General Otolaryngology XXI) p53: tumor suppressor gene involved in cell cycle

regulation and apoptosis; 50-66% of HNSCC

i) Cocaine: inhibits norepi & dobutamine
reuptake, which is responsible for
contain mutations catecholamine side effects
1) Define the following terms regarding genetic transmission
XXII)p16 & p21: normal gene products suppresses cyclin ii) Prilocaine: methemoglobinemia with >600mg
I) Genotype: the genetic constitution of a locus
and cyclin-dependent kinase pathways iii) Hurricaine spray: 20% benzocaine in
II) Phenotype: the observable characteristics of an
XXIII) Cyclin D1: oncogene product accelerates polyethylene glycol base
organism controlled by a specific genetic locus
cell cycle progression
III) Allele: a particular form of a gene on each
XXIV) bcl-2: tumor oncogene, normally inhibits 12) Local anaesthetic toxicity: local effects
chromosome
apoptosis & counteracts p53 XLVIII) Faulty technique: contaminated agent,
IV) Homozygosity: two identical alleles at an autosomal
XXV) RET: proto-oncogene, a cell surface trauma
gene locus
tyrosine kinase receptor involved in signal XLIX) Reactions to local anaesthetic agent
V) Heterozygosity: two different alleles at an autosomal
transduction pathways for cell growth; associated L) Reaction to preservatives: methylparaben,
gene locus
with MEN II metabisulfite
LI) Reaction to vasoconstrictor agents (epinephrine)
2) Describe the common forms of Mendelian inheritance
7) P53 gene
VI) Autosomal dominant inheritance
XXVI) A normal gene, a tumor suppressor, 13) After 4% xylocaine topically to oral cavity wound, you
i) Gene traits are expressed in heterozygotes
normally involved in regulating cell replication and inject 2% xylo with epi. Patient becomes nervous
ii) 50% chance of passing gene to next generation
apoptosis restless, lightheaded, etc. 5 things with initial mgmt
iii) Penetrance
XXVII) Controls cell cycle by binding to cyclin- LII) CNS effects
iv) Expression
dependent kinins and arrests cell replication in G1; i) CNS stimulation: excitement, disorientation,
VII) Autosomal recessive inheritance
can induce apoptosis if DNA repair mechanisms fail rambling speech, can lead to seizures;
i) Heterozygosity implies carrier state
XXVIII) Its absence disrupts control of normal cell brainstem excitement leads to tachycardia,
ii) Disease expressed in homozygous state
replicative function, may lead to neoplastic hypertension, vomiting, sweating
iii) Chance of passing disease onto next
transformation ii) CNS depression: coma, bradycardia,
generation with two heterozygous parents is
XXIX) Located on chromosome 17p13.1 hypotension, apnea
25%; chance of offspring being carriers 50%
iii) Cardiovascular depression: bradycardia,
VIII) Sex linked inheritance
8) Name three augmented penicillins hypotension, shock
i) X-linked most common; mother passes onto
XXX) Amoxicillin-clavulanate iv) Ultimately can have cardiorespiratory arrest &
offspring 50% of time, female offspring are
XXXI) Ticarcillin-clavulanate death
carriers, male offspring homozygous for
XXXII) Ampicillin-sulbactam LIII) Initial management
disease
i) Halt procedure
9) Antibiotics which can cross the blood-brain barrier ii) Avoid giving further depressant meds
3) 5 non-Mendelian inheritance patterns
XXXIII) Flagyl iii) Give oxygen
IX) Mitochondrial inheritance: maternal mitochondria
XXXIV) Ceftriaxone iv) Have IV in place prior to procedure
inherited from ovum
XXXV) Chloramphenicol v) Maintain airway and ventilation
X) Dynamic mutation (trinucleotide repeats)
XXXVI) Ampicillin vi) Fluids/pressors prn
XI) Genetic imprinting: expression depends on parent of
origin
10) Considerations when choosing an antibiotic 14) Pharmacologic action of lidocaine, phenylephrine,
XII) Mosaicism: presence of both normal and abnormal
XXXVII) Specific diagnosis mucolytics, Hismanal, EMLA
cells within the same organism, can be somatic or
XXXVIII) Antibiotic specificity LIV) Lidocaine: blocks neuron Na channels, preventing
germline
XXXIX) Route action potential formation
XIII) Uniparental disomy: offspring inherits both copies of
XL) Side effects LV) Phenylephrine: alpha-adrenergic agonist,
a chromosome pair from a single parent
XLI) Concurrent medical conditions noncatechol sympathomimetic
XLII) Other medications LVI) Mucolytics (N-acetylcystiene): depolymerizes
4) Genes involved in cell growth & cancer
XLIII) Previous drug allergy mucopolysaccharides, making them more soluble
XIV) Protooncogene: normal cell genes that influence cell
XLIV) Cost LVII) Hismanal (H1-receptor blockers): reversible
growth in a positive way
inhibition of histamine receptors
XV) Tumor suppressor gene: encode proteins that
11) Amide vs. ester local anesthetics LVIII)Contents of EMLA: emulsified prilocaine and
normally exert negative regulatory control in a cell
XLV) Amides lidocaine, reliability increases if applied for >1hr
i) Lidocaine, bupivicaine, mepivicaine, prilocaine,
5) Oncogenes classified according to protein’s function
ropivicaine, etidocaine, dibucaine 15) Side effects of corticosteroids
XVI) Growth factor: int-2
ii) Metabolized by liver dealkylation LIX) Fluid imbalance
XVII)Growth factor receptors: erbB/neu
XLVI) Esters LX) Electrolyte disturbances
XVIII) Protein kinases: c-raf
i) Cocaine, procaine, chloroprocaine, tetracaine, LXI) Glycosuria
XIX) Signal transducers for surface growth factor
benzocaine LXII) Susceptibility to infections
receptors: ras
ii) Metabolized by plasma and liver LXIII) Hypertension
XX) Transcription regulator: myc
cholinesterases LXIV) Hyperglycemia
iii) Higher pKa cf. amides, therefore decreased LXV)Peptic ulcer disease
6) What are the most common genes involved in HNSCC?
local uptake LXVI) Osteoporosis
XLVII) Miscellaneous LXVII) Cataracts
 LXVIII) Behavioral disturbances LXXXVII) AD, reduced penetrance, variable CVI) T-dependent activation: antigen is bound, processes
LXIX) Cushingoid habitus expressivity and expressed with surface MHC II; T-cell binds to
LXX)Central obesity LXXXVIII) Sudden increase in Ca in muscle B-cell, expresses gp39 which binds to B-cell CD40
LXXI) Acne sarcoplasm; either increased release or decreased which causes cell proliferation and plasma cell
LXXII) Hirsutism reuptake from sarcoplasmic reticulum differentiation
LXXXIX) Associated with halogenated inhalational CVII)T-independent activation: inefficient, provides mainly
16) Discuss interferons anesthetics, depolarizing muscle relaxants IgM; antigens include carbohydrates from bacterial
LXXIII) Immunomodulatory, anti-inflammatory, XC) Increased BP, HR, temp; muscle rigidity capsule & cell wall
cytotoxic secretory proteins XCI) Investigations: muscle biopsy, CPK, LDH, ALP, urine
LXXIV) Broad range of effects myoglobin 26) Discuss immunoglobulins
i) Antitumor cytotoxicity XCII)Treatment: dantrolene 1mg/kg slow IV push up to CVIII) Anatomy
ii) Inhibition of cell proliferation 10mg/kg, cooling, 100% oxygen i) 2 light chains, 2 heavy chains
iii) Gene activation ii) Light chains of 2 types – kappa & lambda
iv) Modulation of cell surface antigens 21) Discuss antiemetics iii) Heavy chains of 5 types which determines
v) Immune cell activation XCIII) Emetic center in medulla (reticular class of antibody (M, G, A, D, E)
vi) Stimulation of other cytokines & immune formation); Ach & histamine receptors present CIX) IgG
modulators XCIV) Chemoreceptor trigger (CRT) zone in 4th i) 75% of total serum antibodies; 4 subtypes
LXXV) Type I interferons ventricle; dopamine receptors present ii) Crosses placenta to protect fetus
i) IFN-α produced by leukocytes, IFN-ß produced i) Phenothiazines work well, antidopaminergic iii) Can fix complement
by connective tissue cells and anticholinergic CX) IgA
ii) Produced in response to viral infection or ii) Metoclopramide is antidopaminergic i) Predominates in bodily secretions; primary
exposure to ds-RNA, significant antiviral iii) Ondansetron & granisetron: 5HT3 receptor defense against local mucosal infection
effects: decreased viral replication, increased antagonist, found on vagus in CRT zone ii) Dimeric with a secretory component bound to it
cell membrane proteins, decreased lymphocyte CXI) IgM
mitogenesis 22) Discuss expectorants i) Pentameric, predominates in early immune
LXXVI) Type II interferons XCV) Stimulates secretions in respiratory tract response
i) IFN-γ produced by T-lymphocytes in response via vagus ii) IgM & IgD main Ig’s expressed on B-cell
to antigenic stimuli; more potent XCVI) Ammonium salts, iodide salts, guaifenesin surface
immunomodulatory effect than type I CXII)IgD
interferons; 23) What are the 5 antigen presenting cells of the body? i) Found in serum, monomeric
(1) Increases expression of cell membrane XCVII) Monocyte ii) Main function unknown
antigens (including MHC I/II & Fc XCVIII) Macrophage CXIII) IgE
receptors) XCIX) Dendritic cell i) Binds to mast cells & basophils
C) Langerhans cell ii) Triggers inflammatory mediator release from
17) Side effects of interferons CI) B-cell mast cells & basophils
LXXVII) Inflammatory: fatigue, headache, nausea,
fever, chills 24) Discuss cell mediated immunity 27) Discuss complement
LXXVIII) Delayed: leukopenia, alopecia, CII) Major Histocompatibility Complex proteins CXIV) Primary humoral mediator of antigen-
neurotoxicity, polymyalgia, arthralgia, growth i) Class I: present on all cells, binds to CD8 antibody reactions
retardation ii) Class II: present on APC’s and B-cells; bind to CXV) 2 pathways of activation: classic &
LXXIX) Rare: spastic diplegia CD4 alternative
CIII) T cell subclasses CXVI) Biologic activity
18) Name 3 topical and 3 systemic decongestants i) Helper cells (TH) i) Opsonization
LXXX) Topical: phenylephrine (Dristan), (1) Binds to CD4, recognizes foreign antigen ii) Chemotaxis and cell activation by fusion of
oxymetazoline (Afrin), naphazoline, xylometazoline and class II MHC’s requires IL-1 for fragments to neutrophils & macrophages
(otrivin), tetrahydrozoline, cocaine, ephedrine, activation iii) Induces lysis through the membrane attack
propylhexedrine (2) 2 subsets: TH1 stimulates IgM, IgG and complex
LXXXI) Systemic: phenylephrine, IgA & increases CMI response; TH2 more
pseudoephedrine, phenylpropanolamine effective in stimulating antibody secretion 28) The allergic reaction at the cellular level
ii) Delayed Hypersensitivity (TDH) CXVII) Early response (~5 minutes post
19) Discuss the three belladonna derivatives (1) Class II MHC activation, requires IL-2 exposure)
LXXXII) Atropine, scopolamine, glycopyrrolate iii) Cytotoxic (TC) i) Mediated by mast cells & basophils
LXXXIII) Antimuscarinics (1) Binds to CD8, recognizes antigen (1) IgE Fc binds to mast cell, crosslinking of
LXXXIV) Scopolamine & glycopyrrolate potent expressed with Class I MHC IgE triggers activation
antisialogogues iv) Suppressor (TS) (2) Degranulation of mast cell’s preformed
LXXXV) Atropine the most vagolytic, produces mediators (histamine, heparin, tryptase,
greatest increase in HR 25) Discuss humoral immunity beta-glucosaminidase, eosinophil &
CIV) B cells bear surface receptors similar to Ig’s neutrophil chemotactic factors)
20) Discuss malignant hyperthermia CV) Do not need joint recognition of self markers and (3) Synthesis of mediators from membrane
LXXXVI) 1:15,000 children, 1:50-100,000 adults antigen like T cells bound phospholipids (PGs, LTs, PAF)
 CXVIII) Late response (~4 hours post exposure) 35) Oral hairy leukoplakia, what is the chance of getting CLXIII) Most common APUDoma
i) Mediated by neutrophils & eosinophils, reaction AIDS? 2 other oral findings in AIDS CLXIV) Found usually in ileum & bronchi, high
secondary to cytokines CXLVI) OHL due to EBV infection, chances of synchronous & metachronous rate
developing AIDS with HIV positivity within 5 years CLXV) Tumors secrete serotonin
29) Cellular effects of histamine in atopy 100% CLXVI) Symptoms: flushing, diarrhea, cardiac
CXIX) Main mediator of early allergic reaction CXLVII) Oral candidiasis, Kaposi’s sarcoma, valve disease, wheezing
CXX) Causes vasodilation herpes simplex infections CLXVII) Diagnosed by 24hr urine collection for 5-
CXXI) Increases capillary permeability HIAA
CXXII) Bronchoconstriction 36) Discuss multiple sclerosis CLXVIII) Treatment: surgery, pharmacotherapy
CXXIII) Tissue edema CXLVIII) Demyelinating disease of young adults
CXLIX) H&N manifestations: vertigo presenting 43) Describe Churg-Strauss syndrome
30) Contents of eosinophils Sx in 7-10%; nystagmus (mainly horizontal), CLXIX) Allergic granulomatosis & vasculitis
CXXIV) Major basic protein diplopia; deafness rare; bilatereal INO from MLF CLXX) Triad of asthma & allergic rhinitis,
CXXV) Peroxidase lesion suggests MS eosinophilia, systemic vasculitis of small & medium
CXXVI) Neurotoxin CL) Charcot’s triad: nystagmus, scanning speech, arteries
CXXVII) Cationic protein intention tremor CLXXI) 70% have nasal involvement (polyps,
CXXVIII) Charcot Leyden crystal protein CLI) Diagnosis made by MRI findings of demyelinated obstruction, rhinorrhea, crusting)
foci in white matter, abnormal auditory & visual CLXXII) Three phases
31) HIV stuff evoked responses, elevated CSF protein content i) Prodromal: atopy & allergic rhinitis
CXXIX) Family retroviridae ii) 2nd phase: hypereosinophilia, eosinophilic
CXXX) Strong disease correlation with CD4 37) Patient has intermittent diplopia on one side with a tissue infiltration
counts paralyzed medial rectus and unilateral nystagmus: what iii) Final phase: systemic necrotizing vasculitis
CXXXI) Clinical categories is dx and where is the lesion? INO CLXXIII) Treatment: high dose corticosteroids
i) A: asymptomatic, PGL, or acute HIV infection
ii) B: symptomatic condition attributable to HIV 38) Discuss myasthenia gravis 44) Differential diagnosis of nonneoplastic, nontraumatic
infection and associated defects in CMI, but CLII) Autoantibodies towards Ach nicotinic receptor subglottic stenosis
not in A or C CLIII) Symptoms: weakness & fatigue of striated CLXXIV) Wegener’s granulomatosis
iii) C: AIDS muscles (diplopia, dysarthria, dysphagia, ptosis) CLXXV) Amyloidosis
CXXXII) Stratification by CD4 counts CLIV) Diagnosis: history, tensilon test CLXXVI) Sarcoidosis
i) >500 cells/microliter (edrophonium), 85% will have positive anti-AchR CLXXVII) Relapsing polychondritis
ii) 200-499 cells/microliter antibodies
iii) <200 cells/microliter CLV)Treatment: pyridostigmine (Mestinon), thymectomy 45) Discuss amyloidosis
i) Acetyhcholinesterase inhibitors: edrophonium, CLXXVIII) Forms
32) Cervical disease in HIV differential diagnosis neostygmine, pryidostigmine i) Primary systemic (56%): mesenchymal organs
CXXXIII) Progressive generalized lymphadenopathy (heart, tongue, GIT)
(12-45%) 39) What’s Sluder syndrome? ii) Myeloma associated (26%)
CXXXIV) Mycobacterium tuberculosis CLVI) Sphenopalatine neuralgia: localized facial iii) Localized (9%)
CXXXV) Pneumocystiis carinii pain with vasomotor abnormalities (lacrimation, iv) Secondary systemic (8%): secondary to
CXXXVI) Lymphoma rhinorrhea, salivation) chronic destructive disease (TB, RA,
CXXXVII) Kaposi sarcoma osteomyelitis), seen in kidney, adrenals, liver,
40) Discuss pituitary anatomy spleen
33) Indications for open biopsy of lymphadenopathy in HIV CLVII) Boundaries CLXXIX) Pathology
CXXXVIII) FNA that suggests malignancy i) Superior: diaphragam sellae & optic chiasm i) Light microscopy
CXXXIX) FNA negative for malignancy with any of: ii) Anterior/inferior: sphenoid sinus (1) Primary & myeloma: light chain Ig
i) Enlarging node iii) Lateral: cavernous sinuses (2) Secondary: Amyloid associated protein
ii) Asymmetric, localized, unilateral adenopathy CLVIII) Components ii) Biopsy: apple green birefringence with Congo
iii) Nodes >2cm i) Neurohypophysis (posterior): axons of cell Red staining, reversal with potassium
iv) Low CD4 with new lymphadenopathy bodies from supraoptic & paraventricular nuclei permanganate infers secondary amyloid
v) Fever, night sweats, weight loss of hypothalamus; secretes oxytocin & ADH CLXXX) Clinical
vi) Significant mediastinal or abdominal ii) Adenohypophysis (anterior): derived from i) Primary: Tongue most commonly involved
lymphadenopathy Rathke’s pouch (ectoderm); secretes ACTH, ii) Localized: orbit most commonly involved
GH, PRL, FSH/LH, TSH iii) Larynx most common site of deposition in the
34) CD4 counts associated with pathology respiratory tract, trachea next; supraglottis
CXL) NHL: <200 41) Classification of pituitary adenomas involved most often, then glottis
CXLI) KS: <100 CLIX) Class I: microadenoma (<10mm) CLXXXI) Treatment
CXLII) Hodgkin’s: wide range of CD4 CLX) Class II: macroadenoma (>10mm) i) Conservative removal of deposits
CXLIII) Sinonasal lymphoma (HNL): <200 CLXI) Class III: partial destruction of sellar floor ii) Steroids, antimetabolites not helpful
CXLIV) Fungal sinusitis: <150; Aspergillus <50 CLXII) Class IV: total destruction of sellar floor
CXLV) Cryptococcal meningitis: <100 46) H&N manifestations of SLE
42) Describe carcinoid syndrome CLXXXII) Symptoms
 i) Malar rash (50%) ii)Requires tissue diagnosis, most commonly a bodies (cytoplasmic inclusions) within the histiocyte
ii) Painful oral mucosal ulcers nasal biopsy are pathognomonic; CD1 antigen present
iii) Telangiectasias CXCVII) Treatment: CCXIII) Classification
iv) Septal ulceration/perforation (3-5%) i) Prednisone 1mg/kg/day x 4 weeks then taper i) Eosinophilic granuloma
v) Laryngeal/tracheal: true vocal cord ii) Cyclophosphamide 2mg/kg/day for 6-12 (1) Benign chronic course, monoostotic or
thickening/paralysis, cricoarytenoid arthritis, months; if hemorrhagic cystitis occurs may use polyostotic, favors frontal & temporal
subglottic stenosis methotrexate or azathioprine bones; other sites femur, pelvis,
vi) Acute parotid enlargement (10%) iii) Septra vertebrae, ribs
vii) Chronic xerostomia iv) IVIg in immunosuppresion nonresponders (2) Treatment: surgical excision or radiation
viii) Cranial neuropathy (15%) ii) Hand-Schuller-Christian disease
CLXXXIII) Treatment: NSAIDs, antimalarials, 50) 4 histologic findings in Wegener’s (1) More severe chronic disseminated form
glucocorticoids; azathioprine & cyclophosphamide CXCVIII) Small & medium vessel vasculitis (2) Classic triad in 10%: diabetes insipidus,
for resistant cases CXCIX) Fibrinous necrosis exophthalmos, skull lesions
CC) Necrotizing granulomas (3) Treatment: radiation, surgery,
47) H&N manifestations of rheumatoid arthritis CCI) Mixed plasma cell, lymphocyte, histiocyte and chemotherapy, or combination
CLXXXIV) TMJ dysfunction: pain/tender joint or macrophage infiltration (4) 30% overall mortality
overlying muscles iii) Letterer-Siwe disease
CLXXXV) CA joint involvement (86%), findings 51) Describe Sjogren’s syndrome (1) Disseminated and rapidly progressive;
include: CCII) Triad of keratoconjunctivitis, xerostomia, affects patients under 3 years of age
i) Acute inflammation/edema over arytenoids association with other autoimmune disease; altered (2) Symptoms: fever, proptosis, adenopathy,
ii) Decreased mobility & fixed fold in adducted taste, intermittent unilateral/bilateral SG hepatosplenomegaly, multiple bone
position enlargement; absence of A/I disease with other two lesions, anemia, thrombocytopenia,
iii) Arytenoid process tenderness on palpation symptoms known as sicca complex exfoliative dermatitis
iv) Rheumatoid nodule deposition into cords CCIII) Diagnosis (4/6) (3) High mortality rate
v) Subluxed CA joint on CT can be seen i) Ocular symptoms
CLXXXVI) Ossicular: tympanometric alterations ii) Oral symptoms 55) Describe the four stages of rhinoscleroma
CLXXXVII) Cervical pain, decreased ROM iii) Ocular signs (Schirmer test) CCXIV) A chronic granulomatous disease of the
iv) Oral signs nose caused by Klebsiella rhinoscleromatis
48) Behcet’s syndrome v) Minor salivary gland biopsy (lip, septum, hard CCXV) Hallmark histologic sign: Mikulicz cells,
CLXXXVIII) Relapsing/remitting A/I disease triad palate), examine focus score, positive if 1 or large foamy histiocytes; Russell bodies
CLXXXIX) Ulcerations of orogenital mucus more in a 4mm2 field CCXVI) Stages
membranes, painful punched out lesions; typically (1) Focus: 50+ lymphocytes, histiocytes or i) Catarrhal: foul smelling purulent rhinorrhea for
first symptom plasma cells weeks/months
CXC) Iritis/uveitis occurs in 43-72% of patients, vi) Blood tests ii) Atrophic: large foul crusts/plaques simulating
loss of sight in 25% (1) Primary Sjogren’s: SS-A/Ro 60%, SS- those of atrophic rhinitis
CXCI) Progressive SNHL B/La 30%, HLA-DW3, HLA-B8 iii) Granulomatous: large granulomas of URT
CXCII) Treatment: corticosteroid cream for (2) Secondary Sjogren’s: HLA-DW4 iv) Fibrosis: up to complete stenosis of nares, can
ulcers, mydriatics and corticosteroid drops for eyes (3) Other factors (RF, ANA, etc) extend to NP and trachea
CCIV) Radiology (sialography): punctate to CCXVII) Treatment: debridement; long term
49) Discuss Wegener’s granulomatosis globular contrast collections, progresses to complete streptomycin plus tetracycline
CXCIII) Idiopathic A/I disease, a triad of gland destruction
upper/lower airway necrotizing granulomas, systemic CCV) Treatment symptomatic 56) Describe cat scratch disease
vasculitis, focal glomerulonephritis CCXVIII) Caused by Rochalimaea henselae, an
CXCIV) Pulmonary involvement >95%, renal 52) Histopathology of Sjogren’s syndrome intracellular pleomorphic gram-negative bacillus
involvement >85% CCVI) Lymphocyte & histiocyte infiltration seen on Warthin Starry silver staining
CXCV) H&N symptoms CCVII) Acinar atrophy CCXIX) Diagnosis
i) Nasal (90%): crusting, epistaxis, obstruction, CCVIII) Ductal epithelial hyperplasia & metaplasia i) History of cat exposure
septal perforation, saddle nose CCIX) Prominence of myoepithelial components ii) Presence of inoculation site
ii) Otologic (25%): CHL, suppurative OM, SNHL as ductal lumens disappear iii) Regional adenopathy
(can be bilateral & profound) iv) Histologic features on excisional biopsy
iii) Orolaryngeal: gingival hyperplasia & gingivitis, 53) Langerhan’s cells (suppurative & necrotic granulomatous
laryngeal ulceration & edema (25%), subglottic CCX) Macrophage that normally resides in the lymphadenitis)
stenosis (8.5%) epidermis of skin v) Bacteria seen on silver staining
CXCVI) Diagnosis: clinical, pathologic, lab CCXX) Treatment: supportive
findings 54) Histiocytosis X
i) Lab: anemia, increased ESR, CRP, c-ANCA CCXI) Involves temporal bone in 20-60% of 57) A patient has a firm neck mass after dental surgery. FNA
(specificity 90% in systemic vasculitis stage, cases; 25% present with initial otologic symptoms shows sulfur granules. What is this, how do you treat it?
65% in granulomatous phase, 30% in CCXII) Birbeck granules (laminar rod-shaped CCXXI) Actinomyces species
remission patients) organelles within the nuclear cytoplasm) and X
 CCXXII) Clinical: palpable mass most common CCXXXV) Cytokines: polypeptide signal proteins that ii) Cryotherapy
H&N manifestation, 61% have visible sinus tracts, modulate cell function (proliferation, differentiation, iii) Radiotherapy
40% have lymphadenopathy regeneration, wound healing) iv) Laser therapy
i) Often have concurrent dental, sinus or CCXXXVI) Mechanism of action v) Elastic compression
perimandibular disease i) Autocrine: secreted by cells which are vi) Silicone gel sheeting
CCXXIII) Histologic characteristics of modulated by it
Actinomycosis ii) Paracrine: secreted by cells which modulate 66) Wavelengths of lasers
i) Multifilamented, anaerobic gram-positive rods neighboring cell populations CCLIV) Argon 514nm
ii) Sulfur granules (collections of Actinomyces iii) Endocrine: secreted by one population of cells CCLV) KTP 532nm
organisms) with distant effects CCLVI) Flash lamp pumped dye laser (tunable
iii) Granuloma formation CCXXXVII) Categories yellow) 577nm
CCXXIV) Treatment: surgical debridement, i) Angiogenic growth factors: TGF, EGF, PDGF, CCLVII) Argon tunable dye laser (tunable red) 633
penicillin G IV for 2-6 weeks; tetracycline or FGF nm
erythromycin if pen allergic ii) Bone morphogenetic protein CCLVIII) ND:YAG 1064nm
CCLIX) CO2 10600nm
58) Kawasaki disease: 5 investigations, 2 therapies 61) What are the effects of radiation on tissue healing?
