Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
431 Cards in this Set
- Front
- Back
|
Q: Name and describe the 5 phases of the cell cycle
|
A: G1 – 1st Growth phase in preparation for DNA synthesis A: S – DNA Synthesis (most resistant) A: G2 – Cell Growth, duplication of cell proteins & structures A: M – Mitosis (most sensitive) A: G0 – Resting phase |
|
|
Q: What methods are used to introduce genes in gene therapy? |
A: General methods – In vivo (direct introduction of vector with gene into tissues), Ex vivo (removing target tissue/cell portion, Transduction with vector, Reimplantation into patient) A: Viral vectors A: Nonviral vectors – Nonspecific targeting, low transfection rate |
|
|
Q: Name 5 viral vectors |
A: Adenovirus – DNA, nonintegrating episome; immunogenic A: Adeno-Associated virus – ssDNA, when inserts into 19q13.4 causes B-cell leukemia A: Retrovirus – RNA, Lentivirus, risk of insertional mutagenesis A: Herpes – Large DNA, nonintegrating, contains TK for suicide with Acyclovir A: Vaccinia – Large DNA, pox-virus, nonintegrating, immunogenic |
|
|
Q: 5 methods of Targeting Vectors to a tissue/cell type |
A: Tumor-specific Promoter – Activate gene expression in cancer cells (COX-2, hTERT, CEA, AFP, SLPI) A: Non-specific Promoter – Constitutively high level expression (CMV, SV40) A: Indirect, Receptor targeting – Ligand for a specific Receptor A: Indirect, Inverse targeting – Selective Inhibition of infectivity with specific Receptor A: Indirect, Protease targeting – Selective infectivity of cells with specific Protease |
|
|
Q: Name 5 Nonviral vectors |
A: Cationic Liposome A: Plasmid DNA A: Ballistic A: Calcium phosphate precipitation A: Electroporation – Cultured cells exposed to DNA in presence of strong Electrical Pulse 3: Nonspecific targeting, low transfection rate |
|
|
Q: Four areas of research in Gene therapy for Neoplastic disease |
A: Immunomodulation – Modification of TIL’s, enhance immunogenicity in vivo & ex vivo A: Cytotoxic gene therapy – Introduction of Enzymes that convert a Prodrug into a toxic compound HSV-tk (thymidine kinase phosphorylates gangcyclovir into its active compound) Cytosine deaminase (converts prodrug 5-fluorocytosine into 5- fluorouracil) A: Antisense gene therapy – Introduction of Blocking RNA against RNA or DNA targets A: Suppressor gene therapy |
|
|
Q: Two groups of Genes involved in cell Growth & Cancer |
A: Protooncogene – Normal cell genes that influence cell growth in a positive way, if mutated or overexpressed oncogene A: Tumor suppressor gene – Encode proteins that normally exert negative regulatory control in a cell |
|
|
Q: Five Oncogenes classified according to Protein’s Function |
A: Growth factor – int-2 A: Growth factor receptors – erbB/neu A: Signal transducers for surface growth factor receptors – ras A: Protein kinases – b-raf, c-raf A: Transcription regulator – myc |
|
|
Q: What are the 9 most Common Genes involved in HNSCC? |
A: Tumor suppressor genes: p53 – involved in cell cycle regulation and Apoptosis, it is a target for HPV E6 loss, chromosome 17p13, seen in >50% of HNSCC, ass e poor prognosis p16 & p21 – suppresses Cyclin and Cyclin dependent kinase pathways, chromosome 9p21, seen in > 70% of HNSCC, ass e better prognosis (surrogate marker for HPV status) pRB – inhibits Transcription Factor E2F; chromosome 13q, loss in 60% of HNSCC, it is a target for HPV E7 gene A: Oncogenes: ErbB family, Receptor Tyrosine Kinases: Epidermal Growth Factor Receptor (EGFR) - overexpressed in 90% of HNSCC, chromosome 7q11.2, ass e worse prognosis and targeted by cetuximab HER-2/neu Cyclin D1 – phosphorylates Rb accelerates cell cycle progression, chromosome 11q13, overexpression ass e recurrence, nodal metastasis, or death RET –Receptor Tyrosine Kinase involved in cell growth, associated with MEN II C-myc – Transcription regulator bcl-2 – inhibits apoptosis & counteracts p53 3: HPV positivity does not improve prognosis if smoking Hx > 10 pack years |
|
|
Q: Four antagonistic relationships in cancer genes |
A: bcl-2 (oncogene) and p53 (tumor suppressor gene) A: p53 and Cyclin (oncogene) A: p16/p21 (tumor suppressor gene) and Cyclin A: RB (tumor suppressor gene) and TF E2F |
|
|
Q: Functions of p53 gene? |
A: Controls cell cycle by binding to Cyclin-dependent Kinins and arrests cell replication in G1/S junction A: Can induce Apoptosis if DNA Repair mechanisms fail A: Activates DNA repair (BB, CH44) A: Produces factors that prevent angiogenesis (BB, CH44) 3: Located on chromosome 17p13.1 |
|
|
Q: 9 possible mechanisms of Immunosuppression in HNSCC |
A: IgA-blocking antibodies A: Circulating immune complexes A: Antigenic modulation of tumor A: TGF-b A: Suppressor T cells A: Histamine activation of Suppressor T cells A: Exogenous INF A: Tumor production (PGs, p15e, VEGF, GM-CSF, IL-1/10) A: Exogenous Immunosuppressive agents (chemo, XRT) 3: “I C Ant (Modulate) Transform or Suppress His Infinite Tumor Immunosuppression” |
|
|
Q: CT and MRI criteria for diagnosis of Carotid invasion in HNSCC |
A: Effacement of the Fascial plane surrounding greater than 25% of the vessel Circumference A: Tumor involvement of 75% or more of the Circumference of the carotid 3: Best modality between CT, MRI, or U/S remains controversial; MRI = 100% sensitive, 94% specific 3: D.M. Yousem, 2006: CT: The highest accuracy (84.1%) was recorded in 2 types: compression and deformation of the common carotid artery (CCA) or internal carotid artery (ICA) and partial fat or fascia deletion between tumor and the CCA or ICA. Circumferential vessel-wall involvement of greater than 180° on CT had a sensitivity as low as 18.5% but if < 180 peeling the tumor is an alternative to carotid artery resection MRI: 100% sensitive, 94% specific single criterion of involvement of 270° or more of the circumference of the carotid artery was accurate in predicting the surgeon’s inability to peel the tumor off the carotid artery in 100% of the cases Intraluminal tumor, though specific for vascular infiltration and unresectability, was infrequently seen and not very sensitive US and Transcranial Doppler have also been used |
|
|
Q: Incidence of Cerebral Complications following Common Carotid Occlusion |
A: Abrupt ligation = 42% A: Occluded gradually over <7 days = 30.6% A: Occluded gradually over ≥8 days = significantly decreased to 5.3% 3: Unselected ICA interruption – 26% rate of cerebral infarction (depends on patient age) |
|
|
Q: Four Tests to assess the adequacy of Collateral Circulation preop Carotid Resection |
A: 4-vessel angiography (carotids and vertebrals) A: Trial balloon occlusion A: Single-photon emission computed tomography scanning (SPECT, using Tc-99m HMPAO) A: Xenon-133 flow scan |
|
|
Q: Preoperative intervention that may reduce CVA incidence over Simple Carotid Ligation |
A: Permanent balloon occlusion A: Underlying principle is that high Embolization of the carotid eliminates the source of Stump Emboli A: Angiographic placement of permanent balloons or coils in the carotid siphon region just proximal to the ophthalmic artery, closely monitored for 72 hours, 2 weeks prior to carotid resection |
|
|
What are the segments of the ICA? |
A: C1, Cervical A: C2, Petrous A: C3, Lacerum A: C4, Cavernous A: C5, Clinoid A: C6, Ophthalmic A: C7, Communicating A: C’mon Please Let Children Consume Our Candy |
|
|
Q: Define Simultaneous, Synchronous, and Metachronous tumors
|
A: Simultaneous = Diagnosed at same time A: Synchronous tumor = found <6 months later A: Metachronous tumor = found >6 months later |
|
|
Q: Criteria defining a Second Primary |
A: Different Histology A: Different Location A: Each one has its own Metastatses 3: Overall incidence of 2nd primary cancer is ~10%, of which 80% are metachronous and 50% present in the first 2 years |
|
|
Q: Risks of Posttreatment Recurrence, and of 2nd Primary development with continued Smoking and EtOH consumption |
A: 30-50% risk of Locoregional Recurrence A: 10-40% risk of 2nd Primary development |
|
|
Q: Describe the phases of Clinical Trials |
A: Phase I – Tolerance and Pharmacologic properties; determine spectrum of Toxicity, endpoint is the maximally tolerated dose A: Phase II – Efficacy of a drug in a specific Disease and Stage at a defined Dose; define Activity within tolerable levels of toxicity, endpoint is Response Rate A: Phase III – Comparison of 2 therapies in a Randomized manner; endpoints are Response Rate, Response Duration, Disease Free Survival, Overall Survival A: Phase IV: post release to assess long term complications. |
|
|
Q: Response Evaluation Criteria in Solid Tumors (RECIST) |
|
|
|
Q: Six Roles for Chemotherapy in Head & Neck Oncology
|
A: Primary treatment of NPC… A: Organ preservation in Advanced Laryngeal cancer A: Unresectable disease A: Recurrent or metastatic disease A: Post-operative adjuvant therapy A: Investigative therapy |
|
|
Q: Three tumor Factors affecting Chemotherapy success |
A: Tumor burden – Number of tumor cells A: Percentage of cells in a chemo-Responsive phase of cell cycle A: Number of cells with inherent or acquired Resistance to chemotherapeutic agent |
|
|
Q: Mechanism of action and 3 examples of Alkylating agents |
A: Crosslink DNA, interfere with DNA Replication 3: Cyclophosphamide, Chlorambucil, Nitrogen mustard |
|
|
Q: Mechanism of action and 5 examples of DNA Binding chemotherapeutic agents |
A: Covalent DNA Intercalators, interfere with normal DNA function, alter Replication 3: Cisplatinum, Carboplatin, Adriamycin, Bleomycin, Mitomycin |
|
|
Q: Side effects of Cisplatin |
A: Myelosuppression, Nephrotoxicity, Ototoxicity, Neurotoxicity, N/V A: Decreased ototoxicity, neurotoxicity & nephrotoxicity with Carboplatin, myelosuppression main side effect 3: 15-30% single agent partial response 3: Dose in advanced NPC (Concurrent CRTx followed by adjuvant CTx): Cisplatin 100 mg/m2 IV on days 1, 22, and 43 with radiation, then cisplatin 80 mg/m2 IV on day 1 plus fluorouracil (5-FU) 1000 mg/m2/day by continuous IV infusion on days 1-4 every 4wk for 3 cycles (emedicine) |
|
|
Q: Mechanism of action and 4 examples of Antimetabolite chemotherapeutic agents |
A: Actively interfere with Cellular Metabolism, act in S-phase 3: Methotrexate – Interferes with Folate Metabolism, inhibits Dihydrofolate Reductase enzyme, interrupts DNA synthesis in S phase 3: 5-FluoroUracil – S phase Uracil Analogue, either incorporated into DNA and halts replication or is activated and blocks Thymidilate Synthase 3: Hydroxyurea, Gemcitabine |
|
|
Q: Side effects of Methotrexate |
A: Myelosuppression, Mucositis, Dermatitis, N/V/D, Hepatic fibrosis A: Leucovorin (Folinic Acid) rescue 3: 30% partial response rate as a single agent |
|
|
Q: Side effects of 5-FluoroUracil |
A: Myelosuppression, Mucositis, Dermatitis, Diarrhea, Cardiotoxicity 3: 13% single agent partial response |
|
|
Q: Mechanism of action and 3 examples of Vinca Alkaloid chemotherapeutic agents |
A: Interfere with Mitotic Spindle formation (microtubule disruptors) 3: Vincristine, Vinblastine, Vinorelbine |
|
|
Q: Mechanism of action and 2 examples of Taxane chemotherapeutic agents |
A: Stabilize Tubulin Polymers & prevent progression of mitosis/cell division, cause cell cycle arrest in G2 (microtubule stabilizers) 3: Paclitaxel, Docitaxel |
|
|
Q: Side effects of Taxanes |
A: Neuropathy, Muscular pain, Alopecia, Allergic reactions 3: 30-40% Single agent Partial Response rate of Taxanes |
|
|
Q: Mechanism of action and 3 examples of Topoisomerase Inhibitor chemotherapeutic agents |
A: Prevent unwinding of DNA for replication by Inhibiting Topoisomerases I or II 3: Irinotecan (I), Topotecan (I), Etoposide (II) |
|
|
Q: Mechanism of action of Cetuximab (Erbitux) |
A: Anti-EGFR Monoclonal Antibody, inhibits the receptor by Blocking the Ligand Binding site A: 400 mg/m2 wk 1 then 250 mg/m2 wk 2-7 A: no neuro/oto/nephrotoxicity, but can get cardiotoxicity A: other s/e’s include rash (predicts prognosis), hypomagnesemia |
|
|
Q: Three examples of small molecular Tyrosine Kinase Inhibitors and side effects |
A: Gefitinib (Iressa), Erlotinib (Tarceva), and Sunitinib (Sutent), Vandetinib (end stage MTC, acts again VEGF/EGFR) A: Diarrhea, and Acneiform rash (in 50%) which is predictive of better Response Rate and progression-free Survival |
|
|
Q: Four points about Combined Chemotherapy |
A: Higher Response Rates with some combinations A: Overall survival not improved A: Toxicity is more severe A: Cisplatinum & 5FU the “gold standard”, act synergistically; Carbo-Taxol more recently |
|
|
Q: Characteristics of Megavoltage X-rays/Gamma rays (photons) |
A: Low (4-6 MeV) or high (15-25 MeV) energy A: Skin-sparing properties A: Depth-dose properties (Penetration) A: Isodose distribution (Beam Uniformity) |
|
|
Q: Characteristics of Electron Beam XRT |
A: Good for Superficial lesions, deep tissue sparing A: Range of Penetration (cm) = MeV/3 |
|
|
Q: Three Advantages of Brachytherapy |
A: Better dose Localization A: Continuous Fractionation A: Decreased dose to adjacent normal tissue 3: Radioactive source placed in proximity to lesion |
|
|
Q: Brachytherapy source placement (3 types) |
A: Interstitial A: Intracavitary A: Surface mold |
|
|
Q: Brachytherapy time frames of use |
A: Temporary – long lived isotopes used (RIC = Radium, Iridium, Cesium) A: Permanent – short lived isotopes used (PIG = Palladium, Iodine, Gold) |
|
|
Q: Radiotherapy Pearls |
A: Cell Death = Inability to Proliferate; both DNA strands must be knocked out A: Log cell kill = particular radiation Dose will kill the same Proportion of cells A: Therapeutic Window = Dose Response curves between Tumor cell & Tissue damage; relative positions of curves determine safety of tumor control A: Shrinking Field technique; now replaced by concomitant boost? |
|
|
Q: Radiotherapy mechanisms of cell injury (2) |
A: Direct injury – Electron from x-ray absorption causes DNA Damage (1/3) A: Indirect injury – Electron from x-ray creates an Oxygen Free Radical which then damages the DNA (2/3) |
|
|
Q: What are the 4 R’s of radiotherapy injury mechanisms? |
3: Repair – Sublethal injury will be repaired by the cell if it takes no further hits, increased fractionation increases the opportunity for repair 3: Reoxygenation – Presence of oxygen increases the effects of Ionizing Radiation, radiosensitivity stays the same down to 20 mmHg oxygen, below this sensitivity decreases 3: Redistribution – Maximum Radioresistance occurs in late S phase of cell cycle, maximum Radiosensitivity occurs in early M phase, increased fractionation allows increased Redistribution of tumor cells into radiosensitive phases 3: Repopulation – Tumors Accelerate Repopulation after cell reduction from Surgery or Radiation |
|
|
Q: Definition of a Gray and Rad |
A: Gray (Gy) = The absorption of one joule of radiation energy by one kilogram of tissue A: Rad = Radiation absorbed dose; 100 rad = 1 Gy |
|
|
Q: Typical radiation dose |
A: 1.8 – 2.2 Gy given 5x/week for 6-8 weeks |
|
|
Q: Dose limiting factors for Intensity and Total dose |
A: Intensity – Acute toxicity = Mucositis A: Total dose – Late toxicity = Soft tissue Fibrosis |
|
|
Q: Time required post-XRT to call biopsy reliable |
A: 3 months 3: Cell lysis occurs at mitosis, 4-5 divisions occur before Lysis 3: Lethally injured cells and Surviving cells are morphologically identical |
|
|
Q: Five Advantages of Preoperative Radiotherapy for SCC |
A: Better Blood Supply preoperatively, thus are more Radiosensitive A: Unresectable tumors can be made Resectable A: Malignant cells at the periphery are destroyed, thus extent of surgical resection can be diminished A: Tumor Seeding at the time of resection may be decreased due to Decreased Viability A: Fewer and less viable cells Intravascularly & within Lymphatics at the time of surgery may Decrease Distant Metastases |
|
|
Q: 4 Disadvantages of Preoperative Radiotherapy for SCC |
A: Resection and Reconstruction more Difficult due to Fibrosis, Inflammation and decreased Blood Supply A: Obscured tumor Margins by tumor Shrinkage and Inflammatory response A: Wound Healing problems increase as dose >40 Gy A: Lower overall dose (Hart notes) |
|
|
Q: Five Advantages of Postoperative Radiotherapy for SCC |
A: Safer administration of Higher Total Doses of radiation A: Destruction of subclinical Residual tumor A: Surgical resection Easier, Healing is better in non-irradiated tissues A: Distinct tumor Margins which facilitates more accurate & complete surgical removal A: Ability to Direct Radiation specifically at areas Inaccessible by surgery A: Better staging possible |
|
|
Q: Two Disadvantages of Postoperative Radiotherapy for SCC |
3: Surgery may interrupt Blood Flow to remaining tumor cells making them less radiosensitive 3: Wound Breakdown or Infectious Complications may Delay the onset or Prevent radiotherapy delivery |
|
|
Q: Best Postoperative Time interval for Adjuvant XRT |
A: Within 6 weeks |
|
|
Q: General Indications for Postoperative Radiotherapy |
A: T3 or T4 lesion A: Perineural or vascular invasion A: Extracapsular spread A: Multiple histologicaly positive nodes (N2b, 2c) A: Positive resection margins (considered gross residual disease, >106 cells) |
|
|
Q: Distance of tumor to resection Margin that is considered Close |
A: 5 mm 3: Found to have Same Prognostic significance for Recurrence as Positive Margins |
|
|
Q: Six beneficial mechanisms of Chemoradiotherapy |
A: Can act on Different subsets of tumor cells A: Recruit cells from Go into radiation sensitive phases A: Chemo Inhibits Repair of sublethal radiation injury A: Tumor shrinkage decreases Interstitial pressure, thus increases drug and O2 delivery A: Prevents Radiation Resistance A: Cell-cycle Synchronization increases the effectiveness of both therapies 3: “Different cells Go Repair the O-R Sink” |
|
|
Q: Indications for postoperative Chemo |
A: ECS A: Positive margins |
|
|
Q: Toxic CNS doses |
A: Somnolence syndrome A: Myelopathy – 50 Gy in 25 fractions A: Transverse Myelitis – 50 Gy A: Brain Necrosis – 70 Gy |
|
|
Q: Nine Late Complications of Radiotherapy for NPC in 6 different sites |
A: Skin necrosis A: Osteoradionecrosis A: Cataracts – 6 Gy A: Middle ear effusion secondary to ET dysfunction A: Xerostomia – 35 Gy A: Transverse myelitis (50 Gy), somnolence syndrome, brain necrosis (65 Gy) |
|
|
Q: Seven Complications of Radiotherapy for Neck disease |
A: Xerostomia A: Mucositis A: Dental caries A; Osteoradionecrosis – In up to 5% of patients, rare <60 Gy, increased if chemo-XRT A: Soft tissue fibrosis A: Hypothyroidism – 1% clinically overt, 10% occult after 50 Gy in 4 weeks A: Immunosuppression A: Spinal cord Necrosis – Limit to 45-50 Gy in 5 weeks |
|
|
Q: Osteoradionecrosis, 4 treatment modalities |
A: Medical – Local topical care, biopsy, culture & IV antibiotics, nutritional support, Pentoxifylline A: Hyperbaric oxygen A: Debridement & partial mandibular resection, and removal of foreign bodies A: Vascularized tissue transfer (local/regional/free) |
|
|
Q: Three typical osseous findings of mandibular ORN on CT scans |
A: Cortical disruption/thinning A: Disorganization of trabeculation A: Osseous fragmentation 3: Radiolucency, demineralization, sequestrum, moth eaten bone, pathologic fractures |
|
|
Q: Four Intraorbital Complications of Radiotherapy, Maximum Doses where applicable |
A: Cataracts – as little as 6 Gy A: Lacrimal gland injury – ~35 Gy in 3.5 weeks A: Radiation Retinopathy – 50 Gy A: Optic Nerve injury – 50 Gy |
|
|
Q: What Spinal Cord Complication can occur Post-Radiotherapy? Sign/Dose of radiation is associated? |
A: Radiation Myelopathy A: L’Hermitte’s Sign – Electric shock sensations triggered by Flexing the Cervical Spine A: Doses of 50 Gy in 5-6 weeks 3: Also Transverse myelitis, Spinal cord Necrosis? |
|
|
Q: List Cahan’s 4 criteria in the diagnosis of Post-Radiation Sarcoma (PRS) |
A: Histologic features of the original lesion and PRS are completely different A: PRS is located within the field of irradiation A: Tissue from which alleged RT induced tumor arose must have been normal tissue prior to radiation exposure A: Latent period (period between initiation of radiotherapy and histologic diagnosis of second neoplasm) is >4 years |
|
|
Q: Dose of XRT for Microscopic disease and N0 neck |
A: Microscopic dz = 65 Gy A: N0 neck = 55 Gy 3: NCCN (2012): Definitive RT: N0 neck 44-64 Gy N+ 66-74 Gy (same dose as primary site) Postop RT: N0 44-64 Gy N+ 60-66 (same dose as primary site) |
|
|
Q: Definitive RT Fractionation schemes in H&N Ca? |
3: The results of RTOG 9003 led many oncologists to consider accelerated fractionation RT with a concurrent boost preferable to hyperfractionated RT in view of the cost and labor-intensiveness of twice daily RT. 3: Hypofractionation is used in palliative cases or postop in melanoma (e.g. 6-Gy doses for 5 fractions, total dose 30 Gy over 2.5 weeks) |
|
|
Q: Effects of changing RT per-fraction dose & number on acute and late side effects?
