s - painless enlargement, initial hyperthyroidism, then hypothyroidism. Can manage with low dose (eg 50mcg starting) synthroid. Subacute/drQuervains - PAINFUL enlargement. NSAIDs.
62
Expanding neck mass in Hashimoto’s patient?
Lymphoma
63
Symptomatology, at-risk demographic, and management of lymphocytic thyroiditis?
painless enlargement, pregnancy/OCPs at risk. Management is supportive
64
Riedel’s struma - what is it? how to manage?
woody fibrosis of the thyroid including extrathyroidal extension - like sclerosing cholangitis of the thyroid. Management may include isthmusectomy for biopsy, usually cannot resect the rest due to extrathyroidal fibrosis.
65
Bethesda classification? What is NIFTP and its significance?
I - nondiagnostic; risk 5-10%. II - benign; risk ~0-3%. III - atypical lesion/atypical follicular lesion of unknown significance, risk 10-30% (18% if NIFTP not cancer). IV - follicular neoplasm, risk 25-40% (10-40% if NIFTP not cancer). V - suspicious for malignancy, risk 60-75% (45-60%). VI- malignant, like 97-99% (94-96%). NIFTP=noninvasive follicular thyroid neoplasm with papillary like features; intermediate condition that is noninvasive in capsule but nuclear elements similar to PTC
66
What is a hurthle cell? How to manage hurthle cells on FNA?
Hurthle cell is like a follicular cell but with granular features. FNA - consider like follicular cells.
67
What is the clinical significance of hurthle cell carcinoma?
Hurthle cell carcinoma is worse in prognosis and higher risk of distant mets.
68
PTC: a) histopathology? b) 3 unfavorable histological forms? c) significance of RET proto-oncogene? d) significance and clinical implications of BRAF mutation?
a) orphan annie eyes/grooved nuclear margins with prominent nucleoli. b) diffuse sclerosing, tall cell, columnar cell. c) a/w PTC. d) BRAF a/w PTC and with worse prognosis, higher rate of neck mets/distant mets, higher rate of ETE, higher recurrence rate
69
PTC vs follicular: a) higher rate of distant metastasis at diagnosis? b) mode of metastasis? c) unifocal vs multifocal? d) relative incidence of contralateral lobe disease? e) association with iodine-deficient regions?
a) follicular high rate of distant mets. b) PTC lymphatic, follicular hematogenous c) PTC multifocal, follicular unifocal, d) PTC high incidence of contralateral disease, follicular low. e) follicular a/w iodine deficiency
70
TNM staging (AJCC 2018) for thyroid cancer?
T1 = <2cm, T2 2-4cm, T3 > 4cm, ETE no further than straps, T4 into bad things beyond straps. N1 = regional mets. M1 = distant mets. Age <55 can’t be worse than stage 2 (stage 1 M0, stage 2 M1). Age >55 stage 1 - <4cm + no mets. stage 2 - <4cm OR regional mets OR ETE to straps. Stage 3 ETE into neck/larynx/pharynx. Stage IVA - ETE into prevertebral space/carotid sheath, no distant mets. Stage IVB - distant mets.
71
Management of disease adherent to RLN with normal VF function preop?
normal VF function, don’t sacrifice the nerve, try to dissect as much as you can without leaving gross disease.
72
When should RLN be sacrificed in thyroid cancer?
Sacrifice when nerve is already out or gross adherent disease.
73
2-3 indications for post-op RAI?
post-op RAI: incomplete resection (eg tumor left on nerve) or deliberate subtotal, follicular cell carcinoma, high-risk patients with PTC.
74
2-3 indications for post-op external beam radiation?
External Beam: inoperable case, palliate large amounts of central neck disease
75
Name 4 methods of post-operative disease surveillance for well-differentiated thyroid cancer after total thyroidectomy.
thyroglobulin, routine ultrasound, CT scan, I-131 scan, PET/CT
76
mode of inheritance for hereditary MTC?
Autosomal dominant for the most part. There is also sporadic version.
77
Superior vs inferior parathyroid: a) typical location? b) which one is more variable in location? c) dorsal/ventral to RLN?
a) superior - within 1cm of the superior lobe, posterolateral aspect. inferior within 1cm of the inferior lobe. b) inferior more variable. c) superior is dorsal, inferior is ventral to RLN.