CCXXV) Acute febrile illness of childhood, most CCXXXVIII) Acute: severity related to the radiation 67) Describe the qualities of laser light that differentiate it from
common cause of acquired heard disease in fraction; reduction in fibroblast, myofibroblast, radiant light
children endothelial cell proliferation CCLX) Monochromatic: radiant energy emitted all
CCXXVI) Small vessel vasculitis, usually presents CCXXXIX) Intermediate: 3-6 months after radiation, of one wavelength
<5 years of age diminished endothelial & connective tissue CCLXI) Collimated: extremely intense and
CCXXVII) Symptoms: fever, conjunctivitis, oral proliferation unidirectional
ulcers & erythema, erythematous desquamative rash CCXL) Late: related to total radiation dosage; CCLXII) Coherence
of palms & soles, nonsuppurative cervical hyalinization of collagen, rupture of elastic fibrils, i) Temporal: waves oscillate in phase over a given
adenopathy > 1.5cm fibrinous exudate deposition, induction of atypical time
CCXXVIII) 7-20% develop coronary artery aneurysms fibroblasts, hyalinization & sclerosis of blood vessels ii) Spatial: photons equal & parallel along
& have MIs within 2-12 weeks of disease onset wavefront
CCXXIX) Investigations 62) Three effects of steroids on wound healing CCLXIII) Intense
i) CBCD, lytes/BUN/creat CCXLI) Decreased leukocyte & monocyte
ii) Acute phase reactants: ESR, etc. migration & phagocytosis 68) Variables that can be controlled with laser
iii) CXR CCXLII) Inhibition of keratinocyte & fibroblast CCLXIV) Power
iv) Echocardiogram (pericardial effusion, coronary mitosis (slows reepithelialization) CCLXV) Spot size
artery dilation) CCXLIII) Vasoconstriction, results in decreased CCLXVI) Exposure time
v) Abdominal ultrasound (acalculous oxygen & nutrient delivery
cholecystitis) 69) Tissue effects of lasers
CCXXX) Therapy 63) Factors in nutrition that most influence wound healing CCLXVII) Absorption
i) Immunoglobulin CCXLIV) Vitamin A: deficiency causes impaired CCLXVIII) Reflection
ii) Aspirin collagen synthesis & epithelialization CCLXIX) Scattering
CCXLV) Vitamin C: deficiency prevents CCLXX) Transmission
59) Describe the 4 phases of wound healing hydroxylation of proline & lysine
CCXXXI) Coagulation: hemorrhage with exposure of CCXLVI) Zinc: deficiency retards wound healing by 70) Characteristics of the argon, Nd:YAG, CO2 lasers
platelets; formation of platelet plug & degranulation, preventing cell proliferation CCLXXI) Argon
release of mediators that cause vasoconstriction and CCXLVII) Magnesium i) Transmits through clear fluids (eg. vitreous)
chemotaxis CCXLVIII) Arginine ii) Absorbed by Hgb, thus good for pigmented
CCXXXII) Inflammation: infiltration of leukocytes lesions
which scavenge cellular debris, foreign bodies and 64) Three phases of skin graft survival iii) KTP has similar frequency & efficacy
other byproducts; PMNs in first 48 hrs, then CCXLIX) Imbibition: absorption of nutrients from iv) Fiberoptic use
transition to monocyte/macrophages underlying recipient bed CCLXXII) Nd:YAG
CCXXXIII) Fibroplasia: fibroblasts attracted to wound CCL) Inosculation: growth of graft’s blood i) Transmits through clear fluids (eg. can be used
and start extensive collagen synthesis; new capillary vessels to meet preexisting blood vessels of in the bladder)
growth into matrix via angiogenesis recipient bed ii) Deep zone of coagulation (~4mm)
CCXXXIV) Remodelling: inflammation subsides, CCLI) Neovascularization: new blood vessels iii) Fiberoptics
angiogenesis decreases, fibroplasia slows; dynamic form & bridge graft to underlying tissues CCLXXIII) Carbon dioxide
balance reached between collagen synthesis and i) Energy strongly absorbed by water
lysis; over time scar achieves 80% of original 65) Treatment of keloids independent of tissue color
strength CCLII) Keloid: overgrowth of dense fibrous scar ii) Minimal thermal effect on surrounding tissues
that extends beyond the borders of the original skin iii) Disadvantage: cannot pass through fiberoptics
60) Discuss cytokines, their mechanism of action, and types injury
CCLIII) Techniques 71) 8 things to do with a tube fire during laser laryngoscopy?
i) Intralesional steroids CCLXXIV) Stop using laser
 CCLXXV) Turn off the flow of oxygen CCCV) Lasts days to weeks (5) Calcium channel blockers
CCLXXVI) Have saline available to put out the fire CCCVI) Treatment
CCLXXVII) Remove damaged tube i) Somatic therapy: exercise, biofeedback 81) Discuss cluster headache
CCLXXVIII) Reintubate with patient paralyzed to ii) Medications: NSAID’s, acetaminophen, NSAID CCCXXX) Symptoms
facilitate reintubation combinations i) Explosive onset of unilateral
CCLXXIX) Intravenous steroids and antibiotics iii) Preventive: antidepressants, muscle relaxant, periorbital/retroorbital pain, constant with
CCLXXX) Intraoperative bronchoscopy to remove NSAIDs boring/burning quality, lasts 15-180 minutes
any charred debris and assess extent of damage ii) Lacks nausea/vomiting features
CCLXXXI) Delayed extubation, reexamination of 77) Common features of migraine headache iii) Associated autonomic symptoms: nasal
subglottis and trachea to assess extent of further CCCVII) Recurrent attacks of moderate to severe stuffiness, lacrimation, conjunctival injection
airway compromise throbbing pain iv) Strong male predominance
CCCVIII) Sudden onset and limited duration, CCCXXXI) Treatment
72) 4 types of presbycusis, name and mechanism unilateral i) Prophylactic
CCLXXXII) Sensory: atrophy of Organ of Corti, initially CCCIX) Associated symptoms common: (1) Calcium channel blockers
at basal turn; high frequency loss, SDS related to photophobia, phonophobia, nausea & vomiting (2) Ergotamine
frequency range affected CCCX) Strong female predominance (3) Lithium
CCLXXXIII) Neural: atrophy of spiral ganglion cells CCCXI) Family history common (4) Methylsergide
and nerves of spiral lamina; affects all turns of (5) Valproic acid
cochlea, all frequencies, severe discrimination loss 78) Precipitating factors in migraine (6) Antihistamines
CCLXXXIV) Strial/metabolic: atrophy of stria CCCXII) Stress (7) Ranitidine
vascularis, initially at apex of cochlea, flat sensory CCCXIII) Letdown period after stress ii) Acute therapy
loss affecting all frequencies, minimal discrimination CCCXIV) Menses (1) Sumatriptan
loss CCCXV) Pregnancy & OCP (2) Intranasal lidocaine
CCLXXXV) Cochlear conductive: stiffness of basilar CCCXVI) Head & neck infection (3) Oxygen
membrane, affects all turns of the cochlea, high tone CCCXVII) Head trauma/surgery
gradual loss, discrimination related to steepness of CCCXVIII) Dairy products, red wine, nuts, shellfish, 82) Trigeminal neuralgia: symptoms, treatment
slope caffeine withdrawl CCCXXXII) Repeated brief attacks of severe, sharp,
CCCXIX) Vasodilating medications jabbing or lancinating unilateral facial pain, 5-7th
73) 4 clinical laryngeal findings in presbylaryngeus CCCXX) Perfumes, strong odors decades
CCLXXXVI) Yellow/dark gray discoloration of vocal fold CCCXXI) Irregular diet or sleep CCCXXXIII) Typically in mandibular trigeminal division,
CCLXXXVII) Laryngeal edema CCCXXII) Bright sunlight, flickering lights followed by maxillary division; trigger points common
CCLXXXVIII) Vocal fold atrophy; leads to vocal cord CCCXXXIV) No association with facial
bowing and incomplete glottic closure 79) Components of migraine aura numbness/weakness, loss of corneal reflex, change
CCLXXXIX) Arrowhead configuration of glottis CCCXXIII) Scotomata in taste or smell, or other CN impairment
CCCXXIV) Fortification spectra CCCXXXV) Diagnosis
74) Differential diagnosis of early morning headache CCCXXV) Photopsia (flashing lights) i) MRI with contrast
CCXC) OSA CCCXXVI) Paresthesias ii) LP for patients with negative MRI or other
CCXCI) Cluster headache symptoms
CCXCII) Diabetes mellitus 80) Management of migraine CCCXXXVI) Treatment
CCXCIII) Glaucoma CCCXXVII) Abortive medications i) Medical
CCXCIV) Sinusitis i) Sumatriptan (1) Carbamazepine
CCXCV) Bruxism in TMJ syndrome ii) Ergotamine (2) Gabapentin
CCXCVI) Cervical spondylosis iii) Dihydroergotamine (3) Baclofen
iv) Butorphanol (4) Phenytoin
75) Differential diagnosis of headache v) Midring (5) Sodium valproate
CCXCVII) Tension-type vi) NSAIDs ii) Surgical
CCXCVIII) Migraine vii) Lidocaine (1) Percutaneous rhizotomy
i) With aura CCCXXVIII) Acute therapy
ii) Without aura i) Prochlorpeazine 83) Name the 5 main branches of the extratemporal facial
CCXCIX) Cluster ii) Dihydroergotamine nerve
iii) Chlorpromazine CCCXXXVII) Temporal
76) Common features of tension-type headache iv) Haloperidol CCCXXXVIII) Zygomatic
CCC) Bilateral continuous nonpulsatile CCCXXIX) Prevention CCCXXXIX) Buccal
headache i) Lifestyle modification to avoid triggers CCCXL) Marginal mandibular
CCCI) Stress related ii) Prophylaxis in patients with >2 CCCXLI) Cervical
CCCII) Rare associated symptoms migraines/month
(nausea/vomiting) (1) Antidepressants 84) Physiology of saliva
CCCIII) Can continue ADL’s with headache (2) Ergotamines CCCXLII) Functions
CCCIV) Associated with or precipitated by (3) Nonsteroidals i) Lubricate and moisten food
physical or psychological stress (4) Beta-blockers
 ii) Protect mucosa from dessication & chemical 88) Indications & contraindications for sialography CCCLXXI) Echovirus
irritation CCCLIII) Indications CCCLXXII) Influenza
iii) Prevention of caries via supply of inorganic ions i) Suspicion of chronic, recurrent or nonspecific
(calcium, fluoride, phosphate, magnesium) sialoadenitis 95) Describe Heerfordt’s disease (uveoparotid fever)
iv) Antibacterial properties ii) Autoimmune disease: Sjogren’s, Mikulicz’s CCCLXXIII) A variant of sarcoidosis, seen in 3-4th
(1) Secretory IgA syndromes decades
(2) Lactoferrin iii) Sialolithiasis CCCLXXIV) Prodrome of fever, malaise, weakness,
(3) Lysozyme iv) Postop or posttraumatic fistula/stricture/cyst nausea, night sweats
(4) Salivary peroxidase CCCLIV) Contraindications CCCLXXV) Parotitis, uveitis, CN paralysis in 5% of
CCCXLIII) Salivary flow i) Iodine allergy patients (CN VII in 50% of those with paralysis)
i) 24h volume of saliva secretion 1-1.5l ii) Acute sialoadenitis CCCLXXVI) Diagnosis confirmed with high ACE level
ii) Submandibular glands responsible for majority CCCLXXVII) Treatment is corticosteroids; if
of nonstimulated salivary flow (71% in 24 hour 89) Findings for chronic inflammation on sialography nonresponsive, use methotrexate or azathioprine
period) CCCLV) Saccular dilatation of terminal ducts/acini
iii) Stimulated salivary flow: parotid supplies ~66% CCCLVI) Segmental strictures & dilatation 96) Differential diagnosis of sialosis/sialoadenosis (recurrent
of total stimulated flow; overall supplies ~25% CCCLVII) Pseudocyst formation bilateral nontender parotid swelling)
of total 24 hour flow) CCCLXXVIII) Endocrine: diabetes mellitus most
iv) Parotid saliva serous; sublingual gland 90) El Deeb’s predisposing factors for submandibular gland common; ovarian, thyroid, pancreatic insufficiency
mucinous, submandibular gland produces a calculi formation CCCLXXIX) Dystrophic-metabolic: cirrhosis,
mixed serous/mucinous saliva CCCLVIII) Submandibular saliva alcoholism, malnutrition (kwashiorkor, beriberi),
i) High mucin content anorexia
85) 3 muscles originating off the styloid and their ii) Alkaline pH CCCLXXX) Drugs: phenothiazine, isoproterenol,
innervations? iii) Higher percentage of organic matter ethambutol, iodinated compounds, heavy metals
CCCXLIV) Styloglossus (XII) iv) Concentration of calcium & phosphate salts CCCLXXXI) TB
CCCXLV) Stylopharyngeus (IX) v) Low carbon dioxide level CCCLXXXII) Sarcoidosis
CCCXLVI) Stylohyoid (VII) vi) High phosphatase enzyme content
CCCLIX) Anatomy 97) Histologic findings of sialoadenosis
86) Autonomic innervation of the major salivary glands i) Length & irregular course of Wharton’s duct CCCLXXXIII) Acinar hypertrophy, fatty infiltration, or
CCCXLVII) Parasympathetics ii) Dependent position of gland & duct system combination
i) Mediates overall secretion of saliva iii) Position of ductal orifice
ii) Parotid gland iv) Size of orifice smaller than duct lumen 98) Differential diagnosis of recurrent parotid swelling
(1) Nucleus: inferior salivatory CCCLXXXIV) Autoimmune
(2) Preganglionics: CN IX, Jacobsen’s nerve, 91) Why is the parotid gland more susceptible to infection? i) Mikulicz’s disease
lesser superficial petrosal nerve CCCLX) Serous secretions less bacteriostatic than ii) Primary Sjogren’s
(3) Ganglion: otic mucinous secretions, which contain glycoprotein & iii) Secondary Sjogren’s
(4) Postganglionics: auriculotemporal nerve sialic acid that can aggregate bacteria; also contains CCCLXXXV) Nonautoimmune (Mikulicz’s syndrome)
(V3) lysozymes & secretory IgA i) Recurrent sialoadenitis
iii) Submandibular & sublingual glands ii) Sialosis
(1) Nucleus: superior salivatory 92) What is the most common cause of parotid enlargement? iii) Multinodular gland
(2) Preganglionics: nervus intermedius, CCCLXI) Mumps virus – most common viral
chorda tympani disorder of the salivary gland 99) Differential diagnosis of salivary gland cysts
(3) Ganglion: submandibular CCCLXII) Peak incidence 4-6 years, either unilateral CCCLXXXVI) Congenital
(4) Postganglionics: lingual nerve (V3) or bilateral i) Branchial cleft
CCCXLVIII) Sympathetics CCCLXIII) Symptoms: fever, malaise, myalgia, ii) Epidermoid
i) Modulates composition of saliva headache iii) Dermoid
ii) Nucleus: sympathetic chain T1-5 CCCLXIV) Diagnosis: antibodies to hemagluttinin, CCCLXXXVII) Acquired
iii) Preganglionics: sympathetic chain mumps S&V antigens; virus isolation from urine i) Benign lymphoepithelial lesion (AIDS
iv) Ganglion: superior cervical CCCLXV) Complications: uncommon – SSNHL, associated)
v) Postganglionics: run with blood vessels pancreatitis, meningitis, orchitis ii) Mucus retention cyst/mucocele
supplying the glands iii) Sialocele (pseudocyst), associated with trauma
(1) Parotid: external carotid artery 93) Organisms found in acute sialoadenitis
(2) Submandibular: facial artery CCCLXVI) Aerobes: S. aureus, S. pneumoniae, E. 100) Attachments of the pharyngeal constrictor muscles
(3) Sublingual: lingual artery coli, H. influenzae CCCLXXXVIII) All three muscles insert with the
CCCLXVII) Anaerobes: B. melaninogenicus, Strep. corresponding opposite muscle in the midline at the
87) Muscles innervated by marginal mandibular nerve micros pharyngeal raphe
CCCXLIX) Depressor anguli oris CCCLXXXIX) Superior constrictor: Suspended from
CCCL) Depressor labii inferioris 94) Viral causes of sialoadenitis base of skull, medial pterygoid plate,
CCCLI) Orbicularis oris CCCLXVIII) Mumps pterygomandibular raphe, mylohyoid line, lateral
CCCLII) Mentalis CCCLXIX) CMV tongue
CCCLXX) Coxsackie A
 CCCXC) Middle constrictor: hyoid bone, stylohyoid
ligament 108) 4 methods of voluntary control of swallowing 114) Name the four muscles controlling laryngeal elevation
CCCXCI) Inferior constrictor: thyroid & cricoid CDXXVII) Supraglottic swallow: a swallow followed CDXLVI) Digastric (both anterior & posterior bellies)
cartilages by a cough & 2nd swallow before inspiration CDXLVII) Mylohyoid
CDXXVIII) Supra-supraglottic swallow (closure of the CDXLVIII) Geniohyoid
101) Boundaries of the oropharynx entrance to the airway) CDXLIX) Stylohyoid
CCCXCII) Superior: plane through the hard palate CDXXIX) Mendelsohn maneuver: voluntary
CCCXCIII) Inferior: plane through the hyoid elevation of the larynx 115) 2 motor and 2 sensory innervations of the larynx?
CDXXX) Effortful swallow: muscle effort used CDL) Sensory: internal laryngeal branch of SLN
102) Name the four stages of swallowing during oral & pharyngeal phases (supraglottis & glottis), RLN (glottis & subglottis)
CCCXCIV) Oral preparatory CDLI) Motor: external laryngeal branch of SLN
CCCXCV) Oral phase 109) 5 postural effects on swallowing (cricothyroid), RLN (all other intrinsics)
CCCXCVI) Pharyngeal phase CDXXXI) Head rotation to one side closes off that
CCCXCVII) Esophageal phase pyriform sinus to the bolus 116) What five conditions must be met for normal phonation to
CDXXXII) Chin tucking brings anterior wall of occur?
103) Name the six sphincters regulating normal swallowing pharynx posterior, airway entrance narrowed CDLII) Adequate breath support
CCCXCVIII) Lips/oral commissure CDXXXIII) Head tilt to one side directs food down CDLIII) Approximation of the vocal folds
CCCXCIX) The tongue that side of the oral cavity & pharynx CDLIV) Favorable vibratory properties
CD) Soft palate closure with the tongue base CDXXXIV) Lifting chin decreases oral transit time via CDLV) Favorable vocal fold shape
(palatoglossus) gravity CDLVI) Control of length and tension
CDI) Velopharynx CDXXXV) Supine position causes residue to stick to
CDII) Larynx (true cords first, false cords next, pharyngeal walls rather than fall down airway 117) Describe the cover-body theory (Fujimura) and the
then epiglottis & aryepiglottic folds) corresponding vocal cord layers
CDIII) Cricopharyngeus (upper esophageal 110) 5 levels of vocal cord CDLVII) Cover: mucosa (nonkeratinized stratified
sphincter) CDXXXVI) Mucosal layer (nonkeratinized stratified squamous epithelium) and superficial lamina propria
squamous epithelium) (Reinke’s space)
104) Name the four taste bud types CDXXXVII) Lamina propria CDLVIII) Transition: middle & deep layers of lamina
CDIV) Filiform: nonsensory i) Superficial layer (Reinke’s space): fibroblasts, propria
CDV) Fungiform: CN VII scant elastic and collagen fibers CDLIX) Body: vocalis muscle
CDVI) Foliate: CN IX ii) Intermediate layer: mainly elastic fibers, few
CDVII) Circumvallate: CN IX fibroblasts 118) Primary functions of the larynx
iii) Deep layer: collagenous fibers CDLX) Airway protection
105) 4 sensory nerves that supply tongue CDXXXVIII) Vocalis muscle CDLXI) Respiration
CDVIII) Lingual nerve CDLXII) Phonation
CDIX) Facial nerve (chorda tympani) 111) 6 intrinsic muscles of larynx
CDX) Glossopharyngeal nerve CDXXXIX) With quadrangular membrane 119) What is the three (or four) component processes of
CDXI) Vagus nerve i) Thyroepiglottic speech?
ii) Thyroarytenoid (vocalis) CDLXIII) Generator: lungs produce airflow through
106) Pathway of afferent taste fibers from the oral tongue iii) Aryepiglottic URTI
CDXII) Lingual nerve CDXL) With conus elasticus CDLXIV) Phonation: sound production by the vocal
CDXIII) Chorda tympani i) Interartyenoid cords
CDXIV) CN VII ii) Lateral cricoarytenoid CDLXV) Resonance: modulation of phonatory
CDXV) Geniculate ganglion (cell bodies present iii) Posterior cricoarytenoid output by vibration in the chest, pharynx and head
anteriorly) CDXLI) Cricothyroid (disputed) with selective amplification of certain component
CDXVI) Nervus intermedius frequencies
CDXVII) Nucleus tractus solitarius (pons) 112) Superior laryngeal innervation CDLXVI) Articulation: formation of consonants &
CDXVIII) Ventroposteromedial nucleus of the CDXLII) Internal branch: sensory, enters larynx vowels, controlled by lips, tongue, palate, pharynx
thalamus with superior laryngeal artery off of superior thyroid
CDXIX) Cortex: operculum & anterodorsal insula artery through thyrohyoid membrane, supplies false 120) Name the subtypes of lichen planus
cord, pyriform sinus, epiglottis CDLXVII) Plaque
107) Events that occur during the pharyngeal phase of CDXLIII) External branch: motor, supplies CDLXVIII) Atrophic: 1-5% malignancy rate
swallowing cricothyroid CDLXIX) Bullous
CDXX) Breathing cessation CDLXX) Erosive: 1-5% malignancy rate
CDXXI) Palate elevation, closure of 113) What muscles are the main abductor & adductors of the CDLXXI) Reticular
nasopharyngeal isthmus vocal cord? CDLXXII) Lichenoid dysplasia: precancerous lesion
CDXXII) Glottic closure CDXLIV) Abductor: posterior cricoarytenoid,
CDXXIII) Laryngeal elevation supplied by the adductor branch of the recurrent 121) Differential diagnosis of oral cavity vesiculobullous lesions
CDXXIV) Pharyngeal peristalsis laryngeal nerve CDLXXIII) Lupus (DLE > SCLE > SLE)
CDXXV) Cricopharyngeal relaxation CDXLV) 3 intrinsic adductors of larynx: lateral CDLXXIV) HSV stomatitis (primary, secondary)
CDXXVI) Dilation of pharyngoesophageal segment crico-arytenoid, thyroarytenoid/vocalis, interarytenoid CDLXXV) VZV stomatitis (primary, secondary)
 CDLXXVI) Cicatricial pemphigoid (mucosal DIII) Mucosa DXXXIII) Microaerophilic Streptococcus
involvement > cutaneous involvement overall) DIV) Pharyngobasilar fascia DXXXIV) Peptostreptococcus
CDLXXVII) Bullous pemphigoid (cutaneous DV) Buccinator muscle DXXXV) Bacteroides
involvement > mucosal involvement overall) DVI) Buccopharyngeal fascia DXXXVI) Veionella
CDLXXVIII) Pemphigus vulgaris DVII)Buccinator fat pad DXXXVII) Eubacterium
CDLXXIX) Erythema multiforme DVIII) Masseter muscle DXXXVIII) Fusobacterium
CDLXXX) Lichen planus (erosive or bullous form) DIX) SMAS/muscles of facial expression
DX) Subcutaneous tissue 135) Posterior neck spaces
122) Most common drugs associated with toxic epidermal DXI) Skin DXXXIX) Retropharyngeal space: found between
necrolysis visceral layer of deep fascia and alar layer of deep
CDLXXXI) Sulfonamides 128) Describe the canine space fascia; descends to mediastinum at level of carina
CDLXXXII) Barbiturates DXII)Potential space between infraorbital & zygomatic DXL) Danger space: found between alar layer
CDLXXXIII) Phenytoin heads of quadratus labii superior, and this and the and prevertebral layers of deep fascia; descends to
CDLXXXIV) Allopurinol caninus muscle diaphragm
DXIII) Secondary to bicuspid infection DXLI) Prevertebral space: found posterior to
123) 5 syndromes with congenital neurofibromas or fibromas of DXIV) Treatment: dental extraction/root canal, prevertebral fascia, descends to sacrum
tongue and jaw dependent drainage
CDLXXXV) Von Recklinghausen’s disease 136) Pathways of spread to the orbit by dental infections
CDLXXXVI) MEN IIB 129) Define the buccal space boundaries & source of infection DXLII) Teeth infect sinuses, which can track
CDLXXXVII) Cowden’s disease DXV) Boundaries posterior to infratemporal fossa/pterygomaxillary
CDLXXXVIII) Tuberous sclerosis i) Medial: buccinator & buccopharyngeal fasica fossa to inferior orbital fissure, or from maxillary
CDLXXXIX) Melkerson-Rosenthal syndrome (?); ii) Lateral: cheek skin sinus, into ethmoids, then through lamina papyracea
fissured tongue iii) Superior: zygomatic arch DXLIII) Lymphatic seeding
iv) Inferior: inferior border of mandible DXLIV) Venous spread along facial, angular &
124) Diseases causing oral ulcerations v) Anterior: lip muscles ophthalmic arteries
CDXC) Infectious vi) Posterior: pterygmandibular raphe DXLV) Traumatic/congenital dehiscences
i) Recurrent aphthous ulcers DXVI) Secondary to maxillomandibular bicuspid
ii) HSV stomatitis & molar infections 137) Predisposing factors for osteomyelitis of the maxilla &
iii) Syphilis mandible
CDXCI) Autoimmune 130) Primary oral cavity spaces in DSNI DXLVI) Radiotherapy
i) Behcet’s disease: seen in Japanese DXVII) Submental DXLVII) Trauma
populations; uveitis, oral ulcers, genital ulcers DXVIII) Sublingual (anterior teeth, bicuspids, 1st DXLVIII) Systemic disease (DM)
ii) Reiter’s syndrome: conjunctivitis, urethritis, oral molar) DXLIX) Osteodystrophies (Paget’s, fibrous
ulcers, arthritis DXIX) Submandibular (2nd, 3rd molars) dysplasia)
iii) Inflammatory bowel disease DXX) Site of infection determined by level of DL) Endosteal lesions (eg. Cementoma)
iv) Celiac disease tooth roots in relation to mylohyoid line DLI) Dental implants
v) Selective IgA deficiency DLII) Immune compromise
vi) Erythema multiforme 131) Submandibular space contents
CDXCII) Nutritional DXXI) Submandibular gland 138) Treatment strategy for osteomyelitis
i) Vitamin B12 deficiency DXXII) Wharton’s duct DLIII) Appropriate culture directed antibiotics
DXXIII) Facial artery DLIV) Debridement of foreign
125) Name the 6 clinical forms of oral candidiasis DXXIV) Lingual & hypoglossal nerves bodies/sequestra/necrotic tissue
CDXCIII) Pseudomembranous candidiasis (classic DXXV) Fat & lymph nodes DLV)Adjuncts to increase oxygenation (trephination,
presentation) decortication, HBO)
CDXCIV) Acute atrophic candidiasis 132) Ludwig’s angina DLVI) Reconstruction after infection clears
CDXCV) Chronic atrophic candidiasis (most DXXVI) Infection of sublingual, submandibular,
common) submental spaces; usually mixed flora 139) Name the three classes of internal derangements of the
CDXCVI) Hyperplastic candidiasis (increased DXXVII) Airway distress secondary to posteriorly TMJ
epithelial atypia and malignant transformation) displaced tongue, kinks the supraglottis DLVII) Classes
CDXCVII) Median rhomboid glossitis DXXVIII) Treatment: airway control, I&D of i) Anterior displacement with reduction on
CDXCVIII) Mucocutaneous candidiasis abscess/phlegmon opening the mouth: clicking & popping, can be
painless or painful; treat pain with NSAID’s,
126) Differential diagnosis of gingival hypertrophy 133) Describe the masticator space contents bite-block appliance, muscle relaxant prn for
CDXCIX) Poor oral hygiene DXXIX) Masseter, temporal, pterygoid muscles pterygoid spasm
D) Autoimmune: diabetes, Crohn’s DXXX) Trismus hallmark symptom ii) Anterior displacement without reduction on
DI) Drug effects: phenytoin most common, also DXXXI) Maxillomandibular molar origin attempted mouth opening: locking; treat with
cyclosporine A, calcium channel blockers arthroscopic lysis & lavage, or open
DII) Inherited: Cowden’s disease 134) What organisms are most commonly seen in odontogenic mobilization or removal with replacement
oral infections?
127) Describe the layers of the cheek from medial to lateral DXXXII) Aerobic Streptococcus species
 iii) Disc adhesion to the articular eminence: DLXXXVII) Oxygen therapy ii)Nonherediatry causes: medications (ACE-I
limitation of mouth opening; treat with DLXXXVIII) Nasopharyngeal intubation at night most commonly), food, insect bites,
arthroscopic lysis of adhesions & lavage DLXXXIX) Tongue retaining device transfusions, infections
DLVIII) Scale correlates with outcome prognosis DXC) Dental appliances DCXXI) Treatment: oxygenation, epinephrine,
DLIX) Earlier the click, the less displaced the DXCI) CPAP (definitive therapy) steroids, antihistamines, aminophylline; later
disk avoidance, discontinuing medications, etc.