|
Lowering the dose per-fraction (ie 1.2 Gy per fraction) can decrease the late effects (ie: soft tissue fibrosis) Increasing the dose per-fraction (ie 2.5 Gy per fraction) can increase late effects Increasing the number of fractions per day or per week(ie BID) can increase the acute effects (ie skin erythema, mucositis) and acute effects may present earlier E.g. by lowering the dose per fraction and increasing the number of fractions, you can increase the total dose with a decrease in late side effects but results in an increase in acute side effects (Hyperfractionation). However, increasing the total dose with same or higher per-fraction dose will result in more late effects. |
|
|
Q: Compare Hyper and accelerated RT, adv and disadv? |
Hyperfractionation: Higher total dose in the same total time, but delivering it in more fractions with lower doses per fraction as compared to standard fractionation Advantage: Improved loco-regional control Decrease late side effects (see above) Greater total dose, increasing tumor kill Increase tumor cell redistribution and reoxygenation Disadvantage: Inconvenient for pts More acute side effects No OS improvement Accelerated fractionation: Similar total dose delivered in a shorter amount of time using lower dose per fraction as compared to standard fractionation Advantages: Improved loco-regional control Decrease late side effects More convenient than hyperfractionation/BID treatments Reduces tumor repopulation Disadvantages: Slightly more inconvenient than standard fractionation More acute side effects No OS improvement |
|
|
Q: When and for which levels to do an Elective Neck Dissection (or Irradiate) according to Primary Tumors |
A: Nose and Paranasal Sinuses – Never A: Glottis – ≥T3, Unilateral levels II-IV + VI A: Oral cavity – ≥T2, Unilateral levels I-III, unless approaching Midline, Anterior tongue, or FOM (then bilateral) OR T1 with depth >4mm (do unilateral I-III +/- IV) A: Supraglottis – ≥T1, Bilateral levels II-IV A: Subglottis – ≥T1, Bilateral levels II-VI +/- V, & Total Thyroidectomy A: Tonsil – ≥T1, Unilateral levels I-III, & Retropharyngeal nodes A: Base of Tongue – ≥T1, Bilateral levels I-V A: Hypopharynx – ≥T1, Bilateral levels II-V, & Retropharyngeal nodes A: Nasopharynx – ≥T1, Bilateral levels II-V, & Retropharyngeal nodes 3: NCCN (2012): N0 END levels according to site: - OC at least I-III - OP at least II-IV - HP at least II-IV +/- VI - Larynx at least II-IV +/- VI |
|
|
Q: Summarize the VA study |
A: Advanced Laryngeal Cancer, randomized into 2 arms, comparing Surgery + XRT to Chemo + XRT 3: Group 1 = Standard Surgery + Postop XRT 3: Group 2 = Neoadjuvant Cisplatinum + 5-FU, then XRT; but if no (even partial) Response after 2 cycles or Recurrent/Residual disease after XRT => Surgery 3: Overall Survival rate at 2 years Identical = 68% 3: Laryngeal Preservation rate in group 2 = 64% (only 39% had fully functioning larynx) |
|
|
Q: Summarize RTOG 91-11 |
A: Advanced Laryngeal cancer, randomized into 3 arms, looking at Laryngeal Preservation, Locoregional Control, and OS rates 3: Group 1 = Concomitant Cisplatinum + XRT => 88%, 78% 3: Group 2 = Neoadjuvant Cisplatinum + 5-FU, then XRT => 75%, 61% 3: Group 3 = XRT alone => 70%, 56% 3: Overall Survival rate was Similar for all groups => 54-56% at 5 years |
|
|
Q: What is the EORTG 22931 study and RTOG 9501 |
A: Two studies to evaluate the role of post-op RXT alone VS XRT+Concurrent Chemo Randomized high risk patients. EORTG: Improved survival and locoregional control RTOG 9501: Improved locoregional control, no statistically significant increase in survival |
|
|
Q: Karnofsky Performance Scale? |
100 Normal; no complaints; no evidence of disease. 90 Able to carry on normal activity; minor signs or symptoms of disease. 80 Normal activity with effort; some sign or symptoms of disease. 70 Cares for self, unable to carry on normal activity or do active work. 60 Requires occasional assistance, but is able to care for most personal needs. 50 Requires considerable assistance, but is able to care for most personal needs. 40 Disabled; requires special care and assistance. 30 Severely disabled; hospitalization is indicated, although death not imminent. 20 Very sick; hospitalization necessary; active support treatment is necessary. 10 Moribund; fatal processes progressing rapidly. 0 Dead. |
|
|
Q: ECOG/WHO/Zubrod score? |
0 Asymptomatic. (Fully active, able to carry on all predisease activities without restriction). 1 Symptomatic but completely ambulatory. (Restricted in physically strenuous activity but ambulatory and able to carry out work of a light or sedentary nature. For example, light housework, office work). 2 Symptomatic, < 50% in bed during the day. (Ambulatory and capable of all self-care but unable to carry out any work activities. Up and about more than 50% of waking hours). 3 Symptomatic, > 50% in bed, but not bedbound. (Capable of only limited self-care, confined to bed or chair 50% or more of waking hours). 4 Bedbound. (Completely disabled. Cannot carry on any self-care. Totally confined to bed or chair). 5 Death |
|
|
Q: Seven types of Skin Cancer, in descending frequency? |
A: Basal cell cancer (75%) A: Squamous cell cancer (20%) A: Melanomas A: Cutaneous Lymphoma A: Kaposi sarcoma A: Adenexal Carcinoma A: Merkle cell cancer |
|
|
Q: What are the Etiologic risk factors for BCC and cSCC? (Sun GRASSHOPEr) |
A: Sun exposure (UVB 290-320 nm > UVA 320-400 nm) A: Genetic factors: Xeroderma pigmentosum (autosomal recessive genetic defect in which nucleotide excision repair (NER) enzymes are mutated leading to deficient repair of DNA damaged by UV radiation) Others: AD Nevoid BCC syndrome (Gorlin’s Syndrome), B-K Mole syndrome, Atypical mole syndrome, p16 mutation A: Radiodermatitis from previous radiotherapy A: Actinic Keratosis A: Scar from former injury (Marjolin’s ulcers) A: Suppressed immunity (iatrogenic or hemopoietic cancers) A: HPV 16 A: Occupation – Ranchers, farmers, sailors, fishermen (high sun exposure) A: Physical traits – Pale complexion, light hair, blue or green eyes, inability to tan, propensity for sunburn, history of multiple or severe sunburn, Celtic ancestry A: Environmental exposure – Arsenic induced BCC, soot, coal tar, paraffin oil, petroleum oil, and asphalt |
|
|
Q: Describe the Nevoid Basal Cell Carcinoma syndrome (Gorlin syndrome) |
A: Autosomal dominant (9q), rare A: Multiple (hundreds) small cutaneous nodules appear in childhood, as child ages, multiple basal cell carcinomas develop and lesions become aggressive – invasion, destruction, mutilation A: OKC's A: Rib & Vertebral Abnormalities A: Total – BCC, Frontal bossing, Falx cerebri calcification, Mental retardation, Cataracts, OKCs in 75%, Scoliosis, Bifid ribs, Pitting of the palms and soles |
|
|
Q: Histolopathologic characteristics of Basal Cell Carcinoma |
A: Cell typically large, oval or enlongated nucleus, little cytoplasm A: Mucinous connective tissue stroma organized in parallel bundles around tumor masses, causes peripheral pallisading of nuclei and stromal retraction (peritumoral lacunae) A: cleft formation (retraction artifact) from drying/shrinkage of mucin during tissue fixation |
|
|
Q: Five clinical types of Basal Cell Carcinoma |
A: Nodular/noduloulcerative (most common) and Micronodular A: Morphealike/sclerosing (worst prognosis) A: Pigmented – similar appearance & behaviour as noduloulcerative except for brown pigment A: Fibroepithelioma – often seen on back; R/O Cowden’s syndrome A: Superficial multicentric 3: “No More Stupid Fibroepithelioma’s Please” |
|
|
Q: Four histolopathologic classes of Basal Cell Carcinoma (SACK) |
A: Solid – Undifferentiated A: Adenoid – Tubular/Glandular differentiation A: Cystic – Sebaceous gland differentiation A: Keratotic – More biologically aggressive, aka basosquamoid |
|
|
Q: Five histologic classes of cutaneous Squamous Cell Carcinoma (Gee Vat ABS) |
A: Bowenoid – from Bowen’s disease, SCCis A: Adenoid – Adenosquamous, pseudoglandular arrangement A: Generic – well-differentiated, actinic changes A: Spindle cell – pleomorphic, anaplastic, little/no keratinization, lymphoepithelioma-like carcinoma A: Verrucous – white cauliflower like lesion, HPV associated? |
|
|
Q: Histologic classes of H&N SCC (WHO 2005): |
Conventional Verrucous: non-metastasizing variant of well-differentiated SCC characterized by an exophytic, warty, slowly-growing tumor with pushing rather than infiltrative margins (no invasion of BM) Basaloid: high-grade variant of SCC composed of both basaloid and squamous components (Ass e HPV) Papillary: exophytic, papillary growth, and a favorable prognosis Spindle cell (sarcomatoid): biphasic tumor composed of a squamous cell carcinoma and a malignant spindle cell component with a mesenchymal appearance, Acantholytic: uncommon Adenosquamous: rare aggressive neoplasm originates from the surface epithelium and is characterized by both squamous cell carcinoma and true adenocarcinoma; most common in larynx Cuniculatum: rare, proliferation of stratified squamous epithelium in broad processes with keratin cores and keratin-filled crypts which seem to burrow into bone tissue, but lack obvious cytological features of malignancy |
|
|
Q: Define Broder’s Classification of SCC of the Oral cavity |
A: Grade I = 75-100%, Well differentiated A: Grade II = 50-75%, Moderately Well differentiated A: Grade III = 25-50%, Moderately differentiated A: Grade IV = 0-25%, Poorly differentiated 3: Based on cellular differentiation, expressed in percentage of total cellular elements |
|
|
Q: Three Premalignant lesions in cutaneous SCC malignancies |
A: Actinic keratosis A: Bowen’s disease (aka CIS) A: Keratoacanthoma (low grade malignant) - controversial |
|
|
Q: Three BCC and 2 cSCC with worse prognosis |
A: Sclerosing/morpheaform BCC – clinical classification A: Keratotic BCC – histiologic classification A: Recurrent BCC A: Spindle cell SCC A: De novo SCC |
|
|
Q: Nine characteristics of high risk cutaneous SCC (HIGHER RISC) |
A: Histology – poorly differentiated/dedifferentiated A: Invasion to reticular dermis or adipose tissue, >2mm depth, ≥ Clark level IV A: Rapid Growth A: Host immunocompromise A: Ear or hair bearing lip A: Radiated skin A: Recurrent tumor A: Invasion – perineural or lymphatic A: Size >2 cm A: Chronic ulcer/sinus tract, or scar |
|
|
Q: What is the “H” zone of the face? |
A: High risk sites for cutaneous malignancy, overlying embryonic fusion plates 3: upper lip, junction of the ala with the nasolabial fold, nasal ala, the septum, inner canthi & lower eyelids, periauricular region extending to the temple, certain scalp regions |
|
|
Q: What is Leser-Trelat sign, and what cancer is most commonly associated with this?