78
locations for ectopic parathyroid gland? (3 for inferior, 2 for superior)
superior - TE groove/paraesophageal, retroesophageal/retrolaryngeal. inferior - intrathyroidal, thymus, carotid sheath
79
Four functions of PTH in calcium homeostasis?
increase gut absorption of Ca, decrease renal excretion, increase bone resorption of Ca, increase renal production of vitD
80
Hyperparathyroidism: PTH/Ca levels in primary/secondary/tertiary?
PTH and Ca high in primary. PTH high and Ca low in secondary. PTH high and Ca normal in tertiary.
81
MEN disorders associated with hyperPTH?
MEN1 (pituitary, parathyroid, pheo), MEN 2A (parathyroid, MTC, pheo).
82
What is your concern if PTH in the thousands?
parathyroid carcinoma
83
High Ca, high PTH, low urine Ca. Diagnosis?
Benign familial hypocalciuric hypercalcemia
84
Indications for surgery to treat hyperparathyroidism (name 3-5).
Symptomatic hypercalcemia, young age, patient preference for surgery, concern for malignancy, Ca levels >1mg/dL above upper limit of normal, previous episode of life-threatening hypercalcemia
85
Name 2-3 indications for asymptomatic patients >50 years.
GFR 30% normal for age; DEXA score 2 deviation off normal, elevated urine Ca > 400mg/dL
86
How does sestamibi scanning work? What is SPECT? what is SPECT/CT?
It measures washout of technetium, washout is delayed in parathyroid adenomas/hyperplasia compared to thyroid gland/normal parathyroid gland. SPECT = 3D version of sestamibi. SPECT/CT fuses images with thin cut CT.
87
Periapical cyst - a) pathophysiology? b) relationship to teeth c) treatment?
a) arise from a nonvital tooth. b) surrounding apex of tooth c) extraction of diseased tooth and enucleation of cyst
88
Dentigerous cyst - a) pathophysiology? b) relationship to teeth? c) prognosis without treatment? d) management?
a) comes from the enamel of the tooth, epithelial lined b) unerupted crown, typically third molar. c) continued growth if no treatment. d) enucleation/surgical excision +tooth extraction
89
3 clinical variants of ameloblastoma? Which one is most common?
solid, unifocal, multifocal. Solid most common.
90
Histopath buzz word for ameloblastoma?
PIANO KEY appearance (reversed polarization of columnar cells)
91
Malignant ameloblastoma vs ameloblastic carcinoma?
Malignant has distant mets, carcinoma also has local invasion with concomitant histopathological differences. Malignant ameloblastoma doesn’t have pathological differences from regular ameloblastoma but does have mets
92
odontogenic keratocyst: a) contents of aspiration? b) site in mandible? c) histopath findings? d) if multiple, what is syndrome associated/features? mode of inheritance?
a) cheesy/yellow b) posterior mandible c) hyperchromatic palisaded basal cell layer d) Gorlin’s syndrome/familial multiple nevoid basal cell carcinoma syndrome. Auto dominant. Multiple jaw OKCs + basal cell carcinomas
93
Osteoma - a) histopath findings? b) associated syndrome and features? c) mode of inheritance?
a) looks like regular bone b) Gardner’s syndrome - osteomas and colorectal cancer. c) autosomal dominant
94
Osteosarcoma a) age demographic? b) clinical symptoms? c) radiologic buzzword
a) 10-40 years. b) PAIN c) sunburst
95
Fibrous dysplasia: a) two types? associated syndrome / mode of inheritance? b) radiographic buzzword?
a) monostotic or polyostotic. Polyostotic is McCune Allbright. Mode of inheritance is mosaic - can’t be passed on. b) ground glass
96
Paget disease: a) pathophys? b) radiologic buzzword? c) treatment?
a) increased osteoclastic and osteoblastic activity. b) cotton wool c) bisphosphonates/calcitonin
97
two cell types in the carotid body?
chief cells and sustenacular cells
98
path “buzzword” for paragangliomas?
zellballen
99
Mutations in what enzyme are implicated in familial carotid body paraganglioma?
succinyl dehydrogenase.
100
Differences in malignant potential and bilateral vs unilateral occurrence in familial compared to sporadic type?