146) Name the surgical procedures done for OSA
140) Five causes of mandible ankylosis DXCII) Nose: septoplasty, nasal valve 153) 9 granulomatous diseases of the larynx that can simulate
DLX) External trauma reconstruction, turbinectomy cancer
DLXI) Infectious arthritis DXCIII) Nasopharynx: adenoidectomy DCXXII) Tuberculosis
DLXII) Rheumatoid arthritis DXCIV) Oral cavity/oropharynx: geniohyoid DCXXIII) Blastomycosis
DLXIII) Condylar degeneration advancement, mandibular advancement, maxillary DCXXIV) Histoplasmosis
DLXIV) Osteoradionecrosis advancement, tongue base suspension, DCXXV) Sarcoidosis
tonsillectomy, LAUP, UPPP, tongue base reduction, DCXXVI) Syphilis
141) Sleep stages thyrohyoidopexy DCXXVII) Pachyderma laryngis
DLXV) NREM I: light stage, short duration DXCV) Definitive: tracheostomy DCXXVIII) Leprosy
DLXVI) NREM II: defined by sleep spindles/K- DCXXIX) Scleroma
complexes on EEG 147) Success rates for snoring procedures DCXXX) Wegener’s granulomatosis
DLXVII) NREM III & IV: delta sleep, defined by DXCVI) LAUP/UPPP: Immediate results 85-90%
high voltage, slow wave activity success, at 12 months 45-50% success 154) Classic vocal cord positions in vocal cord palsy
DLXVIII) REM sleep DCXXXI) Lateral cord position
148) Complications of UPPP i) Suggests SLN & RLN injury, loss of
142) Sleep syndromes DXCVII) VPI cricothyroid with SLN injury causes increased
DLXIX) Snoring DXCVIII) Postoperative bleeding abduction
DLXX) Upper airway resistance syndrome: DXCIX) Nasopharyngeal stenosis ii) Treated with types I & IV thyroplasty
daytime hypersomnolence with normal PSG DC) Voice change DCXXXII) Paramedian position
DLXXI) Obstructive sleep hypopnea syndrome: DCI) Perioperative upper airway obstruction i) Suggests RLN injury only, implies a lesion
daytime hypersomnolence with hypopneas; >5 DCII) Foreign body sensation below the nodose ganglion
hypopneas/hour on PSG diagnostic DCIII) Death from upper airway compromise ii) Treated with type II thyroplasty
DLXXII) Obstructive sleep apnea syndrome:
daytime hypersomnolence with apneas & hypopneas 149) Contraindications against palatal procedures in mild OSA 155) Therapy for unilateral vocal cord paralysis
DCIV) VPI DCXXXIII) Voice therapy
143) Definition of apnea, hypopnea, AI, AHI, RDI DCV) Bleeding disorder DCXXXIV) Injection techniques
DLXXIII) Apnea: cessation of ventilation >10 DCVI) Voice/swallowing considerations i) Gelfoam if VC recovery expected
seconds DCVII) Submucus cleft palate ii) Polytef if no recovery expected; discontinued
DLXXIV) Hypopnea: episode of hypoventilation >10 due to granuloma formation
seconds, with 30-40% decrease in airflow and 3-4% 150) Indications for permanent tracheostomy in OSA iii) Others include fat, hyaluronic acid
decrease in oxygen saturation DCVIII) Morbid obesity iv) Performed percutaneous, transoral,
DLXXV) Apnea index (AI): number of apneas in an DCIX) Cardiac arrhythmia with apneic events laryngoscopically
hour period; >5 significant DCX) Severe apneas with desaturation DCXXXV) Type I Isshiki thyroplasty (medialization
DLXXVI) Apnea-hypopnea index (AHI): apneas + DCXI) Cor pulmonale thyroplasty)
hypopnea/ sleep hour; >10 significant (Baileys) DCXII) Disabling hypersomnolence DCXXXVI) Arytenoid adduction
DLXXVII) Respiratory disturbance index (RDI): DCXIII) No response to weight loss and avoidance DCXXXVII) Laryngeal reinnervation (ansa hypoglossi
apnea + hypopnea + RERA/sleep hour of sedatives and alcohol transfer)
DCXIV) No response/tolerance to CPAP trial
144) Craniofacial abnormalities associated with OSA DCXV) Chronic alveolar hypoventilation 156) Therapy for bilateral vocal cord paralysis
DLXXVIII) Retrognathia DCXXXVIII) Tracheostomy
DLXXIX) Narrow posterior pharyngeal space 151) Laryngeal diphtheria DCXXXIX) Laser transverse cordectomy &/or
DLXXX) Increased distance between mandibular DCXVI) Caused by Cornybacterium diphtheriae vestibulectomy
plane and hyoid DCXVII) Exudative membranous tonsillitis with DCXL) Arytenoidectomy
DLXXXI) Shortened anterior cranial base fever, dysphonia i) Endolaryngeal (unilat/bilat)
DLXXXII) Enlarged soft palate DCXVIII) Treatment: management of airway (not ii) Extralaryngeal
intubation), diphtheria antitoxin, erythromycin or (1) Woodman lateral approach
145) Medical therapy for OSA tetracycline (2) Anterior thyrotomy approach
DLXXXIII) Progesterone: respiratory stimulant DCXLI) Arytenoidopexy
DLXXXIV) Acetazolamide: increases hydrogen 152) Angioedema DCXLII) Nerve-muscle transposition
concentration in blood DCXIX) Inflammatory reaction with vascular
DLXXXV) Theophylline: increases hypoxic dilation and increased vascular permeability 157) Classification of laryngeal framework (Isshiki) procedures
ventilatory drive DCXX) Causes DCXLIII) Type I: vocal cord medialization
DLXXXVI) Protryptiline i) Hereditary: C1 esterase deficiency DCXLIV) Type II: vocal cord lateralization
 DCXLV) Type III: vocal cord shortening i)Repetitive contact trauma leads to mucosal DCLXXXVIII) Changes in vocal cord length
DCXLVI) Type IV: vocal cord lengthening ulceration, cartilage exposure and inflammation DCLXXXIX) Changes in vocal cord tension
leads to granuloma formation DCXC) Changes in vocal cord mass
158) Complications of vocal cord medialization by injection DCLXX) Risk factors DCXCI) Changes in subglottic air pressure
DCXLVII) Underinjection: requires multiple i) Vocal abuse (chronic cough, throat clearing)
procedures ii) Previous traumatic intubation 170) Diplophonia
DCXLVIII) Overinjection: airway compromise iii) GERD DCXCII) Phonation with two simultaneous
DCXLIX) Improper placement iv) Male sex fundamental frequencies
DCL) Migration of injection material DCLXXI) Treatment options DCXCIII) Divergent travelling wave velocities due to
DCLI) Intrachordal injection: impairs vibratory i) Voice therapy asymmetric stiffness
ability ii) Antireflux medications
DCLII) Granuloma formation (polytef) iii) Intralesional corticosteroids 171) Objective voice measures
iv) Endoscopic CO2 excision DCXCIV) Glottography
159) Guttman’s test v) Botox injection: 12u on side of lesion, 3-5 units i) Photoglottography: change in light
DCLIII) A test for SLN paralysis (cricothyroid contralaterally to prevent overcompensation transillumination measures degree of glottic
paralysis); normally, anterior thyroid cartilage opening
pressure decreases pitch, lateral thyroid cartilage 165) Three benign tumors arising from Schwann cells ii) Electroglottography: change in electrical
pressure increased pitch; with cricothyroid paralysis DCLXXII) Schwannoma: benign, encapsulated, slow conduction measures degree of glottic contact
this reverses growing, rare malignant sarcomatous degeneration DCXCV) Aerodynamic measures
DCLXXIII) Neurofibroma: proliferation of sheath cells i) Open quotient: ratio of duration of open folds to
160) Typical clinical laryngeal findings with LPR on flexible & fibers, nonencapsulated, nodular & diffuse length of the glottic cycle
nasolaryngoscopy DCLXXIV) Paraganglioma ii) Speed quotient: ratio of rise to fall during the
DCLIV) Posterior glottic edema DCLXXV) Granular cell tumor: slow, painless open phase of the glottic cycle
DCLV) Interarytenoid edema & erythema growth, well circumscribed iii) Shift quotient: ratio of time to peak glottic
DCLVI) Vocal fold edema opening over the duration of glottic opening
DCLVII) Mucosal thickening 166) Describe granular cell tumors DCXCVI) Videostroboscopy
DCLVIII) Vocal process ulceration & granuloma DCLXXVI) Arise from schwann cells i) Examines vibratory nature of vocal cords during
DCLXXVII) Two types: mucosal granular cell tumor, phonation; strobe controlled by pitch of
161) Most common causes of stridor in children gingival giant cell tumor phonation or a frequency generator
DCLIX) Laryngeal (60%) DCLXXVIII) Slow, painless growth; well circumscribed DCXCVII) Airflow measures
i) Laryngomalacia (60%) DCLXXIX) Typically solitary, polypoid, sessile, i) Airflow through glottis & subglottic pressure
ii) Subglottic stenosis (20%) papillary or cystic measured, which determines the glottic
iii) VC palsy (13%) DCLXXX) Tongue most common site of origin resistance
iv) Others (7%) DCLXXXI) Histology: large polygonal cells in DCXCVIII) Acoustic measures
DCLX) Tracheal (15%) nests/strands/sheets; infiltrative, no distinct capsule; i) Quantitate vocal harshness
i) Tracheomalacia (45%) defining characteristic are abundant eosinophilic (1) Jitter: cycle to cycle frequency
ii) Vascular compression (45%) cytoplasm filled with granules of varying sizes perturbation
iii) Stenosis (5%) (lysosomes in varying stages of fragmentation); (2) Shimmer: cycle to cycle amplitude
DCLXI) Bronchial & tracheal infections 5% each; keratin pearl formation in some cases perturbation
miscellaneous 15% (pseudoepitheliomatous hyperplasia)
DCLXXXII) Treatment: complete excision (endoscopic 172) Other definitions used in vocal analysis
162) Differential diagnosis of benign vocal cord lesions or open via laryngofissure or conservative resection); DCXCIX) Closed quotient: proportion of the glottic
DCLXII) Polyp (most common) recurrence rate 8%, malignant transformation in 5% cycle during which the glottis is closed
i) Mucoid DCC) Maximum phonation time: maximum
ii) Angiomatous 167) Travelling wave theory in voice production period a subject can maintain audible phonation of a
DCLXIII) Nodule DCLXXXIII) VC vibration occurs in lateral & vertical vowel at comfortable pitch and loudness (men 22-34
i) Cyst planes sec, women 16-25 sec)
ii) Mucus retention DCLXXXIV) Sequence: lower margin separates, DCCI) Phonation quotient: MPT divided by
DCLXIV) Dermoid elliptical volume of air formed in subglottal vault patient’s vital capacity
DCLXV) Granuloma (“glottal puff”), which is released as upper margin
DCLXVI) Sulcus vocalis separates; lower margin returns to midline, then 173) Evaluated criteria on laryngovideostroboscopy (remember
upper margin does also SCAMP)
163) What 2 systemic diseases should be considered in the DCLXXXV) Phase delay: delay between opening of DCCII) Symmetry
differential of a vocal cord lesion? upper and lower vocal cord margins DCCIII) Closure
DCLXVII) Hypothyroidism DCCIV) Amplitude
DCLXVIII) Acromegaly 168) What is the human vocal fundamental frequency? DCCV) Mucosal wave
DCLXXXVI) Men 125 Hz; increases with age DCCVI) Periodicity
164) Vocal cord granuloma: histopathologic origin, 4 risk DCLXXXVII) Women 200-250 Hz; decreases with age DCCVII) Fundamental frequency
factors, 4 treatment options
DCLXIX) Histopathologic origin 169) What mechanisms alter vocal pitch? 174) Normal vocal cord vibration and voice production
 DCCVIII) 2 essential parameters: glottal gap and 180) Describe mechanism of action of botulinum toxin (Botox), ii) Absence of esophageal peristalsis
normal symmetric vocal cord stiffness how does its effect wear off, and what doses are given in iii) Absent LES relaxation
DCCIX) Normal phonatory posture: posterior hyperfunctional laryngeal disorders DCCLII) Scleroderma
commissure closure, symmetric thyroarytenoid DCCXXXIII) Causes irreversible blockage of receptors i) Aperistalsis of lower 2/3s of esophagus
stiffness, equal vertical postion controlling presynaptic release of acetylcholine ii) Absent LES contraction
DCCX) Glottal gap: interarytenoid & lateral DCCXXXIV) Wears off through regeneration of fresh iii) Esophageal dilatation
cricoarytenoid muscles both close and appose the synaptic terminals
vocal cords DCCXXXV) Dose in adductor SD: 1 to 3.75 units 185) Plummer-Vinson syndrome
DCCXI) Normal vocal cord stiffness: DCCXXXVI) Dose in abductor SD: 0.5 to 5 units DCCLIII) Seen in Caucasian females typically of
thyroarytenoid controls stiffness, which increased Scandinavian descent
pitch and resistance; cricothyroid antagonizes 181) Name 5 clinical uses for Botox in the head and neck DCCLIV) Symptoms & signs: dysphagia,
thyroarytenoid, thins & lengthens vocal cord which DCCXXXVII) Spasmodic dysphonia esophageal stricture, glossitis, iron deficiency
increases tension and pitch while decreasing the DCCXXXVIII) Facial dystonias (eg. blepharospasm, anemia, cheilosis, koilonychia, splenomegaly, SCC
area of contact torticollis) of the postcricoid region & cervical esophagus
DCCXXXIX) Vocal cord granulomas DCCLV) Treatment: endoscopic web rupture, iron
175) Strategies for voice therapy DCCXL) Forehead rhytids replacement
DCCXII) Behavior DCCXLI) Ptyalism (drooling)
DCCXIII) Attack DCCXLII) Frey’s syndrome 186) What are the clinical findings in CREST syndrome?
DCCXIV) Pitch DCCXLIII) Cricopharyngeal spasm in laryngectomies DCCLVI) Calcinosis
DCCXV) Rest DCCLVII) Raynaud’s phenomenon
DCCXVI) Relax 182) Indications for the professional voice user to cancel a DCCLVIII) Esophageal stenosis
DCCXVII) Respiration concert, or to persist and use steroids to get through a DCCLIX) Sclerodactyly
DCCXVIII) Rate performance DCCLX) Telangiectasias
DCCXLIV) Conditions requiring cancellation
176) Name 4 common dystonias in the head and neck i) Submucosal hemorrhage 187) Esophageal triangles
DCCXIX) Spasmodic dysphonia ii) Enlarging vocal cord varix DCCLXI) Killian’s dehiscence: space between
DCCXX) Blepharospasm iii) Break in vocal fold mucosa inferior constrictor and cricopharyngeus
DCCXXI) Torticollis iv) Significant systemic illness (Cummings) or space between pars obliquus and
DCCXXII) Oromandibular dystonia v) Severe laryngitis pars fundiformis (horizontal) portions of the
DCCXXIII) Meige’s syndrome: blepharospasm & DCCXLV) Conditions that steroid can be given cricopharyngeus
oromandibular dystonia syndrome i) Edema from episodic abuse DCCLXII) Laimer’s triangle: between circular and
ii) Mild to moderate laryngitis longitudinal fibers of esophagus (KJ Lee) or
177) 3 clinical indicators of a hyperfunctional laryngeal iii) Allergic vocal fold edema posteriorly between the UES and uppermost fibers
dysphonia on indirect laryngoscopy iv) Vocal fold hemorrhage of the esophagus (Cummings)
DCCXXIV) Anteroposterior compression of the larynx DCCLXIII) Killian-Jamison area: lateral dehiscence
DCCXXV) Aryepiglottic fold contraction 183) Achalasia; infection that causes the same symptoms between the cricopharyngeus and esophageal
DCCXXVI) False vocal cord compression DCCXLVI) Degeneration of Auerbach’s plexus muscle fibers through which the RLN runs
DCCXLVII) Symptoms & signs: aperistalsis,
178) Describe spasmodic dysphonia esophageal dilation, failed LES relaxation; 188) Definitions of diverticulae, types, treatment
DCCXXVII) An action induced laryngeal motion progressive disease leads to aperistalsis, fibrosis & DCCLXIV) Types
disorder atrophy of muscle i) True diverticula: involvement of mucosa,
DCCXXVIII) Adductor dysphonia: TA/vocalis complex; DCCXLVIII) Radiographic: esophageal distension, air- submucosa, muscle
choked, strained or strangled voice with abrupt fluid level, aperistalsis, absence of LES relaxation, ii) Pseudodiverticula: involvement of mucosa and
initiation & termination causing short phonation retention of barium submucosa
breaks; vocal tremor, slow speech rate & decreased DCCXLIX) Treatment DCCLXV) Etiology
speech smoothness can all be present i) Early: symptomatic, with Ca-blockers or i) Traction: due to adjacent inflammation or
DCCXXIX) Abductor dysphonia: PCA muscle; nitrates to stimulate LES relaxation neoplasia
breathy, effortful voice quality with abrupt ii) Esophagoscopy routine, pneumatic dilation ii) Pulsion: due to increased intraluminal pressure
termination, causes aphonic segments of speech; common procedure combined with mural weakness
vocal tremor often seen, voice loudness reduced, iii) Surgery: Heller myotomy for failed pneumatic DCCLXVI) Location
speech intelligibility reduced dilatation or those at increased risk of dilation i) Pharyngoesophageal: classic Zenker’s, pulsion
(previous perforation, epiphrenic diverticula, type
179) Describe voice changes in essential tremor adjacent aortic aneurysm) ii) Midesophageal: usually due to traction
DCCXXX) Altered pitch & loudness, phonation DCCL) Chagas disease: systemic parasitic iii) Epiphrenic: usually due to pulsion
stoppages, decreased intelligibility infection that destroys Auerbach’s plexus, similar
DCCXXXI) Tremor absent at rest, attenuated at end presentation as achalasia 189) Management of Zenker’s
of movement, maximal during posturing DCCLXVII) Observation with alternate enteral feeding
DCCXXXII) Treatment: Botox, inject muscles with 184) Manometric findings of achalasia & scleroderma via PEG, NG, kaofeed, etc.; monitoring for aspiration
most tremor DCCLI) Achalasia DCCLXVIII) Surgery
i) Increased LES pressure
 i) Open: diverticulectomy, diverticulopexy, iii) Injury to tracheoesophageal partition
diverticuloplasty, myotomy 194) Contraindications of esophagoscopy iv) Pneumothorax
ii) Endoscopic: myotomy via cautery (Dohlman), DCCXCIII) Combative patient v) Pneumomediastinum
laser, stapling DCCXCIV) Laryngeal edema DCCCXV) Early postoperative
DCCXCV) Chronic corticosteroid use i) Tracheostomy tube obstruction
190) Most common benign esophageal lesions DCCXCVI) Severe erosive burns to esophagus ii) Tracheostomy tube displacement
DCCLXIX) Leiomyoma (most common) DCCXCVII) Aortic aneurysm iii) Infection
DCCLXX) Polyps DCCXCVIII) Severe cervical/thoracic spine iv) Pulmonary edema
DCCLXXI) Hemangioma abnormalities DCCCXVI) Late postoperative
DCCLXXII) Adenoma i) Tracheal stenosis
DCCLXXIII) Neurofibroma 195) Tests for GERD ii) Granulation tissue
DCCLXXIV) Granular cell tumor DCCXCIX) Barium swallow iii) Tracheal-inominate fistula
DCCC) Bernstein test: place NGT, instill N/S for iv) Tracheoesophageal fistula
191) Risk factors for esophageal carcinoma 15 minutes, then 0.1M HCl @ 6cc/min until v) RLN injury
DCCLXXV) Smoking symptomatic or for 45 minutes vi) Sinusitis
DCCLXXVI) EtOH DCCCI) Esophagoscopy & biopsy
DCCLXXVII) Nutritional deficiencies DCCCII) Radionuclide scan 199) Endotracheal tube pearls & complications
DCCLXXVIII) Radiation & chemical exposure (nitrates, DCCCIII) Lipid laden macrophage test DCCCXVII) Most commonly made of polyvinyl chloride
nitrites, petroleum oils) DCCCIV) pH probe: short term or long term (gold DCCCXVIII) Cuff pressure >25mm H2O will
DCCLXXIX) Achalasia standard) compromise mucosal capillary blood flow and cause
DCCLXXX) Plummer-Vinson syndrome necrosis
DCCLXXXI) Tylosis: autosomal dominant, 196) Discuss the symptoms and associations of
hyperkeratosis of palms & soles laryngopharyngeal reflux (LPR) 200) 5 local factors that increase risk for laryngeal damage
DCCLXXXII) Chronic esophagitis/strictures DCCCV) Primary otolaryngologic symptoms of from ETT
DCCLXXXIII) Caustic ingestion GERD DCCCXIX) Cuff pressure too high
DCCLXXXIV) Barrett’s esophagus (15% will develop i) Hoarseness DCCCXX) Too large an ETT for the larynx
adenocarcinoma) ii) Chronic throat clearing DCCCXXI) Length of intubation greater than 7 days in
iii) Globus pharyngeus adults, ~3-4 weeks in pediatrics
192) Esophageal carcinoma iv) Cervical dysphagia DCCCXXII) Blind intubation/poor visualization
DCCLXXXV) SCC most common, adenocarcinoma v) Chronic cough DCCCXXIII) Preexisting laryngeal anatomic
less common vi) Heartburn/regurgitation abnormality
DCCLXXXVI) Symptoms: nonpainful dysphagia & vii) Excess phlegm DCCCXXIV) Presence of GERD
weight loss common; odynophagia, dysphagia, DCCCVI) Associations DCCCXXV) Presence of local infection
anemia, hemorrhage, aspiration pneumonia, VC i) Laryngomalacia
paralysis, adenopathy ii) Vocal cord polyps 201) Risk factors for cardiorespiratory complications in patients
DCCLXXXVII) Diagnosis: CXR, esophagoscopy with iii) Granulation with airway obstruction
brush cytology or biopsy, endoscopic ultrasound, CT iv) Vocal cord nodules DCCCXXVI) Susceptibility of pulmonary vasculature
DCCLXXXVIII) Treatment: radiochemotherapy or surgery; v) Laryngeal & tracheal stenosis DCCCXXVII) Craniofacial malformation
dismal prognosis vi) Laryngospasm/asthma/SIDS DCCCXXVIII) Obesity
vii) Subglottic stenosis (most common association) DCCCXXIX) Congenital heart disease
193) Etiology of esophageal perforation viii) Contact ulcer/granulomas DCCCXXX) Abnormal pharyngeal musculature
DCCLXXXIX) Iatrogenic most common, usually in ix) Carcinoma DCCCXXXI) Concurrent URTI
cervical esophagus x) Pachyderma laryngis
DCCXC) Trauma (blunt, penetrating) 202) Lemierre syndrome
DCCXCI) Inflammatory/neoplastic 197) Indications for tracheotomy DCCCXXXII) IJV thrombophlebitis, usually due to
DCCXCII) Spontaneous DCCCVII) Upper airway obstruction Fusobacterium necrophorum
i) Mallory-Weiss: present with UGI bleed DCCCVIII) Inability of patient to handle own DCCCXXXIII) Symptoms & signs: spiking fever,
secondary to vomiting/retching, develop secretions engorged optic disks, increased CSF pressure,
nonpenetrating mucosal tear at lower DCCCIX) Facilitation with intubation SCM tenderness, neck stiffness, metastatic lung
esophagus/cardia, tears submucosal arteries, DCCCX) Difficulties with intubation abscesses, septic arthritis
usually causes significant bleed and DCCCXI) Prolonged intubation DCCCXXXIV) Greisinger’s sign (edema of the
hypovolemic shock in 50%; bleeding usually DCCCXII) Adjunct to HNS with possible airway postauricular soft tissues overlying the mastoid
stops, may require endoscopic cautery or compromise process as a result of thrombosis of the mastoid
vasoconstrictor application DCCCXIII) Adjunct to management of severe facial emissary vein)
ii) Boerhaave: spontaneous esophageal rupture fractures DCCCXXXV) Toby-Ayer Queckenstadt test
due to vomiting, coughing, heavy lifting or (compression of the jugular vein on the intact side
straining; typically left sided & transmural; 198) Complications of tracheotomy causes a rise in CSF pressure, whereas
symptoms typical for mediastinitis; treatment by DCCCXIV) Intraoperative compression of the obstructed side does not raise
surgical drainage of mediastinum/pleura, repair i) Great vessel injury the CSF pressure)
of perforation, nutritional support ii) Laryngeal damage (improper placement)
 DCCCXXXVI) Treatment: drainage of infection, ligation DCCCLXI) Treatment: Incision & drainage of DCCCLXXXVII) Reapproximation done with 8-0
of IJV; anticoagulation controversial hematoma, reduction of neocartilage formation, to 10-0 monofilament suture under microscopy
pressure dressing application for 7-10 days
203) Etiologies of deep space neck infections 216) What types of facial nerve repair are there?
DCCCXXXVII) Dental/salivary infection 209) Factors to consider when repairing the auricle after a total DCCCLXXXVIII) Epineural
DCCCXXXVIII) URTI avulsion DCCCLXXXIX) Perineural
DCCCXXXIX) Trauma DCCCLXII) Status of the avulsed portion: size, DCCCXC) Interfascicular
DCCCXL) Foreign bodies viability?
DCCCXLI) Instrumentation DCCCLXIII) Status of the remaining tissue: if severe, 217) What anatomic landmark determines likelihood of parotid
DCCCXLII) Spread of localized/superficial infection may need some healing to occur prior to duct trauma?
DCCCXLIII) IV drug abuse reconstruction DCCCXCI) Vertical lacerations below anterior border
DCCCLXIV) Timing of repair: need for delay if wound of masseter muscle likely to injure the parotid duct
204) Review the layers of the deep cervical fascia contaminated (eg. animal, human bites)
DCCCXLIV) Superficial/investing DCCCLXV) Best use of remaining tissues 218) Methods of repairing the parotid duct
i) From nuchal line & mandible to the clavicles DCCCLXVI) Careful planning of reconstruction DCCCXCII) Ideal: soft polymeric silicone or
ii) Envelops trapezius, SCM, parotid & SMG polyethylene 22G catheter threaded through
DCCCXLV) Middle 210) Signs & symptoms of laryngeal trauma Stensen’s duct, repair of duct with 6-0 or 7-0
i) Muscular layer: surrounds strap muscles DCCCLXVII) Symptoms: hoarseness, pain, dyspnea, monofilament suture under the microscope, suture
ii) Visceral layer: surrounds trachea, esophagus, dysphagia the stent to the buccal mucosa for 10-14 days
thyroid; superiorly ensheathes constrictors & DCCCLXVIII) Signs: stridor, hemoptysis, subcutaneous DCCCXCIII) Less ideal
buccinator muscle emphysema, laryngeal tenderness, loss of thyroid (1) Tying off the duct: gland atrophies after a
DCCCXLVI) Deep cartilage eminence, vocal fold immobility, laryngeal period of swelling, pain, possibly infection
i) Prevertebral: from skull base to coccyx, fuses hematoma, laryngeal edema, laryngeal lacerations (2) Rerouting more proximally in the oral
with transverse processes cavity: technically more difficult
ii) Alar: lies between prevertebral & visceral layer 211) Indications for medical management of traumatic
of middle cervical fascia; extends from skull laryngeal injuries 219) Management of eyelid lacerations
base to T2 level where it fuses with visceral DCCCLXIX) Edema DCCCXCIV) Primary closure with <25% loss
layer DCCCLXX) Small hematoma formation DCCCXCV) Lateral canthotomy provides 5-10mm of
DCCCLXXI) Undisplaced single stable fracture length
205) Bacterial flora of deep space neck infections DCCCLXXII) Lacerations with no cartilage exposure DCCCXCVI) Grafts: from contralateral eyelid,
DCCCXLVII) Usually due to mixed flora DCCCLXXIII) Healthy vocal cord movement supraclavicular area, postauricular area
DCCCXLVIII) Aerobes: Strep (viridans, beta-hemolytic), DCCCLXXIV) No injury to anterior commissure
Staph (aureus, epidermidis), Neisseria, Klebsiella, 220) Oral commissure burn
Haemophilus 212) Indications for open repair of traumatic laryngeal injuries DCCCXCVII) Prolonged wait to allow demarcation (10-
DCCCXLIX) Anaerobes: Bacteroides, DCCCLXXV) Anterior commissure injury 14d)
Peptostreptococcus, Peptococcus, Fusobacterium, DCCCLXXVI) Exposed cartilage DCCCXCVIII) Excision after demarcated
Eikenella, Veillonella DCCCLXXVII) Multiple or displaced fractures of cricoid DCCCXCIX) Contracture a long-term complication,
and/or thyroid leads to microstomia; prevent by fitting an oral
206) CT characteristics of deep space neck DCCCLXXVIII) Vocal cord paralysis applicance
infections/abscesses DCCCLXXIX) Airway compromise requiring CM) Possible repair with Estlander flap depending on
DCCCL) Low attenuation intubation/tracheotomy tissue loss
DCCCLI) Contrast enhancement of abscess wall DCCCLXXX) Concordant injury to neck requiring
DCCCLII) Tissue edema surgical exploration 221) Areas of inherent mandible weakness
DCCCLIII) Cystic/loculated appearance CMI) 3rd molar region (angle)
213) Indications for stenting in laryngeal trauma CMII) Mental foramen (parasymphyseal)
207) Mosher’s landmarks for surgical approaches to the DCCCLXXXI) Anterior commissure involvement CMIII) Condylar neck
infected neck DCCCLXXXII) Multiple displaced laryngeal fractures
DCCCLIV) Lateral tip of greater cornu of hyoid DCCCLXXXIII) Multiple severe endolaryngeal lacerations 222) Angle’s classification of teeth occlusion
DCCCLV) Cricoid cartilage DCCCLXXXIV) Architecture of larynx not maintained by CMIV) Defines position of maxillary first molar
DCCCLVI) Styloid process open fracture fixation mesial buccal cusp’s relation to buccal groove of
DCCCLVII) Anterior border of SCM mandibular 1st molar
DCCCLVIII) Posterior belly of digastric 214) Fix facial nerve proximal to what line? i) Type I, normal occlusion: cusp fits into groove
DCCCLXXXV) Line running through lateral canthus ii) Type II, retrognathism/overbite: cusp anterior to
208) Etiology of a cauliflower ear, how to treat it (Baileys, Cummings, KJ Lee) and through mental groove
DCCCLIX) Subperichondrial auricular hematoma foramen (Cummings soft tissue trauma chapter) iii) Type III, prognathism/underbite: cusp posterior
formation, will devascularize cartilage to groove
DCCCLX) If not treated in a timely fashion, leads to 215) Strategies for fixing the traumatized facial nerve CMV) Only describes anteroposterior dental
neocartilage formation and distortion of ear shape DCCCLXXXVI) Distal excitability lost after ~72 hours, relationships
ideal to fix before then; if primary repair impossible,
clip/tag ends for future repair
223) Define the normal transverse and anterior dental CMXXI) Nonunion ii) Enophthalmos
relationships CMXXII) Malunion iii) Extraocular muscle entrapment
CMVI) Transverse: buccal cusps of mandibular CMXXIII) Subluxation of the condyle
molars should be between the buccal and palatal CMXXIV) Unfavorable mandibular fracture 233) Orbital anatomy considerations in facial trauma
cusps of the maxillary molars CMXXV) Tooth impaction in the fracture line CMXLIII) No true medial rim
CMVII) Anterior dental: maxillary anterior dentition CMXXVI) Undiagnosed second fracture of mandible CMXLIV) Maximum diameter ~15mm posterior to
should be 1-3mm anterior to mandibular anterior or maxilla inferior orbital rim
dentition with central incisal overlap of 1-3mm CMXXVII) Osteomyelitis CMXLV) Maximum height of orbital roof convexity 5
CMXXVIII) Error in fragment alignment mm
224) Describe mandible fractures (in general) CMXLVI) Maximim depth of orbital floor concavity
CMVIII) Favorable: when muscles draw fragments 229) Describe the buttress system of the midface 3mm
together & reduce the fracture CMXXIX) Vertical buttresses
CMIX) Unfavorable: when fragments are i) Nasomaxillary 234) What amount of orbital injury will cause enophthalmos?
distracted ii) Zygomaticomaxillary (greatest occlusal load) CMXLVII) Disruption of the orbital floor exceeding 2
CMX) Fractures can be vertically or horizontally iii) Pterygomaxillary sq. cm
favorable or unfavorable CMXXX) Verticals suspended from thick frontal bar, CMXLVIII) Bone volume changes exceeding 1.5
CMXI) Angle fractures almost always horizontally reinforced by inferior orbital rims, maxillary alveolus cubic cm (5% of orbital volume)
unfavorable, masseter, medial pterygoid, temporalis & hard palate, zygomatic processes of temporal CMXLIX) Considerable fat and soft tissue
muscles contribute bone, greater sphenoid wings displacement (teardrop sign on Waters view)
CMXII) Body & symphysis/parasymphysis usually
vertically unfavorable, mylohyoid muscle main 230) Describe the LeFort fractures 235) Symptoms of orbital apex syndrome
distracting muscle CMXXXI) LeFort noted that facial fractures occurred CML) Opthalmoplegia, ptosis, pupillary dilation
in 3 typical patterns, often bilateral, could be mixed; CMLI) Blindness & decreased visual acuity
225) Physical signs of a unilateral condylar/neck fracture all involved fracture of the pterygoid plates (involves optic nerve)
CMXIII) Ipsilateral premature contact of molars CMXXXII) Types CMLII) Anaesthesia of upper eyelid & forehead
CMXIV) Contralateral open bite deformity i) LeFort I: palate-face dysjunction, lower face &
CMXV) Deviation of jaw to ipsilateral side maxillae move separately 236) What muscles are responsible for (upper) eyelid
ii) LeFort II: pyramidal dysjunction, maxillary & movements?