|
A: A shower of Seborrheic Keratoses as a sign of internal malignancy, most commonly Colonic Adenocarcinoma |
|
|
A: N, M & clinical staging as other H&N sites except Stage IV has no a, b, c
|
1 |
|
|
Q: Outline the management options for Cutaneous malignancies |
A: Observation A: Medical – Topical 5-FU, imiquimod, Retinoic acid, Interferon-α A: Surgical – Electrodessication & curettage, Excision, Cryosurgery, Photodynamic therapy, Mohs surgery A: Radiotherapy – Generally not indicated due to duration, complications, carcinogenesis, lack of margin control, increased aggressiveness of recurrences A: Elective Neck dissection in CSCC (not BCC): controversial but may be considered in T3, 4 and high risk lesions Posterior scalp and upper neck: Posterolateral SND (II-V + postauricular + suboccipital LN) Preauricular, anterior scalp and temporal region: SND levels: parotid and facial, II, III, Va + ext. jugular nodes Anterior and lateral face: SND levels: parotid and facial, levels I - III |
|
|
Q: Thirteen indications for Moh’s surgery in BCC
|
A: Aggressive Histology or growth pattern – Morpheaform or Keratotic for BCC; infiltrative type, sclerosing and keratinizing (Basosquamous or metatypical), Poorly differentiated SCC A: Incompletely excised tumor A: Tumors with poorly defined Margins A: Immunosuppressed patients A: High risk location (H zone) A: Skin cancer in Irradiated skin A: Recurrent tumor A: Tumors with Neurotropism A: Size >0.6 cm in high risk area, or >1 cm on scalp, face, neck A: Young patients, Cosmetically important area A: Tumors potentially involving Vital structures 3: “HIGHER RISC, Cosmetic, Vital, with Positive Margins” |
|
|
Q: What are the tumors treatable with Mohs’ surgery? |
A: BCC A: Cutaneous SCC A: Selected mucosal SCC A: Bowen’s disease (Queyrats on the glans penis) A: Keratoacanthoma A: Verrucous carcinoma A: Microcystic or other adnexal neoplasms A: Dermatofibrosarcoma protuberans A: Malignant fibrous histiocytoma A: Atypical fibroxanthoma A: Extramammary Paget’s disease A: Merkel cell carcinoma A: Cutaneous rhabdomyosarcoma 3: “BCCs, SCCs, Premalignants, Adnexals, MCC, DFSP, MFH, AFX, cRMS, EMP” |
|
|
Q: Five indications for Radiation for Skin tumors
|
A: Massive tumors (SCC >2 cm) A: Very aggressive (Merkels cell) A: Invasive (bone, muscle, cartilage, and nerve) A: Resection margins uncertain or positive A: Multiple recurrences A: Marjolin’s ulcer A: To the neck – Multiple positive nodes, extracapsular spread and lymphovascular invasion 3: Contraindicated in: Xeroderma pigmentosum, Gorlin, SLE, scleroderma & relatively in verrucous Ca |
|
|
Nonmelanoma Skin Cancer of the Head and Neck recommended surgical margins? |
A: If < 2 cm and low risk at least 4 mm margin A: If ≥ 2 cm and / or high risk at least 6-10 mm margin and may consider frozen section or Mohs Sx |
|
|
Q: Merkel Cell carcinoma characteristics |
A: Poorly Differentiated histology A: Neuroendocrine origin A: High Recurrence rate A: High Lymphatic met rate, Need to Treat lymphatics A: Requires post op XRT after wide resection |
|
|
Q: Four skin lesions associated with a higher risk of melanoma? |
A: Multiple benign nevi (>20 increases relative risk to 12:1) A: Congenital nevi (especially giant types >20 cm) A: Junctional nevi A: Dysplastic nevi > 5 (dysplastic nevus syndrome, aka Familial atypical multiple mole–melanoma (FAMMM) syndrome) 3: 50-70% of all melanoma arise from preexisting benign nevi 3: “Multiple CJDs” |
|
|
Q: 4 main types of Melanoma, best prognosis, most common, etc. And other rarer types of melanoma |
A: Superficial spreading – 75%, Intermediate prognosis, late invasion A: Nodular – 15-20%, Worst prognosis due to vertical growth, early invasion A: Lentigo Maligna Melanoma – 4-10%, Best prognosis, only 30% ever metastasize A: Mucosal – ~2% of all H&N melanoma, 50% arise in nasal cavity A: Acral Lentiginous (Blacks, soles and palms, not from sun) Not much in head and neck A: Desmoplastic/Neurotropic – <1% of all cases, but 75% occur in the head & neck, amelanotic A: Metastatic with unknown primary 3: Head & neck melanoma ~20% of total incidence “SNL is MAD” |
|
|
Q: What is a Hutchinson’s freckle? |
A: Lentigo Maligna, or melanoma In Situ 3: Associated with Solar damage & atypical melanocytes, Radial spread along dermal/epidermal Junction, focal Nests of cells 3: Overall probability of developing into melanoma ~5%; presence of a Nodule carries likelihood of invasion of 100% |
|
|
Q: Describe the Breslow classification and the associated risk of regional metastasis
|
A: <0.75 mm = 0% (Clark 1) A: 0.76-1.5 mm = 25% (clark 2-3) A: 1.51-4 mm (subdivided into 3a 1.51-3 mm, and 3b 3.01-4 mm) = 50% (clark 4) A: >4 mm = 75% (clark 5) |
|
|
Q: Describe the Clark classification |
A: Level I = Within Epidermis only A: Level II = Invasion into Papillary dermis (through basement membrane) A: Level III = Invasion to Papillary-Reticular dermis interface A: Level IV = Invasion into Reticular dermis A: Level V = Invasion into Subcutaneous tissues |
|
|
Q: What is the most important factor in overall survival in melanoma |
A: Presence or absence of Lymph Node Metastasis |
|
|
Q: What is the 2010 AJCC TNM staging for melanoma? |
* Satellite mets: tumor aggregates separated from primary by normal tissue and is ≤ 2 cm from primary. In transit mets are the same but > 2 cm away from primary. |
|
|
Q: Six Methods of identifying Occult Nodal disease in Melanoma |
A: Ultrasound A: CT/MRI A: SPECT or PET A: ELND = No benefit found except in 1-2 mm thick lesions in patients <60 years of age A: Sentinel LNB – Should be offered to Stage IB, IIA/B/C |
|
|
Q: Identify the Histochemical Markers for SCC |
A: Cytokeratin autoantibodies |
|
|
Q: Identify the 5 Histochemical Markers for Melanoma |
A: S100 A: HMB-45 A: Melan-A/MART-1 A: Tyrosinase A: Vimentin |
|
|
Q: Identify the Histochemical Markers for Lymphoma |
A: Leukocyte Common Antigen (LCA)/Panleukocyte autoantibodies A: CDs (clusters of differentiation) |
|
|
Q: Resection margins based on melanoma thickness (NCCN 2012) |
A: Tis = 0.5cm A: ≤1 mm = 1 cm A: 1.01-2 mm = 1-2 cm A: >2 mm = 2 cm |
|
|
Q: Five Indications for Radiotherapy in Melanoma |
A: Elderly poor candidate for operative resection A: Extensive Facial LMM which would require significant resection A: Postop adjuvant for High risk lesions, defined as >1.5 mm depth or ulcerated lesion A: Positive Regional Metastasis A: Desmoplastic histology |
|
|
Q: Six indications for systemic therapy in Melanoma |
A: Agents: interferon, ipilimumab, dacarbazine, imatinib,.. A: High Risk patients finished Primary Therapy – primary Ulcerated lesions, >4 mm depth or Clark level IV, Satellitosis, in- Transit Metastases, Nodal metastases A: Distant Metastases on presentation A: B-raf oncogene positive in >65% of cutaneous melanoma Vemurafenib (Braf enzyme inhibitor), indicated for metastatic melanoma that is positive for B-raf V600 mutation |
|
|
Q: Seven Environmental Risk Factors for Sinonasal malignancy |
Hardwood dust – Mahogany Nickel-refining processes Leather tanning Mineral oils Industrial fumes – Formaldehyde, Chlorophenol, Chromium, Isopropyl oils, Lacquer paints, Soldering and welding, Radium dial Painting Asbestos Cigarette smoke |
|
|
Q: Ddx of a Sinonasal lesion |
A: Benign Epithelial – Vestibular (squamous/keratotic) papilloma, Schneiderian papilloma (inverted, fungifom, cylindrical), Adenoma A: Benign Nonepithelial – Fibroma, Osteoma, Chondroma, Hemangioma A: Malignant Epithelial – SCC (most common), Adenocarcinoma, Adenoid cystic, Olfactory neuroblastoma, SNUC, Melanoma A: Malignant Nonepithelial – Liposarcoma, Fibrosarcoma, Rhabdomyosarcoma, Leiomyosarcoma, Osteogenic sarcoma, Chondrosarcoma, Hemangiopericytoma, Neurogenic sarcoma, Lymphoma, Extramedullary plasmacytoma, Giant cell tumor 3: Nonepithelial tissues are Fat, Fibrous, Muscle, Bone, Cartilage, Vessels, Nerve and White cells. |
|
|
Q: Schneiderian papilloma types and locations |
A: Inverted (50%) – Lateral wall A: Fungiform/Everted (47%) – Septal A: Cylindrical/Columnar/Oncocytic (3%) – Lateral wall 3: Bony destruction common even though benign, malignant change seen in ~10%, low for septal, highest for Lateral wall 3: Therapy – Total surgical removal, either Medial Maxillectomy (recurrence rate ~9%), or Transnasal/ESS |
|
|
Q: Discuss Sinonasal SCC |
A: Most common sinonasal malignancy (85%) A: Maxillay > Ethmoid > Sphenoid > Frontal A: Incidence of Regional and Distant mets = 10 and 7% respectively A: Regional lymph nodes = Facial, Parotid, Submandibular A: Treatment – Surgical resection +/- Chemo/XRT A: Prognosis – 50% at 5 yrs |
|
|
Q: Discuss Sinonasal Adenocarcinoma |
A: Second most common sinonasal malignancy A: Male predominace ~6:1, 5th-6th decade, usually arises in Middle Meatus A: Papillary, Sessile, and Alveolar mucoid |
|
|
Q: Discuss Sinonasal Undifferentiated Carcinoma (SNUC) |
A: Rare aggressive malignancy commonly affecting the Anterior Skull Base A: Incidence of Regional and Distant mets = 20 and 10% respectively A: Treatment – Surgical resection + Chemo-XRT A: Prognosis – Disease free survival up to 29% at 2 yrs, 9% longterm |
|
|
Q: Discuss the Histopathology of Esthesioneuroblastoma |
A: Sheets of Small Round Blue cells, Scant cytoplasm and Hyperchromatic nuclei A: Neurofibrils, Flexner-Wintersteiner Rosettes and Homer-Wright Pseudorosettes A: Neurosecretory Granules on electron microscopy A: Immunohistochemistry typically positive for neural markers - Neuron specific enolase (most consistent), S-100, Synaptophysin, +/- Chromogranin 3: Mets rare at presentation, but Regional and Distants mets may arise in 15-30% 3: iso- or hypointense to muscle and mucosa on T1 images and heterogeneously hyperintense on T2 images |
|
|
Q: Kadish staging for Esthesioneuroblastoma and 5-year survivals |
A: A – Confined to Nasal cavity, 85% A: B – Extension into Paranasal sinuses, 70% A: C – Spread Beyond nasal cavity/sinuses (orbit, BOS, intracranial, neck LNs), 45% |
|
|
Q: UCLA staging for Esthesioneuroblastoma (modified Biller staging) |
T1 representing nasal/paranasal disease, no sphenoid or superior ethmoid T2 including sphenoid, sup. ethmoid and/or extension to the cribriform plate T3 indicating orbital or anterior cranial fossa invasion without dural invasion T4 indicating dural invasion into brain |
|
|
Q: Biller staging for Esthesioneuroblastoma |
A: T1 – Involves nasal/paranasal sinuses (except sphenoid) A: T2 – Extension into ACF or Orbit A: T3 – Extension into Brain, resectable with margin A: T4 – Unresectable |
|
|
Q: Define Ohngren’s line |
A: Line between Medial Canthus and Angle of Mandible that divides Maxillary sinus for staging A: prognosis poorer if posterosuperior to this line |
|
|
Q: Tumor staging of Maxillary sinus cancer (AJCC 2010) |
A: Nodal and Staging systems the usual |
|
|
Q: Tumor staging for Nasal cavity/Ethmoid sinus cancer (AJCC 2010) |
A: Nodal and Staging systems the usual |
|
|
Q: Six Absolute and 2 Relative Contraindications for Craniofacial Resection |
A: Absolute – A: Medical or nutritionally unfit A: Distant metastasis A: Prevertebral fascia invasion A: Invasion of Optic Chiasm or both optic nerves A: Cavernous sinus invasion by high grade lesion A: Carotid invasion in a high risk patient A: Relative – A: Dural invasion A: Intracranial nerve involvement by Adenoid Cystic |
|
|
Q: Most common cause of unilateral or bilateral proptosis in adults |
A: Grave’s orbitopathy |
|
|
Q: Most common primary benign and malignant orbital tumors in adults |
A: Cavernous hemangioma A: Lymphoma |
|
|
Q: Most common cause of unilateral proptosis in children |
A: Complication of sinusitis |
|
|
Q: Most common benign and malignant orbital tumors in children |
A: Dermoid (most common cyst), capillary hemangioma most common tumor A: Rhabdomyosarcoma |
|
|
Q: Five most common Primary Orbital Tumors overall |
A: Meningioma (30% of all cases primary) A: Hemangioma A: Lymphoma A: Inflammatory tumors A: Optic nerve glioma 3: “Men Have Lived In Orbit” 3: Hemangioma (tumor) & Dermoid (cyst) most common in kids, followed by Rhabdomyosarcoma |
|
|
Q: Ddx of orbital tumors, primary and secondary |
A: Epithelial – Dermoid cyst, simple epithelial (conjunctival) cyst, mucocele, lacrimal (50% benign = PA, 50% malignant = ACC, MEC, mixed, AdenoCA), SCC, BCC (90% of eyelid tumors), mets A: Mesenchymal – Fibrous dysplasia, rhabdomyosarcoma, osteoma, osteosarcoma A: Vascular – Hemangioma (cavernous or capillary), lymphangioma A: Neural – Meningioma, schwannoma, optic nerve glioma A: Hematopoietic – Lymphoma, leukemia (Chloroma), histiocytosis A: Inflammatory – Pseudotumor, Grave’s (most common in adults), infection (viral, bacterial, fungal), vasculitis (WG, PAN, TA, SLE) 3: Epithelial Fat Fibrous Muscle Bone Cartilage Vessel Nerve and White cells |
|
|
Q: Metastatic tumors of the orbit |
A: Breast, lung, prostate, GI, renal cell, thyroid, melanoma 3: In other words, most common cancers; represent 8% of all orbital tumors, 25% will be the presenting manifestation of the original cancer |
|
|
Q: Difference between Proptosis and Exophthalmos |
A: Proptosis = Pushing of the globe A: Exophthalmos = Uniform expansion of the orbital contents |
|
|
Q: Other causes of unilateral Proptosis in adults and children |
A: Sinusitis complications (most common in children) A: Orbital fracture A: Lymphoma |
|
|
Q: Average volume of the orbital cavity |
A: 30ml 3: 5ml increase in size (16%) will cause 5mm proptosis |
|
|
Q: Describe Grave’s Ophthalmopathy |
A: 3 to 1 female predominance, 5th–6th decades, incidence ~10- 45% (!), most severe forms with CN II involvement rare, ~2-5% of Graves’ patients require surgical intervention 3: Due to Thyroid Stimulating Immunoglobulins, T-lymphocyte Infiltration into orbital tissues, Fibroblast response causes Glycosaminoglycan (GAGs) and Collagen deposition in the Extraocular Muscles leading to Fibrosis and Ophthalmoplegia |
|
|
Q: Wermer’s classification of Grave’s ophthalmopathy (NO SPECS) |
A: 0 = Normal A: I = only signs, no symptoms (lid retraction, lid lag, and stare) A: II = Soft tissue Swelling with symptoms and signs (deep conjunctival injection, mild chemosis, edema of caruncle or periorbita) A: III = Proptosis (≥3 mm, use exophthalmometer) with or w/o symptoms A: IV = Extraocular muscle involvement (inferior and medial rectus most commonly, use forced duction test) A: V = Corneal exposure A: VI = Sight loss |
|
|
Q: What is Pathognomic for Graves’s orbitopathy on physical exam? |
A: Hyperemia over the Lateral Rectus muscle |
|
|
Q: What are the 2 Extraocular muscles most commonly affected in Grave’s ophthalmopathy? |
A: Inferior rectus A: Medial rectus |
|
|
Q: Medical management of Grave’s orbitopathy |
A: Local Eye care – Eyedrops, nocturnal eye taping, sunglasses A: Thyroid therapy – Antithyroid drugs (PTU, Methimazole), radioiodine ablation, thyroidectomy A: Steroid therapy – For acute vision loss in Graves orbitopathy, Prednisone 80-120 mg qd x 2 weeks with slow taper following this A: Immunosuppressives – Cyclosporine, Cyclophosphamide experimental for autoimmune aspects A: Radiotherapy – Indicated for late sequelae of stable thyroid orbitopathy, 20 Gy in 10 fractions (2 weeks), good-excellent response in 35-92%, not for acute/subacute phases, for those who can’t tolerate, refuse, or fail surgery 3: Beta-blockers – Propranolol can be used as adjunct for severe symptoms in Grave’s |
|
|
Q: Indications for orbital decompression in Graves orbitopathy |
A: Altered vision – Decreasing acuity, field defects, abnormal visual evoked potentials, disk edema; typically after failed course of steroids A: Corneal exposure keratitis not responding to medical therapy A: Cosmetic decompression only if eye findings stable for at least 6 months |
|
|
Q: Seven surgical options for Grave’s orbitopathy |
A: Naffziger (superior orbital plate decompression into anterior cranial fossa) – Through anterior craniotomy A: Kronlein (lateral orbital plate) – Through coronal, direct rim incision or lateral canthotomy A: Hirsch (inferior orbital plate) – Through subciliary and/or Caldwell-Luc incision A: Sewall (medial orbital decompression) – Through coronal incision or external ethmoidectomy approach A: Walsh-Ogura – Transantral decompression of medial & inferior orbit, most widely used, as it is extracranial, decompresses two orbital walls into the largest empty space, allows gravity to aid in the expansion A: Orbital fat removal – Through upper lid crease and subciliary approaches; ~6 mm maximum reduction in proptosis possible; caution around inferior oblique A: Endoscopic orbital decompression |
|
|
Q: What is a Chloroma? |
A: Also called Granulocytic Sarcoma, an immature myeloid cell collection seen in AML & CML, green color secondary to myeloperoxidase A: Symptoms – Painless proptosis & violaceous lid swelling over weeks A: Treatment – Systemic chemotherapy, will develop into leukemia without treatment A: Prognosis – Poor, death usually within 18 months |