Familial is more likely to be benign and more likely to be bilateral
101
What is the Shamblin classification?
Classification of carotid body tumor. I - small and easily dissected from capsule. II- partially surround, able to dissect. III - encapsulates and difficult to dissect
102
Defining features of malignancy in carotid body tumors?
Pain is highly suggestive. Region and distant mets are diagnostic. Local invasion/high-risk features are not diagnostic without mets.
103
Radiologic buzz words on CTA and MRI for carotid body tumor?
Lyre sign, salt and pepper flow voids.
104
Role of preop embolization in carotid body tumor?
Preop embolization not helpful for carotid body tumor overall. CTA may be helpful for evaluating circle of willis when carotid sacrifice is expected.
105
What is first bite syndrome?
Pain in the parotid region upon first bite - due to damage to the cervical sympathetics. Gets better over the course of the day.
106
What is baroreflex syndrome? What cranial nerve mediates this?
essentially like autonomic instability due to loss of baroreceptor mediated control. CN IX mediates.
107
Vagal paragangliomas: Rate of malignancy compared to carotid body tumors (higher or lower)?
More likely to be malignant.
108
Which ganglion do vagal paragangliomas typically arise from (inferior vs superior/middle)?
Typically arise from inferior nodose.
109
Approach to surgery vs RT in vagal paragangliomas?
Surgery if nerves are already out. RT if nerves are functional.
110
Histological patterns in Schwannoma (2)? What’s the difference between them?
Antoni A (verocay bodies, solid component). Antoni B (sparse stromal tissue).
111
Where do most extratemporal H&N schwannomas occur and what nerves do they arise from?
Most H&N schwannomas occur in the parapharyngeal space and arise from X and sympathetic chain.
112
How does UV light cause DNA damage?
photodamage to pyridine DNA base pairs (T/C).
113
Difference between UVA and UVB? Which one is a more potent cause of damage? Which one is rated in sunblock? which one is primary in tanning beds?
UVB shorter wavelength and more potent damage. UVA slightly longer and still with phototoxicity potential. UVB rated in sunblock. Tanning beds predominantly UVA but have UVB as well in some cases.
114
Risk factors for melanoma: Name 2-3 examples.
Fitzpatrick I, >3 blistering sunburns before 17 years of age, h/o actinic keratosis, family history, tanning bed use.
115
What benign skin condition is a risk factor for malignant melanoma?
Actinic keratosis
116
Name 2 hereditary syndromes a/w malignant melanoma/skin cancer. Implicated mutation?
Familial dysplastic nevus syndrome; CDKN2A implicated. Xerodoma pigmentosum - a heterogeneous group of mutations leading to inability to clear phototoxic damage (specifically thymidine dimers). Disrupted nucleotide excision repair. AR.
117
Name 2-3 genetic derangements implicated in melanoma.
PTEN, BRAF, P13K, cKit, Ras family.
118
Mutations in which protein are implicated in 50-70% of melanomas?
BRAF implicated
119
Name 3 pre-malignant skin lesions. Which one is considered melanoma in situ?
lentigo maligna, dysplastic nevus, congenital nevus. Lengtigo maligna = melanoma in situ, radial growth without vertical growth
120
Name the 6 melanoma subtypes. Which one is most common? Which one has no radial growth phase? Which one is known for high rates of perineural spread without lymphatic spread? Which one is often nonpigmented?
lentigo maligna melanoma, superficial spreading (most common), nodular (no radial growth phase), desmoplastic (often nonpigmented, high perineural spread), acral lentiginous, mucosal
121
Benign skin lesions: a) “stuck on” appearance b) name 3 benign melanocytic lesions
a) seborrheic keratosis b) mongolian spot, lentigo maligna, dysplastic nevus, blue nevus, melanotic nevus (hamartomatous)
122
What is keratoacanthoma?
keratoacanthoma - low grade squamous cell carcinoma.
123
What is a Merkel cell carcinoma?
Merkel cell - neuroendocrine skin ca, worse prognosis
124
Histopath IHC markers positive in melanoma (4)?
S100, HMB45, vimectin, melan-A. CK negative
125
Role of serum LDH in melanoma?
Can monitor for metastasis
126
Contrast Clark level vs Breslow staging.