226) General management of mandible fractures nasal regions move separately from rest of CMLIII) Orbicularis oris: pretarsal segment most
CMXVI) Antibiotics for any case involving teeth midface & skull important for blinking, innervated by CN VII
bearing segments until gingival or mucosa healed iii) LeFort III: craniofacial dysjunction, includes all CMLIV) Levator palpebrae superioris: innervated
CMXVII) Closed reduction the vertical buttresses attaching the midface to by CN III
i) Most favorable fractures the skull base CMLV) Muller’s muscle: innervated by
ii) 4-6 weeks of IMF sympathetics
CMXVIII) Open reduction 231) 7 bones that make up orbit
i) For fractures with fragment displacement CMXXXIII) Frontal 237) Fracture patterns in nasal trauma
despite closed reduction CMXXXIV) Zygomatic CMLVI) C shaped across cartilaginous septum
ii) Classification CMXXXV) Maxillary CMLVII) Distal end of nasal bone with C-shaped
(1) Rigid: recon plate, compression plate, lag CMXXXVI) Lacrimal bony septum
screw CMXXXVII) Ethmoid CMLVIII) Midnasal bone with C-shaped bony
(2) Semirigid: miniplates CMXXXVIII) Palatine septum
(3) Nonrigid: interosseous wiring CMXXXIX) Sphenoid CMLIX) Anterior nasal spine
CMLX) Multiple or stellate fractures
227) Indications for ORIF of condylar neck fractures 232) Orbital blowout fractures
CMXIX) Absolute indications CMXL) Etiology 238) Indications for closed/open reduction of nasal fractures
i) Condyle displaced into MCF i) Due to impact forces centered over the globe, CMLXI) Closed reduction
ii) Lateral extracapsular condyle displacement causes rapid increase in intraorbital pressure i) Unilateral or bilateral nasal bone fracture
iii) Failure of closed techniques to establish good that “blows out” the thin bone of concave floor ii) Nasal pyramid deviation <50% nasal bridge
occlusion of orbital floor width
iv) Foreign body in the TMJ CMXLI) Common signs & symptoms CMLXII) Open reduction
CMXX) Relative indications i) Decreased visual acuity i) Extensive fracture/dislocation of nasal
i) Bicondylar fractures in the elderly edentulous ii) Diplopia bones/fractures
patient iii) Hypesthesia of infraorbital nerve ii) Nasal pyramid deviation >50% of nasal bridge
ii) Bicondylar fractures with associated iv) Orbital emphysema width
comminuted unstable midfacial fractures v) Periorbital ecchymosis iii) Open septal fracture
iii) Unilateral/bilateral fractures when closed vi) Enopthalmos (sunken-in globe) iv) Persistent deformity after closed reduction
reduction not indicated for medical reasions vii) Inferior rectus entrapment v) Dislocation of the caudal septum
(epilepsy, pregnancy) CMXLII) Indications for surgical repair vi) Anterior spine fracture
i) Rapid onset of serious intraorbital hemorrhage
228) Reasons for malocclusion after a mandibular fracture with decreased visual acuity 239) Complications of nasal fractures
 CMLXIII) Early: epistaxis, hematoma, infection
CMLXIV) Late: perforation, saddle nose,
fibrosis/scar, obstruction
CMLXV) Emergency: CSF leak, visual impairment,
severe epistaxis, hematoma in a child, nasal
obstruction in a newborn
240) Components of tears
CMLXVI) Lipid layer: from Meibomian glands
CMLXVII) Aqueous portion: from lacrimal gland
CMLXVIII) Mucin: from goblet cells
241) Anatomy of the suspensory system of the eye
CMLXIX) Medial canthal ligament
i) Anchors eyelid structures to medial wall,
maintains configuration of palpebral opening
ii) Anterior horizontal component: strongest,
attached to anterior lacrimal crest
iii) Anterior vertical component: attached superior
to anterior horizontal component
iv) Posterior horizontal component: weakest
attachment, attached to posterior lacrimal crest
CMLXX) Lateral canthal ligament
i) Anchors eyelid structures to lateral wall
ii) Attaches to Whitnall’s tubercle, bony spur just
inside and above midpoint of lateral orbital rim
242) Define the normal interpupillary distance, telecanthus,
hypertelorism, pseudohypertelorism, signs of MCT
disruption
CMLXXI) Normal interpupillary distance: ~60-70mm
CMLXXII) Telecanthus: intercanthal distance greater
than half the interpupillary distance (>35mm)
CMLXXIII) Hypertelorism: abnormal increase in
interpupillary distance, usually due to
overdevelopment of the lesser wings of the sphenoid
CMLXXIV) Pseudohypertelorism: an apparent
increase in the interorbital distance due to lateral
displacement of the inner canthi
CMLXXV) Signs of MCT disruption: telecanthus,
narrowed & blunted palpebral fissure, epiphora
243) Name four signs of an NOE fracture
CMLXXVI) Pig nose deformity
CMLXXVII) Palpable mobile fracture
CMLXXVIII) Telecanthus
CMLXXIX) Posterior displacement of nasal bones
244) Reconstruction of NOE fracture/MCL tear
CMLXXX) Low velocity: unilateral, reduce fragment
transconjunctivally (occ. sublabially), fixate with
microplates and screws; occ. will need transnasal
wiring
CMLXXXI) Medium velocity: partial avulsion of MCL
common, realignment & fixation may require
transconjunctival, sublabial, coronal incisions
CMLXXXII) High velocity: often comminution of NOE
with avulsion of all components of MCL; will require
microplate fixation with MCL repair
i) MCL repair done by evaluating vectors and MI) Dyskeratosis: Production of keratin at lower layers
using transnasal wires to attach ligaments MII) Dysplasia: Change affecting the size, shape and
through drillholes to opposite location of NOE orientational relationship
MIII) Ectopic: Normal appearing tissue in an abnormal
245) Classification of frontal sinus fractures location
CMLXXXIII) Anterior table MIV) Hamartoma: Circumscribed overgrowth of tissues,
CMLXXXIV) Posterior table normally present in that part of the body
CMLXXXV) Frontonasal duct MV) Hyperkeratosis: Increased thickness of keratinized
layers
246) Injury to the nasofrontal duct correlates on CT with: MVI) Hyperplasia: Increase in the number of cells per unit
CMLXXXVI) Frontal sinus floor fractures 83% of the of tissue or organ of origin
time MVII) Hypertrophy: Increase in individual cell
CMLXXXVII) Anterior ethmoid fractures 67% of the size
time MVIII) Keratoacanthosis: Large acanthoma,
CMLXXXVIII) Thus, if there is an NOE injury or injury to surface keratosis
the floor or posterior wall of the frontal sinus, be MIX) Metaplasia: differentiation of one cell into another
suspicious of a nasofrontal duct injury MX) Metastasis: Secondary discontinuous cancerous
growths
247) Define the levels of the neck in blunt & penetrating trauma MXI) Neoplasm: Proliferation of cells and formation of a
CMLXXXIX) Zone I: clavicles to inferior border of the mass
cricoid MXII) Parakeratosis: migration of the nucleus to
CMXC) Zone II: inferior border of the cricoid to the the surface of a cell
angle of the mandible MXIII) Pleomorphism: More than one form of a
CMXCI) Zone III: angle of mandible to skull base single cell type
MXIV) Repair: Cell proliferation to repair and
248) Management of neck trauma: general principles restore toward normal structure and function
CMXCII) Zone I MXV) Tumor: Any swelling from whatever cause
i) Asymptomatic: angiography,
esophagolaryngoscopy, then observation or
neck exploration given findings
ii) Symptomatic: angiography, then neck
exploration
CMXCIII) Zone II
i) Asymptomatic: directed exam (angiography,
esophagoscopy and/or laryngoscopy) then
either surgical exploration or serial exams and
close observation
ii) Symptomatic: neck exploration
CMXCIV) Zone III
i) Asymptomatic: angiography, esophago-
laryngoscopy, then observation or neck
exploration given findings
ii) Symptomatic: angiography, then either neck
exploration or interventional radiology
249) Definitions from highlights & pearls in KJ Lee
CMXCV) Acanthosis: increased thickness of prickle
cell layer
CMXCVI) Anaplasia: change in a cell or tissue to a
less highly differentiated form
CMXCVII) Atrophy: diminution in the size of cells,
organ, or tissue after a stage of full development
CMXCVIII) Carcinoma in situ: growth disturbance in
which there is sufficient atypicality of the epithelial
cells and their arrangement to warrant the diagnosis
of cancer in the absence of invasion
CMXCIX) Choristoma: similar to hamartoma except
the component tissues are not normally present in
that part of the body
M) Desmoplasia: connective tissue reaction to tumor
 Nose & Paranasal Sinuses MXXXVI)
i)
Findings
Hypogonadotropic hypogonadism
ML) Nasal valve competency tested with the Cottle
maneuver
ii) Micropenis
250) What are the six cell types found in olfactory epithelium?
iii) Cryptorchidism 261) Discuss nasal airway evaluation
MXVI) Ciliated bipolar receptor cells (increase
iv) Unilateral renal agenesis MLI) Rhinomanometry
surface area, lack dynein arms and do not beat)
v) Agenesis of the olfactory lobes (anosmia) i) Measures the resistance to airflow in the nose
MXVII) Microvillar cells: 1/10th as frequent as
vi) Deafness ii) Cannot identify specific sites of obstruction
bipolar cells, may have a receptor function (unknown
vii) Midline facial deformities iii) Technique
currently)
viii) Diabetes (1) Anterior rhinomanometry: occlusion of one
MXVIII) Sustentacular cells: microvilli, insulate
nostril with an inflatable cuffed pressure
bipolar cells, deactivate odorants, protect epithelium
257) Etiology of olfactory dysfunction sensor measures nasopharyngeal
from foreign agents, regulate mucus composition
MXXXVII) Obstructive nasal disease (23%): polyps, pressure; nonphysiologic, as all airflow
MXIX) Lining epithelium of Bowman’s glands &
edema, tumors, nasal deformity happens through one nostril
ducts
MXXXVIII) Postinfectious (19%): viral injury to (2) Posterior rhinomanometry: placement of
MXX) Horizontal (dark) basal cells
olfactory neurons pressure catheter in mouth which can
MXXI) Globose (light) basal cells
MXXXIX) Head trauma (15%): shearing of accurately measure nasopharyngeal
filaments, olfactory bulb contusion, frontal lobe injury pressure
251) Differences between olfactory and respiratory epithelium
MXL) Toxins/medications (3%) iv) Total nasal resistance greater than 0.3Pa/cm2
MXXII) Olfactory epithelium is thicker (60-70nm)
MXLI) Miscellaneous (21%): aging, congenital, usually is symptomatic
than respiratory epithelium (20-30nm)
neoplastic, psychogenic, other v) Marked reduction in resistance after
MXXIII) Olfactory epithelium has cilia that lack
MXLII) Idiopathic (21%) decongestion infers mucosal disease; <35%
dynein arms
reduction in resistance infers a structural cause
MXXIV) At physiologic flow rates olfactory
258) Name the 4 main functions of the nasal airway MLII)Acoustic rhinometry
epithelium gets ~15% of nasal airflow, 50% flows
MXLIII) To provide heat & moisture for warming & i) Analyzes sound pulses reflected from the
through middle & inferior meatuses
humidifying inspired air airway, can accurately identify narrow airway
MXLIV) To alter airway resistence through segments
252) Describe Foster Kennedy syndrome
congestion & decongestion of the mucosa ii) Does not rely on nasal airflow, but cannot
MXXV) Due to tumors of the olfactory groove or
MXLV) To clean & filter inspired air measure the effects of narrow regions on
sphenoid ridge
MXLVI) To sense the environment through the airflow dynamics or resistance
MXXVI) Ipsilateral anosmia/hyposmia, ipsilateral
specialized & general sensory nerves (olfactory & iii) Maximum narrowing lies within first 2 cm,
optic atrophy, central papilledema
trigeminal) corresponds to the nasal valve and the pyriform
aperture at the level of the head of the inferior
253) Methods of olfactory testing
259) Describe the autonomic supply to the nasal mucosa turbinate
MXXVII) Subjective odorant testing
MXLVII) Sympathetics: preganglionics from
MXXVIII) Standardized psychophysical tests, eg.
sympathetic chain synapse in the superior cervical 262) Foramen of maxilla
UPSIT test, highly reliable
ganglion; postganglionics travel with ICA, split off as MLIII) Infraorbital
MXXIX) Electrophysiologic tests
deep petrosal nerve and joins with greater superficial MLIV) Superior alveolar canal
i) Odor event-related potentials (OERP):
petrosal nerve to form the vidian nerve MLV) Maxillary ostium
experimental, identifies brain EEG activity after
i) Vasoconstrictor tone MLVI) Accessary maxillary ostium
odor presentation; far field potentials, cannot
MXLVIII) Parasympathetics: arise in superior MLVII) Incisive canal
identify site of lesion
salivatory nucleus, preganglionics travel in nervus
ii) Electoolfactogram: electrode placed on
intermedius and branches off at the geniculate 263) Name the etiology of vasomotor rhinitis (nonstructural,
olfactory epithelium identifies summated
ganglion as the greater superficial petrosal nerve noninflammatory, nonautoimmune, nonallergic causes)
generator potentials of olfactory receptor
and becomes the vidian nerve, synapses at the MLVIII) Drugs
neurons
pterygopalatine ganglion, postganglionics distributed i) Antihypertensives
with sympathetics through maxillary trigeminal ii) Topicals: cocaine & nasal spray abuse
254) How does injury to olfaction occur?
branches to the nose MLIX) Hormonal
MXXX) Access of odorant changed
i) Vasodilation of capacitance & resistance i) OCP
MXXXI) Damage to olfactory nerve & receptors
vessels, also mediate nasal secretion ii) Pregnancy (estrogen effect in 2nd trimester)
MXXXII) Damage to central olfactory pathways
iii) Hypothyroidism
260) Nasal valve & nasal area MLX) Emotional causes
255) What’s the Moffett position?
MXLIX) Nasal valve: extends from caudal end of MLXI) Temperature mediated
MXXXIII) Improves efficacy of nasal steroid
upper lateral cartilages to anterior end of inferior MLXII) Environmental/Irritative rhinitis
application by laying upside down with one’s head
turbinates MLXIII) Gustatory rhinitis
hanging over the side
i) Influenced by nasal septum, upper lateral MLXIV) Endstage vascular atony of chronic
cartilage, pyriform aperture, anterior inferior allergic or inflammatory rhinitis
256) Kallmann’s syndrome
turbinate (cross sectional area 0.73 cm2) MLXV) Recumbency rhinitis
MXXXIV) Transmitted X-linked (Cummings)
ii) Nasal valve angle: junction between nasal MLXVI) Paradoxic nasal obstruction and nasal
MXXXV) Deficiency of hypothalamic GnRH
septum and caudal edge of upper lateral cycle
secretion
cartilage (10-15 degrees)
 MLXVII) Nonairflow rhinitis (postlaryngectomy, iii)
Intradermal testing: more sensitive &
choanal atresia, adenoid hyperplasia) reproducible 274) 3 Differences between mucosa of nose and sinuses
MLXVIII) Compensatory hypertrophic rhinitis iv) Serial dilution endpoint testing: intradermal test, MCI) Ciliated cells more concentrated at the ostia
MLXIX) Eosinophilic/basophilic nonallergic rhinitis determines more specific levels of atopy, used MCII) Increased number of goblet cells present
(NARES): similar to allergic rhinitis, lacks the IgE to determine immunotherapy concentrations in the nose
mediated immunopathologic events MLXXXV) Direct measurement of allergen-specific
MLXX) Idiopathic IgE in serum 275) 5 etiologic factors for polypoid nasal lesions
i) Serum incubated with known antigens on a MCIII) Allergy
264) Etiology of vasomotor rhinitis during pregnancy matrix; excess serum washed off, and residual MCIV) Cystic fibrosis
MLXXI) 20% of pregnancies, usually 1st & 3rd complexes incubated with anti-IgE and a MCV) Samter’s triad
trimesters marker MCVI) Kartegener’s syndrome
MLXXII) Increased estrogen levels inhibits (1) Radioactive marker: RAST test MCVII) Fungal atopy
acetylcholinesterase activity, leads to increasedAch (2) Fluorescent marker: ELISA
in parasympathetic nervous system, causes swelling ii) More specific but less sensitive cf. skin tests, 276) Nasal polyposis and asthma, drug that makes it worse,
& edema of nasal mucosa takes longer to do (days) what mechanism, what triad?
MLXXIII) Treatment: oral antihistamines & MCVIII) ASA
decongestants 270) Treatment strategy for allergy MCIX) Samter’s triad
MLXXXVI) Avoidance MCX) Thought to block oxidative
265) Define atrophic rhinitis MLXXXVII) Pharmacotherapy phosphorylation; anti-inflammatory actions due to
MLXXIV) Classified as a transformation of the i) Topical decongestants blockage of cyclooxygenase enzyme; polyp formation
respiratory pseudostratified columnar epithelium to a ii) Systemic decongestants influenced by stimulation of 5-lipoxygenase, which
keritanized squamous epithelium that sloughs off iii) Cromolyn (mast cell stabilizer, decreases influx causes leukotriene overproduction
of calcium)
266) Differential of granulomatous lesions of the sinonasal tract iv) Steroids (spray, turbinate injection): considered 277) What are the most common benign nasal cavity lesions in
MLXXV) Autoimmune 1st line therapy order of frequency?
i) Wegener’s v) Immunotherapy MCXI) Osteoma (most commonly in the frontal
ii) Sarcoidosis sinus)
iii) Relapsing polychondritis 271) 5 effects of corticosteroids in allergic rhinosinusitis MCXII) Hemangioma
MLXXVI) Infectious MLXXXVIII) Decreased capillary permeability MCXIII) Papilloma
i) TB (vasoconstriction) MCXIV) Angiofibroma
ii) Leprosy MLXXXIX) Decreased glandular response to
iii) Sporotrichosis cholinergic stimulation 278) 5 types of nasopharyngeal cysts
iv) Blastomycosis MXC) Interferes with arachidonic acid MCXV) Rathke’s pouch cyst: remnant of
v) Histoplasmosis metabolism (decreases PG/LT/TX production) invaginated ectoderm that forms the anterior pituitary
vi) Coccidiomycosis MXCI) Decreased influx of eosinophils, basophils gland; located high in nasopharynx near
vii) Rhinoscleroma & T-lymphocytes into the nasal epithelium sphenovomeral junction
MXCII) Stabilize lysosomal membranes MCXVI) Thornwaldt’s cyst: inferior to Rathke’s
267) How to detect eosinophilia on nasal smears MXCIII) Block action of migratory inhibitory factor pouch, remnant of caudal notochord; filled with
MLXXVII) Acquire sample of nasal mucus (wax jellylike material
paper or swab), smear on slide 272) What are the indications for immunotherapy in allergic MCXVII) Intraadenoidal: from median pharyngeal
MLXXVIII) Stain with Hansel stain (eosin & sinusitis? recess, opens onto adenoid bed
methylene blue) MXCIV) IgE mediated symptoms not readily MCXVIII) Extraadenoidal: deep within
MLXXIX) Positive criteria: >25% eosinophil content, controlled by pharmacologic means pharyngobasilar fascia, remnant of the pharyngeal
or if eosinophils, mast cells & goblet cells are MXCV) Symptoms persisting for greater than one bursa; usual findings are a cuff of granulation tissue
present season rostral to the pharyngeal tubercle
MXCVI) Severe symptomatology MCXIX) Branchial cleft cyst: arises from 1st & 2nd
268) Describe the Gell & Coombs 4 hypersensitivity reactions MXCVII) Symptoms caused by allergens not easily pharyngeal pouches, usually paired, present on
MLXXX) Type I: Immediate avoided lateral walls; treated by excision
MLXXXI) Type II: Cytotoxic MXCVIII) Motivated patients willing to undergo a
MLXXXII) Type III: Immune complex program that may last up to 5 years 279) Describe the four cell types making up the nasal
MLXXXIII) Type IV: Delayed epithelium
273) What is the mechanism of action of immunotherapy? MCXX) Pseudostratified ciliated columnar
269) Methods of testing for atopy MXCIX) Parenteral administration of antigens epithelium: 50-200 cilia per cell beating 10-
MLXXXIV) Skin tests: detect presence of IgE- identified on appropriate in vivo or in vitro tests to 20/second at physiologic temperature, moves mucus
mediated allergy; takes little time to do (~1 hr), but stimulate formation of allergen-specific IgG blocking 3-35mm/minute
uncomfortable, risk of anaphylaxis antibodies which will compete with IgE for binding MCXXI) Pseudostratified nonciliated columnar
i) Scratch tests: neither sensitive nor sites on mast cells or basophils epithelium: possess microvilli that expand the
reproducible MC) Typically twice a week until a response is noted, then surface area of the epithelium
ii) Prick tests: not sensitive for low levels of atopy q1 weeks x 1 year, q2 weeks x 2 years, q3 weekly x MCXXII) Goblet cells
3 years MCXXIII) Basal cells
 MCXXIV) Other cell types 286) Holman-Miller sign MCLXVII) Otologic, tracheal, renal involvement rare
i) Stratified squamous epithelium in nasal MCXLVI) Anterior bowing of posterior maxillary in lymphoma
vestibule sinus wall & enlargement of superior orbital fissure,
ii) Olfactory epithelium found along roof of nose indicates JNA invasion of pterygopalatine fossa 293) Differential diagnosis of fibroosseous lesions
MCLXVIII) Osteoma
280) Mucous layer in upper resp tract, 2 layers and function of 287) Biopsy of which 4 nasal masses are at significant risk of MCLXIX) Osteochondroma
each hemorrhage? MCLXX) Ossifying fibroma
MCXXV) Sol layer: thin periciliary layer which allows MCXLVII) JNA MCLXXI) Fibrous dysplasia
cilia to be mobile; produced by microvilli MCXLVIII) Hemangiopericytoma
MCXXVI) Gel layer: thick layer of mucoglycoproteins MCXLIX) Hemangioma 294) Discuss hemangioperictyoma
in which cilia embed themselves; produced by goblet MCL) AV malformations MCLXXII) Originate from pericytes of Zimmermann
cells and submucosal glands, propelled by cliliated MCLXXIII) Occurs wherever there are capillaries,
epithelium 288) Potential complications of radiotherapy for management of MSK and skin predilection
JNA? MCLXXIV) Unpredictable, considered malignant &
281) 3 stages of sphenoid sinus pneumatization MCLI) Radiotherapy used in past successfully infiltrative
MCXXVII) Pneumatization starts between 5 & 7 for primary therapy, recurrences, inoperable tumors MCLXXV) Treatment: wide surgical excision;
years of age, complete by 20-25 years MCLII) Complications radiotherapy palliative, no initial role unless margins
MCXXVIII) Stages i) Failure of treatment positive or lesion unresectable
i) Conchal (3%) ii) Induction of malignancy
ii) Presellar (11%) iii) Failure of facial growth centers 295) Contraindications to IV iodinated contrast for CT
iii) Sellar (86%) iv) Cataract formation MCLXXVI) Absolute
i) Previous adverse reaction
282) Incidental findings of sphenoid sinusitis on imaging: what 289) Difference between a mucocele and a mucus retention ii) Severe renal insufficiency
do you do? cyst MCLXXVII) Relative
MCXXIX) Consider the optic complications, 25% of MCLIII) Mucocele: a chronic, cystic lesion of the i) Mild renal insufficiency
patients with sphenoid sinusitis have neurophthalmic paranasal sinuses lined with pseudostratified or low ii) Atopy
dysfunction columnar epithelium containing occasional goblet iii) Asthma
cells iv) Advanced age
283) What factors are present in nasal secretions which fight MCLIV) Mucus retention cyst: retained mucus v) Dehydration
infection? within a blocked goblet cell, lined by sinus mucosa vi) Cardiac disease
MCXXX) IgA rather than a true epithelium vii) Use of beta-blockers
MCXXXI) IgG
MCXXXII) Interferon 290) Differential diagnosis of small round cells on nasal biopsy 296) 2 benefits, 2 limitations of MRI for sinuses
MCXXXIII) Lysozyme MCLV) Rhabdomyosarcoma MCLXXVIII) Benefits
MCXXXIV) Lactoferrin MCLVI) Esthesioneuroblastoma i) Differentiation of soft tissue involvement
MCLVII) Lymphoma ii) Differentiation of soft tissue from fluids
284) What local factors influence nasal ciliary motility? MCLVIII) Melanoma iii) Multiplanar capabilities with minimal patient
MCXXXV) Primary ciliary abnormalities MCLIX) Poorly differentiated carcinoma (SNUC) movement
MCXXXVI) Temperatures <18 C MCLX) Hemangiopericytoma iv) No exposure to radiation
MCXXXVII) Excessive acidic or basic environment MCLXI) Immature teratoma MCLXXIX) Limitations
(optimal ciliary function @ pH 7.0) MCLXII) Carcinoid i) Poor visualization of bony involvement
MCXXXVIII) Mucosal to mucosal surface contact ii) Increased cost cf. CT scan
MCXXXIX) Allergy 291) 60 year old female with blocked nose, npx. Bx is LCA iii) Limitations due to metal
MCXL) Rhinitis medicamentosa (chronic abuse) positive cytokeratin negative. What is this? What is ruled
MCXLI) Humidity <50% out? 297) General advantages & disadvantages of MRI
MCXLII) Dehydration MCLXIII) Lymphoma; SCC ruled out by negativity of MCLXXX) Advantages
MCXLIII) Hypertonic or hypotonic solutions cytokeratin i) Better soft tissue definition than CT
MCXLIV) Infection (viral, bacterial) ii) Multiplanar capability
292) 3 histologic and clinical differences of T-cell lymphoma iii) Clear delineation of arteries, veins, major
285) 5 clinical features of Kartagener’s (immotile cilia) and Wegener’s granulomatosis of the nose cranial nerves
syndrome, abnormalities in cilia? MCLXIV) Wegner’s has diffuse nasal ulcerations iv) Less invasive than CT
MCXLV) Autosomal recessive inherited lack of whereas lymphoma lesions are focal, localized & v) Absence of ionizing radiation
dynein arms in A-tubules (9+2 microtubule structure) explosive vi) Absence of beam-hardening artifacts from
i) Sinusitis MCLXV) Wegner’s has a small & medium vessel dental implants
ii) Bronchiectasis vasculitis, lymphoma has a polymorphic lymphoid MCLXXXI) Disadvantages
iii) Chronic cough infiltrate with angiocentric & angioinvasive features i) Prolonged data collection times
iv) Situs inversus & dextrocardia MCLXVI) Wegner’s has an inflammatory cell ii) Higher sensitivity to patient motion
v) Infertility (male) infiltrate, lymphoma has a primarily lymphocytic iii) Scanning not possible with history of
vi) Otitis media infiltrate pacemakers, certain implants, metallic foreign
bodies
 iv) Inferior bony detail ii) Chronic invasive
v) Claustrophobia may prohibit examination MCCV) Noninvasive 309) Etiologic agents in acute sinusitis
vi) Higher equipment cost & exam cost i) Allergic fungal MCCXVIII) Pneumococcus
ii) Mycetoma MCCXIX) H. influenzae
298) CT, MRI findings for common nasal pathology iii) Saprophytic MCCXX) M. catarhallis
MCLXXXII) Mycetoma: hyperintense on CT, MCCXXI) S. pyogenes
hypointense on T1/T2 304) Definition of allergic fungal sinusitis for diganosis (Bent & MCCXXII) Peptostreptococcus
MCLXXXIII) Allergic mucin: hyperintense on CT, Kuhn) MCCXXIII) Fusobacterium
hypointense on T2 (lack of water) MCCVI) Testing or history positive for fungal atopy MCCXXIV) Bacteroides
MCLXXXIV) Polyps: low density on CT, hypointense on MCCVII) Nasal polyps
T1, hyperintense on T2 MCCVIII) CT scan with hyperdense material in 310) Etiologic agents in chronic sinusitis
MCLXXXV) Mucocele: any pattern depending on sinus cavity and possible sinus wall erosion or MCCXXV) Greatly increased role of anaerobes
hydration; typically hypointense on CT, hyperintense expansion of the sinus cavity (Peptococcus, Bacteroides, Peptostreptococcus)
on T1 (when dehydrated), hyperintense secretions MCCIX) Allergic mucin with eosinophil MCCXXVI) Pneumococcus, H. flu, Moraxella still
on T2 with hypointense central area preponderance common, but S. aureus & Pseudomonas play larger
MCLXXXVI) Fibrous dysplasia: featureless trabecular MCCX) Identification of fungus in mucous by role
pattern on CT, hypo to hyper on T1, T2 homogenous stain, culture, ELISA, PCR
(like air) MCCXI) No evidence of invasion by fungus 311) Antibiotic therapy for community-acquired bacterial
sinusitis
527) Describe the structures involved in the osteomeatal unit 305) 4 histopathologic findings of allergic mucin in fungal MCCXXVII) First line
(OMU) sinusitis? i) Amoxicillin
I) Uncinate process i) Eosinophils ii) Erythromycin-sulfisoxasole
II) Ethmoid bulla ii) Fungal elements & hyphae iii) Keflex & Septra
III) Infundibulum iii) Charcot-Leyden crystals (byproduct of MCCXXVIII) Second line
IV) Middle turbinate eosinophil degranulation) i) Clavulin
V) Maxillary sinus ostium iv) Necrotic inflammatory cellular debris ii) Extended macrolides (clarithromycin,
azithromycin)
299) Anatomic variations influencing incidence of sinusitis 306) What fungi are most commonly seen in allergic fungal iii) Cephalosporins (cefpodoxime, cefuroxime,
MCLXXXVII) Conchal bullosa sinusitis? cefprozil)
MCLXXXVIII) Septal deviation and spur MCCXII) Aspergillus (most common) iv) Quinolones (ciprofloxacin, levofloxacin)
MCLXXXIX) Lateral convexity of the middle turbinate MCCXIII) Demitaceous species
MCXC) Haller cells i) Alternaria 312) Indications for surgical intervention in acute bacterial
MCXCI) Prominent agger nasi cells ii) Bioplaris sinusitis
MCXCII) Prominent ethmoidal bulla iii) Curvularia MCCXXIX) Impending complications of sinusitis
MCXCIII) Pneumatization and inversion of the iv) Cladosporium MCCXXX) Severe pain
uncinate plate v) Dreshleria MCCXXXI) Nonresponse to medical therapy
MCCXXXII) Immunosuppressed patient
300) Name the 4 structures visible on the walls of the sphenoid 307) Characteristics of fungal hyphae in invasive fungal
sinus sinusitis 313) 4 chemical mediators in chronic sinusitis
MCXCIV) Optic nerve: projects into sinus less MCCXIV) Mucor: broad & ribbonlike (10-15 um), MCCXXXIII) Leukotrienes
commonly, ~50%; bone dehiscent ~4% of time irregular, rarely septated; order Mucorales in MCCXXXIV) Prostaglandins
MCXCV) Internal carotid artery: medial deflection Zygomycetes class, most virulent and common is MCCXXXV) Interleukins
into lateral wall called the carotid sulcus, present 65- Rhizopus oryzae MCCXXXVI) PAF
98% of time; bone dehiscent in ~7-22% i) More commonly seen in diabetic ketoacidotic MCCXXXVII) TNF
MCXCVI) Maxillary division of trigeminal nerve patients
MCXCVII) Vidian nerve MCCXV) Aspergillus: narrow hyphae, regular 314) What is the management of a frontal sinusitis and brain
septations, 45 degree branching; most virulent & abscess in 10 year old?