|
|
Q: Describe Optic Nerve Glioma |
A: 2nd most common pediatric orbital tumor A: Cell origin – Fibrillary astrocyte, associated with neurofibromatosis in 18-50% A: Radiographic – CT fusiform, lobular, isodense homogenous enlargement of optic nerve; MRI T1 hypo, T2 hyper A: Treatment – Observation vs. resection depending on whether indolent or progressive growth |
|
|
Q: Describe Orbital Pseudotumor |
A: Inflammation of unknown etiology, diffuse or localized (muscle, lacrimal gland, sclera, optic nerve) A: Symptoms – Pain increased with movement, Proptosis A: Signs – Eyelid edema, chemosis, diplopia, vision loss (20%) A: Radiographic – CT enlargement of involved structures; EOM tendons involved unlike in Graves ophthalmopathy; MRI T1 iso to muscle with gad enhancement, T2 hyper to fat A: Treatment – Corticosteroids, rarely cyclophosphamide, cyclosporine, or XRT; biopsy treatment failures! |
|
|
Q: Enlarging Lacrimal gland pathology |
A: Infectious – Acute bacterial (Staph, Strep), chronic bacterial (trachoma, syphilis, TB), viral (HSV, EBV, mumps) A: Epithelial – Pleomorphic adenoma most common (50%); other 50% malignant (adenoid cystic, mucoepidermoid, malignant mixed, adenocarcinoma) A: Hematopoietic – Benign lymphoid hyperplasia (20% get systemic lymphoma), atypical lymphoid hyperplasia (40% get systemic lymphoma), lymphoma (50% localized), leukemia A: Idiopathic – Sarcoid |
|
|
Q: Most common Benign Salivary gland tumors in Children |
A: Hemangioma A: Pleomorphic adenoma A: Lymphangioma A: Neurogenic |
|
|
Q: Most common Malignant Salivary gland tumors in Children |
A: Mucoepidermoid carcinoma A: Acinic cell A: Adenocarcinoma A: Undifferentiated carcinoma A: Adenoid cystic |
|
|
Q: Ddx of Benign Salivary gland neoplasms in Adults |
A: Pleomorphic adenoma A: Warthin’s tumor A: Oncocytoma A: Monomorphic adenoma A: Myoepithelioma |
|
|
Q: Nine Risk factors for Salivary gland malignancy |
A: XRT (low dose) A: Full-mouth dental x-rays A: EBV A: Skin CA? A: Rubber industry A: Nickel A: Silica dust A: Hair dye A: Kerosene cooking fuel A: Vegetables preserved in salt |
|
|
Q: Parts of a salivary gland tubuloacinar unit (MAISE) |
A: Myoepithelial cell A: Acinus A: Intercalated duct A: Striated duct A: Excretory duct 3: - Multicellular Theory: each neoplasm originates from a distinct cell type within the salivary gland unit e.g. oncocytic tumors from striated ducts. - Bicellular Theory: all neoplastic cells differentiate from basal (reserve) cells of either excretory (mucoepidermoid, SCC) or intercalated (pleomorphic, others) ducts |
|
|
Q: Parotid tumors arising from Myoepithelial cells |
A: Monomorphic adenoma A: Pleomorphic adenoma A: Adenoid cystic |
|
|
Q: Parotid tumors arising from Acinar cells |
A: Acinic cell carcinoma |
|
|
Q: Parotid tumors arising from Intercalated duct cells |
A: Adenocarcinoma A: Pleomorphic adenoma |
|
|
Q: Parotid tumors arising from Striated duct cells A: Warthin’s tumor A: Oncocytoma Q: Parotid tumors arising from Excretory duct cells |
A: Mucoepidermoid A: Squamous A: PAc A PAd WOMS: M A I SE |
|
|
Q: Pleomorphic adenoma locations |
A: Parotid > Hard palate (minor salivary gland) > SMG > MSGs (upper lip) A: 90% superficial to FN, 10% deep to stylomandibular ligament 3: If tumor extends from parotid to PPS through stylomandibular tunnel dumbbell appearance. If entirely deep to ligament rounded appearance. |
|
|
Q: Pleomorphic adenoma Histology |
A: Gross = well encapsulated, smooth, rubbery A: Microscopic = incomplete encapsulation, pseudopod extensions A: Mixture of epithelium, myoepithlium and mesenchymal stroma A: Epithelial growth patterns – Cystic, Papillary, Small nests, Solid sheets, Ductal structures, Anastomosing Trabeculae A: Myoepithelial cells – Spindle shaped, hyperchromatic nuclei, may be multiple cell layers thick A: Mesenchymal stroma morphologies – Fibroid, Myxoid, Mucoid, Chondroid, Osteoid |
|
|
Q: Describe the difference between Malignant Mixed and CA ex-pleomorphic adenoma |
A: Malignant mixed tumors display malignant transformation in both epithelial (carcinoma) and stromal (sarcoma) components, whereas CA ex-pleomorphic adenoma only displays malignant transformation in its epithelial component A: There should be evidence of underlying benign pleomorphic adenoma in CA ex-pleomorphic 3: Malignant transformation of pleomorphic adenoma is 1.5% in the first 5 years. Increases to 10% in > 15 yrs. |
|
|
Q: Warthin’s tumor (papillary cystadenoma lymphomatosum, adenolymphoma) epidemiology |
A: Whites A: Male/Female = 5/1 A: 5-6th decades A: Radiation & smoking influence A: 10% of parotid tumors, 10% bilateral, 10% multicentric 3: Almost exclusive to parotid gland |
|
|
Q: Warthin’s tumor (papillary cystadenoma lymphomatosum, adenolymphoma) Histology |
A: High density of mitochondria on EM A: Gross = Smooth with well-defined capsule A: Microscopic = Biphasic, epithelial cells forming Papillary projections into Cystic spaces with a background of Lymphoid stroma A: Epithelium = Double cell layer of Oncocytic cells with nuclei of cystic side (columnar luminal cells) toward cystic space and nuclei of basement membrane (cuboidal basal cells) side toward basement membrane (i.e. nuclei away from each other) A: Lymphoid stroma = Lymphocytes with follicles and germinal Centers |
|
|
Q: Oncocytoma Histology
|
A: Cell of origin is an oncocyte: large epithelial cells with granular eosinophilic cytoplasm from mitochondrial hyperplasia. A: Almost exclusive to parotid A: Gross = Slow growing, circumscribed but encapsulated A: Microscopic = Brown, plump, granular eosinophilic cells with small indented nuclei & high mitochondrial density (no lymphoid component as seen in warthin’s) A: Electron microscopy = Mitochondrial hyperplasia |
|
|
Q: Monomorphic adenoma Histology |
A: Glycogen rich A: Basal cell (most common) A: Myoepithelioma (Pasha) A: Canalicular (upper lip) A: Clear cell (R/O metastatic renal cell CA) A: Membranous (Pasha) A: Sebaceous A: Gross = Well circumscribed and encapsulated A: Microscopic = Basal cell, rows of peripheral pallisading cells 3: “M.A. Gladly Backed My Canadian Club Membership” |
|
|
Q: What are the 3 most common subtypes of monomorphic adenoma |
A: basal cell adenoma (occur in parotid and upper lip) A: clear cell adenoma A: glycogen rich adenoma BCG! |
|
|
Q: Histologic subtypes of Myoepithelioma |
A: Spindle pattern A: Plasmacytoid A: Combination |
|
|
Q: Mucoepidermoid carcinoma |
A: Location = Parotid > MSG (palate) > SMG A: Low, Intermediate, or High Grade = Ratio of Mucinous (low grade) to Epidermoid cells A: Treatment – Stage I and II = Wide local excision; Stage III and IV = Radical excision, neck dissection and post op XRT A: Mucoepidermoid Histologic Grading A: Low grade – More Mucous cells, fewer epidermoid cells, with prominent cysts and mature cellular elements; behave like benign neoplasm but capable of local invasion & metastasis A: Intermediate grade – Mucous cells = Epidermoid cells, fewer and smaller cysts, increasing pleomorphism and mitotic figures A: High grade – More Epidermoid cells, fewer mucous cells; requires IHC staining for Mucin to differentiate from SCC 3: MRI: T2 intermediate to low (Pleomorphic is high) with or without invasion 3: most common pediatric SG Ca 3: Stains: Mucicarmine, PAS, alcian blue |
|
|
Q: Adenoid cystic carcinoma |
A: Most common malignancy of SMG, SLG, and MSGs; second most common malignancy overall A: Gross – Monolobular, either no capsule or partially encapsulated; infiltrates surrounding tissue A: Micro – Basaloid epithelium arranged in cylindric formations, eosinophilic hyaline stroma (blue goo) A: Histologic subtypes – Solid (worst prognosis), Tubular (best prognosis), Cribriform (intermediate prognosis, most common subtype) A: Grade depends on percentage of Solid elements; low grade <30% solid, high grade >30% solid A: Perineural invasion a typical feature A: Treatment – Surgery with postop XRT, neck dissection only if N+ |
|
|
Q: Acinic cell carcinoma |
A: Second most common salivary gland cancer in children A: Derived from serous acinar cells, thus for location Parotid >> SMG, rare in MSG A: Gross – well circumscribed, fibrous capsule A: Histologic – 2 types, one resembles Serous acinar cells, other has a Clear cytoplasm; Amyloid a hallmark pathologic finding A: Configurations – Solid, papillary cystic, follicular, microcystic, vacuolated A: Treatment – Surgery (no neck dissection), with post op XRT if residual disease |
|
|
Q: Adenocarcinoma |
A: Location = MSG > parotid A: Aggressive tumors, likely to recur & metastasize A: Gross – firm/hard, attached to surrounding tissue A: Micro – cylindric cells of variable height, form papillae, acini, solid masses; mucin producing A: Treatment – Aggressive surgical resection, with post op XRT, elective ND if extensive local disease or high grade lesions |
|
|
Q: Histologic classification of Adenocarcinoma |
A: Depends on degree of glandular structure cellular differentitation A: Grade I – Well-formed ductal structures A: Grade III – Solid growth pattern with few glandular characteristics |
|
|
Q: Three things must rule out in parotid SCC |
A: High grade Mucoepidermoid ca A: Metastatic SCC to intraglandular nodes A: Direct extension of cSCC to parotid 3: Treatment – Surgical resection with ND, with post op XRT |
|
|
Q: Polymorphous Low Grade (PLGA) |
A: 2nd most common Ca of the MSG’s (does not occur in major SG) A: Seen on palate (Junc of hard & soft P), buccal mucosa, upper lip A: Most have perineural invasion A: Gross – firm, painless mucosalized mass A: Histo – Concentric whorling of the nests around each other in a single-file arrangement, eye of the storm or Indian filing pattern A: Treatment: Surgical excision, no neck dissection unless N+ & rarely results in death |
|
|
Q: Name 4 Low Grade salivary gland malignancies |
A: Acinic cell ca A: Low grade mucoepidermoid A: Polymorphous low grade adenocarcinoma A: Low grade Adenoid Cystic Ca |
|
|
Q: Name 6 High grade salivary gland malignancies? |
A: SCC A: High grade mucoepidermoid A: AdenoCa NOS A: CaExPleomorphic adenoma A: Salivary duct Ca A: Undifferentiated Ca |
|
|
Q: Hot lesions on Technetium scans |
A: Warthin’s tumor A: Oncocytoma 3: High mitochondrial content (striated duct) |
|
|
Q: Most common Bilateral lesions |
A: Warthin’s (10% of cases) A: Acinic cell (3% of cases) A: Oncocytoma 3: “Bilateral lesions are WACO!” |
|
|
Q: Major salivary gland T staging (AJCC 2010) |
A: Nodal and Staging the usual |
|
|
Q: Seven signs or symptoms which would support a malignant diagnosis for parotid mass |
A: Facial nerve paralysis/paresis A: Fixation to overlying/underlying structures A: Overlying skin ulceration/infection A: Localized pain or trismus A: Cervical adenopathy A: Metastatic disease A: Large size (>5cm)? >4cm |
|
|
Q: Three reasons for surgical excision of a benign salivary gland lesion diagnosed on FNAB |
A: Impact on cosmesis & continued growth of lesion A: Definitive diagnosis (FNA can be wrong) A: Chance of malignant transformation over time |
|
|
Q: Five methods are used to identify the facial nerve during parotidectomy? |
A: Tragal pointer (1cm deep, anterior and inferior) A: Tympanomastoid suture A: Retrograde dissection from a distal branch A: Identification within mastoid bone (mastoidectomy) A: Digastric muscle attachment to the digastric groove |
|
|
1
|
A: High grade Ca A: LN mets present A: Deep lobe involved |
|
|
Q: What levels should be addressed for salivary gland malignancy with a No neck |
A: Parotid – I, II, III, IV (some debate about V) A: Submandibular – I, II, III 3: in N+ disease MRND ipsilateral only |
|
|
Q: Seven Indications for Radiotherapy in Salivary gland malignancies |
A: High grade tumors = SCC, AdenoCA, Undifferentiaed, High grade mucoepidermoid, Malignant mixed A: Positive margins – Unresectable or incomplete resection A: Extraparotid spread – T3 or T4 A: Lymph node mets A: Extracapsular spread A: Facial nerve dysfunction caused by cancer (Perineural spread) A: Recurrent tumor 3: All malignant tumors except T1N0 or T2N0 disease with low grade histology (low grade mucoepidermoid, acinic cell) and negative resection margins 3: Use Neutron beam for primary site in Adenoid Cystic carcinoma |
|
|
1
|
A: T3&T4: Extension to extraglandular tissues or size ≥4 cm A: High grade tumors = SCC, AdenoCA, Undifferentiated, High grade mucoepidermoid A: SMG Ca (21% chance of LN mets) |
|
|
Q: Pathophysiology & diagnosis of Frey’s syndrome (aka. Gustatory sweating) |
A: Aberrant reinnervation of postganglionic parasympathetic nerves to the sweat glands of the face A: 10% of patients overtly symptomatic A: Diagnosis: Minor’s starch iodine test |
|
|
Q: Pathway for Frey’s syndrome |
A: Inferior salivatory nucleus A: CN IX A: Jacobson’s nerve (leaves skull base via inferior tympanic canaliculus) A: LSPN (enters skull base via foramen ovale) A: Otic ganglion A: Auriculotemporal nerve A: Parotid and sweat glands |
|
|
Q: Treatment options Frey’s syndrome |
A: Antiperspirant A: Topical anticholinergic (Scopolamine cream, glycopyrrolate, or atropine) A: Botox A: Tympanic neurectomy, fascial graft, SCM flap, free flap |
|
|
Q: Describe the lesser petrosal nerve |
A: from jacobsons plexus to otic ganglion (parasympathetic to parotid) |
|
|
Q: Histologic features of necrotizing sialometaplasia |
A: Preserved lobular architecture A: Lobular infarction with or without mucus extravasation A: Inflammation secondary to extravasated mucus A: Pseudoepitheliomatous hyperplasia at periphery of lesion A: Squamous metaplasia of ducts & acini Found mostly on the posterior hard palate, is due to necrosis of minor salivary glands due to trauma (often palatal infiltrations of local anaesthetic or trauma during intubation) or idiopathic. Often painless, condition is self-limiting and should resolve in 6 – 10 weeks. |
|
|
Q: Percentage of tumors that occur in the different salivary glands and percentage which are benign |
A: 80% Parotid – 80% A: 15% Submandibular – 50% A: 5% Sublingual – 20% |
|
|
Q: Seven subsites of the oral cavity |
A: Upper & lower lips A: Oral tongue A: Upper & lower alveolus A: Buccal mucosa A: Floor of mouth A: Retromolar trigone A: Hard palate |
|
|
Q: 8 muscles from 1st arch |
A: Masseter A: Temporalis A: Medial pterygoid A: Lateral pterygoid A: Anterior belly of digastric A: Tensor tympani A: Tensor veli palatini A: Mylohyoid |
|
|
Q: Boundaries of the Oral cavity |
A: Anteriorly – Vermilion border A: Posteriorly – Posterior border of hard palate, intersection of retromolar trigone and anterior pillar, circumvallate line of the tongue |
|
|
Q: Eight functions of the oral cavity |
A: Mastication A: Taste A: Deglutition A: Oral competence A: Articulation A: Respiration A: Airway protection A: Oral hygiene |
|
|
Q: Five Anatomic structures running between the skull base & superior constrictor |
A: Tensor veli palatini A: Levator veli palatini A: Eustachian tube A: Ascending pharyngeal artery A: Ascending palatine artery |
|
|
Q: Anatomic associations between the superior & middle constrictors |
A: Glossopharyngeal nerve (IX) A: Stylopharyngeus A: Stylohyoid ligament A: Lingual artery |
|
|
Q: Anatomic associations between the middle & inferior constrictors (space closed by thyrohyoid membrane) |
A: Superior laryngeal artery & vein A: Internal branch of the superior laryngeal nerve |
|
|
Q: Anatomic associations between the inferior constrictor & esophagus |
A: Recurrent laryngeal nerve A: Inferior laryngeal artery & vein |
|
|
Q: Attachments of Superior, Middle and Inferior constrictor muscles |
A: Superior: Skull base, Pterygomandibular raphe, Lateral tongue, transverse process C-spine A: Middle: Stylohyoid ligament, hyoid bone, transverse process of C-spine A: Inferior: Thyroid/cricoid cartilage, transverse process of C-Spine |
|
|
Q: Four risk factors for lip cancer |
A: Sun exposure A: Smoking A: Chronic alcoholism A: Poor dental hygiene |
|
|
Q: TNM staging for lip & oral cavity cancer (AJCC 2010) |
|
|
|
Q: Seven poor prognostic indicators for lip cancer |
A: Cervical metastasis (below are RFs for occult regional mets, thus criteria for SND I-III ± IV) A: Size > 2 cm A: Thickness > 4 mm A: Mandibular invasion A: Perineural invasion A: Commissure lesion A: Recurrent tumors A: Poorly differentiated histology |
|
|
Q: Seven indications for postop XRT for lip cancer |
A: T3 or T4 tumor A: Recurrent tumor A: Positive margins A: Perineural invasion A: Multiple level cervical mets A: >1 LNs positive A: Extracapsular spread |
|
|
Q: Ideal reconstruction of the lip |
A: Sensate A: Intact sphincter function for control of watertight continent seal A: Sufficient opening for food, dentures, oral hygiene A: Aesthetically acceptable |
|
|
Q: Three indications for Vermilionectomy |
A: CIS A: Diffuse premalignant disease (Actinic cheilitis) A: Multicentric disease |
|
|
Q: Three conditions for Mohs excision of lip cancer |