Clark level looks at depth of invasion based on layer of skin. Breslow is depth in mm from surface of skin.
127
How to determine appropriate surgical margins in WLE of melanoma?
1mm depth -> 1cm margin. 1-2mm = 1-2cm margin. >2mm -> 2cm margin.
128
when should therapeutic ND be offered in malignant melanoma?
palpable lymphadenopathy/gross disease, +SLN.
129
when should superficial parotidectomy be considered/offered in malignant melanoma?
sufficient depth/ulceration/palpable LAD with parotid in the drainage pathway in lesions anterior to the EAC
130
Name 2-3 indications for SLN biopsy.
SLN: 1-4mm lesion, invasion of reticular dermis or subQ tissue, ulcerated lesion.
131
Name 2-3 indications for external beam radiation.
EBR: positive lymph nodes, recurrence s/p prior neck dissection, inability/refusal to have neck dissection with T2b to T4 disease
132
4 most common sites of mucosal melanoma, in decreasing order of commonality? Which one has the best prognosis? Which one has the worst?
Nasal cavity > paranasal sinuses > oral cavity > nasopharynx. Nasal cavity best. Paranasal sinuses worst.
133
Dysplasia: a) diff between mild/mod/severe/CIS? b) potential for malignant transformation between mild/mod vs severe?
It’s related to the degree/proportion of epithelium with cellular atypia. <1/3 - mild. <2/3 mod. >2/3 severe. CIS = neoplasm w/o BM invasion. b) mild/mod <10%, Severe ~18-30%.
134
Histological cell type of: a) supraglottis b) glottis c) subglottis
a) pseudostratified columnar b) stratified squamous epithelium c) pseudostratified columnar
135
Laryngeal SCC: Lymphatic drainage pattern of supraglottic vs glottic vs subglottic and likelihood of nodal metastasis at presentation?
a) supraglottic = bilateral and common. glottic = rare/minimal. subglottic = typically rare
136
Name 2-3 contraindications for supraglottic laryngectomy or endoscopic glottic surgery.
poor pulmonary status, VF paralysis, interarytenoid involvement, cartilage invasion.
137
Benefit of preserving arytenoid complex in glottic surgery?
Preserving arytenoid arytenoid complex helps with voicing and swallowing.
138
Management of the neck in supraglottic vs glottic early stage cancer?
supraglottic - bilateral elective neck dissection. glottic - no elective neck dissection.
139
Management if anterior commissure involved?
If anterior commissure involved, consider supracricoid laryngectomy with preservation of cricoid + one arytenoid.
140
Discuss implications of 1991 VA study in management of advanced laryngeal cancer.
1991 VA - surgery +post op vs primary chemoradiation, no survival differences. 60% laryngeal preservation with chemorads. Higher rate of crossover with T4 tumors, gross cartilage invasion, VF fixation.
141
Discuss implications of 2003 RTOG study in management of advanced laryngeal cancer.
2003 RTOG compared induction chemo + rads vs chemoradiation, radiation alone. Chemorads was best for laryngectomy free survival and locoregional control.
142
Management of the cN0 neck in T3 or T4 glottic cancers? What if complete response to chemorads?
Elective neck on the side of the lesion. Does not need salvage neck/elective neck if complete response.
143
2004 RTOG and EORTC findings on postop adjuvant therapy?
Both studies showed efficacy for postop chemorads for high-risk patients (eg positive margins, ECS, perineural disease)
144
Name 2-3 complications of TL.
pharyngocutaneous fistula, stomal stenosis, hypothyroidism.
145
Name 2-3 complications of chemoradiation.
Xerostomia, nonfunctional larynx, hypothyroidism.
146
Follow-up: a) frequency after treatment completion? b) what lab needs to be checked regularly? c) how soon after completion can a PET/CT be considered?
a) 1-3 months for a year, then 4-6 months until 5 years, then 6-12 months. b) TSH c) 10 weeks
147
Verrucous carcinoma: a) histological buzz word for behavior? b) treatment? c) management of the neck? d) postop adjuvant therapy? e) potential for metastasis?
a) pushing borders. b) WLE c) no neck dissection. d) no postop adjuvant therapy e) no mets unless there is a focus of SCC