301) Pathophysiologic mechanisms of infectious sinus disease frequent species found in those with invasive fungal MCCXXXVIII) CT
MCXCVIII) Ostial patency sinusitis; typically A. fumigatus in North America MCCXXXIX) Neurosurgical consult
MCXCIX) Ciliary function i) More commonly seen in immune compromised MCCXL) Surgical debridement of sinuses
MCC) Status of nasal secretions patients with neutropenia
315) What are the frontal veins of Breschet in the frontal bone
302) Timeframe of rhinosinusitis 308) DM pt with sugars out of control, acute onset sharp R and what is their significance?
MCCI) Acute: 1 day to 4 weeks facial pain, opacification of right maxillary sinus with bony MCCXLI) Perforating veins connecting the
MCCII) Subacute: 4 to 12 weeks destruction, what is dx and what would you see on intracranial and extracranial venous draining
MCCIII) Chronic: Greater than 12 weeks anterior rhinoscopy systems
MCCXVI) Mucormycosis; necrosis of nasal mucosa, MCCXLII) A potential pathway of hematologic spread
303) 5 types of fungal sinusitis classification ischemic infarction, granular serosanguinous of infection
MCCIV) Invasive rhinorrhea; fungal hyphae may be seen
i) Acute invasive (mucormycosis) MCCXVII) Stains: Gomorri silver methenamine, KOH
 MCCXLIII) If not cleared in frontal sinus obliteration, iii) CSF leak repair 326) Describe the embryologic derivations of the
can harbor mucosa and cause mucopyocele iv) Anterior skull base lesion ethmoturbinals
formation MCCLXI) Complications MCCLXXIX) 1st ethmoturbinal: uncinate process
i) Bleeding/crusting MCCLXXX) 2nd ethmoturbinal: ethmoid bulla
316) Sinusitis pathways of spread ii) Epiphora MCCLXXXI) 3rd ethmoturbinal: basal lamella &
MCCXLIV) Hematogenous spread: retrograde iii) Frontal sinusitis attachment of middle turbinate to lateral nasal wall
thrombophlebitis through valveless veins (veins of iv) Diplopia or blindness MCCLXXXII) 4th ethmoturbinal: attachment of superior
Breschet) v) CSF leak turbinate to lateral nasal wall
MCCXLV) Direct extension vi) Intracranial hemorrhage MCCLXXXIII) 5th & 6th: usually fuse and degenerate, but
i) Preformed pathways: eg. natural dehiscence of occasionally can form a supreme turbinate
lamina 321) Major landmarks along the medial orbital wall
ii) Traumatic/surgical pathways: eg. traumatic MCCLXII) Blood vessels found along the 327) Development of the paranasal sinuses
dehiscence of lamina papyracea frontoethmoid suture, which divides the ACF from MCCLXXXIV) Maxillary
iii) Osteomyelitis: eg. Pott’s puffy tumor the ethmoid sinuses i) Present at birth, conspicuous growth by 3
MCCLXIII) Anterior ethmoid artery ~14-22mm years
317) Chandler classification of orbital complications in sinusitis posterior to the anterior lacrimal crest ii) Inferior expansion starts at time of permanent
MCCXLVI) Preseptal cellulitis (maxillolacrimal suture) dentition (7-8 years)
MCCXLVII) Orbital cellulitis MCCLXIV) Posterior ethmoid artery ~10-12mm iii) Reaches adult size by midadolescence
MCCXLVIII) Subperiosteal abscess posterior to the anterior ethmoid artery MCCLXXXV) Ethmoids
MCCXLIX) Orbital abscess MCCLXV) Optic nerve ~6mm (4-7mm) posterior to i) Present at birth
MCCL) Cavernous sinus thrombosis the posterior ethmoid artery ii) Pneumatization begins significantly at 3-7
years, reaches adult form by 12-14 years
318) Organisms seen in orbital/periorbital cellulitis 322) 3 approaches to frontal mucocele, adv/disadv of each MCCLXXXVI) Sphenoid
MCCLI) H. influenzae MCCLXVI) Lynch frontoethmoidectomy: i) Does not pneumatize and become clinically
MCCLII) S. aureus ethmoidectomy plus removal of entire frontal sinus significant until 4-5 years
MCCLIII) Group A Streptococci floor ii) Growth complete by midadolescence, variable
MCCLIV) S. pneumoniae MCCLXVII) Osteoplastic flap: Advantage – eradication pneumatization
MCCLV) Bacteroides species of disease and mucosa; Disadvantage – requires MCCLXXXVII) Frontal
MCCLVI) Peptostreptococci coronal approach, disfiguring i) Not present at birth, begins growth in the 3rd
MCCLVII) Veionella MCCLXVIII) Endoscopic: Adv – all incisions made year, continues into adolescence;
intranasally; Disadv – cannot access sinuses to pneumatization higly variable
319) Indications and complications of the Caldwell Luc eradicate mucosa, osteomas
procedure 328) Define the following sinuses and air cells
MCCLVIII) Indications 323) Indications for osteoplastic flap obliteration of the frontal MCCLXXXVIII) Suprabullar recess: air cell space left
i) Chronic maxillary sinusitis sinus between the ethmoid bulla and the fovea ethmoidalis
ii) Maxillary sinus disease refractory to MCCLXIX) Osteomyelitis when the bulla does not extend up to the fovea
endoscopic surgery MCCLXX) Frontal sinus tumor MCCLXXXIX) Sinus lateralis/retrobullar recess: air cell
iii) Antrochoanal polyp MCCLXXI) Chronic frontal sinusitis with persistent space found between the posterior surface of the
iv) Multiseptate maxillary mucocele symptoms despite previous intervention ethmoid bulla and the vertical portion of the basal
v) Maxillary sinus foreign body or mycetoma MCCLXXII) Frontal sinus fracture with comminuted lamella
vi) Approaches to pterygomaxllary space (Imax anterior table MCCXC) Sinus terminalis: uncinate process
ligation, vidian neurectomy, biopsy of skull base terminates in the lamina papyracea, frontal recess
lesions) 324) Historical open frontal sinus procedures drains medial to the uncinate process, this sinus is
vii) Trauma repair MCCLXXIII) Killian: removal of floor and anterior wall, essentially a superior ending of the infundibulum
viii) Oroantral fistula repair retain frontal bar (blind pocket)
ix) Orbital decompression of Grave’s MCCLXXIV) Reidel: entire floor & frontal wall of sinus MCCXCI) Agger nasi cell: remnant of 1st
ophthalmopathy are removed; significant cosmetic deformity ethmoturbinal, found superior, lateral & anterior to
MCCLIX) Complications MCCLXXV) Lothrop/Chaput-Mayer: intersinus septum attachment of the middle turbinate; can also refer to
i) Cheek edema & ecchymosis taken down ethmoid cells anterior to the frontal duct
ii) Hypesthesia of infraorbital n. distribution MCCXCII) Haller cell: an infraorbital ethmoid cell,
iii) Epiphora 325) Keros classification of lateral cribriform plate lamella pneumatizes into the maxilla
iv) Oroantral fistula length MCCXCIII) Onodi cell: aka. sphenoethmoidal cell, a
MCCLXXVI) Type 1: cribriform plate 1-3mm below posterior ethmoid air cell pneumatizing into the
320) Indications & complications of external fovea sphenoid
frontoethmoidectomy MCCLXXVII) Type 2: cribriform plate 4-6mm below
MCCLX) Indications fovea 329) What is a frontal cell?
i) Frontoethmoid mucopyocele or sinusitis with MCCLXXVIII) Type 3: cribriform plate 7-16mm below MCCXCIV) An anterior ethmoid cell above the agger
orbital involvement fovea nasi that can obstruct the nasofrontal recess or the
ii) Revision surgery with absent or distorted frontal sinus
landmarks MCCXCV) Types
 i) Type I: single frontal recess cell above agger MCCCXIII) Caused by sphenoid sinusitis, neoplasm, MCCCXXVIII) Woodruff’s plexus (naso-nasopharyngeal
nasi but below the floor of the frontal sinus trauma plexus): located in posterior nasal cavity along lateral
ii) Type II: multiple cells in frontal recess above MCCCXIV) Involves CN III, IV, V1, VI; CN II usually wall inferior to the inferior turbinate
agger nasi but below floor of frontal sinus not involved as it is in its own canal i) Pharyngeal branch of the internal maxillary
iii) Type III: single cell pneumatizing cephalad into MCCCXV) Symptoms artery
frontal sinus i) Orbital pain & photophobia ii) Posterior lateral nasal artery
iv) Type IV: Single isolated cell within the frontal ii) Ophthalmoplegia & upper eyelid paralysis
sinus iii) Failure of accommodation 339) Management of epistaxis
iv) Proptosis MCCCXXIX) Medical
330) Surgical approaches to the sphenoid sinus v) Forehead paresthesia/hypoesthesia i) Cauterization: silver nitrate, electrocautery
MCCXCVI) Transseptal ii) Packing: anterior, posterior, combined, balloon
i) Sublabial transseptal 335) Describe the features of cavernous sinus syndrome packs
ii) Intranasal transseptal MCCCXVI) Caused by ethmoiditis, 80% mortality rate iii) Greater palatine canal injection
iii) External rhinoplasty transseptal MCCCXVII) Symptoms: orbital pain (V1), venous MCCCXXX) Radiologic
MCCXCVII) Transantral congestion of retina, lids, conjunctiva, proptosis & i) Embolization of internal maxillary & facial
MCCXCVIII) Transethmoidal exophthalmos; photophobia, CN II, III, IV, V1 arteries
i) Internal involvement MCCCXXXI) Surgical
ii) External MCCCXVIII) Treatment: antibiotics, anticoagulation i) Maxillary artery ligation: transantral or transoral
MCCXCIX) Endoscopic (ideal for inflammatory ii) Sphenopalatine artery ligation: transantral,
disease) 336) 3 useful landmarks for revision ESS? endoscopic
i) Intranasal sphenoethmoidectomy MCCCXIX) Superior attachment of middle turbinate iii) Ethmoid artery ligation: Lynch
ii) Transantral sphenoethmoidectomy MCCCXX) Maxillary ostium frontoethmoidectomy approach
MCCC) Transpalatal: ideal for tumors involving the MCCCXXI) Sphenoid sinus ostium iv) External carotid artery ligation
nasopharynx, posterior pharyngeal wall, and MCCCXXII) Skull base
choanae MCCCXXIII) Lamina papyracea 340) 2 vessels that must be ligated in a transantral maxillary
MCCCXXIV) Roof of maxillary sinus artery ligation to prevent recurrent epistaxis from
331) 4 anterior to posterior bony lamina encountered in ESS collaterals
MCCCI) Uncinate process 337) Blood supply to the nose MCCCXXXII) Sphenopalatine artery
MCCCII) Ethmoid bulla MCCCXXV) Internal carotid artery branches MCCCXXXIII) Descending palatine artery
MCCCIII) Vertical portion of the basal lamella i) Anterior ethmoid artery
MCCCIV) Anterior wall of sphenoid sinus ii) Posterior ethmoid artery 341) Complications of posterior nasal packing
iii) Each divides into a medial branch (Little’s area MCCCXXXIV) Airway obstruction & exacerbation of OSA
332) Bony components of the medial orbital wall & septum) and a lateral branch (superior & MCCCXXXV) Dyspnea
MCCCV) Frontal process of the maxilla middle turbinates) MCCCXXXVI) Sinusitis
MCCCVI) Lacrimal bone MCCCXXVI) External carotid artery branches MCCCXXXVII) Otitis media
MCCCVII) Lamina papyracea of the ethmoid i) Terminal branches of the internal maxillary MCCCXXXVIII)Toxic shock syndrome
MCCCVIII) Sphenoid bone (just anterior to the optic artery MCCCXXXIX) Septal or alar necrosis
canal) (1) Sphenopalatine artery: supplies septum
(2) Posterior nasal artery: supplies lateral 342) Osler Weber Rendu syndrome (hereditary hemorrhagic
333) Your postop ESS patient develops a postoperative orbital nasal wall telangiectasia)
hematoma. What are your management considerations? (3) Pharyngeal branch: supplies posterior MCCCXL) Autosomal dominant
MCCCIX) Fast (arterial) vs. slow (venous) nose & nasopharynx MCCCXLI) Multiple telangiectasias of the skin and
hematoma formation (4) Descending palatine artery: splits into mucosa
MCCCX) Proptosis, pupil changes, vision loss greater and lesser palatine arteries; MCCCXLII) Present with recurrent epistaxis,
indications for immediate intervention greater palatine artery supplies anterior pulmonary, GI & CNS bleeds
MCCCXI) Medical treatment septum & floor of nose through the MCCCXLIII) Treatment: manage anemia/acute bleeds;
i) Ophthalmology consultation incisive branch septal dermoplasty for epistaxis
ii) Orbital massage ii) Superior labial artery: a branch off the superior
iii) Mannitol 1-2mg/kg in 20% infusion labial, supplies the septum and ala
iv) Steroids (controversial)
v) Acetazolamide 338) Describe the two nasal vascular arterial plexuses and their
vi) Timolol ophthalmic drops blood supply
MCCCXII) Surgical treatment MCCCXXVII) Little’s area/Kiesselbach’s plexus: found
i) Lateral canthotomy on the anterior septum
ii) Medial external (Lynch) decompression i) Anterior ethmoid artery
iii) Endoscopic decompression ii) Sphenopalatine artery
iv) Anterior chamber paracentesis iii) Greater palatine artery
iv) Nasal branch of the superior labial artery
334) 4 features of superior orbital fissure syndrome
 Facial Plastics & Reconstructive MCCCLXII) Zone II/III failure with intact zone I;
endothelial & parenchymal swelling & intravascular
MCCCLXXXIII) Platysma: occipital, postauricular, facial,
superior thyroid, transverse cervical
stasis MCCCLXXXIV) Temporoparietal: superficial
343) Discuss titanium as a facial implant material
MCCCLXIII) Xanthine oxidase: responsible for temporal artery & vein
MCCCXLIV) Lightweight, resists corrosion
conversion of hypoxantine to uric acid after MCCCLXXXV) Postauricular: posterior auricular artery
MCCCXLV) Most biocompatible; soft, deformed by
restoration of oxygen to hypoxic tissue, produces MCCCLXXXVI) Forehead: used for oropharynx
loading forces
superoxide ions recon, based on superficial temporal artery
MCCCXLVI) Forms titanium oxide on surface (10nm),
interacts with protein for binding
349) Oxygen free radical scavengers 354) Advantages of free flaps over local or regional flaps
MCCCLXIV) Allopurinol (xanthine oxidase inhibitors) MCCCLXXXVII) Two team approach
344) Biocompatibility of facial implants
MCCCLXV) Superoxide dismutase MCCCLXXXVIII) Immediate single stage
MCCCXLVII) Cells don’t adhere directly
MCCCLXVI) Deferoxamine reconstruction
MCCCXLVIII) Substances in extracellular matrix binds
MCCCLXVII) Vitamins E, A, C MCCCLXXXIX) Large number of donor sites
the cell to the surface (fibronectin, vitronectin,
MCCCLXVIII) Glutathione available
globulin, proteoglycans)
MCCCXC) Unrestricted positioning and reach
MCCCXLIX) Extracellular matrix in bone around bone
350) What are the advantages & disadvantages of local flaps MCCCXCI) Large amount of composite tissue
must mineralize for compression
MCCCLXIX) Advantages MCCCXCII) Potential for sensate, motor & secretory
(1) Use of local tissue with better donor site function
345) Name the four zones of the circulatory system applied to
match MCCCXCIII) Improved vascularity and healing
flap perfusion
(2) One stage in most cases MCCCXCIV) Can cover any defect (larger tumor free
MCCCL) Zone I: cardiopulmonary system, arteries
(3) Low donor site morbidity margins)
& veins, lymphatic system
MCCCLXX) Disadvantages MCCCXCV) Permits primary placement of
i) Supplies flap through musculocutaneous,
(1) Random pattern blood supply with limited osseointegrated implants
septocutaneous branches
length
MCCCLI) Zone II: capillary circulation
(2) Distortion surrounding structures due to 355) Characteristics of an ideal free flap
i) Flow controlled by precapillary & preshunt
donor site closure in some instances MCCCXCVI) Minimal donor site morbidity
sphincters
(3) Not enough bulk for deep defects MCCCXCVII) Two team approach for resection and
ii) Precapillary sphincters under control by local
harvest of flap
hypoxia & metabolic byproducts
351) What are the three main types of local flaps MCCCXCVIII) Adequate length and caliber of vessels
iii) Preshunt sphincters under autonomic control
MCCCLXXI) Pivotal MCCCXCIX) Tissue composition similar to that of
(norepinephrine)
i) Rotation (curvilinear) defect
MCCCLII) Zone III: interstitial space & mechanisms
ii) Transposition (linear): rhomboid, Dufourmental, MCD) Bulk and color matched to that of defect
of nutrient delivery, including capillary wall
bilobed MCDI) Innervation with sensation/motor function
i) Diffusion & convection (bulk flow)
iii) Interpolated (linear, base located some feasible
MCCCLIII) Zone IV: cells and its membranes
distance away from defect) MCDII) Excellent cosmetic potential
MCCCLXXII) Advancement MCDIII) Donor site previously unviolated
346) Classification of local skin flaps based on blood supply
i) Monopedicled MCDIV) Potential for osseointegration
MCCCLIV) Random cutaneous: no named vessels,
ii) Bipedicled
rely on dermal and subdermal plexus vessels
iii) V-Y 356) 5 useful signs for monitoring a cutaneous free flap
supplied by musculocutaneous arteries near the
iv) Hinged MCDV) Color
base of the flap
MCDVI) Temperature
MCCCLV) Arterial cutaneous/axial pattern:
352) Reconstruction of large skin defect under the eye MCDVII) Capillary refill
incorporates a named subcutaneous artery running
MCCCLXXIII) Full thickness skin graft MCDVIII) Swelling
along length of the longitudinal axis of flap
MCCCLXXIV) Laterally based upper lid graft MCDIX) Palpable pulse
MCCCLVI) Myocutaneous/fasciocutaneous:
MCCCLXXV) Cutler-Beard flap MCDX) Needle stick
incorporates a segmental vessel that sends
perforating vessels to overlying muscle & skin
353) Blood supply of regional skin flaps 357) Mechanisms of dextran
MCCCLXXVI) Deltopectoral: 1st-4th perforators from IMA MCDXI) Decreased viscosity leads to improved
347) Mechanisms of the delay phenomenon in local flaps
MCCCLXXVII) Paramedian forehead: supratrochlear & capillary blood flow
MCCCLVII) Closure of arteriovenous shunts (due to
supraorbital arteries MCDXII) Decreased platelet adhesiveness
development of autonomous tone or regrowth of
MCCCLXXVIII) Nape of neck: occipital artery MCDXIII) Alters fibrin structure
sympathetics along flap base, or increased
MCCCLXXIX) Nasolabial: angular branch of the facial MCDXIV) Antithrombotic effect starts 2-4 hours
sensitivity to circulating catecholamines)
artery after infusion starts
MCCCLVIII) Reorientation of vessels along axis of the
MCCCLXXX) Pectoralis major: thoracoacromial artery,
flap
lateral thoracic (supplies inferior 1/5th), IMA 358) Neurovascular supply of common fasciocutanous free
MCCCLIX) Increase in vessel caliber
perforators flaps
MCCCLX) Increased vessel numbers
MCCCLXXXI) Trapezius: occipital, suprascapular, MCDXV) Radial forearm
MCCCLXI) Conditioning of distal flap to ischemia
transverse cervical arteries i) Artery: radial artery; perforators travel in lateral
MCCCLXXXII) SCM: occipital artery, superior thyroid intermuscular septum (brachioradialis-flexor
348) Discuss the no-reflow phenomenon
artery, branch from the thyrocervical trunk carpi radialis)
 ii) Venous: venae comitantes or cephalic vein 362) What types of allografts are used in mandibular MCDXLVII) Fibula
iii) Nerve: lateral antebrachial cutaneous reconstruction i) Vascular: peroneal artery & vein; perforators
MCDXVI) Lateral arm MCDXXVII) Pins & wires (Kirschner wire, Steinmann run in posterior intermuscular septum
i) Artery: terminal branch of profunda brachii and pins; no longer used anymore due to instability) ii) Nerve: peroneal communicating branch
posterior radial collateral artery, travels in spiral MCDXXVIII) Alloplast appliances: trays made of iii) Bone: up to 25cm of bone available,
groove, septocutaneous perforators travel in silicone, polyurethane-reinforced Dacron polyester contourable due to segmental blood supply
lateral intermuscular septum mesh; used as spacer trays or carriers for bone iv) Blood supply to skin not completely reliable;
ii) Venous: venae comitantes of above vessels grafts loss in 5-10% of cases
iii) Nerve: posterior cutaneous nerve of the MCDXXIX) Bone plates & screws: stainless steel, MCDXLVIII) Iliac crest
forearm cobalt-chromium, titanium; used most commonly in i) Artery: deep circumflex iliac artery off of
MCDXVII) Lateral thigh mandibular reconstruction external iliac artery; internal oblique supplied by
i) Artery: 3rd perforator of the profunda femoris, ascending branch of DCIA
travels in intermuscular septum 363) What are the three types of autogenous bone grafts used ii) Venous: deep circumflex iliac vein usually
ii) Nerve: lateral femoral cutaneous nerve of the in secondary mandibular reconstruction? composed of 2 venae comitantes
thigh MCDXXX) Cortical: lamellar plates of bone, provides iii) Natural shape conforms to that of native
MCDXVIII) Anterolateral thigh the least amount of viable cells, requires long mandible
i) Artery: lateral circumflex femoral, descending periods for revascularization, provides best rigid MCDXLIX) Scapula
branch support for mandible reconstruction; excellent i) Artery: circumflex scapular artery off of
ii) Venous: venae comitantes source of BMP for transformation of pluripotential subscapular artery, divides into transverse &
cells into osteoblastic cells descending branches to supply two separate
359) Neurovascular supply of muscle & myocutaneous free MCDXXXI) Cancellous: medullary bone and bone skin paddles (scapular & parascapular)
flaps marrow, provides the highest concentration of viable ii) Bone: separate thoracodorsal blood supply to
MCDXIX) Rectus abdominis cells which can produce new bone, requires shortest bony component, 10-12cm length from inferior
i) Vascular: deep (superior &) inferior epigastric period for revascularization lateral aspect of bone
arteries & veins; inferior pedicle larger and MCDXXXII) Particulate cortical bone and cancellous (1) Not suitable for osseointegration
provides the musculocutaneous perforators marrow contains both medullary and cortical bone, MCDL) Radial forearm
supplying the skin which provides a tradeoff between support and a i) Up to 10cm and 40% of radial circumference
ii) Nerve: any of the intercostal nerves viable transferable cell population (best osteogenic can be taken
MCDXX) Latissimus dorsi potential); requires a crib for stability (1) Not suitable for osseointegration
i) Vascular: thoracodorsal vessels, off of MCDLI) Lateral arm flap
subscapular vessels 364) Goals of primary mandibular reconstruction i) Up to 10cm and one-sixth of humeral
ii) Nerve: thoracodorsal nerve MCDXXXIII) Restore mandibular continuity circumference can be taken
iii) Can be elevated as a free or regional pedicled MCDXXXIV) Restore lower facial contour MCDLII) Dorsalis pedis
flap MCDXXXV) Maintain mobility of residual tongue i) Artery: dorsalis pedis artery
MCDXXI) Gracilis MCDXXXVI) Reconstruct anatomic configuration of ii) Nerve: superficial peroneal nerve
i) Artery: terminal branch of adductor artery, sulcus iii) Thin sensate cutaneous flap from dosal foot
which arises from profunda femoris MCDXXXVII) Provide rehabilitation with a functional iv) 2nd metatarsal included for osseocutaneous flap
ii) Vein: venae comitantes, join or drain separately lower denture MCDLIII) Rib
into profunda femoris vein MCDXXXVIII) Improve mastication, deglutition, speech i) Intercostal vascular pedicle
iii) Nerve: anterior branch of the obturator nerve MCDXXXIX) Restore sensation to denervated lower lip ii) Marginal blood supply to skin
(motor supply) MCDXL) Restore sensation to resurfaced portions
iv) Primary use is for facial reanimation of oral cavity 367) What are the three classes of dentures used for dental
rehabilitation post-mandibulectomy?