A: Stage 1 or 2 disease A: Thickness ≤2.5 mm A: No muscle involvement 3: Beyond this, there will be regional mets, or there will be functional impairment |
|
|
Q: Three broad repair options for Partial Thickness Lip defects |
A: CO2 Laser lip shave and mucosalization by secondary intention A: Advancement flaps – Labial buccal or V-Y A: Two-stage techniques – Bipedicle visor flaps from opposing lips, ventral tongue, or cross-lip mucosal flaps |
|
|
Q: Repair options for Lower Lip defects |
A: ≤50% – Primary closure (wedge, W plasty, M plasty) A: 50-66% – Karapandzic flap (orbicularis oris myocutaneous flap) Abbe flap Estlander flap (if commissure involved) A: >66% – Bernard-Burow advancement flap for midline defects Gillies fan flap = Full thickness nasolabial transposition flap for lateral defect Regional, Distant, or Microvascular free flap if inadequate adjacent cheek tissue |
|
|
Q: Repair options for Upper Lip defects
|
A: ≤50% – Perialar crescentic excisions and primary advancement closure for midline defects Primary closure for lateral A: 50-66% – Karapandzic flap for midline Abbe flap Estlander flap (if commissure involved) A: >66% – Webster modification of Bernard-Burow advancement flap for midline Gillies fan flap (full thickness nasolabial transposition) Temporal forehead flap, Regional flap, or Microvascular free flap if inadequate adjacent cheek tissue |
|
|
Q: Ddx of Leukoplakia on oral mucosa
|
A: Hyperkeratosis A: Lichen planus A: Leukoedema A: Hairy leukoplakia A: White spongy nevus A: Candidiasis A: SLE A: Psoriasis A: Secondary syphilis A: Geographic tongue A: Koplik spots (Measles) A: Fordyce granules |
|
|
Q: what are Fordyce granules? |
A: Ectopic sebaceous glands (naturally occurring) |
|
|
Q: Histologic features of Leukoplakia |
A: Hyperkeratosis – Increased Thickness of keratinized layers A: Parakeratosis – orderly but abn, nucleated cells in keratin layer A: Dyskeratosis – Production of Keratin at lower layers A: No Pleomorphism – therefore no More than one form of a single cell type A: No Anaplasia – therefore no Change in a cell or tissue to a Less differentiated form A: No Desmoplasia – therefore no Connective tissue Reaction to tumor 3: Rare mitotic figures and normal maturation |
|
|
Q: Ddx of a red lesion in the oral cavity |
A: Erythroplakia A: Pyogenic granuloma A: Papilloma A: Inflammatory papillary hyperplasia A: Pigmented nevi A: Kaposi’s sarcoma A: Leukemia A: Hemangiosarcoma A: Mycosis fungoides A: Polycythemia rubra vera |
|
|
Q: Five prognostic factors in oral cavity cancer imparting a worse prognosis |
A: Increasing Stage A: Increasing tumor Thickness A: Perineural invasion A: Angiolymphatic invasion A: DNA ploidy |
|
|
Q: Ddx of non-epidermoid oral cavity cancer? |
A: Lymphoma A: Melanoma A: Kaposi’s sarcoma A: Minor salivary gland cancer 3: 10% occurrence |
|
|
Q: Define Eagle syndrome |
A: Caused by elongated styloid or calcification of stylohyoid ligament, causes irritation of V, VII, IX, X nerves; normal finding in 4% of population A: Symptoms – Throat pain, facial pain, carotodynia, otalgia, globus, dysphagia, increased salivation A: Treatment – Removal of styloid process via intraoral or external approach |
|
|
Q: Ddx of Maxillary & Mandibular cysts |
A: Inflammatory (85%) – Periapical/Radicular cyst Lateral periodontal cyst A: Developmental Odontogenic (10%) – Dentigerous/Follicular cyst Odontogenic keratocyst Eruption cyst Alveolar cyst of infants Gingival cyst of adults A: Nonodontogenic (5%) – Nasopalatine duct cyst Nasolacrimal duct cyst Midpalatal cyst of infants Nasolabial cyst Aneurysmal bone cavity Stafne lingual cortical defect Idiopathic (Traumatic) bone cyst |
|
|
Q: Ddx of Multiloculated Bone/Jaw Cyst (MACHO) |
A: Myxoma A: Ameloblastoma A: Aneurysmal bone cyst A: Cherubism A: Central giant cell granuloma A: Hemangioma A: OKC |
|
|
Q: Describe Periapical/Radicular cyst |
A: Most common maxillary/mandibular cyst, arise from nonvital root/pulp infection A: From rests of Malassez A: Treatment – root canal |
|
|
Q: Describe Dentigerous/Follicular cyst |
A: Second most common maxillary/mandibular cyst, enlargement of follicle of impacted tooth A: Treatment – Enucleation & curettage |
|
|
Q: Describe Odontogenic Keratocyst |
A: Cystic neoplasm that causes bone destruction, frequent Recurrence A: Rests of Serres are remnants of dental lamina A: Treatment – Enucleation & curettage |
|
|
Q: Ddx of Odontogenic tumors |
A: Benign Epithelial tumors – Ameloblastoma, Ameloblastic fibroma, Ameloblastic fibroodontoma, Ameloblastic odontoma, Calcifying epithelial odontogenic tumor (Pindborg), Odontogenic adenomatoid tumor, calcifying odontogenic cyst (Gorlin), Odontoma (complex, compound) A: Benign Mesenchymal tumors – Odontogenic fibroma, Odontogenic myxoma, Cementoma, Cementifying fibroma, Benign cementoblastoma, Periapical cementoosseous dysplasia, Dentinoma A: Malignant tumors – Malignant ameloblastoma, Ameloblastic fibrosarcoma, Ameloblastic dentinosarcoma, Ameloblastic odontosarcoma |
|
|
Q: Subclassify Ameloblastomas |
A: Peripheral vs. Central A: Unicystic, Plexiform unicystic, or Multicystic 3: Plexiform unicystic more aggressive, requires excision with 3 cm margins |
|
|
Q: Six Histologic patterns of Ameloblastomas |
A: Follicular or Simple (most common) A: Plexiform A: Acanthomatous A: Desmoplastic A: Granular cell A: Basal cell 3: Histologic findings include cystic spaces lined with tall columnar epithelium, filled with stellate reticulum, surrounded by a dense fibrous stroma |
|
|
Q: Six CT signs of Nodal Metastasis |
A: Central necrosis (most accurate CT criterion) A: Diameter >10 mm in short diameter (>15 mm for jugulodigastric & SM, > 8 mm in RP LN) A: Extracapsular spread A: Spherical shape – LS ratio <2 (95% Accuracy, BJR 1995, Vol 68, Issue 807:266-70) A: Nodal grouping (> 3 LNs in one area) A: Rim enhancement 3: U/S characteristics of mets: - Spherical shape - Loss of fatty hilum - Extracapsular spread - Hypoechoic and heterogeneous - Central necrosis - Mixed vascularity |
|
|
Q: Name the 5 structures that cross over the internal carotid lateral to it |
A: Hypoglossal nerve A: Glossopharyngeal nerve A: Pharyngeal branch of vagus A: Superior laryngeal branch of vagus A: Occipital artery A: Posterior auricular artery A: Posterior belly of digastric A: Stylo-everything – Stylopharyngeus, styloglossus, stylohyoid muscle and ligament |
|
|
Q: Name the 5 structures that run between the external and internal carotid arteries
|
A: Pharyngeal branch of the glossopharyngeal nerve A: Pharyngeal branch of the vagus A: Stylopharyngeus A: Styloglossus A: Stylohyoid ligament |
|
|
Q: Six main branches of the vagus nerve in the neck and subdivisions |
A: Meningeal A: Auricular (Arnold’s nerve, exists tympanomastoid suture line, supplies posterior and inferior EAC, and lower TM, causes referred otalgia!) (Anterior EAC V3, superior EAC VII) A: Pharyngeal (from nodose ganglion, runs between ICA & ECA, to join pharyngeal branch of CN IX) A: Superior laryngeal below nodose (External and Internal) A: Cervical cardiac (sympathetics to cardiac plexus in upper and lower neck) A: Recurrent laryngeal nerve |
|
|
Q: Four cutaneous branches of the cervical plexus |
A: Lesser occipital (C2,3) A: Greater auricular (C2,3) A: Transverse cervical (C2,3) A: Supraclavicular (C3,4; divided into anterior, middle, and posterior) |
|
|
Q: Venous drainage of the superficial head & neck |
A: Retromandibular vein (posterior facial vein)– formed from junction of superficial temporal and pterygoid plexus veins, splits to join the external jugular and the common facial vein A: Common facial vein – formed from junction of anterior facial and branch from retromandibular vein, drains into internal jugular vein at the level of the hyoid |
|
|
Q: Describe the borders of Level Ia in the neck |
A: Superior – mandibular symphysis A: Inferior – body of hyoid A: Lateral – anterior belly of ipsilateral digastric A: Medial – midline |
|
|
Q: Describe the borders of Level Ib in the neck |
A: Lateral – body of mandible A: Medial – anterior belly of digastric A: Posterior – stylohyoid muscle A: Floor – posterior belly of digastric |
|
|
Q: Describe the borders of Level IIa in the neck |
A: Superior – skull base A: Inferior – hyoid (clinical) or carotid bifurcation (anat) A: Medial – stylohyoid muscle A: Posterior: plane defined by CN XI |
|
|
Q: Describe the borders of Level IIb (Submuscular recess) in the neck |
A: Superior – skull base A: Inferior – hyoid (clinical) or carotid bifurcation (anat) A: Medial – plane defined by CN XI A: Posterior – posterior border of SCM |
|
|
Q: Describe the borders of Level III in the neck |
A: Superior – hyoid (clinical) or carotid bifurcation (anatomic) A: Inferior – lower border of the cricoid (clinical) or omohyoid over IJV (anatomic) A: Medial – lateral border of sternohyoid A: Lateral – posterior border of SCM |
|
|
Q: Describe the borders of Level IV in the neck |
A: Superior – lower border of the cricoid (clinical) or omohyoid crossing over IJV (anatomic) A: Inferior – clavicle A: Anterior – lateral border of sternohyoid A: Lateral – posterior border of SCM |
|
|
Q: Describe the borders of Level Va in the neck |
A: Superior – Apex of convergence of the trapezius and SCM muscles A: Inferior – horizontal plane through inferior border of cricoid A: Medial – posterior border of SCM A: Lateral – anterior border of trapezius |
|
|
Q: Describe the borders of Level Vb in the neck |
A: Superior – horizontal plane through inferior border of cricoid A: Inferior – clavicle A: Medial – posterior border of SCM A: Lateral – anterior border of trapezius |
|
|
Describe the borders of Level VI (Prelaryngeal/Delphian, pretracheal, paratracheal) in the neck |
A: Superior – hyoid bone A: Inferior – suprasternal notch A: Lateral – common carotids |
|
|
Q: Classification of neck dissections |
A: Radical A: Modified radical (types I, II, III/Functional) A: Selective – Lateral (II, III, IV), Posterolateral (II, III, IV, V), Anterolateral (II, III, IV, VI), Supraomohyoid (I, II, III) A: Extended |
|
|
Q: Management of an exposed carotid |
A: Risk factors – Prior radiation, Malnutrition, Diabetes, Fistula/Infection A: Inpatient considerations – Design incisions properly (avoid trifurcations), Perioperative antibiotics, Adequate tissue coverage (regional/free flaps) |
|
|
Q: Management of carotid blowout |
A: Manual pressure to stop bleeding A: Blood products/IV fluids A: OR ligation of carotid +/- Fogarty catheterization (embolization) to help control bleed |
|
|
Q: Risk factors for postoperative major vessel rupture (FEARR!) |
A: Fistula/infection A: Exposure of vessel A: Adventitia removed A: Recurrent tumor A: Radiation |
|
|
Q: Components of Chyle |
Odorless Milky appearance that separates into a creamy layer when left to stand Specific gravity greater than 1.012 Total fat composition of 0.4-4 g/L Total protein greater than 30 g/L pH greater than 7.0 Sterile fluid Lipophilic globules when stained with Sudan III WBC differential of predominately lymphocytes |
|
|
Q: Management of the Chylous fistula |
A: When encountered intraoperatively, ligate it off A: Postoperative Head elevation A: Closed suction drainage A: Pressure dressing A: octeotride/somatostatin: minimizes lymph fluid excretion A: Alter diet with MCT’s – directly absorbed into portal system, avoids breakdown of LCT’s into FFAs & glycerol which are transported in chylomicrons A: Monitor and correct electrolytes A: +/- Surgery vs tetracycline sclerosing therapy for failures |
|
|
Q: Indication for early surgical intervention for chylous fistula |
A: >600 ml in 24 hours A: Persistent >1 week A: Chylothorax A: Cachexia |
|
|
Q: What are the 5 signs of Horner’s syndrome? |
A: Ptosis A: Meiosis A: Anhidrosis A: Enophthalmos A: Loss of the Ciliospinal reflex – therefore absence of dilation of the ipsilateral pupil to a pain stimulus applied to the neck |
|
|
Q: Sensitivity & specificity for physical exam, CT, and combined for detecting neck disease in HNSCC |
A: Clinical exam – sensitivity 74%, specificity 81%, accuracy 77% A: CT – sensitivity 83%, specificity 83%, accuracy 83% A: Combined – sensitivity 92% 3: Remember sensitivities in order = 74%, 83%, 92%; just add 9! |
|
|
Q: Describe the Embryology of the Thyroid gland |
A: 4 weeks GA – Endoderm on the floor of the pharynx between the 1st & 2nd arches invaginates and descends into the mesenchyme of the neck; this diverticulum is situated between the Tuberculum impar (forms the oral tongue along with the ligual swellings) and the Copula (forms the base of tongue) A: 4.5 weeks GA – The connection between the ventral thyroid diverticulum and the floor of the pharynx (Foramen Cecum) disappears; the diverticulum develops into the median thyroid anlage A: 6 weeks GA – The thyroglossal duct has completely degenerated, and cellular proliferation results in the right and left thyroid lobes, separated by an isthmus; in up to 50% of individuals, the distal aspect of the duct persists as a pyramidal lobe A: The Ultimobranchial body of the 4th arch fuses and is incorporated into the supero-lateral aspects of the thyroid lobes, and forms the parafollicular C-cells which secrete calcitonin |
|
|
Q: Seven steps in thyroid metabolism |
A: Uptake of Iodine by thyroid – ↑ by TSH A: Coupling of Iodine to Thryroglobulin (organification) – ↑ by TSH A: Storage of MIT/DIT in colloid – ↑ by TSH A: Re-absorption of MIT/DIT A: Formation of T3 and T4 form MIT/DIT – ↑ by TSH A: Release of T3 and T4 into serum – ↑ by TSH A: Breakdown of T3 and T4 to release Iodine |
|
|
Q: Percentage of thyroid hormone as T4 |
A: 98% |
|
|
Q: Four effects of TSH on thyroid cells |
A: ↑ Iodine transport into cell A: ↑ TG synthesis and proteolysis A: ↑ formation of MIT & DIT (organification) A: Storage of T3 & T4 in the gland as colloid A: ↑ hydrolysis of the stored TG to release T3 and T4 into circulation 3: Maintains structure of thyroid cells, and stimulates gland size and vascularity |
|
|
Q: Nine thyroid hormone functions (CHROME NCL) |
A: ↑ CO, HR A: ↑ Heat production A: ↑ RBC mass A: ↑ O2 consumption A: ↑ metabolic rate (calorigenesis) A: Epinephrine potentiation A: Neural growth and development (*Neonatal brain) A: ↓ Cholesterol A: metabolism of Lipids, carbs, & protein |
|
|
Q: Risk factors for hypothyroidism |
A: Old age A: Female sex A: Grave’s disease A: Drugs – lithium iodide, amiodarone, iodide containing drugs A: Surgery – postthyroidectomy A: Hashimoto’s disease A: Autoimmune disease A: Euthyroid goiter A: Laryngectomy with/without irradiation A: Prior head & neck radiotherapy management 3: “Old Female Grave Diggers Smoke Hash And Eat Lotsa Peanuts!” |
|
|
Q: Five head & neck signs & symptoms of hypothyroidism |
A: Hearing loss: sensorineural, mixed, conductive A: Tinnitus A: Vertigo A: Enlarged tongue A: Hoarseness (mucopolysaccharide infiltration) A: Blurred vision |
|
|
Q: Graves’ disease triad |
A: Diffuse toxic goiter A: Infiltrative ophthalmopathy A: Infiltrative dermopathy (pretibial myxedema) |
|
|
Q: Medical management of Graves’ disease (PIPI) |
A: Thionamides – oral use only, indicated in young patients, pregnant patients (PTU 1st trimester, Methimazole in 2/3rd trimesters) but surgery procedure of choice in preggos, severe thyrotoxicity prior to OR or radioactive iodine ablation Propylthiouracil: inhibits thyroid peroxidase (decreases central T4/T3 production), decreases peripheral T4 to T3 conversion by inhibiting type I deiodinase; severe liver side effects, therefore not first line anymore. Class D drug (evidence of human fetal risk), but used in life threatening situations. Methimazole: same central effects as PTU but no peripheral effect A: I-131 – most common, C/I in pregnancy A: Β-blockers (Propranolol) – Decreases sympathetic overdrive, used as an adjunctive treatment A: Iodide (Lugol’s) – Wolf-Chaikoff effect: inhibits organification & thyroid hormone release, decreases vascularity; most useful in thyroid storm, C/I in R/A |
|
|
Q: Define the Jod-Basedow phenomenon |
A: Development of overt hyperthyroidism in subclinical patients due to exogenous iodide administration |
|
|
Q: Management of Thyroid Storm (PPID) |
A: PTU 800-1000mg NG qd A: Propranolol IV (block adrenergic effects and peripheral conversion) A: sodium Iodide 1g IV (inhibits hormone release) A: Dexamethasone 2mg IV q6h (suppresses the H-P-T axis & peripheral hormone conversion) 3: Admit to ICU, IVF, cooling blankets |
|
|
Q: Classification of Benign Thyroid Disease |
A: Nontoxic – Diffuse, Nodular Goiter A: Toxic – Toxic multinodular goiter, Toxic adenoma, Graves Disease A: Inflammatory |
|
|
Q: Inflammatory thyroiditides (SHARP) |
A: Subacute/de Quervain’s – Viral etiology, most common cause of painful thyroiditis A: Hashimoto’s (autoimmune) – Most common; anti-TPO (90%) & anti-TG (50%) antibodies A: Acute suppurative A: Riedel’s thyroiditis A: Painless/Silent thyrotoxic thyroiditis |
|
|
Q: Four Antibodies that may be present in Hashimoto’s thyroiditis |
A: Anti-TPO Ab (90%) (TPO, key enzyme in organification) A: Anti Thyroglobulin (TG) Ab (50%) A: Anti microsomal Ab (90%) A: Anti TSH Ab (may be seen) |
|
|
Q: Indications for surgery in euthyroid goiter |
A: Symptoms – Compressive (airway, esophagus), recurrent painful hemorrhage A: Diagnosis – Inability to exclude cancer on FNA A: Cosmesis A: Substernal extension? |
|
|
Q: Six most common thyroid malignancies |
A: Papillary 80% A: Follicular 10-15% A: Medullary 5% A: Anaplastic <5% A: Lymphoma A: Metastasis |
|
|
Q: Discuss Papillary thyroid cancer |
A: Represents 80%, multicentric in 80%, A: 3rd & 4th decades, F: M = 3:1 A: Poorly encapsulated A: High locoregional metastasis to nodes (37-65%), lower rate of distant metastasis (2-17%) A: Age and Size are important prognostic factors; whereas vascular invasion and nodal metastasis are not significant A: Can display mucinous, ciliary, or squamous metaplasia |
|
|
Q: Histologic subtypes of PTC with worse prognosis |
A: Usual Papillary A: Encapsulated A: Follicular A: Poorly differentiated/Insular cell A: Tall cell (aggressive) A: Columnar cell (aggressive) A: Hurthle cell /Oxyphillic /Oncocytic (variant of Follicular, worst of the WDTCs) A: Diffuse sclerosing (aggressive) 3: LN metastasis increases risk of local recurrence, not mortality; 5 year survival = 70-90% |
|
|
Q: Histologic subtype of PTC with better prognosis |
A: Encapsulated 3: Others include papillary microcarcinoma (<1 cm), follicular, diffuse follicular & macrofollicular |
|
|
Q: Histology of Papillary thyroid carcinoma |
A: Multicentricity A: Papillary formations with fibrovascular cores A: Elongated Follicles A: Psammoma bodies – Laminated calcific densities A: Nuclei – Enlarged, Irregularly shaped, Overlapping/Crowding, Ground glass chromatin (Optically cleared/Orphan Annie eyes), Margination of chromatin along nuclear membrane, abundant nuclear Grooves, intranuclear Cytoplasmic inclusions/Vacuoles, loss of basal Polarity, and prominent Nucleoli? A: Immunohistochem: BRAF, HBME-1, TTF-1 (thyroid transcription factor-1), Gelactin-3, Thyroglobulin, cytokeratin A: Inspissated colloid A: Intratumoral fibrosis Important is Papillary with psammoma bodies, nuclear grooves and nuclear inclusions, and nuclear crowding, orphan annie eyes |
|
|
Q: Discuss Follicular thyroid carcinoma |
A: Represents 10-15% (including Hurthle cell subtype) A: >4th decade, F: M 3:1 A: Varying degrees of Capsular and Vascular invasion (required for carcinoma diagnosis); other suggestive features are Necrosis, high Mitotic rate, and widespread Nuclear atypia; multicentricity uncommon A: IHC usually not necessary, but Tg, TTF-1, Cytokeratin, HBME- 1, and Galectin-3 are positive A: Histologic variants – Oxyphilic (Hurthle), Clear cell A: Lower rate of nodal metastasis (20%), higher rate of distant metastasis (65%) A: Size not a prognostic factor, angioinvasion a poor prognosis; 5 year survival 70% |
|
|
Q: Discuss Medullary thyroid carcinoma |
A: Represents ~5% A: 80% sporadic, 20% familial (better prognosis); RET protooncogene on chromosome 10q11.2, autosomal dominant A: Familial >90% bilateral, sporadic 30% bilateral A: Age of onset younger (20-30) in familial; mean age 50 in sporadic A: Early lymph node metastasis (50% at presentation) A: Histologic features – unencapsulated, hyalinized bands of collagen, Amyloid deposits, Granular cytoplasm, coarsely clumped chromatin, and prominent Nucleoli A: Markers – Calcitonin (most sensitive & specific), CEA, NSE (neuron specific enolase), Chromogranin, Synaptophysin A: Total thyroidectomy for MEN IIA by 5-6 years, for MEN IIB by 6 months of age; 131I not indicated (not effective) A: 5 year survival 88%, 10 year survival 65% A: Vandetinib: kinase inhibitor against VEGF/EGFR, indicated for late stage MTC for pts who are ineligible for surgery |
|
|
Q: Histology of Medullary thyroid carcinoma |
A: Nests of small round cells with abundant granular cytoplasm A: Presence of Amyloid A: Dense, irregular areas of calcification in superior poles thyroid Think embryology: ultimobranchial body of 4th arch fuses with superior poles which harbors the parafollicular C-cells for calcitonin A: IHC – Calcitonin (most sensitive & specific), NSE, Chromogranin, Synaptophysin, CEA (sensitive, not specific) |
|
|
Q: Discuss MEN I (Werner/Wermer syndrome) |
A: Autosomal dominant, altered tumor suppressor gene (menin) found on chromosome 11 A: Pituitary lesions (prolactinoma) 65%, Parathyroid adenomas/hyperplasia 90%, pancreatic islet cell tumors (gastrinoma) |
|
|
Q: Discuss MEN II |
A: Autosomal dominant, caused by RET protooncogene mutation on chromosome 10 (tyrosine kinase), 5 different point mutations identified A: Medullary thyroid carcinoma (100%), Pheochromocytoma (in ~50% of patients) plus: IIA (Sipple) – Parathyroid adenoma/hyperplasia & hyperparathyroidism (10-30% (KJ) or 85% of patients) IIB (Wagenmann-Froboese) – Marfanoid habitus, multiple mucosal neuromas, hyperplastic corneal nerves |
|
|
Q: Timing of thyroidectomy in children whose genetic screen is positive for MEN type 2 |
A: MEN 2A (Sipple) around 6 years of age A: MEN 2B (Wagenmann-Froboese) around 6 months of age 3: Risk of developing MCT during lifetime >90% |
|
|
Q: Ten clinical signs of Marfan’s syndrome |
A: Long spidery fingers, scoliosis, hammer toe, pigeon breast, dolichocephaly, low hairline, tall & thin body structure, lens displacement, aortic root dilatation, may have SNHL, CHL or mixed HL A: Autosomal dominant |
|
|
Q: What is the Pheochromocytoma rule of 10s? |
A: 10% bilateral A: 10% malignant A: 10% extraadrenal |
|
|
Q: Discuss Anaplastic thyroid carcinoma |
A: Represents ~5% A: >65 years of age A: Risk factor is previous thyroid tumors = Papillary CA (typically a transformation of this subtype), Follicular CA, Follicular Adenoma A: Two genes associated = p53 and BRAF A: Histology – Bizarre, Giant & Spindle cells in various proportions, high mitotic rate, necrosis, infiltration A: 10% survival after 1 year |
|
|
Q: Discuss thyroid Lymphoma |
A: Represents ~5%, more common than anaplastic carcinoma A: Hashimoto’s disease increases patients risk 70x A: Almost always NHL, Immunoblastic most common subtype |
|
|
Q: Name the WHO Architectural (growth patterns) subtypes of thyroid Follicular Adenoma |
A: Microfollicular (fetal) A: Macrofollicular (colloid) A: Normofollicular (simple) A: Trabecular (embryonal) A: Solid (embryonal) A: Atypical |
|
|
Q: Name the WHO Histologic subtypes of thyroid Follicular Adenoma (CHAOS) |
A: Clear cell A: Hyalinizing trabecular A: Atypical A: Oxyphilic/Oncocytic (Hurthle) cell A: Signet-ring |
|
|
Q: Define an adequate FNAB for thyroid |
A: >6 properly prepared smears with 15-20 groups of well-preserved clumps of follicular epithelium |
|
|
Q: Accuracy of FNAB at identifying each thyroid tumor histology |
A: Anaplastic & Medullary = 90% A: Papillary = 80% A: Follicular = 40%? 3: FNAB cannot diagnose follicular cancer because Vascular &/or Extracapsular invasion are required on pathology to make this diagnosis |
|
|
Q: Hurthle cells on FNAB, 4 possibilities |
A: Follicular adenoma A: Follicular carcinoma/Hurthle cell carcinoma A: Hashimoto’s thyroiditis A: Papillary carcinoma 3: Other lesions include Grave’s, post-XRT, Aging, Papillary, and Medullary carcinoma (Wenig, p. 894) |
|
|
Q: Clear cells on FNAB, 3 possibilities |
A: Follicular adenoma A: Follicular carcinoma A: Metastatic Renal Cell carcinoma 3: RCC can be distinguished by lack of Colloid on PAS, Tg and TTF-I stains negative, CD10 and RCC marker stains positive |
|
|
Q: Bethesda Classification |
|
|
|
Q: AJCC 2010 staging for thyroid carcinoma
|
|
|
|
Q: Six patient risk factors for diagnosis of thyroid cancer |
A: Family history of thyroid cancer A: History of radiation exposure A: Male gender A: Age >45 A: Previous history of thyroid cancer A: Ethnicity (Hawaiian, Philipino) |
|
|
Q: Seven concerns on history, physical, or testing for diagnosis of thyroid cancer |
A: Enlarging A: Size >3 cm A: Dysphagia A: Hoarseness A: Cervical adenopathy A: Fixation to skin A: Microcalcifications, increased vascularity on U/S |
|
|
Q: Risk factors for worse prognosis for well differentiated thyroid cancer |
A: Older age (men >40, women >50) has worse prognosis A: Size of primary – >5cm worse, <1.5cm improved prognosis; thus size >1.5cm consider worse A: Extrathyroidal extension A: Distant metastases adversely affects prognosis A: Unifocal more likely to be malignant versus multifocal disease; mutifocality increases with age A: Cervical metastases – does not impact overall survival but does increase chances of local recurrence |
|
|
Q: Three risk profiles scales for well differentiated thyroid cancer |
A: AMES (Lahey) – Age, distant Metastasis, Extrathyroidal extension, Size A: AGES (Mayo) – Age, Grade, Extrathyroidal extension, Size A: MACIS – distant Metastases, Age, Completeness of resection, extrathyroidal Invasion, Size |
|
|
Q: Most important prognostic factors for Papillary thyroid cancer-MASH (MD Anderson) |
A: presence of distant Metastatic diseases A: Age A: Sex A: Histology of the cancer |
|
|
Q: Significant prognostic factors for Follicular thyroid ca |
A: Invasion of blood vessels and capsule (has significant effect the prognosis in the first 10 years) |
|
|
Q: Most aggressive WDTC |
A: Hurthle cell (50-60% five year survival) |
|
|
Q: Two Lab markers of recurrent WDTC |
A: Thyroglobulin A: Anti-Thyroglobulin antibody |
|
|
Q: What are the boundaries of Lore’s triangle, and what does it identify? |
A: Identifies location of RLN in the neck during thyroidectomy A: Medial – tracheal sidewall A: Lateral – carotid sheath A: Superior – surface of retracted thyroid pole inferiorly |
|
|
Q: Four branches of the thyrocervical trunk |
A: Ascending cervical – supplies prevertebral muscle region A: Transverse cervical – supplies the trapezius muscle (mid and lower island flap) A: Inferior thyroid – to inferior pole of thyroid gland A: Suprascapular 3: Originates off of the 1st portion of the subclavian artery |
|
|
Q: Management of preoperative hyperthyroidism
|
A: Suppressive therapy with thionamides (PTU, methimazole, carbimazole) used until patient normothyroid A: Iodides, lithium used 10-14 days prior to surgery once normothyroid to inhibit synthesis & release of hormone A: Β-blockers used 48-72 hours before surgery to suppress sympathetic manifestations of thyrotoxicosis |
|
|
Q: Side effects of 131I (BP BATCH) |
A: Breast cancer A: Pulmonary fibrosis A: Bladder cancer A: AML A: Thyroid crisis/Thyroiditis (give steroids to avoid this) A: Chromosomal abnormalities/Gonadal dysfunction A: Hypoparathyroidism |
|
|
Q: Three thyroid tumors that are hard to diagnose with the best FNA |
A: Follicular carcinoma A: Lymphoma A: Poorly diff/Met? |
|
|
Q: Three instances when median sternotomy will likely be necessary for a retrosternal goiter |
A: Cannot feel the mass in the neck A: Goiter very low or POSTERIOR in the mediastinum A: Cannot finger dissect the retrosternal mass |
|
|
Q: Effects of Parathyroid Hormone |
A: ↑ serum calcium, ↓ serum phosphates A: Bone – ↑ osteoclasts A: Kidney– ↑ calcium reabsorption, ↓ phosphate reabsorption, ↑ 1, 25-(OH) 2-D3 synthesis A: Gut – ↑ calcium absorption via vitamin D stimulation |
|
|
Q: Effect of Calcitonin |
A: ↓ serum calcium by inhibiting Osteoclast function A: Inhibits Ca absorption in gut A: Increases excretion of Ca and phosphate in kidney |
|
|
Q: Blood supply to superior & inferior parathyroid glands |
A: Superior and inferior parathyroid arteries, originating from inferior thyroid artery (86% of time), some contribution from superior thyroid artery (10-20%) |
|
|
Q: Most common number of parathyroids |
A: ~85% have 4 parathyroids A: ~10% have >4 A: ~5% have <4 |
|
|
Q: Etiologies of Hyperparathyroidism |
A: Primary (High Calcium, low phosphate)– Adenoma or Hyperplasia A: Secondary (Normal/low calcium, High Phosphate)– Gland hyperplasia due to malfunction of other organ system; CRF, MM, OI, PD, bone mets (PTBLK), pituitary basophilism, Vit D deficiency A: Tertiary (Normal/high Calcium, Variable Phosphate PO4 tends to be high if Calcium is high) – Autonomous PTH production ; After cause of secondary HPT has been corrected |
|
|
Q: Incidence of PTH pathologies in primary hyperparathyroidism |
A: Adenoma – 85% A: Hyperplasia – 10% A: Multiple adenoma – 5% A: Carcinoma – <1% |
|
|
Q: Normal anatomic locations of the parathyroids |
A: Superior pair – usually on deep surface of thyroid within 1cm of RLN entry at cricothyroid joint OR 1 cm above intersection of RLN and inf thyroid artery (within 2 cm of this point) A: Inferior pair – usually within 1-2 cm of inferior thyroid artery entry into thyroid gland |
|
|
Q: Six alternative sites for parathyroid gland location |
A: Retroesophageal (most common location for ectopic superior glands) A: Superior mediastinal (most common location for ectopic inferior glands) A: Intrathymic A: Intrathyroidal A: Carotid sheath A: Tracheoesophageal |
|
|
Q: Four noninvasive localization studies for parathyroid adenoma |
A: Ultrasonography – 22-82% sensitive A: CT – 47-76% sensitive A: MRI – 50-80% sensitive A: Sestamibi scan – 70-90% sensitive |
|
|
Q: Three invasive localization studies for parathyroid adenoma |
A: Arteriography (TC trunk, Int mammary & carotids) A: Digital subtraction angiography – for multiple gland disease in revision cases, 60-70% sensitive A: Selective venous catheterization, 80% sensitive (two fold rise in PTH) A: U/S-guided FNA 3: Intraoperative localization methods (Cummings): - Intraop U/S - Injection of Methylene or toluidine blue - Gamma probes (after Tc99m injection 2 hrs preop, radiation >20% than surgical bed is +ve) - Intraop PTH &frozen section - Urinary adenosine monophosphate |
|
|
Q: Nine indications for surgery with primary hyperparathyroidism (1990 NIH consensus statement) |
A: Any overt Manifestations of hypercalcemia: Muscle weakness, Osteitis fibrosa cystica, Renal calculi +/– radiograph, Life threatening hypercalcemic crisis, Psychiatric problems OR Asymptomatic with: A: Serum calcium >3 mmol/L or >0.25 mmol/L above normal (>12 mg/dl or >1 mg/dl above normal) A: Hypercalciuria (>400 mg/24h = >10mmol/d) A: Decreased creatinine clearance (>30%) A: Osteoporosis >2.5 SDs A: Age <50 years A: Consistent followup unlikely A: Patient requests surgery A: Coexistent illness complicates management |
|
|
Q: Indications for surgery with asymptomatic primary hyperparathyroidism (2008 NIH consensus statement adapted by Third International Workshop) |
Serum calcium >12 mg/dl (>3 mmol/L) (ie 1-1.6mg/dl above normal) Decreased creatinine clearance <60ml/min Age <50 years Osteoporosis > 2SDs or previous fracture Patient requests surgery Consistent followup unlikely Coexistent illness complicates management |
|
|
Q: Four indications for parathyroidectomy due to CRF (CRRF) |
A: Calciphylaxis (tissue calcification) unresponsive to hemodialysis or meds A: Refractory bone pain/pruritus A: Renal osteodystrophy A: pathologic Fractures |
|
|
Q: Three surgical options for parathyroid hyperplasia |
A: Subtotal parathyroidectomy – preferred if patient doesn’t have MEN or renal failure A: Total parathyroidectomy with autotransplantation – CRF A: Total parathyroidectomy with cryopreservation of 1 gland – CRF or MEN |
|
|
Q: Management of hypercalcemic crisis (http://www.aafp.org/afp/2003/0501/p1959.html) |
A: Saline hydration & electrolyte correction A: Furosemide diuresis A: Glucocorticoids A: Calcitonin (inhibits osteoclasts) 5 IU/Kg IM A: Bisphosphonates (inhibits osteoclasts) – Pamidronate 60 mg IV over 4 hours A: Organic phosphates: 8 mg IV, PO, PR A: Mithramycin (MOA poorly understood but works well) 25 mcg/Kg IV over 4 hours A: Gallium nitrate (inhibits osteoclasts) A: Hemodialysis for life threatening situations 3: Symptoms – weakness, anorexia, N/V, drowsiness, confusion, stupor, coma 3: Causes – CHIMPANZEES C = Calcium supplementation H = Hyperparathyroidism I = Iatrogenic (Drugs such as Thiazides, or Immobility after surgery) M = Milk Alkali syndrome P = Paget disease of the bone, also OI A = Acromegaly and Addison's Disease N = Neoplasia (common cause): MM, bone mets Z = Zollinger-Ellison Syndrome (MEN Type I) E = Excessive Vitamin D E = Excessive Vitamin A S = Sarcoidosis |
|
|
Q: Enzyme stimulated by PTH to activate vitamin D |
A: 1-alpha-hydroxylase |
|
|
Q: Four lab findings with tertiary hyperparathyroidism |
A: Elevated PTH A: Low or normal Ca? (We agreed Normal/high Ca) A: Low Vit. D A: Hyperphosphatemia (particularly when high Ca) |
|
|
Q: Eight investigations other than Ca and intact PTH that should preformed with dx of hyperPTH (AABBCC TUG A PUP!) |
A: Albumin A: Alkaline phosphatase A: Bone densitometry A: BUN and CR A: Calcitonin (R/O MEN IIA) A: TFT A: 24 h Urine Ca (R/O familial hypocaluric hypercalcemia) A: Gastrin (R/O MEN I) A: ACE (R/O Sarcoid) A: Phosphorous A: Urine catecholamines (R/O MEN IIA) A: Prolactin (R/O MEN I) |
|
|
Q: Medical management of hyperPTH |