360) Neurovascular supply of visceral free flaps 365) Characteristics of the ideal qualities of the bony MCDLIV) Tissue borne prosthesis: simplest,
MCDXXII) Jejunum component of a vascularized composite free tissue complete or partial, stabilized by remaining teeth and
i) Vascular: based on single vascular arcade from transfer a broad denture supporting area
SMA (usually 2nd arcade) MCDXLI) Adequate length to restore a segmental MCDLV) Implant assisted prosthesis:
ii) Peristalsis maintained by action of autonomic defect of nearly any length osseointegrated posts help stabilize the dentures
plexuses MCDXLII) Natural shape or easy contourability to against lateral displacement forces with use; mores
MCDXXIII) Gastroomental match the mandibular defect stable than conventional dentures, cheaper than
i) Vascular: based on right gastroepiploic artery MCDXLIII) Well vascularized implant-borne prosthetics
MCDXLIV) Vascular anatomy that is well preserved MCDLVI) Fixed implant-borne prosthesis: most
361) Hyperbaric oxygen (HBO) mechanism of action while contouring the graft stable form of restoration, supported by 5-6 fixtures
MCDXXIV) Increases amount of oxygen dissolved in MCDXLV) Sufficient height and width for reliable attached to transepithelial connector implants,
solution placement of endosteal dental implants for prosthetic denture does not come into contact with the
MCDXXV) Increases diffusion distance from rehabilitation underlying mucosa
capillaries MCDXLVI) No significant functional or esthetic
MCDXXVI) Increases role of neovascularization defects at the donor site after harvest 368) Anticoagulation in free flaps
MCDLVII) Heparin
366) Neurovascular supply of bone composite free flaps
 i) Binds to antithrombin III, inactivated thrombin,
other esterases; increases electronegative
potential of endothelium, thus decreases
platelet adhesiveness
MCDLVIII) Aspirin
i) Inhibits cyclooxygenase, interferes with PGH2
synthesis
MCDLIX) Dextran
i) Antithrombin & antifibrin effects
MCDLX) Medicinal leech
i) Indication: venous congestion
ii) Hementin (local anesthetic), hirudin (inhibits
fibrinogen to fibrin conversion)
iii) Aeromonas hydrophile: gram negative ß-
lactamase producing commensal, casuses
necrotic soft tissue flap infection in 10-15%)
369) Viscoelastic properties of skin
MCDLXI) Stress relaxation
i) Occurs when skin stretched to a given
constant length; over time, force required to
maintain this constant length decreases
MCDLXII) Creep
i) Biologic: seen in pregnancy, lymphedema,
morbid obesity, gradual stress stretches skin,
muscles, nerves, blood vessels, lymphatics;
increase lengths by cell division and collagen &
elastin synthesis
ii) Mechanical: due to dehydration of tissue by
displacing fluid & MPS ground substance,
realignment of collagen, microfragmentation of
elastin, migration of undermined tissue into
field defect by stretching force
370) Tissue expansion
MCDLXIII) Expanders: round, rectangular, crescentic
MCDLXIV) Match geometric shape of expander to the
shape of the expansion site & planned flap
MCDLXV) Area of expander ~2.5x that of the defect
to be closed; amount of flap advancement either half
the base diameter of the expander or half the
diameter of the expansion dome
MCDLXVI) Expansion starts ~3 weeks after implant
insertion, 6-12 weeks to reach maximum expansion
MCDLXVII) Complications/emergencies
i) Hematoma: truly emergent; return to OR for
evacuation, stop bleeding, possibly reinsert
expander
ii) Skin necrosis
iii) Implant exposure
iv) Extrusion
v) Bone remodeling/neurovascular compromise:
remove expander or perform surgery ASAP
371) 5 things to consider when hiding facial incisions
MCDLXVIII) Hair bearing requires incision parallel to
follicles
MCDLXIX) Scars best hidden if within or parallel to
RSTL’s
MCDLXX) Junction of aesthetic subunits
MCDLXXI) Use of squamomucosal incisions MDIII) Facial width:length 3:4
(margins of orifices) MDIV) Width divided into fifths, each ~1 eye
MCDLXXII) Locations that can be hidden by hair width from canthus to canthus
MDV) Height divided into thirds: trichion-
372) Five things to consider to minimize scar tissue formation glabella, glabella-subnasale, subnasale-menton
when repairing facial laceration MDVI) Gonzalez-Ulloa’s line: perpendicular from
MCDLXXIII) Tissue eversion Frankfort line, midforehead, subnasale, upper/lower
MCDLXXIV) Absorbable vs. nonabsorbable sutures lips, pogonion all lie on the line
MCDLXXV) Patient’s propensity for keloid/hypertrophic MDVII) Frankfort horizontal line: upper EAC
scar margin through infraorbital rim
MCDLXXVI) Patient’s natural complexion, eg. light vs.
dark skin 380) Eye analysis
MCDLXXVII) Minimal tension on incision line MDVIII) Interpalpebral distance = ~1eye width
MCDLXXVIII) Clean wound, avoidance of infection MDIX) Intercanthal distance (30-35mm) = ½
interpupillary distance (60-70mm)
373) Indications for scar revision
MCDLXXIX) Scars >2cm in length or wider than 2mm 381) Nose analysis
MCDLXXX) Distortion of normal anatomy MDX) Nasal width from alar groove to alar
MCDLXXXI) Does not lie in RSTL groove =70% the length of the nose (from nasion to
tip defining point); nasal width equal to intercanthal
374) Characteristics of the ideal scar distance
MCDLXXXII) Flat, level with skin MDXI) Profile measures
MCDLXXXIII) Narrow i) Contour: should be relatively straight
MCDLXXXIV) Parallel to RSTLs ii) Projection: extent of tip protrusion from the
MCDLXXXV) Same color anterior facial plane
MCDLXXXVI) No long unbroken segments iii) Rotation: angle of inclination of the nasolabial
angle
375) Methods of scar irregularization iv) Length: dorsum measured from nasion to tip
MCDLXXXVII) Z-plasty: single or compound; best for defining point
scars across concavities (ie. webbing or banding)
MCDLXXXVIII) W-plasty: best for long scars along curves 382) Methods of determining tip projection
(eg. angle of mandible); base <6mm, sides <6.5mm MDXII) Powell & Humphries: height measured
MCDLXXXIX) Geometric broken line: best technique for from nasion to subnasale, perpendicular drawn
long unbroken facial scars; shapes should be <5- through tip defining point, ratio of N-X/X-Tp ideally
6mm in any dimension 2.8:1
MDXIII) Goode: line drawn through nasion to alar-
376) Three indications for Z-plasty facial groove, perpendicular drawn through tip
MCDXC) Rotation of the dominant axis of a scar, defining point, ratio of N-Tp/N-Y ideally 0.55-0.6:1
especially those that cross RSTLs MDXIV) Crumley & Lancer: defined relationship of
MCDXCI) Reduction of scars distorting anatomic tip projection, nasal length, vertical height as a right
landmarks triangle whose sides follow a 3:4;5 ratio
MCDXCII) Avoidance of a web or band across a MDXV) Simon: tip projection (measured from tip
concavity defining point to subnasale) and length of the upper
lip (measured from subnasale to upper vermilion
377) 5 advantages of Z-plasty border) should be equal
MCDXCIII) Axis of scar changes
MCDXCIV) Lengthens scar 383) Chin position analysis
MCDXCV) Tension redistribution MDXVI) Vertical from inferior vermilion border
MCDXCVI) Defect closure determines position; males’ pognonion should be
MCDXCVII) Tissue brought in tangential to line, females 2-3mm posterior to the line
MDXVII) Length: menton to suprasternal notch
378) Theoretic increases in length with varying Z-plasty angles should be 50% of the head height (from vertex to
MCDXCVIII) Less than 30 degrees: tip necrosis menton)
MCDXCIX) 30 degrees: 25%
MD) 45 degrees: 50% 384) Hinderer’s method for malar eminence position
MDI) 60 degrees: 75% MDXVIII) Two lines; one from lateral canthus to
MDII) Greater than 75 degrees: redundant lateral commissure, other from tragion to lateral ala
standing cones MDXIX) Malar prominence should be in upper
lateral angle formed from the lines’ intersection
379) General facial analysis stuff
385) Lips analysis ii) Levator labii superioris alaque nasi
MDXX) Upper lips: from subnasale to stomion = iii) Anomalous nasi 395) Describe the incisions, approaches and techniques used
1/3 lower facial third MDXLVI) Depressors in surgery of the nasal tip
MDXXI) Lower lips: from stomion to menton = 2/3 i) Alar nasalis MDLXIII) Incisions: methods of gaining access to
lower facial third ii) Depressor septi the underlying supporting structures
MDXXII) Upper lip fuller, projects slightly more than MDXLVII) Compressors i) Transcartilaginous
lower i) Transverse nasalis ii) Intracartilaginous
MDXXIII) Lips should be anterior to line through ii) Compressor narium minor iii) Marginal
subnasale & pogonion MDXLVIII) Minor dilators MDLXIV) Approaches: methods of gaining exposure
MDXXIV) Oral commissure on same vertical line as i) Dilator naris anterior to nasal skeletal structures
medial limbus i) Delivery: for more abnormal or asymmetric tip
391) Name the 3 major and 6 minor tip supports anatomy, allows presentation of the alar
386) Ear analysis MDXLIX) Major cartilages as bipedicled chondrocutaneous
MDXXV) Height ~6cm i) Resiliency of medial & lateral crura flaps for surgical modification
MDXXVI) Top of helix at same level as lateral brow, ii) Medial crural attachment to septum ii) Nondelivery: for conservative/minimal tip
helical root at same level as lateral canthus, inferior iii) Alar attachment to upper lateral cartilages refinement, disturbs little of the normal anatomy
attachment at same level as alar-facial junction MDL) Minor (1) Cartilage splitting
MDXXVII) Long axis posteriorly inclined 20 degrees i) Interdomal soft tissue attachments (2) Retrograde
MDXXVIII) Protrusion from posterior skull 20 ii) Cartilaginous dorsum iii) Open (External)
degrees, approximately 10-20mm iii) Soft tissue/sesamoid complex attachment to MDLXV) Techniques: surgical modifications to the
MDXXIX) Width 0.55-0.6 of the height pyriform wall nose: reconstruction, excision, augmentation,
iv) Alar cartilage attachments to overlying skin & reorientation
387) Identify the profile angles for facial analysis soft tissue i) Volume reduction with:
MDXXX) Nasofrontal angle: vertex at the nasion, v) Bony nasal spine (1) Residual complete strip: whenever
formed by lines through the glabella and nasal vi) Membraneous septum possible, ideal to leave a complete strip of
dorsum; measures ~120-135 degrees lateral crus of at least 5mm in width
MDXXXI) Nasofacial angle: angle defined by 392) What anatomic variations are there in the attachment of (2) Weakened complete strip: for further
intersection of a line drawn through the glabella and the upper and lower lateral nasal cartilages? refining of tip, done by conservative cross
pogonion and 2nd along the nasal dorsum; measures MDLI) Cephalic end of lower lateral cartilage hatching, morselization, or incomplete
36 degrees ideally usually overlies the caudal end of the upper lateral noncoalescent dome incisions
MDXXXII) Nasolabial angle: vertex at the subnasale, cartilages (3) Suture modification of complete strip
formed by lines through the columellar point and the i) Interlocking scroll 52% (4) Interrupted strip: for severe tip
upper vermilion border; measures 90-105 degrees in ii) Overlapping 20% deformities, increased risk of asymmetric
men, 100-120 degrees in women; this angle defines iii) End-to-end 17% healing & scarring, causes increased
the amount of tip rotation iv) Opposed scroll 11% cephalic tip rotation
MDXXXIII) Mentocervical angle: measures the angle
at the gnathion (pogonion-gnathion-menton); 393) Indications for external (open) rhinoplasty 396) Methods of increasing tip projection in rhinoplasty
measures 80-90 degrees or 100 degrees MDLII) Cases that require extended surgical MDLXVI) Complete strip techniques with avoidance
MDXXXIV) Nasomental angle: vertex at tip defining exposure for diagnostic/technical reasons of complete transfixion incision
point, tangents drawn through nasion and pogonion; i) Asymmetric nasal tip cartilages or middle nasal MDLXVII) Columellar strut grafts placed between the
120-132 degrees vault medial crura
ii) Structural deficiency MDLXVIII) Shield grafts overlying the dome
388) What angles make up the aesthetic triangle of Powell & iii) Marked overprojection MDLXIX) Plumping grafts to the columellar-labial
Humphries? iv) Significant underprojection angle
MDXXXV) Nasofrontal angle MDLIII) Crooked nose MDLXX) Excision of excessive interdomal soft
MDXXXVI) Nasolabial angle MDLIV) Secondary & revision rhinoplasty tissue and suturing of the domes & medial crura
MDXXXVII) Mentocervical angle MDLV) Cleft lip nasal deformity together
MDXXXVIII) Nasomental angle MDLVI) Saddle nose deformity MDLXXI) Vertical dome division (Goldman tip)
MDLVII) Benign nasal tumors MDLXXII) Toriumi: lateral crural steal (with increased
389) List the aesthetic subunits of the nose MDLVIII) Closure of septal perforation rotation), tip graft, plumping grafts, premaxillary
MDXXXIX) Dorsum MDLIX) Teaching graft, septocolumellar sutures (buried), columellar
MDXL) Sidewalls (2) strut (variable effect), caudal extension graft
MDXLI) Tip 394) Describe the blood flow to the nasal tip
MDXLII) Nasal ala (2) MDLX) Dorsal nasal artery (2): branch of the 397) Methods of enhancing tip rotation in rhinoplasty
MDXLIII) Soft tissue facet (2) facial artery superiorly, runs along dorsum near the MDLXXIII) Interrupted strip technique (fosters
MDXLIV) Columella midline cephalic tip rotation; residual complete strip
MDLXI) Lateral nasal arteriy (2): branch of the techniques resist cephalic tip rotation)
390) Name the important muscles of the nose facial artery MDLXXIV) Caudal septal shortening
MDXLV) Elevators MDLXII) Columellar artery (2): branch of the MDLXXV) Excision of overlong upper lateral
i) Procerus superior labial artery cartilages
 MDLXXVI) Septal shortening with high septal MDXCV) Restore rotation & projection to the lower i) Nasal bone disparity
transfixion third of the nose ii) Subluxated upper lateral cartilage
MDLXXVII) Reduction of convex caudal medial crura MDXCVI) Resection of caudal septum with excess iii) Overexcised upper lateral cartilage
MDLXXVIII) Reduction of the membranous columellar vestibular skin iv) Nasal septal deviations
skin MDXCVII) Trim the caudal medial crura MDCIX) Therapy
MDLXXIX) Toriumi: lateral crural steal, transdomal i) Appropriate nasal bone restructuring
suture that recruits lateral crura medially, base-up 403) Etiology and treatment of nasal tip bosselation ii) Onlay grafts
resection of caudal septum (variable effect), cephalic MDXCVIII) Etiology iii) Spreader grafts
resection (variable effect), lateral crural overlay, i) Primary nasal tip asymmetry iv) Septal corrections
columellar strut (variable effect), plumping grafts ii) Iatrogenically created sharp edges
(variable effect), illusions of rotation (increased iii) Too narrow a rim strip 409) Fat compartments of upper/lower eyelids
double break, plumping grafts) MDXCIX) Therapy MDCX) Upper lid: either central & nasal, or central
i) Raise low side & medial
398) Characteristics of the unilateral cleft lip nasal deformity ii) Lower high side MDCXI) Lower lid: either temporal, central &
MDLXXX) Deviation of nose to affected side iii) Combination of above medial, or lateral, central and medial
MDLXXXI) Lower dome MDCXII) Upper medial & central compartments
MDLXXXII) Flattened or crimped lateral crus 404) Etiology and treatment of nasal tip pinching divided by superior oblique
MDLXXXIII) Caudal displacement of alar rim MDC) Etiology: overresection of lateral crural MDCXIII) Lower central & medial compartments
MDLXXXIV) Horizontal nostril axis cartilage divided by inferior oblique, central & lateral
MDLXXXV) Loss of nasal sill MDCI) Therapy: replacement with nasal septal compartments divided by fascial sling
MDLXXXVI) Depressed or missing bony floor cartilage, precise pocket formation
410) Name the 3 parts of the orbicularis oculi muscle
399) Etiology of saddle nose deformity 405) Etiology and treatment of alar retraction MDCXIV) Pretarsal: overlying tarsal plate
MDLXXXVII) Congenital MDCII) Etiology MDCXV) Preseptal: overlying orbital septum
i) Achondroplasia i) Congenital causes MDCXVI) Orbital: overlying bone surrounding the
ii) Apert’s syndrome ii) Poor alar-columellar relationship orbit
MDLXXXVIII) Acquired iii) Overresection of lateral crural cartilage and
i) Traumatic membrane 411) What are the layers of the upper lid at the lid margin?
ii) Postinfectious (septal hematoma) MDCIII) Treatment MDCXVII) Skin
iii) Iatrogenic (post-SMR or SRP) i) Shorten columella MDCXVIII) Orbicularis oculi
ii) Shorten contralateral ala MDCXIX) Tarsal plate
400) Therapeutic options for saddle nose deformity iii) Cartilage graft for minimal retraction MDCXX) Conjunctiva
MDLXXXIX) Nasal tip retrodisplacement (for tip iv) Composite graft for extensive retraction
overprojection) 412) What are the layers of the upper lid above the eyelid
MDXC) Lateral osteotomies 406) Etiology and treatment of columellar retraction crease?
MDXCI) Grafts MDCIV) Etiology MDCXXI) Skin
i) Autogenous graft with bone/rib grafts i) Congenital MDCXXII) Orbicularis oculi
ii) Allografts: silastic, proplast, GoreTex, ii) Alar-columellar disproportion MDCXXIII) Orbital septum
mersilene iii) Traumatic MDCXXIV) Orbital fat pad
iii) Homograft iv) Iatrogenic MDCXXV) Levator aponeurosis
(1) Demineralized bone: significant long term MDCV) Treatment MDCXXVI) Muller’s muscle
resorption i) Raise ala MDCXXVII) Conjunctiva
(2) Irradiated cartilage: unnatural feel, long ii) Cartilage graft
term resorption iii) Composite graft 413) Things to evaluate when planning a blepharoplasty
(3) Acellular dermis (Alloderm) MDCXXVIII) Upper lid
407) What causes a “polly-beak” (supratip swelling) deformity, i) Brow ptosis, possible need for browplasty?
401) Alar base resection (Weir): anatomy, indications and what are the therapeutic options? ii) Skin type determines aggressiveness of
MDXCII) Used to reduce nasal width MDCVI) Etiology resection
MDXCIII) Anatomy i) Excessive cartilaginous dorsum iii) Presence of lagopthlamos
i) Nasal sill: nostril rim between attachment of ii) Excessive dorsal bony resection iv) Test for presence of Bell phenomenon
medial crus and attachment of ala to the face iii) Excessive tip cartilage resection leading to loss MDCXXIX) Lower lid
ii) Flare: amount of alar tissue lateral to the alar- of tip support i) Is problem due to fat pseudoherniation only, or
facial junction iv) Excess supratip scar tissue formation is there skin & muscle redundancy also?
MDXCIV) Indications MDCVII) Treatment ii) Snap test
i) Reduction in nasal tip projection in Caucasian i) Supratip scar excision
rhinoplasty ii) Augmentation of tip support & projection 414) What are the most common muscles injured in
ii) Nasal width reduction in nonwhite rhinoplasty iii) Augmentation of dorsal profile blepharoplasty?
MDCXXX) Upper lid – superior oblique
402) Correction of the hanging columella 408) Etiology and therapy for midnasal asymmetry MDCXXXI) Lower lid – inferior oblique
MDCVIII) Etiology
415) Complications of blepharoplasty MDCLIX) Skin ptosis: management requires i)Mustarde technique: placement of horizontal
MDCXXXII) Milia formation redraping of the skin mattress sutures to create an antihelical fold
MDCXXXIII) Scleral show/ectropion MDCLX) Subcutaneous fat/submental fat ii) Converse technique: creation of island of
MDCXXXIV) Hematoma accumulation: management through liposuction, cartilage to produce a normal appearing fold;
MDCXXXV) Subconjunctival ecchymosis either endoscopic or open more permanent auricle retraction, more
MDCXXXVI) Chemosis MDCLXI) Platysma banding/atrophy: platysmaplasty permanent correction of antihelix
MDCXXXVII) Lagophthalmos with anterior/posterior tightening, submental tuck iii) Farrior technique
MDCXXXVIII) Ptosis MDCLXII) Retrognathia: suspension of tightened iv) Pitanguy technique: creation of island flap with
platysma from mandible, chin implant conchal setback suture
416) Histologic changes in aging skin MDCLXIII) Pathologic hyoid: ideally should be v) Furnas conchal mastoid suture technique:
MDCXXXIX) Thinning of the dermis posterior and high up (at level of C4); if not, can cut method of choice in reduction of prominent
MDCXL) Decreased moisture content & cellular ¾ of anterior belly of digastric for preferential conchal bowls
cohesion of the stratum corneum posterior belly action, or delineate acute MDCLXXXVI) Complications
MDCXLI) Effacement of rete ridges cervicomental contour by suture suspension i) Hematoma (easiest to detect but most
MDCXLII) Decrease in melanocytes & Langerhans emergent)
cells 421) Considerations for surgery of the aging forehead ii) Inadequate correction (most common)
MDCXLIII) Elastic fibers of dermis become thin & MDCLXIV) Brow ptosis iii) Chondritis (most feared)
fragmented MDCLXV) Presence of rhytids
MDCXLIV) Thickened dermal collagen but overall MDCLXVI) Hairline patterns 426) 5 stages for microtia/aural atresia repair
decrease in amount MDCLXVII) Skin type MDCLXXXVII) Stage I: auricular reconstruction (Brent or
MDCXLV) Reduced vascular supply MDCLXVIII) Brow asymmetries Nagata)
MDCXLVI) Smaller sebaceous glands MDCLXIX) Bony contour MDCLXXXVIII) Stage II: lobule transposition
MDCLXXXIX) Stage III: atresia repair (by otologist)
417) The facial nerve innervates the facial mimetic muscles 422) Surgical approaches to the forehead MDCXC) Stage IV: tragal reconstruction
from their deep surfaces except for which three? MDCLXX) Endoscopic MDCXCI) Stage V: auricular elevation
MDCXLVII) Buccinator MDCLXXI) Coronal
MDCXLVIII) Levator anguli oris MDCLXXII) Trichophytic 427) Evaluation of the chin
MDCXLIX) Mentalis MDCLXXIII) Pretrichial MDCXCII) Legan’s angle: tangent through subnasale
MDCLXXIV) Midforehead: browplasty, rhytidectomy & glabella, 2nd tangent from subnasale through
418) Rhytidectomy general points MDCLXXV) Direct browplasty, browpexy pogonion; angle normally 12 +/- 4 degrees
MDCL) General anaesthetic MDCXCIII) Merrifield Z angle: Frankfort line, line
MDCLI) Ideal patient has strong angular bony 423) Muscles encountered in forehead rhytidectomy from deep through anterior aspect of lip and pogonion, angle
facial structure, thin skin with mobile subcutaneous to superficial, which muscles are cut and how? formed from two lines normally 80 +/- 5 degrees
tissue, minimal subcut. fat, long columnar neck, MDCLXXVI) Muscles MDCXCIV) Gonzales-Ulloa Zero meridian
cephalically positioned hyoid, long strong mandible, i) Frontalis
well defined cervicomental angle (90 degrees) ii) Corrugator supercilii: causes vertical rhytids 428) Management of the retrognathic chin
MDCLII) SMAS suspension key, either imbrication iii) Procerus: causes horizontal rhytids MDCXCV) Alloplast: simpler, removable, fewer
or plication; superior and posterior vectors of pull iv) Orbicularis oculi: typically spared during complications; subperiosteal placement
MDCLIII) Deep plane rhytidectomy: to correct aging rhytidectomy i) Intraoral: bothersome sutures, geniobuccal
changes of melolabial fold and malar area MDCLXXVII) Management scar contracture, intraoral contamination
MDCLIV) Combination of rhytidectomy with i) Frontalis: horizontal relaxing incisions made ii) Extraoral: external scar
submental liposuction and platysmaplasty between midpupillary lines MDCXCVI) Sliding genioplasty: indications are excess
ii) Corrugator & procerus: excised to eliminate or insufficient vertical mandibular height, extreme
419) Complications of rhytidectomy glabellar frown lines microgenia, hemifacial atrophy, mandibular
MDCLV) Nerve damage asymmetry, failed implant previously
i) Most common sensory nerve injured is the 424) Changes in the aged nose
greater auricular MDCLXXVIII) Nasolabial angle below 90 degrees 429) Chemical peels, general thoughts
ii) Facial nerve damage: uncommon, frontal MDCLXXIX) Elongation of lower & midportions of the MDCXCVII) Classified by layer of penetration
branch (Baileys), marginal mandibular nose (epidermis to stratum corneum or to stratum basale,
(Cummings) and buccal at risk; avoided by not MDCLXXX) Alar cartilage flattens & fragments papillary dermis, papillary-reticular junction, reticular
elevating past the anterior border of the parotid MDCLXXXI) Loss of attachments between upper & dermis)
MDCLVI) Hematoma: most common complication lower cartilages MDCXCVIII) Variables
(8.5%) MDCLXXXII) Cartilage ossification i) Agent & concentration used
MDCLVII) Incision problems: avoid tension on MDCLXXXIII) Nasal bones osteoporotic ii) Application method, number of layers
incision lines MDCLXXXIV) Skin thinner and less elastic iii) Prepeel keratolytics (retinoids, α-hydroxy acids)
MDCLVIII) Alopecia (1) Tretinoin (retinoic acid) thickens
425) Describe the 5 methods used in otoplasty and the most epidermis, thins stratum corneum,
420) Management of the aging neck: anatomic factors and their common complications reverses keratinocyte atypia
treatment MDCLXXXV) Surgical techniques iv) Degreasing agents
v) Occlusion/semiocclusion
 vi) Skin thickness MDCCXVI) UVA passes through window glass, MDCCXLVI) DHT influences bear growth and pattern
vii) Pilosebaceous gland activity & density constant intensity through year, 90% of solar baldness
radiation reaching surface
430) Depth of peels MDCCXVII) Sun damage 440) Etiology of alopecia
MDCXCIX) Superficial: into epidermis and superficial i) UVB: sunburn & skin cancer MDCCXLVII) Male pattern baldness
papillary dermis; to freshen appearance ii) UVA: deeper penetration into dermis, causes MDCCXLVIII) Autoimmune disease
MDCC) Medium: injures entire epidermis and to photoaging (breaks down collagen & elastin, MDCCXLIX) Burns
the papillary and upper reticular dermis; for patients damages superficial blood vessels, immune MDCCL) Chemotherapy
with actinic keratoses, moderate rhytids, suppression, increases cancer stimulating MDCCLI) Dermatologic disorders (eg. psoriasis)
dyschromias present in the epidermis and upper effects of UVB, role in melanoma formation) MDCCLII) Radiation exposure
dermis MDCCXVIII) Sunscreens MDCCLIII) Neoplasms
MDCCI) Deep: injures epidermis, papillary dermis i) Organic: UV filters secondary to conjugate MDCCLIV) Traction
and to midreticular dermis; for heavy wrinkles, solar double bonds
lentigines, lines secondary to photodamage, ii) Physical: reflect & scatter light (eg. zinc oxide) 441) Management of alopecia
superficial premalignant keratoses iii) SPF#: derived from testing under artificial light, MDCCLV) Medical
for UVB only i) Finasteride: 5α-reductase inhibitor
431) Types of chemical peel agents ii) Minoxidil: local vasodilator, potassium-like
MDCCII) Glycolic acid: sugarcane derived α- 435) Complications of chemical peels & dermabrasion agonist that reduces cytoplasmic free calcium
hydroxy acid, 20-70% concentrations, superficial MDCCXIX) Pigment abnormalities MDCCLVI) Surgical
peeling agent; penetration dependent upon skin MDCCXX) Increased sun sensitivity i) Hair bearing autografts
contact MDCCXXI) Hypertrophic scar (1) Follicular unit grafts
MDCCIII) TCA: coagulates protein in skin, MDCCXXII) HSV reactivation or dissemination (2) Micrografts: 1-2 hairs
neutralized by serum, less hypopigmentation, no MDCCXXIII) Persistent erythema (3) Minigrafts: 3-8 hairs
cardiotoxic effects MDCCXXIV) Dermatitis (4) Standard grafts: 15-25 hairs
i) 10-20% superficial MDCCXXV) Milia ii) Scalp reduction
ii) 30-40% medium MDCCXXVI) Foreign body granuloma iii) Extensive scalp reduction: bilateral
iii) 45-50% deep MDCCXXVII) Full thickness skin loss occipitoparietal or occipitotemporal flaps
MDCCIV) Jessner: resorcinol, salicylic acid, lactic iv) Pedicled flaps: Juri’s delayed temporo-
acid in ethanol 436) Describe Gardner syndrome parietooccipital flap
MDCCV) Phenol peels: deep peel, causes MDCCXXVIII) Multiple epidermal cysts, 40% malignant v) Tissue expansion
pigmentation changes degeneration
MDCCXXIX) Facial bone osteomas, cutaneous
432) Indications for chemical peels fibromas, lipomas, leiomyomas of stomach & ileum
MDCCVI) Actinic keratosis
MDCCVII) Photoaging 437) Describe Cowden’s disease
MDCCVIII) Pigment changes MDCCXXX) Autosomal dominant
MDCCIX) Lentigines MDCCXXXI) Multiple trichilemmomas, gingival
MDCCX) Epidermal growth fibromatosis
MDCCXI) Fine rhytids MDCCXXXII) Hamartomas of breast, thyroid & GI tract
MDCCXII) Acne management & scarring MDCCXXXIII) Greatly increased risk of breast cancer,
thyroid adenomas and cancer
433) Contraindications to chemical peels
MDCCXIII) Absolute 438) Telangiectasia associations
i) Hepatorenal disease MDCCXXXIV) Scleroderma
ii) Cardiac disease MDCCXXXV) Dermatomyositis
iii) Unstable psychiatric disease MDCCXXXVI) Radiation dermatitis
iv) Allergy MDCCXXXVII) Chronic alcoholism
v) Active herpes simplex MDCCXXXVIII)Liver disease
MDCCXIV) Relative MDCCXXXIX) Pregnancy
i) Physical restriction MDCCXL) Childhood
ii) Radiotherapy to face MDCCXLI) Osler-Weber-Rendu syndrome
iii) Keloid former MDCCXLII) Carcinoid
iv) Fitzpatrick types IV to VI
v) Latent herpes simplex 439) Stuff about hair
vi) Telangiectasias MDCCXLIII) 100,000 hairs on the head
vii) Medication use (estrogen, warfarins) MDCCXLIV) Growth cycle ~1000 days; 90% anagen
viii) HIV (low CD4) phase, 10% telogen phase
MDCCXLV) Testosterone influences axillary & pubic
434) Sunlight & photoaging hair growth
MDCCXV) UVB 290-320nm, UVA 320-400nm
 Head and Neck MDCCLXXIV) Simultaneous: diagnosed at same time
MDCCLXXV) Synchronous tumor: found within 6
MDCCXCII) Topoisomerase inhibitors: prevent
unwinding of DNA for replication; irinotecan,
months topotecan
442) Cell cycle
MDCCLXXVI) Metachronous tumor: found after 6
MDCCLVII) G1: 1st growth phase in preparation for
months 450) Discuss the common HNSCC chemotherapy agents
DNA synthesis
MDCCLXXVII) 85% of 2nd primaries occur within 2 years; MDCCXCIII) Methotrexate
MDCCLVIII) S: DNA synthesis
5% of 2nd primaries occur after 3 years i) Binds to dihydrofolate reductase, interrupts
MDCCLIX) G2: cell growth, duplication of cell
MDCCLXXVIII) Continued smoking and EtOH DNA synthesis
proteins & structures
consumption: 30-50% risk of locoregional ii) S-phase mechanism
MDCCLX) M: mitosis
recurrence posttreatment, 10-40% risk of 2nd primary iii) Side effects: myelosuppression, mucositis,
MDCCLXI) G0: resting phase
development dermatitis, N/V/D, hepatic fibrosis
iv) Leukovorin rescue
443) What methods are used to introduce genes in gene
447) Phases of clinical trials v) 30% partial response rate as a single agent
therapy?