A: Ca, Cr, U/A, PTH q6month A: Bone density qyear A: Restrict oral Ca intake <1 g/day |
|
|
Q: Management of hyperPTH associated with renal failure |
A: Calcium salts (Phosphate binder for hyperphosphatemia) A: Vit. D (because hypovit D) |
|
|
Q: Danger of Primary hyperparathyroidism in pregnancy |
A: Neonatal tetany 3: Ca crosses placenta, PTH doesn’t; newborn’s PTH is suppressed and serum Ca drops soon after delivery 3: Note: In 22q11 spectrum (VCF, DiGeorge), get neonatal hypoparathyroidism and subsequent hypocalcemia, and also neonatal tetany |
|
|
Q: What does primary hyperparathyroidism in infancy present with? |
A: Respiratory distress A: Hypotonia A: Skeletal demineralization |
|
|
Q: What is hyperparathyroidism-jaw tumor syndrome? |
A: Autosomal dominant A: Hyperparathyroidism – solitary or multiple adenomas, 10% will present as parathyroid carcinoma; severe hypercalcemia as a teenager A: Jaw – cemento-ossifying fibromas A: Renal – cysts, hamartomas, Wilms’ tumor (nephroblastoma) |
|
|
Q: Causes of congenital hypoparathyroidism (due to agenesis) |
A: Deletion 22q11.2 spectrum – DiGeorge’s, Velocardiofacial syndrome |
|
|
Q: What week embryologically does thyroid development begin and end |
A: 4th week to 10th week (TGD disappears) |
|
|
Q: Define tubercles of Zuckerkandl |
A: Posterior extensions of each thyroid lobe |
|
|
Q: Histological features of Hurthle cells |
A: Follicular cells with rich granular eosinophilic cytoplasm |
|
|
Q: Three general classes of papillary thyroid ca |
A: Occult (less than 1.5 cm) – associated with good prognosis A: Intrathyroidal A: Extrathyroidal |
|
|
Name two syndromes associated with Papillary thyroid ca |
A: Gardner A: Cowden |
|
|
Q: What are Orphan Annie eyes? |
A: Vesicular, “ground-glass” nuclei |
|
|
Q: Three patterns of calcification of thyroid masses |
A: Rim (eggshell) – Benign A: Bilateral superolateral – Medullary Ca A: Extensive irregular – Multinodular goiter |
|
|
Q: Conditions for partial thyroidectomy (hemithyroidectomy with isthmusectomy) |
A: Unifocal, intrathyroidal, and nonmetastatic papillary carcinomas <1.0 cm in diameter A: No previous radiation A: Contralateral lobe is clinical normal |
|
|
Q: Indications for near total thyroidectomy? |
A: Microcarcinomas with multifocality A: Local lymph node mets (will get I-131 post op) |
|
|
Q: Three indications for post op XRT for thyroid Ca |
A: Advanced locoregional WDTC whether superficial excision is complete or incomplete A: Tumor no longer picks up radioiodine A: Palliation of unresectable bone metastasis |
|
|
Q: N+ disease in WDTC – what type of neck dissection |
A: Level II-VI A: Level I only if clinically positive A: N0 – Central compartment (upper mediastinum to hyoid, laterally to Carotids) |
|
|
Q: Hurthle cell carcinoma management |
A: Total Thyroidectomy A: Post op thyroid suppression (TSH receptors on tumor surface) A: Generally unresponsive to I-131 and radiosensitive |
|
|
Q: Management of neck disease for Medullary thyroid ca |
A: N0 – central compartment (upper mediastinum to hyoid, laterally to Carotids) A: N+ – include II-VI |
|
|
Q: Classification of hypothyroidism |
A: Primary (Gland) A: Secondary (Pituitary) A: Tertiary (Hypothalamus) A: Peripheral resistance |
|
|
Q: Epithelium of the nasopharynx |
A: Pseudostratified columnar majority at birth, slowly replaced by stratified squamous in adolescence A: Transitional cell, found at junction of the two epithelial linings |
|
|
Q: NPC histology and clinical features WHO |
A: Keratinizing (Type I) – Squamous, 25% in nonendemic areas, 1-2% in endemic areas; distinct intercellular bridges, keratin production; worst prognosis = 10% 5 year survival A: Nonkeratinizing (Type II) – Squamous/Transitional, 12% in nonendemic areas; little/no keratinization present; papillary morphology; ~60% 5 year survival A: Undifferentiated (Type III) – Lymphoepithelioma, 63% in nonendemic areas, 95% in endemic areas; clear, enlarged nuclei; ~60% 5 year survival |
|
|
Q: Risk factors for NPC |
A: Genetics – HLA-A2, B17, Bw46 (only in Orientals) A: Geographic – southeast Asia (Kwantung/Guangdong, Hong Kong, Taiwan) A: Environmental – Nitrosamines, salted preserved foods A: Infectious – EBV |
|
|
Q: What are the 6 top signs & symptoms of NPC? |
A: Neck mass (60%) A: Ear plugging/fullness (41%) A: Conductive hearing loss (37%) A: Epistaxis (30%) A: Nasal obstruction (29%) A: Cranial nerve palsy (18%), usually VI, or V initially |
|
|
Q: What three indirect immunofluorescence tests for antibodies to EBV play a role in NPC diagnosis and therapy? |
A: Viral Capsid Antigen (IgA, 95% Sensitive) & Early Antigen (IgA, 95% Specific) – Most specific tests for diagnosis, titers ~85% positive in cases of WHO II & III NPC A: ADCC (antibody-dependent cellular cytotoxicity) titers – can be used to predict prognosis of WHO II & III NPC, significant relationship between lower titers & progression, poor prognosis |
|
|
Q: TNM Staging for Nasopharynx (AJCC 2010) |
|
|
|
Q: Ho & Neel’s 5 adverse prognostic indicators for NPC |
A: Length & symptomatology of disease (>2 months) A: Extension beyond the nasopharynx A: Low neck disease (Levels IV/V) A: Keratinizing histology A: Distant metastasis |
|
|
Q: Overall survival for NPC postradiotherapy |
A: In general, 5 year survival ~60%, worse for type I and better for types II/III A: Survival continues to decreased past 10 years |
|
|
Q: Boundaries of the oropharynx |
A: Superior – horizontal plane through the hard palate A: Inferior – horizontal plane through the hyoid A: Anterior – circumvallate papillae |
|
|
Q: Four subsites of the oropharynx |
A: Base of tongue A: Soft palate A: Tonsillar area (most common location) A: Posterior and lateral pharyngeal wall A: glossotonsillar sulci (part of tonsillar area?) |
|
|
Q: Five muscles of soft palate |
A: Palatoglossus A: Palatopharyngeus A: Musculus uvulae A: Levator veli palatini A: Tensor veli palatini (innervated by V) |
|
|
Q: Nerve ganglia for anterior tongue/base of tongue/hypopharynx involved in referred otalgia |
A: Anterior tongue – V3, from Gasserian ganglion A: Posterior tongue – IX, from superior petrosal ganglion and inferior ganglion A: Hypopharynx – X, from superior (jugular) ganglion and inferior (nodose) ganglion |
|
|
Q: T staging for Oropharyngeal carcinoma (AJCC 2010) |
A: Nodal and Staging same |
|
|
Q: Surgical approaches for management of oropharyngeal carcinoma |
A: Transoral – Oral, Visor lip & cheek flap, Upper/Lower cheek flap, Mandibular lingual release A: Transpharyngeal – Suprahyoid, Subhyoid, or Lateral (high or low) pharyngotomy A: Transmandibular – Midline labiomandibular glossotomy (good only for small midline BOT lesions), Mandibulotomy/Mandibular swing (midline or lateral), Mandibulectomy (composite resection) |
|
|
Q: Indications for radiation therapy for oropharyngeal cancer
|
A: Primary modality for T1 & T2 lesions with equal cure rate as surgery |
|
|
Q: Indications for combined therapy for oropharyngeal cancer |
A: Primary lesion – T3/T4, perineural/vascular invasion, positive/close margins A: Neck – N2, N3; or N0/N1 (clinical) with 2+ histologically positive nodes/nodes at multiple sites, Extracapsular invasion, Perineural or vascular invasion |
|
|
Q: Boundaries of the hypopharynx |
A: Superior – horizontal plane through the hyoid A: Inferior – horizontal plane through inferior margin of cricoid |
|
|
Q: Three subsites of the hypopharynx |
A: Piriform sinus A: Posterior pharyngeal wall A: Postcricoid region |
|
|
Q: Staging for hypopharyngeal carcinoma (AJCC 2010) |
A: Nodal and Staging same |
|
|
Q: Management of hypopharyngeal carcinoma |
A: Early – XRT, Surgery, or both A: Late – Surgery + postop Chemo-XRT |
|
|
Q: Surgical approaches to the Posterior pharyngeal wall |
A: Suprahyoid (transhyoid) pharyngotomy A: Lateral pharyngotomy A: Combined Suprahyoid and Lateral pharyngotomy A: Median labiomandibular glossotomy |
|
|
Q: Surgical options for cancer of the Pyriform sinus |
A: T1 lesions in high medial area – partial laryngopharyngectomy A: T2+ lesions – usually require total laryngectomy, partial pharyngectomy if lateral extension present |
|
|
Q: Surgical option for cancer of the Postcricoid area |
A: Total laryngectomy, partial pharyngectomy, and cervical esophagectomy |
|
|
1
|
A: Partial pharyngectomy: - Extension of tumor to more than one wall of the pyriform - Extension to pyriform apex - Involvement of larynx A: Partial LP: - Extension to pyriform apex - Extension to postcricoid region & CP - Ipsilateral TVC palsy |
|
|
Q: List 10 risk factors for cervical esophageal Ca |
A: Smoking – 4.5x increased risk A: ETOH – 11x increased risk, synergistic with smoking A: Nitrosamines A: Prior H&N carcinoma A: Barrett’s esophagus – distal ↑ 5-15% increased risk of adenocarcinoma A: Caustic burn/scar/stricture A: Achalasia A: Plummer-Vinson syndrome A: Oculopharyngeal muscular dystrophy: AD, ptosis, dysphagia, proximal limb weakness A: Pernicious anemia A: Tylosis (thickening palms and soles) A: Scleroderma |
|
|
Q: Describe the TNM Staging of Esophageal cancer (AJCC 2010) |
|
|
|
Q: Four methods of reconstructing the cervical esophagus, advantages & disadvantages |
A: Free jejunum – Adv = mucosalized tubed structure that reestablishes conduit; Disadv = requires laparotomy, requires microvascular anastomosis, often unable to achieve TE speech. Preferred for total pharyngoesophageal defects, not ideal if significant base of tongue resected A: Colonic interposition (not a first choice reconstructive alternative) – Adv = mucosalized tube structure that reestablishes food conduit; Disadv = requires laparotomy, high morbidity/mortality from postoperative infection A: Gastric pullup/transposition – Adv = single anastamotic line, can perform total esophagectomy for margins; Disadv = morbidity with the pullup (pneumothorax), postoperative early satiety/dumping/emesis, mortality is 5-15%. Preferred for resections that extend into the cervical esophagus A: Free microvascular transfer (radial forearm, lateral thigh) |
|
|
Q: Five categories of early laryngeal squamous malignancy |
A: Hyperkeratosis A: Hyperkeratosis with atypia (? same as dysplasia) A: Carcinoma in-situ – chance of developing SCC with CIS or severe dysplasia ~16% if left untreated A: Superficial invasive carcinoma A: Invasive carcinoma |
|
|
Q: Identify 6 Histologic features found in Dysplasia of the oral cavity |
A: Loss of cellular Polarity A: Cellular/nuclear Pleomorphism A: Enlarged Nucleoli A: Increased Nuclear: Cytoplasmic Ratio A: Increased Mitoses/Mitotic spindling A: Presence of abnormal mitotic figures A: No penetration through the Basement Membrane |
|
|
Q: Five common subtypes of Head & Neck SCC (BAG SVP) |
A: Basaloid (poor prognosis) A: Adenosquamous A: Giant cell A: Spindle cell A: Verrucous A: Papillary |
|
|
Q: Boundaries of the Preepiglottic space |
A: Superior – hyoepiglottic ligament and vallecular mucosa A: Anterior – thyrohyoid membrane and thyroid cartillage A: Posterior – epiglottis A: Inferior – thyroepiglottic ligament A: Lateral – Paraglottic space |
|
|
Q: Boundaries of the Paraglottic space (#3 in figure below)
|
A: Lateral – thyroid cartilage (anterior) and mucosa over medial wall of pyriform fossa (posteriorly) A: Superior – (Medial) quadrangular membrane, most superior aspect is aryepiglottic folds A: Inferior – (medial) conus elasticus, (Lateral) cricothyroid membrane A: Anterior- pre-epiglottic space |
|
|
Q: Name 7 histologic barriers to laryngeal carcinoma spread
|
A: Thyroid and cricoid cartilages with overlying perichondrium A: Conus elasticus A: Quadrangular membrane A: Ventricle A: Hyoepiglottic ligament A: Thyrohyoid membrane |
|
|
Q: T Staging for Glottic carcinoma (AJCC 2010) |
A: Nodal and Staging same |
|
|
Q: Name the 6 treatment options for early glottic cancer; which one has best voice function? |
A: Radiation (best voice function, preserves normal anatomic relationships) A: Endoscopic cordectomy – cold steel, or laser A: Laryngofissure and cordectomy A: Vertical partial laryngectomy A: Hemilaryngectomy |
|
|
Q: Three contraindications for laser microlaryngeal excision of early glottic carcinoma |
1
|
|
|
Q: Four Indications for VPL/laryngoplasty in early glottis carcinoma |
A: Anterior commissure involvement A: Extension to the vocal process of the arytenoid A: Select superficial transglottic lesions?? A: Carcinoma recurring after radiotherapy |
|
|
Q: Nine Contraindications for VPL/laryngoplasty in early glottis carcinoma |
A: Fixed vocal cord A: Cartilage invasion – Thyroid or Cricoid A: Posterior commissure involvement A: Involvement of Both arytenoids A: Bulky transglottic lesions A: Lesion extending above the free edge of the false vocal cords superiorly A: More than 10 mm of subglottic extension anteriorly and 5 mm posteriorly A: More than 5 mm (1/3) of contralateral true vocal cord involvement A: Poor pulmonary reserve (FEV1/FVC <50%) |
|
|
Q: List 8 factors for treatment of glottic Ca with VPL instead of XRT |
A: Radioresistant tumors (eg verrucous carcinoma) A: Salivary gland malignancies A: Benign laryngeal tumors A: Patients deemed unreliable for 6 weeks of XRT A: Young patients (due to the theoretical increased risk of late radiation-induced sarcoma) A: Neck nodes >2 cm in size favors primary surgery for both neck and primary A: Obese A: T1 extending to anterior commissure |
|
|
Q: Most common reconstruction after VPL |
A: Bipedicled Strap muscle flap |
|
|
Q: Eight Criteria for Hemilaryngectomy for recurrent cancer after radiotherapy |
A: Mobile cord A: Lesion limited to one cord, may involve anterior commissure A: Body of arytenoid free of tumor A: Subglottic extension no more than 10mm anterior/5mm post A: The lesion must extend no higher than the lateral wall of the ventricle A: No cartilage invasion A: Recurrence correlating with initial tumor A: The entire area of pre-XRT tumor involvement must be encompassed in the resection |
|
|
Q: T staging for Supraglottic carcinoma (AJCC 2010)
|
A: Nodal and Staging same |
|
|
Q: Six Criteria for Supraglottic laryngectomy |
A: T1, T2, some T3 lesions (preepiglottic space involvement or minimal medial piriform sinus(T2) involvement) A: Mobile vocal cords A: Anterior commissure uninvolved by cancer (>5 mm) A: Thyroid cartilage uninvolved by cancer A: Surmountable nodal metastasis A: General good health |
|
|
Q: Nine Contraindications to Supraglottic laryngectomy
|
A: Vocal cord fixation (absolute contraindication) A: Bilateral arytenoids cartilage involvement (absolute contraindication) A: Involvement at the glottic level A: Tumor within 5 mm of anterior commissure A: Ventricle or pyriform apex involvement A: Thyroid or cricoid cartilage involvement A: Involvement of the tongue base to within 1 cm of the circumvallate papillae A: Poor medical condition – extreme age, poor pulmonary function A: Prior irradiation (relative) |
|
|
Q: Indications for SCPL-CHP (SCPL-CHEP for glottic Ca) |
A: T2-T3 supraglottic carcinoma A: Floor of ventricle involvement A: Anterior commissure involvement A: Impaired vocal cord or arytenoids mobility A: Preepiglottic invasion A: Paraglottic space invasion below the glottic level A: Selected T4 supraglottic carcinoma A: Transglottic glottic carcinoma?? (Not if into subglottis) A: Radiation failure for glottic and supraglottic carcinoma |
|
|
Q: Contraindications for SCPL-CHP in supraglottic carcinomas |
A: Hyoid invasion A: Massive preepiglottic space invasion with vallecula involvement A: Tongue base invasion A: Arytenoid fixation A: Subglottic extension to cricoid A: Pharyngeal or interarytenoid involvement A: Extensive thyroid cartilage invasion A: Inadequate pulmonary reserve A: Resectable by supraglottic laryngectomy |
|
|
Q: Contraindication to any organ preserving laryngeal surgery
|
A: Cricoarytenoid joint involvement |
|
|
Q: Five components of the Cricoarytenoid unit |
A: Arytenoid cartilage A: Cricoid cartilage A: Associated musculature A: Superior laryngeal nerve A: Recurrent laryngeal nerve for that unit |
|
|
Q: Staging for Subglottic carcinoma (AJCC 2010) |
A: Nodal and Staging same |
|
|
Q: Indications for hemithyroidectomy or subtotal thyroidectomy in carcinoma of the larynx/hypopharynx |
A: Palpable disease present A: Subglottic carcinoma or Glottic with greater than 1cm subglottic extension A: T4 glottic carcinoma (cartilage destruction) A: T4 pyriform sinus carcinoma 3: Positive Delphian node |
|
|
Q: Five measures in the Prevention of tracheal stomal Stenosis |
A: Tensionless anastomosis A: Cut the medial heads of the SCM A: Bevelled tracheal cuts, yet leave entire tracheal ring intact at anastomosis A: Use of a laryngectomy tracheostomal tube A: Bilaterally suture outer tracheal wall to clavicular periosteum 3: prevent Infection & radiation which predispose to stenosis |
|
|
Q: Eight Alaryngeal Communication Methods |
A: Writing A: Gesturing A: Mouthing words A: AAC computer-based program, Alphabet boards A: Buccal-Pharyngeal speech A: Artificial Laryngeal devices A: Esophageal speech A: Tracheo-Esophageal speech |
|
|
Q: Three methods of Voice post-laryngectomy |
A: Artificial Larynx – Pneumatic vs. Electronic devices = Transcervical (Electrolarynx), Transoral (Cooper-Rand), or Intraoral (Ultra Voice) A: Esophageal speech - Low fundamental frequency (65Hz), short duration (80cc air), effort to produce Injectional technique – air pushed into esophagus Inhalation technique – air inhaled (sucked) into esophagus A: Tracheoesophageal puncture – Primary (at time of resection), Secondary |
|
|
Q: Five Reasons for Alaryngeal TE speech failure |
A: Inadequate air supply – Decreased respiratory support, improper stoma occlusion A: Puncture site closure A: Prosthesis failure – Position, patency, size, type, degradation, infection A: Reflex pharyngeal constrictor spasm – Constrictors reflexively contract when dilated A: Non vibrating pharyngoesophageal segment – Postradiation, reconstructed segment |
|
|
Q: Management of Dysfluent speech |
A: Speech therapy A: Dilate or repuncture A: Use correctly sized prosthesis with ideal airflow characteristics A: Pharyngeal constrictor myotomy, neurectomy, Botox injection A: Allow edema to subside, provide external pressure |
|
|
Q: Most common cause of TEP failure after successfully establishing speech |
A: Candidal infection of prosthesis A: Premature failure of prosthesis due to valve degradation with aspiration of liquids through prosthesis A: Treatment – Nystatin oral suspension |
|
|
Q: Pearls on Tracheal tumors |
A: 75% malignant in adults, 90% benign in pediatrics A: Chondroma most common benign lesion in adults A: SCC & Adenoid Cystic most common (75%) malignant tumors; SCC 60% in males; Adenoid cystic 60% in females A: Others adenocarcinoma, chondrosarcoma, rhabdomyosarcoma, small cell, melanoma A: Gentle inhalational induction, rigid bronchoscopy, and endotracheal debridement A: Do not free more than 2 cm of trachea circumferentially if that part remaining (risk of devascularization) A: Tension-free end-to-end anastomosis with coated polyglactin suture A: Strap muscle flap for innominate artery protection A: Postop radiation for SCC & Adenoid Cystic |
|
|
Q: Three methods of palliation for a high Tracheal Adenoid Cystic carcinoma |
A: Tracheostomy A: Laser debulking A: Endoscopically inserted stent |
|
|
Q: Six tracheal lengthening techniques |
A: Blunt dissection of larynx & trachea (anterior & posterior) – 3- 5cm A: Incision of alternating annular ligaments – 2.5cm A: Suprahyoid laryngeal release – 5cm A: Infrahyoid laryngeal release (usually causes dysphagia, risk to SLNs) A: Release of inferior pulmonary ligament/hilum A: Cervical flexion suture (Grillo/Guardian stitch) A: Reanastomosis of left mainstem bronchus onto bronchus intermedius – 2.7cm 3: Airway 10-13cm long, 16-20 rings present, can excise 6.5 cm maximum |
|
|
Q: Structures of the superior orbital fissure and tendon of Zinn |
A: Optic nerve, ophthalmic artery (optic canal) A: CN III (superior & inferior divisions), CN VI, nasociliary division of V1, sympathetics to ciliary ganglion A: CN IV, lacrimal and frontal divisions of V1, superior ophthalmic vein (outside annulus of Zinn) A: D – Zygomaticofacial and zygomaticotemporal divisions of V2, inferior ophthalmic vein (outside annulus of Zinn and in inferior orbital fissure) |
|
|
Q: Three branches of V1, what these pass through, what they provide innervation to |
A: Frontal – enters the superior orbital fissure (SOF) lateral to tendon of Zinn, divides into supratrochlear and supraorbital nerves to supply forehead and scalp A: Lacrimal – enters the SOF lateral to tendon of Zinn, supplies lacrimal gland (postsynaptic autonomic efferents) and lateral eyelid A: Nasociliary – enters the SOF medial to tendon of Zinn, supplies tip of nose through external branch of anterior ethmoidal nerve, root of nose through infratrochlear nerve, corneal surface sensation |
|
|
Q: Contents of Jugular Foramen |
A: Anterior – Inferior petrosal sinus, CN IX and Jacobson’s nerve (passes through inferior tympanic canaliculus between jugular and carotid foramina A: Middle (pars nervosa) – CN X/XI A: Posterior (pars vasculara) – IJV, meningeal branches from occipital and ascending pharyngeal arteries, Nodes of Krause |
|
|
Q: Boundaries of the Infratemporal Fossa |
A: Anterior – posterior surface of the maxilla A: Superior – greater wing of the sphenoid bone, foramen ovale & spinosum A: Medial – lateral pterygoid plate, pterygomaxillary fissure A: Posterior – articular tubercle of temporal bone, sphenoid spine A: Lateral – coronoid process and ramus of the mandible A: Inferior – alveolar border of the maxilla |
|
|
Q: Borders of parapharyngeal space and its connections |
A: Superior – skull base along the sphenoid A: Inferior – greater cornu of hyoid A: Lateral – fascia covering the medial pterygoid, ramus of the mandible, and deep surface of the parotid A: Medial – buccopharyngeal fascia covering the superior constrictor A: Anterior – pterygomandibular raphe A: Posterior – carotid sheath posterolaterally, retropharyngeal space posteromedially 3: Connects to paralingual, parotid, carotid, masticator, retropharyngeal, submandibular spaces |
|
|
Q: Contents of the parapharyngeal space |
A: Styloid process, or the tensor-styloid fascia attaching the TVP to the styloid, divides space into two compartments (aponeurosis of Zuckerkandl and Testut) A: Prestyloid – Fat, deep lobe of parotid, internal maxillary artery, & branches of V3 (lingual, inferior alveolar, auriculotemporal), LNs A: Poststyloid – CN’s IX-XII, IJV, ICA, sympathetic chain |
|
|
Q: Five surgical approaches to the parapharyngeal space |
A: Transoral – seldom used, poor access A: Transfacial/transparotid – total parotidectomy performed A: Cervical parotid A: Transcervical – submandibular incision A: Transmandibular – midline mandibular osteotomy with lateral swing 3: Other possibilities may include Infratemporal fossa, or Transcervical-transmastoid approaches? |
|
|
Q: Four ancillary procedures which assist in exposing the parapharyngeal space |
A: Submandibular gland swing or excision (for transcervical) A: Separation of styloid structures (stylohyoid, styloglossus, stylopharyngeus, and stylomandibular ligament) provides access to carotid at skull base A: Separation of sphenomandibular ligament A: Disarticulation of the TMJ |
|
|
Q: Two routes of deep parotid lesions to enter the PPS |
A: Posterior to stylomandibular ligament – round shaped lesion A: Anterior to stylomandibular ligament (ie via the tunnel) – dumbbell shaped mass 3: Stylomandibular tunnel – defined by posterior border of ramus of mandible, skull base and stylomandibular ligament |
|
|
Q: Ddx of parapharyngeal space
|
A: Deep lobe parotid tumors (45%) A: Neurogenic tumors (30%) – Schwannoma, Neurofibroma, Paraganglioma A: Lymphoma (25%) A: Vascular (3%) – Hemangiopericytoma, Hemangioendothelioma, AVM, ICA aneurysm A: Minor salivary gland tumors – most frequently malignant, occasionally pleomorphic adenoma A: Other – Brachial cleft cyst, Lipoma, Teratoma |
|
|
Q: Ddx of Poststyloid parapharyngeal space tumors (8) |
A: Nerve sheath tumors A: Paraganlioma A: LN (met) A: Meningioma A: Hemangioma A: Chondrosarcoma A: Rhabdomyosarcoma A: Perineural mets A: Lymphoma 3: Prestyloid almost all salivary; look for fat plane |
|
|
Q: Discuss primary salivary gland pathologies within parapharyngeal space |
A: Most common PPS tumor (45%), seen in pre-styloid space A: Pleomorphic adenoma most common, and mucoepidermoid most common malignant A: Can be parotid or minor salivary gland (look for fat plane between parotid and tumor); either displace carotid posteriorly |
|
|
Q: Discuss primary neurogenic pathologies within parapharyngeal space |
A: Schwannoma – Most common neurogenic tumor, most common poststyloid mass; Vagus > Sympathetic chain; anterior displacement of carotid A: Paragangliomas – 2nd most common neurogenic PPS tumor, seen in poststyloid space; arise from Nodose ganglion of vagus (most common in PPS)/carotid body/inferiorly from jugular bulb, less commonly glossopharyngeal/superior or inferior laryngeal; Familial in about 10% (PGL1 gene on 11q23, can be part of MENIIA or IIB), bilateral/multiple 10%, malignancy 5%, secretory 3%; Vagal – displace carotid anteriorly; Carotid body – Lyre sign A: Neurofibroma – 3rd most common neurogenic tumor of PPS, origin = Schwann cells and perineural fibroblasts, unencapsulated/involve nerve; higher malignancy rate associated with NF Type I |
|
|
Q: List the Paraganglia of the Head and Neck, beginning with the most common sites of Paragangliomas |
A: Carotid body A: Tympanic A: Jugular bulb A: Intravagal A: Glossopharyngeal A: Superior laryngeal A: Inferior laryngeal A: Nasal A: Nasopharyngeal A: Orbital A: Subclavian A: Aortico-pulmonary A: Coronary |
|
|
Q: What are the 2 most common cranial nerves to be affected by a carotid body tumour? |
A: Vagus (X) A: Hypoglossal (XII) |
|
|
Q: Work up of paraganglioma |
A: CT A: MRI A: 24 urine collection of vanillymandelic acid and metanephrines, if positive… A: serum catecholamines A: Indium-111 pentetreotide (somatostatin/octreotide analog) or Iodide-131 metaiodobenzyl guanidine (MIBG) scan looking for multiple lesions; CT or U/S abdomen to R/O pheochromocytoma A: Angiography (and pre-op embolization) |
|
|
Q: Five reasons for Angiography in the workup of Carotid Body tumors |
A: Delineate the primary blood supply to the tumor A: Identify any collateral feeding vessels A: Evaluate the feasibility of pre-op embolization A: Evaluate for the presence of carotid involvement A: Evaluate for the presence of multifocal disease |
|
|
Q: What is the Shamblin classification of Carotid Body tumors? |
A: Type I – Not encasing the carotid A: Type II – Partially encasing the carotid A: Type III – Completely encasing the carotid |
|
|
Q: At what rate/year do these tumors tend to grow?
|
A: 1-4 mm/year 3: Study by Jansen (Cancer, 2000) showed a mean doubling time of 7 years |
|
|
Q: Three management options for Paraganglioma |
A: Observation – Small, stable, asymptomatic, elderly A: XRT/Gamma-knife-only slows progression A: Surgery – Resection in subadventitial plane +/- Vascular replacement (Saphenous, Synthetic, or STA to MCA bypass) +/- Embolization +/- Regional neck dissection if malignant |
|
|
Q: Three pros and 4 cons of radiotherapy for Paraganglioma |
A: Pros – Lower/No risk to cranial nerves Lower/No risk of stroke Most tumours will stop growing A: Cons – Risk of microvascular and carotid artery disease Risk of radiation induced malignancies May have to operate in radiated bed Risk of Osteoradionecrosis |
|
|
Q: Six steps to be done preoperatively for a secreting Carotid body tumor |
A: Type and cross match (consider autologous blood) A: ICU bed A: Balloon occlusion test A: Consult vascular surgery A: Embolization (24-48 hours before) A: Alpha and beta antagonists |
|
|
Q: Ten potential surgical complications in the resection of Carotid Body tumors |
A: Bleeding A: Hematoma A: CVA A: Injury to CN XII A: Injury to CN X A: Injury to CN VII, IX, XI A: Horner’s syndrome A: First Bite Syndrome: facial pain characterized by a severe cramping or spasm in the parotid region with the first bite of each meal that diminishes over the next several bites A: Cardiovascular collapse (secreting carotid body tumour) A: Death |
|
|
Q: Carotid body vs carotid sinus |
A: Carotid body: chemoreceptors (pH and temperature) A: Carotid sinus: baroreceptors (HR and BP) |
|
|
Q: Outline the steps in the surgical resection of Carotid Body tumors
|
A: Oblique neck incision made anterior to SCM, subplatysmal flap elevation to provide wide exposure of the carotid system A Limited selective neck dissection is performed; the IJV is retracted sampling of regional nodes for metastasis, CNXI, CNX, and CNXII identified and preserved; division of ansa cervicalis, CN XII can be retracted superiorly A: Common, external and internal carotid arteries proximal and distal to the tumour are controlled; if the external carotid is involved within the tumour, it can be sacrificed A: Subadventitial dissection in the plane of Gordon-Taylor; tumour is dissected away from the surface of the internal carotid, excessive bleeding may be avoided by ligation of the small tumour-feeding vessels on the posterior aspect of the carotid bifurcation; the tumor freed from the bifurcation is retracted superiorly to allow dissection of the superior laryngeal nerve away from the deep surface of the tumour A: If more exposure is needed superiorly, the digastrics is taken down along with the stylohyoid muscle A: If the carotid is involved with the tumour, it is sacrificed and replaced with either a venous or synthetic graft |
|
|
Q: MRI findings of parapharyngeal space tumors |
A: Pleomorphic adenoma – Low signal T1, high signal T2, displace carotid posteriorly A: Schwannoma – High signal T2, enhances with gad, displace carotid anteriorly A: Paraganglioma – Salt and Pepper appearance due to Flow Voids T1 and T2, displace carotid anteriorly |
|
|
Q: Boundaries of the pterygopalatine fossa |
A: Anterior – posterior wall of the maxilla A: Posterior – sphenoid bone, base of pterygoid process, inferior portion of anterior aspect of greater wing A: Medial – perpendicular plate of Palatine bone A: Superior – undersurface of sphenoid bone and orbital process of palatine bone, opens into inferior orbital fissure A: Lateral – Pterygomaxillary fissure |
|
|
Q: Eight openings of the pterygopalatine fossa and connections where applicable |
A: Inferior orbital fissure – Orbit A: Pterygomaxillary fissure – Infratemporal fossa A: Sphenopalatine foramen – Nose A: Foramen rotundum – Middle cranial fossa A: Pterygoid canal (Vidian N) A: Pharyngeal canal A: Greater palatine canal – Oral cavity A: Lesser palatine canal – Oral cavity |
|
|
Q: Branches of the internal maxillary artery |
A: First part (5) – lies medial to the mandible, all branches go through foramina = Anterior tympanic, Deep auricular, Middle meningeal, Accessory meningeal, Inferior alveolar A: Second part (5) – lies lateral to lateral pterygoid, all branches supply muscles = Deep temporal (anterior & posterior), Medial pterygoid branch, Lateral pterygoid branch, Massseteric artery, Buccal artery A: Third part (6) – lies within pterygomaxillary fossa = Posterior superior alveolar, Infraorbital, Descending palatine (forms greater and lesser palatine), Vidian/pterygoid canal, Pharyngeal, Sphenopalatine |
|
|
Q: Describe general principles of Osseointegration |
A: Rehabilitation of oral/maxillofacial or other head and neck defects with permanently implanted hardware, typically after resection & other therapy (chemo/RT) A: First surgery – Titanium implants placed into bone and allowed to integrate (form stable relationship) with bone A: 2nd surgery – Implants exposed and abutments placed which will connect the implant to the bone |
|
|
Q: Describe the Sisson classification of stomal recurrence |
A: Type I – Tumor involves superior ½ of the stoma without esophageal involvement A: Type II – Tumor involves superior ½ of the stoma with esophageal involvement, or the inferior ½ of the stoma A: Type III – Tumor involves the inferior ½ of the stoma and extends to the mediastinum A: Type IV – Tumor extends beneath the clavicle |
|
|
Q: Six Indications to perform a detailed metastatic workup in Head and Neck Cancer |
A: ≥4 lymph nodes metastases A: Level 4 lymph nodes metastases A: Bilateral lymph nodes metastases A: Lymph nodes metastases ≥6 cm in size A: Recurrent disease A: Second primary cancer |
|
|
Q: Likelihood of malignancy for a cystic neck mass in someone >40 years old, and top 3 differential |
A: 80% A: Thyroid cancer A: Cancer in Waldeyer’s ring (oropharynx or nasopharynx) A: Branchiogenic cancer |
|
|
Q: Six criteria to call SCC Poorly Differentiated |
A: Loss of Intercellular Bridges A: Loss of Keratinization A: Increased Number of Mitoses A: Abnormal Mitoses A: Multinucleated cells A: Nuclear and cellular Polymorphism |
|
|
Q: Discuss Field Cancerization and 2 Theories of possible explanations |
A: Premalignant changes and the propensity for second primary tumor development in the mucosal surface in the region adjacent to an invasive tumor A: Theory 1 – The areas of abnormality represent independent clones, with a unique pattern of genetic alterations A: Theory 2 – The areas of abnormality are genetically related and originate from a common cellular clone, with lateral spread of progenitor clones throughout squamous mucosal surfaces; predominant theory as per genetic studies 3: Subsequent alterations may demonstrate discordance, so the final pattern may be different. Therefore, the concept of field cancerization is likely a reflection that at least a proportion of lesions derived from lateral migration and subsequent expansion of clonally related cells develop histologic alterations surrounding the primary lesion, and ultimately lead to an increased incidence of subsequent primary tumors. |