MDCCLXXIX) Phase I: tolerance and pharmacologic MDCCXCIV) Cisplatin
MDCCLXII) General methods
properties; determine toxicity with clinical intent of i) Covalent DNA intercalator, interferes with
i) In vivo: direct introduction of vector with gene
tumor shrinkage and palliation normal DNA function
into tissues
MDCCLXXX) Phase II: determine efficacy of a drug in a ii) Side effects: N/V, nephrotoxicity, ototoxicity,
ii) Ex vivo: removing target tissue/cell portion,
specific disease and stage at a defined dose; to neurotoxicity, myelosuppression
transduction with vecor, reimplantation into
define its activity within tolerable levels of toxicity; iii) 15-30% single agent partial response
patient
endpoint is response rate iv) Carboplatin: decreased neurotoxicity &
MDCCLXIII) Viral vectors
MDCCLXXXI) Phase III: Comparison of 2 therapies in a nephrotoxicity, myelosuppression main side
i) Retrovirus: risk of insertional mutagenesis
randomized manner; endpoints are response rate, effect
ii) Adenovirus: nonintegrating episome;
disease free survival, response duration, overall MDCCXCV) 5-fluorouracil
immunogenic
survival i) S phase uracil analogue, 2 mechanisms of
iii) Adeno-associated virus
action that interrupt DNA synthesis
iv) Herpes: nonintegrating, immunogenic
448) Clinical response rates ii) Side effects: myelosuppression, mucositis,
v) Vaccinia: nonintegrating, immunogenic
MDCCLXXXII) Complete: complete disappearance of all dermatitis, diarrhea, cardiotoxicity
MDCCLXIV) Nonviral vectors: nonspecific targeting,
clinically detectable disease; must last a minimum of iii) 13% single agent partial response
low transfection rate
28 days MDCCXCVI) Taxanes
i) Cationic liposome
MDCCLXXXIII) Partial: >50% reduction in tumor size, i) Stabilize tubulin polymers, prevent cell division,
ii) Plasmid DNA
must last a minimum of 28 days cause cell cycle arrest in G2
iii) Ballistic
MDCCLXXXIV) Minor response: <50% ii) High single agent partial response rates, 30-
iv) Calcium phosphate precipitation
regression in size 40%
v) Electroporation: cultured cells exposed to DNA
MDCCLXXXV) Stable disease: no appreciable change in
in presence of strong electrical pulse
dimensions 451) Combined chemotherapy
MDCCLXXXVI) Progressive disease: MDCCXCVII) Higher response rates with some
444) Gene therapy in neoplastic disease: 4 areas of research
appearance of any new lesions or >25% increase in combinations
MDCCLXV) Immunomodulation: modification of TIL’s,
size of known lesions MDCCXCVIII) Toxicity is more severe
enhance immunogenicity in vivo & ex vivo
MDCCXCIX) Overall survival not improved
MDCCLXVI) Cytotoxic gene therapy: introduction of
449) Overview of chemotherapeutic agents MDCCC) Cisplatinum & 5FU the “gold standard”
enzymes that convert a prodrug into a toxic
MDCCLXXXVII) Alkylating agents: crosslink
compound
DNA, interfere with DNA replication; 452) Types of external beam radiation
i) HSV-tk: thymidine kinase phosphorylated
cyclophosphamide, nitrogen mustard, chlorambucil MDCCCI) Megavoltage x-rays/gamma rays
gangcyclovir into its active compound
MDCCLXXXVIII) DNA binders: also bind to DNA (photons)
ii) Cytosine deaminase: converts prodrug 5-
& alter replication; cisplatinum, carboplatin, i) Low (4-6MeV) or high (15-25MeV) energy
fluorocytosine into 5-fluorouracil
doxorubicin, bleomycin mitomycin ii) Characteristics
MDCCLXVII) Suppressor gene therapy
MDCCLXXXIX) Antimetabolites: actively (1) Skin-sparing properties
MDCCLXVIII) Antisense gene therapy: introduction of
interfere with cellular metabolism (2) Depth-dose properties
blocking RNA against RNA or DNA targets
i) Methotrexate: interferes with folate metabolism, (3) Isodose distribution (beam uniformity)
inhibits dihydrofolate reductase enzyme MDCCCII) Electrons
445) Radiography for diagnosis of carotid invasion in HNSCC
ii) 5-fluorouracil: uracil analogue, either i) Good for superficial lesions, deep tissue
MDCCLXIX) CT criterion: >25% effacement of
incorporated into DNA and halts replication or sparing
circumference of artery; accurately excludes
is activated and blocks thymidilate synthase
patients, but false positive rate 94%
iii) Hydroxyurea 453) Brachytherapy highlights
MDCCLXX) MRI: 100% sensitive, 94% specific
iv) Gemcitabine MDCCCIII) Radioactive source placed in proximity to
MDCCXC) Vinca alkaloids: interfere with mitotic lesion; advantages are better dose localization and
446) Criteria defining a second primary
spindle formation; vincristine, vinblastine, vinorelbine continuous fractionation
MDCCLXXI) Different histology
MDCCXCI) Taxanes: stabilize tubulin polymers & MDCCCIV) Source placement
MDCCLXXII) Different location
prevent progression of mitosis; paclitaxel, docitaxel i) Interstitial
MDCCLXXIII) Each one has its own metastatses
ii) Intracavitary
 iii) Surface mold
MDCCCV) Time frame of use
i) Temporary: long lived isotopes used
ii) Permanent: short lived isotopes used
454) Radiotherapy pearls to remember
MDCCCVI) Cell death = inability to proliferate; both
DNA strands must be knocked out
MDCCCVII) Log cell kill: particular radiation dose will
kill the same proportion of cells
MDCCCVIII) Mechanisms of cell injury
i) Direct injury: electron from x-ray absorption
causes DNA damage
ii) Indirect injury: electron from x-ray absorption
creates an oxygen free radical with then
damages the DNA
MDCCCIX) Therapeutic window: dose response
curves between tumor cell & tissue damage; relative
positions of curves determine safety of tumor control
MDCCCX) Shrinking field technique
455) What are the 4 R’s of radiotherapy injury mechanisms?
MDCCCXI) Repair (sublethal injury)
i) Nonlethal injury will be repaired by the cell if it
takes no further hits
ii) Biologic effect of radiation influenced by
fractionation; increased number of fractions
increases the opportunity for repair
MDCCCXII) Reoxygenation (tumor cell hypoxia)
i) Presence of oxygen increases the effects of
ionizing radiation
ii) Radiosensitivity in oxygen: stays the same
down to 20mmHg, below this sensitivity
decreases
MDCCCXIII) Redistribution (cell cycle effects)
i) Maximum radioresistance occurs in late phase
ii) Maximum radiosensitivity occurs in early M
phase
iii) Increased fractionation allows increased
redistribution of tumor cells into radiosensitive
phases
MDCCCXIV) Repopulation
i) Tumors accem lerate repopulation after cell
reduction from surgery or radiation
456) What are the advantages & disadvantages of preoperative
radiotherapy for SCC?
MDCCCXV) Advantages
i) Unresectable tumors can be made resectable
ii) Tumor cells have better blood supply
preoperatively thus are more radiosensitive
iii) Malignant cells at the periphery of the
neoplasm are destroyed, thus extent of surgical
resection can be diminished
iv) Tumor seeding at the time of resection may be
decreased due to decreased viability
v) Fewer and less viable cells intravascularly &
within lymphatics at the time of surgery may
decrease the frequency of distant metastases
MDCCCXVI) Disadvantages
i) Wound healing problems increase as dose 461) Osteoradionecrosis, three treatment modalities
>40Gy MDCCCXLI) Hyperbaric oxygen
ii) Resection and reconstruction more difficult due MDCCCXLII) Debridement & partial mandibular
to fibrosis, inflammation and decreased blood resection
supply MDCCCXLIII) Vascularized tissue transfer
iii) Obscured tumor margins by tumor shrinkage (local/regional/free)
and inflammatory response MDCCCXLIV) Local topical care
457) What are the advantages & disadvantages of 462) 4 intraorbital complications of radiotherapy, maximum
postoperative radiotherapy for SCC? doses where applicable
MDCCCXVII) Advantages MDCCCXLV) Cataracts (doses as little as 6 Gy)
i) Safer administration of higher total doses of MDCCCXLVI) Radiation retinopathy: 55-60 Gy
radiation MDCCCXLVII) Optic nerve injury: 55-60 Gy
ii) Destruction of subclinical residual tumor MDCCCXLVIII) Lacrimal gland injury: ~35 Gy in 3.5
iii) Surgical resection easier, healing is better in weeks
nonirradiated tissues
iv) Distinct tumor margins which facilitates more 463) What spinal cord complication can occur post-
accurate & complete surgical removal radiotherapy? What sign is associated with it? What is
v) Ability to direct radiation specifically at areas the dose of radiation associated with it?
inaccessible by surgery MDCCCXLIX) Radiation myelopathy
MDCCCXVIII) Disadvantages MDCCCL) Lhermette’s sign: electric shock
i) Surgery may interrupt blood flow to remaining sensations triggered by flexing the cervical spine
tumor cells making them less radiosensitive MDCCCLI) Can occur after doses of 50-60 Gy in 5-6
ii) Wound breakdown or infection may delay the weeks
onset or prevent radiotherapy delivery
464) What are the etiologic risk factors for basal and
458) General indications for postoperative radiotherapy squamous cell carcinoma? (Sun GRASSPEr)
MDCCCXIX) T3 lesion MDCCCLII) Sun exposure (UVB 290-320nm)
MDCCCXX) T4 lesion MDCCCLIII) Genetic factors: xeroderma pigmentosum,
MDCCCXXI) Perineural or vascular invasion AD nevoid BCC syndrome
MDCCCXXII) Extracapsular spread MDCCCLIV) Occupation: ranchers, farmers, sailors,
MDCCCXXIII) Multiple histologicaly positive nodes fishermen (high sun exposure)
MDCCCXXIV) Positive resection margins MDCCCLV) Radiodermatitis from previous
radiotherapy
459) 6 late complications of radiotherapy for NPC in 6 different MDCCCLVI) Actinic keratosis
sites MDCCCLVII) Former injury: scar carcinoma, Marjolin’s
MDCCCXXV) Skin necrosis ulcers
MDCCCXXVI) Osteoradionecrosis MDCCCLVIII) Suppressed immunity: iatrogenic or
MDCCCXXVII) Cataracts (6 Gy) hemopoietic cancers
MDCCCXXVIII) Middle ear effusion secondary MDCCCLIX) Environmental exposure: arsenic induced
to ET dysfunction BCC; others – soot, coal tar, paraffin oil, petroleum
MDCCCXXIX) Xerostomia (35 Gy) oil, asphalt
MDCCCXXX) Transverse myelitis (45-50 Gy) MDCCCLX) Physical traits: pale complexion, light hair,
MDCCCXXXI) Somnolence syndrome blue or green eyes, inability to tan, propensity for
MDCCCXXXII) Brain necrosis (65-70Gy) sunburn, history of multiple or severe sunburn,
Celtic ancestry
460) Complications of radiotherapy for neck disease
MDCCCXXXIII) Xerostomia (5-6cGy in 5-6 465) 5 clinical types of basal cell carcinoma
weeks) MDCCCLXI) Nodular/noduloulcerative: most common
MDCCCXXXIV) Dental caries MDCCCLXII) Morphealike/sclerosing: worst prognosis
MDCCCXXXV)Osteoradionecrosis (in up to 5% of MDCCCLXIII) Superficial multicentric
patients) MDCCCLXIV) Pigmented: similar appearance &
MDCCCXXXVI) Mucositis behaviour as noduloulcerative except for brown
MDCCCXXXVII) Soft tissue fibrosis pigment
MDCCCXXXVIII) Hypothyroidism (1% clinically MDCCCLXV) Fibroepithelioma: often seen on back
overt, 10% occult after 50Gy in 4 weeks)
MDCCCXXXIX) Immunosuppresion 466) Describe the nevoid basal cell carcinoma syndrome
MDCCCXL) Spinal cord necrosis (limit to 45-50Gy in 5 (Gorlin syndrome)
weeks) MDCCCLXVI) Autosomal dominant (chromosome 9q)
 MDCCCLXVII) Multiple (hundreds) small cutaneous MDCCCLXXXVIII) Spindle cell SCC MCMXI) Immunosuppressed patients
nodules appear in childhood, as child ages, MDCCCLXXXIX) De novo SCC MCMXII) Incompletely excised tumor
neoplasia develops and lesions become aggressive MCMXIII) Tumors in young patients where cosmesis
– invasion, destruction, mutilation 472) Characteristics of high risk cutaneous SCC (Rowe, is an issue
MDCCCLXVIII)Other characteristics: jaw cysts Carroll, Clay) MCMXIV) Tumors potentially involving vital
(odontogenic keratocysts) in 5%, bifid ribs, frontal MDCCCXC) Invasion to reticular dermis or adipose structures
bossing, mental retardation, scoliosis, falx MDCCCXCI) Poorly differentiated histology
calcification MDCCCXCII) Immunocompromised patient 477) What are the tumors treatable with Mohs’ surgery?
MDCCCXCIII) Tumor size >2cm MCMXV) BCC
467) Histolopathologic characteristics & classes of basal cell MDCCCXCIV) Lip or ear location MCMXVI) SCC
carcinoma MDCCCXCV) Tumor arising from scar, radiated skin, MCMXVII) Bowen’s disease
MDCCCLXIX) Characteristics chronic ulcer/sinus tract MCMXVIII) Erythroplasia of Queyrat
i) Cell typically large, oval or enlongated nucleus, MDCCCXCVI) Recurrent tumor MCMXIX) Keratoacanthoma
little cytoplasm MDCCCXCVII) Perineural invasion MCMXX) Verrucous carcinoma
ii) Mucinous connective tissue stroma organized MDCCCXCVIII) Rapid growth MCMXXI) Microcystic adnexal carcinoma
in parallel bundles around tumor masses, MCMXXII) Other adnexal neoplasms
causes peripheral pallisading and stromal 473) What is the “H” zone of the face? MCMXXIII) Dermatofibrosarcoma protuberans
retraction (peritumoral lacunae) MDCCCXCIX) High risk sites for cutaneous malignancy MCMXXIV) Malignant fibrous histiocytoma
MDCCCLXX) Classes (SCAK or SACK) MCM) Junction of the ala with the nasolabial fold, MCMXXV) Atypical fibroxanthoma
i) Solid: no differentiation the septum, nasal ala, inner canthi & lower eyelids of MCMXXVI) Extramammary Paget’s disease
ii) Cystic: sebaceous gland differentiation periorbital region, periauricular region extending to MCMXXVII) Merkel cell carcinoma
iii) Adenoid: tubular/glandular differentiation the temple, certain scalp regions MCMXXVIII) Cutaneous rhabdomyosarcoma
iv) Keratotic: more biologically aggressive
474) A man in his 40’s suddenly develops hundreds of little 478) Indications for radiation for skin tumors
468) Histologic classes of squamous cell carcinoma (Batsakis) brown/brownish-black raised pedunculated lesions. What MCMXXIX) Massive tumors
MDCCCLXXI) Generic: actinic changes sign is this, what are the lumps, and what cancer is most MCMXXX) Very aggressive
MDCCCLXXII) Adenoid: pseudoglandular arrangement commonly associated with this? MCMXXXI) Invasive
MDCCCLXXIII)Bowenoid: consistent with Bowen’s MCMI) Leser-Trelat sign: a sign of internal MCMXXXII) Resection margins uncertain
disease malignancy, showers of seborrheic keratoses appear MCMXXXIII) Gross tumor left behind
MDCCCLXXIV) Verrucous: white cauliflowerlike MCMII) Most commonly associated with colonic MCMXXXIV) Multiple recurrences
lesion adenocarcinoma
MDCCCLXXV) Spindle cell: anaplastic, little/no 479) Which skin lesions are associated with a higher risk of
keratinization 475) Management of cutaneous malignancies melanoma?
MCMIII) Medical MCMXXXV) 50-70% of all melanoma arise from
OR i) Observation preexisting benign nevi
ii) Topical: 5-FU, retinoic acid MCMXXXVI) Junctional nevi
MDCCCLXXVI) Keratinized MCMIV) Surgical MCMXXXVII) Dysplastic nevi (dysplastic nevus
MDCCCLXXVII) Nonkeratinized i) Electrodessication & curettage syndrome)
MDCCCLXXVIII) Verrucous ii) Excisional surgery MCMXXXVIII) Congenital nevi (especially giant types -
MDCCCLXXIX) Adenosquamous iii) Cryosurgery >20cm)
MDCCCLXXX) Spindle cell iv) Photodynamic therapy MCMXXXIX) Presence of high numbers of benign nevi
v) Interferon-α (>20 melanocytic nevi increases relative risk to 12:1)
469) Define Broder’s classification of SCC of the oral cavity vi) Radiotherapy: generally not indicated cuz of
MDCCCLXXXI) Based on cellular length of therapy, complications, secondary 480) 4 types of melanoma, best prognosis, most common
differentiation, expressed in percentage of total carcinogenesis, lack of margin control, MCMXL) Head & neck melanoma ~20% of total
cellular elements increased aggressiveness of recurrences incidence
i) Grade I: 75-100%, well differentiated vii) Mohs’ surgery MCMXLI) Types
ii) Grade II: 50-75%, moderately well differentiated i) Superficial spreading: 75%, kaleidoscopic
iii) Grade III: 25-50%, moderately differentiated 476) 5 reasons to use Moh’s surgery in BCC (indications for color, intermediate prognosis, late invasion
iv) Grade IV: 0-25%, poorly differentiated Mohs’ surgery) ii) Lentigo maligna: 4-10%, best prognosis, only
MCMV) Recurrent tumor 30% ever metastasize
470) Premalignant lesions in cutaneous malignancies MCMVI) Size greater than 0.6 cm high risk or iii) Nodular: 15-30%, worst prognosis, early
MDCCCLXXXII) Actinic keratosis >1cm on the scalp, face, neck invasion
MDCCCLXXXIII) Bowen’s disease MCMVII) High risk location: central face, ear, chin, iv) Mucosal: ~10% of H&N melanoma
MDCCCLXXXIV) Keratoacanthoma mandible (1) 2% of all head & neck melanoma
MCMVIII) Aggressive growth pattern of BCC (2) 50% arise in nasal cavity; other sites
471) Cutaneous malignancies with worse prognosis (morpheaform or keratotic) or poorly differentiated include parnasal sinuses, nasopharynx,
MDCCCLXXXV) Sclerosing/morpheaform BCC SCC oral cavity, oropharynx
MDCCCLXXXVI) Keratotic BCC MCMIX) Tumors with poorly defined margins v) Desmoplastic
MDCCCLXXXVII) Recurrent BCC MCMX) Tumors with neurotropism
 (1) Histiologic variant, <1% of all cases; 75% iv) N3: 4+ metastatic nodes, matted nodes, or in MCMLXX) Differentiates adjacent soft tissue
occur in the head & neck transit metastases/satellites with metastatic involvement
(2) Amelanotic clinically; affinity for nodes MCMLXXI) Differentiates obstructed sinus filled with
neurotropism MCMLVI) Metastasis staging fluid from a space occupying lesion
vi) Acral lentiginous i) M0: No distant metastasis MCMLXXII) Can image sagitally
vii) Metastatic with unknown primary ii) M1a: Distant skin, subcutaneous, or nodal MCMLXXIII) Avoids radiation
metastases; normal LDH MCMLXXIV) Demonstrates perineural invasion
481) What is a Hutchinson’s freckle? iii) M1b: Lung metastases; normal LDH
MCMXLII) Lentigo maligna, or melanoma in situ iv) M1c: all other visceral metastases, normal 489) A patient has a unilateral polypoid nasal cavity lesion.
MCMXLIII) Associated with solar damage & atypical LDH; any distant metastasis, elevated LDH What is your diagnosis?
melanocytes MCMLVII) TNM Staging MCMLXXV) Inverted papilloma (Schneiderian
MCMXLIV) Radial spread along dermal/epidermal i) Stage 0: Tis, N0, M0 papilloma)
junction, focal nests of cells ii) Stage I: T1 or T2, N0, M0 i) Proliferation of squamous epithelium through
MCMXLV) Overall probability of developing into iii) Stage II: T3 or T4, N0, M0 fingerlike projections into underlying stroma;
melanoma ~5%; presence of a nodule carries iv) Stage III: Any pT, N1 or N2, M0 bony destruction/erosion common
likelihood of invasion of 100% v) Stage IV: Any pT, any pN, M1 ii) Origin
(1) 50% lateral wall
482) Definitions of depth of melanoma invasion 485) Identification of occult nodal disease (2) 47% septal
MCMXLVI) Depth of invasion the most important MCMLVIII) Ultrasound (3) 3% cylindrical type
factor in histologic staging MCMLIX) CT iii) Malignant change seen in ~10%, low for septal,
MCMXLVII) Breslow’s classification MCMLX) MRI highest for lateral wall
i) <0.75mm MCMLXI) SPECT or PET iv) Therapy: total surgical removal, either via
ii) 0.76-1.5mm MCMLXII) ELND: no benefit found except in 1-2mm medial maxillectomy (recurrence rate ~9%),
iii) 1.51-4mm (subdivided into 3a 1.51-3mm, and thick lesions in patients <60 years of age transnasal/ESS (recurrence rate ~43%)
3b 3.01-4mm) MCMLXIII) SLNB
iv) >4mm 490) Staging for esthesioneuroblastoma
MCMXLVIII) Clark’s classification 486) Identify the pathology with the following histochemical MCMLXXVI) Kadish
i) Within epidermis only markers i) A – Confined to nasal cavity
ii) Invasion into papillary dermis MCMLXIV) SCC: cytokeratin autoantibodies ii) B – Extension into paranasal sinuses
iii) Invasion to papillary-reticular dermis MCMLXV) Melanoma: S100, HMB-45, vimentin auto- iii) C – Spread beyond nasal cavity/sinuses
iv) Invasion into reticular dermis antibodies (intracranial)
v) Invasion into subcutaneous tissues MCMLXVI) Lymphoma: LCA/panleukocyte MCMLXXVII) Biller
autoantibodies i) T1 – involves nasal/paranasal sinuses (except
483) Risk of regional metastasis based on lesion thickness sphenoid)
MCMXLIX) Most important factor in overall survival is 487) Treatment strategy for melanoma ii) T2 – extension into ACF or orbit
presence or absence of lymph node metastasis MCMLXVII) Full thickness surgical resection iii) T3 – extension into brain, resectable with
MCML) <0.75mm – 0% risk i) Margins (Baileys) margin
MCMLI) 0.76-1.49mm – 25% risk (1) Tis: 0.5cm iv) T4 – unresectable
MCMLII) 1.50 – 3.99mm – 60% risk (2) 1-2mm: 1 cm MCMLXXVIII) UCLA
MCMLIII) >4mm – 65% risk (3) 2-4mm: 2 cm i) T1 – involves nasal/paranasal sinuses (except
(4) >4mm: >2cm sphenoid), spares most superior ethmoid cells
484) What is the TNM (1997) staging for melanoma? MCMLXVIII) Radiotherapy: not indicated for primary ii) T2 – T1 plus sphenoid, extends into cribriform
MCMLIV) Tumor staging therapy, indications include: iii) T3 – extension to ACF/orbit
(1) T1: <1.0mm (a, without ulceration and i) Elderly poor candidate for operative resection iv) T4 – extension to brain
mitosis <1/mm2; b, with ulceration and ii) Extensive facial LMM which would require
mitosis >1/mm2) significant resection 491) Define Ohngren’s line
(2) T2: 1.01-2.0mm (a, without ulceration; b, iii) Postop adjuvant for high risk lesions, defined MCMLXXIX) Line between medial canthus and angle of
with ulceration) as >1.5mm depth or ulcerated lesion mandible that divides maxillary sinus into a
(3) T3: 2.01-4.0mm (a, without ulceration; b, iv) Positive regional metastasis suprastructure and an infrastructure for staging
with ulceration) v) Desmoplastic histology
(4) >4.0mm (a, without ulceration; b, with MCMLXIX) Systemic therapy: 2 indications 492) Tumor staging of maxillary sinus cancer (UICC 2002)
ulceration) i) High risk patients finished primary therapy: MCMLXXX) T1: limited to antral mucosa with no
MCMLV) Nodal staging high risk includes primary ulcerated lesions, erosion or destruction of bone
i) N0: 0 nodes >4mm depth or Clark level IV, satellitosis, in- MCMLXXXI) T2: bone erosion/destruction, includes
ii) N1: 1 node (a, micrometastasis; b, transit metastases, nodal metastases extension to hard palate and/or middle nasal meatus,
macrometastasis) ii) Presence of distant metastases on except extension to posterior wall of maxillary sinus
iii) N2: 2-3 nodes (a, micrometastasis; b, presentation & pterygoid plates
macrometastasis; c, in transite MCMLXXXII) T3: tumor invades any of following: bone
metastases/satellites without metastatic nodes) 488) Why is MRI better than CT for paranasal sinus ca? of posterior maxillary sinus wall, subcutaneous
 tissues, floor or medial wall of orbit, pterygoid fossa, vi) Lymphoma i) Hyperemia over lateral rectus muscle
ethmoid sinuses vii) Extramedullary plasmacytoma pathognomonic for dysthyroid orbitopathy
MCMLXXXIII) T4a: tumor invades any of: anterior orbital viii) Hemangiopericytoma MMXXIV) T-lymphocyte infiltration into orbital
wall, skin of cheek, pterygoid plates, infratemporal tissues, fibroblast response releases the GAGs and
fossa, cribriform plate, sphenoid sinus, frontal sinus 496) Five most common primary orbital tumors causes collagen deposition in the EOMs leading to
MCMLXXXIV) T4b: tumor invades orbital apex, dura, MCMXCVI) Overall fibrosis and ophthalmoplegia
brain, MCF, CN’s other than V2, nasopharynx, clivus i) Meningioma (30% of all cases primary)
ii) Hemangioma 503) Stages of Grave’s ophthalmopathy
493) Tumor staging for nasal cavity/ethmoid sinus cancer iii) Lymphoma MMXXV) 0: normal
(UICC 2002) iv) Inflammatory tumors MMXXVI) I: proptosis only, no signs
MCMLXXXV) T1: Restricted to 1 subsite of nasal cavity v) Optic nerve glioma MMXXVII) II: symptoms present
or ethmoid sinus, with or without bony invasion MCMXCVII) Pediatrics: hemangioma & optic nerve MMXXVIII) III: proptosis >3mm
MCMLXXXVI) T2: Involves 2 subsites in a single site, or glioma most common lesions MMXXIX) IV: extraocular muscle involvement
extends to involve an adjacent site within the MMXXX) V: corneal involvement
nasoethmoidal complex, with or without bony 497) Differential diagnosis of primary orbital tumors MMXXXI) VI: vision loss
invasion MCMXCVIII) Vascular: hemangioma, lymphangioma
MCMLXXXVII) T3: Extends to invade medial wall or floor MCMXCIX) Hematopoietic: lymphoma, leukemia, 504) Medical management of Grave’s orbitopathy
of orbit, maxillary sinus, palate, or cribriform plate histiocytosis MMXXXII) Thyroid therapy (antithyroid drugs,
MCMLXXXVIII)T4a: Invades any of following – anterior MM) Neural: schwannoma, optic nerve glioma radioiodine ablation, thyroidectomy)
orbital contents, skin of nose or cheek, pterygoid MMI) Mesenchymal: rhabdomyosarcoma, MMXXXIII) Local therapy: eyedrops, nocturnal eye
plates, sphenoid or frontal sinuses fibrous dysplasia, osteoma, osteosarcoma taping, sunglasses
MCMLXXXIX) T4bb: Invades any of following – orbital MMII) Inflammatory: pseudotumor MMXXXIV) Steroid therapy: initial therapy for acute
apex, dura, brain, MCF, CN’s other than V2, MMIII) Cysts: dermoid, simple epithelial vision loss in Graves orbitopathy, prednisone 80-
nasopharynx, clivus 120mg qd x2 weeks with slow taper following this
498) Differential diagnosis of secondary orbital tumors MMXXXV) Immunosuppressives: cyclosporine,
494) Contraindications for craniofacial resection MMIV) Mucocele (>80% from frontal or ethmoid) cyclophosphamide used experimentally to alter
MCMXC) Absolute MMV) SCC autoimmune aspects of disease
i) Medical or nutritionally unfit MMVI) Meningioma (70% of all cases secondary) MMXXXVI) Radiotherapy: indicated for late sequelae
ii) Distant metastasis MMVII) BCC (90% of all eyelid malignancies) of stable thyroid orbitopathy; 20Gy in 10 fractions,
iii) Prevertebral fascia invasion MMVIII) Vascular malformation good-excellent response in 35-92%
iv) Cavernous sinus invasion by high grade lesion i) Not much use during acute/subacute phases of
v) Carotid invasion in a high risk patient 499) Metastatic tumors of the orbit disease
vi) Invasion of optic chiasm or both optic nerves MMIX) 8% of all orbital tumors, 25% will be the ii) Reserved for those who can’t tolerate, refuse,
MCMXCI) Relative presenting manifestation of the original cancer or fail surgery
i) Dural invasion MMX) Breast, lung, prostate, GI, renal cell,
ii) Intracranial nerve involvement by adenoid cystic thyroid, melanoma 505) Indications for orbital decompression in Graves
orbitopathy
495) Differential diagnosis of a sinonasal lesion 500) Causes of unilateral proptosis in adults and children MMXXXVII) Functional: decreasing visual acuity,
MCMXCII) Benign epithelial MMXI) Rhabdomyosarcoma visual field defects, abnormal visual evoked
i) Vestibular papilloma MMXII) Grave’s ophthalmopathy potentials, disk edema; typically after failed course of
ii) Schneiderian papilloma MMXIII) Pseudotumor steroids
iii) Adenoma MMXIV) Hemangioma MMXXXVIII) Corneal exposure with keratitis not
MCMXCIII) Malignant MMXV) Orbital fracture responding to medical therapy
i) SCC (most common tumor) MMXVI) Sinusitis complications MMXXXIX) Cosmetic decompression only if eye
ii) Adenocarcinoma MMXVII) Lymphoma findings stable for at least 6 months
iii) Adenoid cystic
iv) Melanoma 501) Average volume of the orbital cavity 506) Surgery for Grave’s orbitopathy
v) Olfactory neuroblastoma MMXVIII) 30ml MMXL) Kronlein (lateral orbital plate); approached
vi) SNUC MMXIX) 5ml increase in size (16%) will cause 4- through coronal direct rim incision or lateral
MCMXCIV) Benign nonepithelial (most common 5mm proptosis canthotomy
benign lesions) MMXLI) Naffziger (superior orbital plate
i) Osteoma 502) Describe Grave’s ophthalmopathy decompression into anterior cranial fossa);
ii) Fibroma MMXX) 3:1 F:M predominance, 5th–6th decades approached through anterior craniotomy
iii) Chondroma MMXXI) Incidence ~10-45% (!), most severe MMXLII) Hirsch (inferior orbital plate); approached
MCMXCV) Malignant nonepithelial forms with CN II involvement rare, ~2-5% of Graves’ through subciliary and/or Caldwell-Luc incision
i) Neurogenic sarcoma patients require surgical intervention MMXLIII) Sewall (medial orbital decompression);
ii) Rhabdomyosarcoma MMXXII) Due to thyroid stimulating approached through coronal incision or external
iii) Fibrosarcoma immunoglobulins ethmoidectomy approach
iv) Osteogenic sarcoma MMXXIII) Buildup of glycosaminoglycans in MMXLIV) Walsh-Ogura: transantral decompression
v) Chondrosarcoma extraocular muscles of medial & inferior orbit, most widely used, as it is
 extracranial, decompresses two orbital walls into the ii) Epithelial: pleomorphic adenoma most common i) Location: parotid>SMG>MSGs
largest empty space, allows gravity to aid in the (50%); other 50% malignant, includes adenoid ii)Gross: well encapsulated, smooth, rubbery
expansion cystic, malignant mixed, adenocarcinoma iii)
Epithelial & mesenchymal elements
MMXLV) Orbital fat removal: approached through iv)Epithelial trabecular pattern
upper lid crease and subciliary approaches; ~6mm 511) Most common salivary gland tumors in children v) Diverse stromal morphology: mucoid,
maximum reduction in proptosis possible; caution MMLXIV) Benign chondroid, myxoid, osteoid
around inferior oblique i) Hemangioma vi) Microscopic: incomplete encapsulation,
ii) Pleomorphic adenoma pseudopod extensions through capsule
507) What is a chloroma? iii) Lymphangioma MMLXXVIII) Warthin’s tumor (papillary cystadenoma
MMXLVI) aka. granulocytic sarcoma, an immature iv) Neurogenic lymphomatosum)
myeloid cell collection seen in conjunction with AML MMLXV) Malignant i) Whites, predominance in 5-6th decades,
& CML i) Mucoepidermoid carcinoma radiation & smoking influence; M:F 5:1
MMXLVII) Green color secondary to ii) Acinic cell ii) 5-10% of parotid tumors, 10% bilateral, 10%
myeloperoxidase iii) Adenocarcinoma multicentric
MMXLVIII) Symptoms: painless proptosis & iv) Undifferentiated carcinoma iii) High density of mitochondria on EM
violaceous lid swelling over weeks v) Adenoid cystic iv) Gross: smooth with well defined capsule
MMXLIX) Treatment: systemic chemotherapy, will v) Histology: biphasic composition
develop into leukemia without treatment 512) Etiologic risk factors for salivary gland neoplasms (1) Abundant lymphoid sheets with
MML) Prognosis poor, death usually within 18 MMLXVI) Low dose radiation conspicuous follicles and germinal
months MMLXVII) Smoking associated with Warthin’s only centres
MMLXVIII) Occupational exposure to wood dust (2) Lining epithelium consisting of a bilayer of
508) Optic nerve glioma linked to increased MSG neoplasms (especially oncocytic papillary cells
MMLI) 2nd most common pediatric orbital tumor adenocarcinoma of the nasal cavity & paranasal MMLXXIX) Oncocytoma
MMLII) Cell origin: fibrillary astrocyte sinuses) i) Almost exclusive to parotid
MMLIII) Associated with neurofibromatosis in 18- ii) Slow growing, circumscribed but
50% 513) Label the following parts of a salivary gland tubuloacinar unencapsulated
MMLIV) Radiographic: CT fusiform, lobular, unit iii) Brown, plump, granular eosinophilic cells with
isodense homogenous enlargement; MRI T1 hypo, small indented nuclei & high mitochondrial
T2 hyper density
MMLV) Treatment: observation vs. resection MMLXXX) Monomorphic adenoma
depending on whether indolent or progressive i) Basal cell: most common
growth ii) Clear cell
iii) Glycogen rich
509) Orbital pseudotumor iv) Other rare types
MMLVI) Inflammation of unknown etiology, diffuse
or localized (muscle, lacrimal gland, sclera, optic 516) Malignant salivary gland tumor histologies
nerve) MMLXXXI) Mucoepidermoid carcinoma
MMLVII) Symptoms: pain increased with i) Location: parotid > MSG (palate) > SMG
movement, proptosis ii) Grade either low or high, depends on ratio of
MMLVIII) Signs: eyelid edema, chemosis, diplopia, mucinous to epidermoid components
vision loss (20%) I) A: secretory duct iii) Low grade: high ratio of mucinous to
MMLIX) CT will show enlargement of involved II) B: striated duct epidermoid cells, behave like benign neoplasm
structures; lacks characteristic enlargement of III) C: intercalated duct but capable of local invasion & metastasis
extraocular muscles typical for Graves IV) D: acinus iv) High grade: low ratio of mucinous to
ophthalmopathy V) E: myoepithelial cell epidermoid cells, resembles SCC
MMLX) MR: T1 iso to muscle with gad MMLXXXII) Adenoid cystic carcinoma
enhancement, T2 hyper to fat 514) Cellular origin of parotid tumors i) Most common malignancy of SMG and MSG’s
MMLXI) Treatment: corticosteroids MMLXIX) Acinic cell: acinar cells ii) Gross: monolobular, either no capsule or
MMLXX) Adenoid cystic: myoepithelial partially encapsulated; infiltrates surrounding
510) Enlarging lacrimal gland pathology MMLXXI) Pleomorphic adenoma: myoepithelial & tissue
MMLXII) Infectious intercalated iii) Micro: basaloid epithelium arranged in cylindric
i) Acute bacterial: Staph, Strep MMLXXII) Adenocarcinoma: intercalated or striated formations, eosinophilic hyaline stroma
ii) Acute viral: herpes, mumps, mono duct iv) Histologic subtypes
iii) Chronic bacterial: trachoma, syphilis, TB, MMLXXIII) Warthin’s: striated (1) Solid (worst prognosis)
sarcoid MMLXXIV) Oncocytoma: striated (2) Tubular (best prognosis)
MMLXIII) Neoplastic MMLXXV) Squamous: excretory duct (3) Cribriform (intermediate prognosis, most
i) Lymphoproliferative: benign lymphoid MMLXXVI) Mucoepidermoid: excretory duct common subtype)
hyperplasia, atypical lymphoid hyperplasia, v) Grade depends on percentage of tumor made
lymphoma, leukemia 515) Benign salivary gland tumor histologies up of solid elements; low grade <30% solid,
MMLXXVII) Pleomorphic adenoma high grade >30% solid
 vi) Perineural invasion a typical feature vi) Metastatic disease v) Jacobson’s nerve (leaves skull base via inferior
MMLXXXIII) Acinic cell carcinoma vii) Large size: >5cm tympanic canaliculus)
i) Derived from serous cells, thus for location vi) CN IX
parotid >> SMG, rare in MSG 521) Name three reasons to recommend surgical excision of a vii) Inferior salivatory nucleus
ii) Gross: well circumscribed, fibrous capsule benign salivary gland lesion diagnosed on FNA MMCXXI) Treatment
iii) Histo: two types, one resembles serous acinar MMXCIX) Impact on cosmesis & continued growth i) Antiperspirant
cells, other has a clear cytoplasm; amyloid a of lesion ii) Scopolamine cream
hallmark pathologic finding MMC) FNAB not 100% accurate in diagnosis iii) Topical anticholinergic (glycopyrrolate or
iv) Configurations: papillary, follicular, cystic, MMCI) Chance of malignant transformation over atropine)
vacuolated time iv) Botox
MMLXXXIV) Adenocarcinoma
i) Location: MSG > parotid 522) What methods are used to identify the facial nerve during 526) Histologic features of necrotizing sialometaplasia
ii) Aggressive tumors, likely to recur & parotidectomy? MMCXXII) Lobular infarction with or without mucus
metastasize MMCII) Tragal pointer extravasation
iii) Gross: firm/hard, attached to surrounding MMCIII) Tympanomastoid suture MMCXXIII) Pseudoepitheliomatous hyperplasia at
tissue MMCIV) Retrograde dissection from a distal periphery of lesion
iv) Micro: cylindric cells of variable height, form branch MMCXXIV) Squamous metapasia of ducts & acini
papillae, acini, solid masses; mucin producing MMCV) Identification of nerve within mastoid bone MMCXXV) Inflammation secondary to extravasated
MMLXXXV) PLGA MMCVI) Digastric muscle attachment to the mucus
i) 2nd most common tumor of the MSG’s digastric groove MMCXXVI) Preserved lobular architecture
ii) Seen on palate, buccal mucosa, upper lip
iii) Gross: firm, painless mucosalized mass 523) Indications for neck dissection for salivary gland 527) Subsites of the oral cavity
iv) Histo: variable tumor cell differentiation & neoplasms MMCXXVII) Upper & lower lips
organization, mitotic figures & necrosis unusual MMCVII) Cervical metastasis MMCXXVIII) Oral tongue
MMCVIII) Tumors >4cm MMCXXIX) Upper & lower alveolus
517) Hot lesions on technetium scans MMCIX) High grade malignancies MMCXXX) Buccal mucosa
MMLXXXVI) Warthin’s tumor i) High grade mucoepidermoid carcinoma MMCXXXI) Floor of mouth
MMLXXXVII) Oncocytoma ii) Adenoid cystic carcinoma MMCXXXII) Retromolar trigone
iii) Mucinous adenocarcinoma MMCXXXIII) Hard palate
518) Most common bilateral lesions iv) Small/large cell carcinoma
MMLXXXVIII) Warthin’s (10% of cases) v) Metastasizing pleomorphic adenoma 528) 8 muscles from 1st arch
MMLXXXIX) Acinic cell (3% of cases) vi) Carcinosarcoma MMCXXXIV)Masseter
MMXC) Oncocytoma vii) Primary squamous cell carcinoma MMCXXXV) Temporalis
viii) Undifferentiated carcinoma MMCXXXVI)Medial pterygoid
519) Parotid tumor staging (UICC 6th edition) MMCXXXVII) Lateral pterygoid
MMXCI) T1: Tumor <2cm without 524) Indications for radiotherapy in salivary gland malignancies MMCXXXVIII) Anterior belly of digastric
extraparenchymal extension MMCX) Recommended for all patients with MMCXXXIX)Tensor tympani
MMXCII) T2: Tumor 2-4cm without malignant tumors except T1N0 orT2N0 disease with MMCXL) Tensor veli palatini
extraparenchymal extension low grade histology (low grade mucoepidermoid, MMCXLI) Mylohyoid
MMXCIII) T3: Tumor more than 4 cm and/or tumor acinic cell) and negative resection margins
with extraparenchymal extension MMCXI) Unresectable or incomplete resection 529) Boundaries of the oral cavity
MMXCIV) T4a: Tumor invades skin, mandible, ear MMCXII) Ulceration or fixed to tissues MMCXLII) Anteriorly: vermilion border
canal, facial nerve MMCXIII) Size larger than 4cm MMCXLIII) Posteriorly: posterior border of hard
MMXCV) T4b: Tumor invades base of skull, MMCXIV) Multiple tumor nodules palate, intersection of retromolar trigone and anterior
pterygoid plates, or encases carotid artery MMCXV) Facial nerve dysfunction caused by pillar, circumvallate line of the tongue
MMXCVI) Extraparenchymal extension: clinical or cancer
macroscopic evidence of invasion of soft tissues or MMCXVI) Extension to extraglandular tissues 530) Functions of the oral cavity
nerve, except those listed under T4A and 4b MMCXLIV) Mastication
525) Pathway for Frey’s syndrome (aka. Gustatory sweating) MMCXLV) Deglutition
520) What is the percent chance of a 2cm parotid mass being MMCXVII) Aberrant reinnervation of postganglionic MMCXLVI) Oral competence
malignant? Name 5 signs or symptoms which would parasympathetic nerves to the sweat glands of the MMCXLVII)
support a malignant diagnosis face MMCXLVIII) Articulation
MMXCVII) 15-25% chance of malignancy in isolated MMCXVIII) 10% of patients overtly symptomatic MMCXLIX) Respiration
parotid mass MMCXIX) Diagnosis: Minor’s starch iodine test MMCL) Airway protection
MMXCVIII) Signs suggesting a malignant diagnosis MMCXX) Afferent pathway MMCLI) Oral hygiene
i) Facial nerve paralysis/paresis i) Parotid and sweat glands
ii) Fixation to overlying/underlying structures ii) Auriculotemporal nerve 531) Anatomic associations of the pharyngeal constrictors
iii) Overlying skin ulceration/infection iii) Otic ganglion MMCLII) Between skull base & superior constrictor
iv) Localized pain or trismus iv) LSPN (enters skull base via foramen ovale) i) Tensor veli palatini
v) Cervical adenopathy ii) Levator veli palatini
 iii) Eustachian tube iv) Estlander flap (if commissure involved) MMCCVI) Increasing stage
iv) Ascending pharyngeal artery MMCLXXIX) Greater than 66% MMCCVII) Increasing tumor thickness
v) Ascending palatine artery i) Midline: advancement flap via Webster MMCCVIII) Perineural invasion
MMCLIII) Between superior & middle constrictors modification of Bernard-Burow; Gilles fan flap; MMCCIX) Intralymphatic invasion
i) Glossopharyngeal nerve gate flap MMCCX) Vascular invasion
ii) Stylopharyngeus ii) Lateral: full thickness nasolabial transposition MMCCXI) DNA ploidy
iii) Stylohyoid ligament flap
iv) Lingual artery iii) If inadequate adjacent cheek tissue, use 542) Treatment of neoplasms of the oral cavity by level of
MMCLIV) Between middle & inferior constrictors regional, distant, or microfascular free flap staging
(space closed by thyrohyoid membrane) MMCCXII) T1 & T2 lesions
i) Superior laryngeal artery & vein 537) Repair of upper lip defects i) Equal survival with surgical excision vs.
ii) Internal laryngeal nerve MMCLXXX) Up to 50% radiation therapy
MMCLV) Between inferior constrictor & esophagus i) Midline: perialar crescentic excisions and ii) Consider patient’s health, preference, mobility
i) Recurrent laryngeal nerve primary advancement closure MMCCXIII) Larger T1 & T2 lesions with N0 neck
ii) Inferior laryngeal artery & vein ii) Lateral: primary closure i) Treat with supraomohyoid neck dissection or
MMCLXXXI) 50-66% radiation therapy
532) Risk factors for lip cancer i) Full thickness pedicled flap from lower lip MMCCXIV) T3 & T4 lesions
MMCLVI) Sun exposure ii) Karapandzic flap i) Combination therapy, either pre- or
MMCLVII) Smoking iii) Abbe flap postoperative radiation
MMCLVIII) Poor dental hygiene iv) Estlander flap (if commissure involved) ii) Modified radical/radical neck dissection for all
MMCLIX) Chronic alcoholism MMCLXXXII) Greater than 66% cases, with decision based on number of
i) Midline: advancement flap closure via nodes, extracapsular spread, fixation to
533) TNM staging for lip & oral cavity cancer (UICC 6th edition) Dieffenbach or Webster techniques adjoining tissues/structures
MMCLX) T1: Tumor 2cm or less in greatest ii) Lateral: full thickness nasolabial transposition
dimension flap 543) Differential diagnosis of nonepidermoid oral cavity cancer
MMCLXI) T2: Tumor 2-4cm in greatest dimension iii) If inadequate adjacent cheek tissue, use MMCCXV) 10% occurrence
MMCLXII) T3: Tumor >4cm in greatest dimension temporal forehead flap, regional flap, free flap MMCCXVI) Lymphoma
MMCLXIII) T4a (lip): Tumor invades through cortical MMCCXVII) Melanoma
bone, inferior alveolar nerve, floor of mouth, or skin 538) A patient comes in with a white patch on their oral MMCCXVIII) Kaposi’s sarcoma
MMCLXIV) T4a (oral cavity): Tumor invades through mucosa. What is the differential diagnosis? MMCCXIX) Minor salivary gland cancer
cortical bone, deep/extrinsic muscles of tongue, MMCLXXXIII) Leukoplakia
maxillary sinus, or skin of face MMCLXXXIV) Lichen planus 544) Eagle syndrome
MMCLXV) T4b (lip and oral cavity): Tumor invades MMCLXXXV) Leukoedema MMCCXX) Caused by elongated styloid or
masticator space, pterygoid plates, skull base, or MMCLXXXVI) White spongy nevus calcification of stylohyoid ligament, causes irritation
encases carotid artery MMCLXXXVII) Candidiasis of V,VII,IX,X nerves; normal finding in 4% of
MMCLXXXVIII)SLE population
534) Poor prognostic indicators for lip cancer MMCLXXXIX) Psoriasis MMCCXXI) Symptoms: throat pain, globus,
MMCLXVI) Size > 3cm dysphagia, facial pain, increased salivation,
MMCLXVII) Perineural invasion 539) Histologic features of leukoplakia carotodynia, otalgia
MMCLXVIII) Cervical metastasis MMCXC) Hyperkeratosis MMCCXXII) Therapy: removal of styloid process via
MMCLXIX) Recurrent tumors MMCXCI) Parakeratosis intraoral or external approach
MMCLXX) Poorly differentiated histology MMCXCII) Dyskeratosis
MMCLXXI) Mandibular invasion MMCXCIII) No pleomorphism 545) Differential diagnosis of maxillary & mandibular cysts
MMCLXXII) Commissure lesion MMCXCIV) No anaplasia MMCCXXIII) Inflammatory (85%)
MMCXCV) No desmoplasia i) Periapical cyst: most common; arise from
535) Ideal reconstruction of the lip nonvital root/pulp infection; treat with root canal
MMCLXXIII) Sensate 540) Differential diagnosis of a red lesion in the oral cavity ii) Lateral inflammatory periodontal cyst
MMCLXXIV) Intact sphincter function for control of MMCXCVI) Erythroplakia MMCCXXIV) Developmental (10%)
watertight continent seal MMCXCVII) Pyogenic granuloma i) Odontogenic
MMCLXXV) Sufficient opening for food, dentures, oral MMCXCVIII) Papilloma (1) Dentigerous/follicular cyst: 2nd most
hygiene MMCXCIX) Pigmented nevi common, cystic enlargement of follicle of
MMCLXXVI) Aesthetically acceptable MMCC) Inflammatory papillary hyperplasia impacted tooth; treat with enucleation &
MMCCI) Kaposi’s sarcoma curettage
536) Repair of lower lip defects MMCCII) Leukemia (2) Odontogenic keratocyst: cystic neoplasm
MMCLXXVII) Up to 50%: primary closure MMCCIII) Hemangiosarcoma that causes bone destruction, frequent
MMCLXXVIII) 50-66% MMCCIV) Mycosis fungoides recurrence; enucleate & curettage
i) Full thickness pedicled flap from upper lip MMCCV) Polycythemia rubra vera (3) Eruption cyst
ii) Karapandzic flap (orbicularis oris (4) Alveolar cyst of infants
myocutaneous flap) 541) Prognostic factors in oral cavity cancer imparting a worse (5) Gingival cyst of adults
iii) Abbe flap prognosis (6) Developmental lateral periodontal cyst
 ii)Nonodontogenic MMCCXXXIX) Multiple nodes ii) Inferior: body of hyoid
(1) Nasopalatine duct cyst MMCCXL) Extracapsular spread iii) Medial: anterior belly of contralateral digastric
(2) Midpalatal cyst of infants iv) Lateral: anterior belly of ipsilateral digastric
(3) Nasolabial cyst 549) Branches of ECA MMCCLXVIII) Level Ib
MMCCXXV) Nonodontogenic cysts (5%) MMCCXLI) Superior thyroid (anterior) i) Superior: body of mandible
i) Aneurysmal bone cavity MMCCXLII) Ascending pharyngeal (posterior) ii) Inferior: posterior belly of digastric
ii) Stafne lingual cortical defect MMCCXLIII) Lingual (anterior) iii) Medial: anterior belly of digastric
iii) Idiopathic bone cyst MMCCXLIV) Facial (anterior) iv) Posterior: stylohyoid muscle
MMCCXLV) Occipital (posterior) MMCCLXIX) Level IIa
546) Differential diagnosis of odontogenic tumors MMCCXLVI) Posterior auricular (posterior) i) Superior: skull base
MMCCXXVI) Benign epithelial tumors MMCCXLVII) Superficial temporal (terminal) ii) Inferior: hyoid (clinical) or carotid bifurcation
i) Ameloblastoma MMCCXLVIII) Internal maxillary (anterior) (anat)
(1) Peripheral iii) Medial: stylohyoid muscle
(2) Central 550) Name the 5 structures that cross over the internal carotid iv) Lateral: plane defined by CN XI
(a) Unicystic lateral to it MMCCLXX) Level IIb
(b) Plexiform unicystic MMCCXLIX) Hypoglossal nerve i) Superior: skull base
(c) Multicystic (solid): requires MMCCL) Occipital artery ii) Inferior: hyoid (clinical) or carotid bifurcation
marginal/partial resection MMCCLI) Posterior belly of digastric (anat)
ii) Calcifying epithelial odontogenic tumor MMCCLII) Stylohyoid muscle iii) Medial: plane defined by CN XI
(Pindborg) MMCCLIII) Posterior auricular artery iv) Lateral: lateral border of SCM
iii) Odontogenic adenomatoid tumor MMCCLXXI) Level III
iv) Calcifying odontogenic cyst (Gorlin) 551) Name the 4 structures that run between the external and i) Superior: hyoid (clinical) or carotid bifurcation
v) Ameloblastic fibroma internal carotid arteries (anatomic)
vi) Ameloblastic fibroodontoma MMCCLIV) Glossopharyngeus ii) Inferior: cricothyroid membrane (clinical) or
vii) Ameloblastic odontoma MMCCLV) Pharyngeal branch of the vagus omohyoid over IJV (anatomic)
viii) Odontoma (complex, compound) MMCCLVI) Stylopharyngeus iii) Medial: lateral border of sternohyoid
MMCCXXVII) Benign mesenchymal odontogenic tumors MMCCLVII) Stylohyoid ligament iv) Lateral: posterior border of SCM
i) Odontogenic fibroma MMCCLXXII) Level IV
ii) Odontogenic myxoma 552) Branches of the vagus nerve i) Superior: cricothyroid membrane (clinical) or
iii) Cementoma MMCCLVIII) Pharyngeal omohyoid crossing over IJV (anatomic)
iv) Periapical cementoosseous dysplasia MMCCLIX) Superior laryngeal ii) Inferior: clavicle
v) Cementifying fibroma i) External iii) Anterior: lateral border of sternohyoid
vi) Benign cementoblastoma ii) Internal iv) Lateral: posterior border of SCM
vii) Dentinoma MMCCLX) Recurrent laryngeal MMCCLXXIII) Level Va
MMCCXXVIII) Malignant odontogenic tumors i) Tracheal i) Superior: Apex of convergence of the trapezius
i) Malignant ameloblastoma ii) Esophageal and SCM muscles
ii) Ameloblastic fibrosarcoma iii) Pharyngeal ii) Inferior: horizontal plane through inferior border
iii) Ameloblastic dentinosarcoma of cricoid
iv) Ameloblastic odontosarcoma 553) Cutaneous branches of the cervical plexus iii) Medial: posterior border of SCM
MMCCLXI) Lesser occipital (C2,3) iv) Lateral: anterior border of trapezius
547) What are the nodal (N) stagings for HNSCC by TNM MMCCLXII) Great auricular (C2,3) MMCCLXXIV) Level Vb
classification? MMCCLXIII) Anterior cutaneous nerve of the neck i) Superior: horizontal plane through inferior
MMCCXXIX) Nx: nodal status cannot be assessed (C2,3) border of cricoid
MMCCXXX) N0: no nodal metastasis MMCCLXIV) Supraclavicular (C3,4) ii) Inferior: clavicle
MMCCXXXI) N1: single nodal metastasis <3cm in iii) Medial: posterior border of SCM
greatest diameter 554) Venous drainage of the superficial head & neck iv) Lateral: anterior border of trapezius
MMCCXXXII) N2a: single ipsilateral metastasis 3-6cm MMCCLXV) Retromandibular vein: formed from MMCCLXXV) Level VI
in greatest diameter junction of superficial temporal and pterygoid plexus i) Superior: hyoid bone
MMCCXXXIII) N2b: multiple ipsilateral metastases none veins ii) Inferior: suprasternal notch
>6cm in greatest diameter i) Splits into two branches to feed external jugular iii) Region found between common carotids
MMCCXXXIV) N2c: single or multiple contralateral and the common facial vein
metastases none >6cm in greatest diameter MMCCLXVI) Common facial vein: formed from junction 556) Classification of neck dissections
MMCCXXXV) N3: metastasis greater than 6cm in of facial (external maxillary) and branch from MMCCLXXVI) Comprehensive
diameter retromandibular vein i) Radical
i) Drains into internal jugular vein at the level of ii) Modified radical (types I, II, III)
548) Radiographic signs of nodal metastasis the hyoid MMCCLXXVII) Selective (describe level)
MMCCXXXVI) Central necrosis (most accurate CT i) Lateral (II, III, IV)
criterion) or rim enhancement 555) Describe the borders of the levels of the neck ii) Posterolateral (II, III, IV, V)
MMCCXXXVII) Spherical shape MMCCLXVII) Level Ia iii) Anterolateral (I, II, III)
MMCCXXXVIII) Diameter >10mm or >15mm i) Superior: symphysis MMCCLXXVIII)Extended
 562) Sensitivity & specificity for physical exam, CT, and MMCCCXXXV) Propylthiouracil: provides
557) Management of an exposed carotid combined for detecting neck disease in HNSCC thyroid peroxidase substrate, decreases peripheral
MMCCLXXIX) Risk factors MMCCXCIX) Clinical exam: sensitivity 74%, specificity T4 to T3 conversion; liver side effects
i) Prior radiation 81%, accuracy 77% MMCCCXXXVI) MMI: thyroid peroxidase
ii) Malnutrition MMCCC) CT: sensitivity 83%, specificity 83%, substrate
iii) Diabetes accuracy 83% MMCCCXXXVII) Thionamides: oral use only,
MMCCLXXX) Inpatient considerations MMCCCI) Combined: sensitivity 91% indicated in young patients, pregnant patients,
i) Design incisions properly severe thyrotoxicity prior to OR or radioactive iodine
ii) Perioperative antibiotics 563) Physiology of TSH (4 effects on the thyroid cell) ablation
iii) Adequate tissue coverage (regional/free flaps) MMCCCII)  Iodine transport into cell MMCCCXXXVIII) Β-blockers: decreases
MMCCLXXXI) Obsolete methods of management MMCCCIII)  formation of MIT & DIT sympathetic overdrive, used as an adjunctive
i) Dermal flap MMCCCIV)  T3 and T4 release treatment
ii) Scalene local flap MMCCCV)  TG synthesis and proteolysis MMCCCXXXIX) Iodide: inhibits organification &
iii) Levator scapulae flap MMCCCVI) Maintains structure of thyroid cells thyroid hormone release, decreases vascularity;
iv) Pharyngostomes for controlled salivary fistulas MMCCCVII) Stimulates gland size and vascularity most useful in thyroid storm
MMCCLXXXII) Management i) Wolf-Chaikoff effect: a transient antithyroid
i) Manual pressure to stop bleeding 564) Thyroid hormone functions effect of iodides
ii) Blood products/IV fluids MMCCCVIII)  calorigenesis / metabolic rate ii) Jod-Basedow phenomenon: development of
iii) OR ligation of carotid +/- Fogarty overt hyperthyroidism in subclinical patients
MMCCCIX)  O2 consumption
catheterization to help control bleed due to exogenous iodide administration
MMCCCX)  heat production
MMCCCXI) Potentates epinephrine
558) Risk factors for postoperative major vessel rupture 569) Management of thyroid storm
MMCCCXII) Growth and development (*neonatal brain)
MMCCLXXXIII)Fistula/infection MMCCCXL) Mania, progresses to lethargy,
MMCCCXIII) Metabolism of protein, carbs, lipids
MMCCLXXXIV) Exposure of vessel obdundation, coma; heart failure & atrial fibrillation;
MMCCLXXXV) Adventitia removed MMCCCXIV)  Cholesterol jaundice, diarrhea
MMCCLXXXVI) Recurrent tumor MMCCCXV)  RBC mass MMCCCXLI) Precipitated by stress
MMCCLXXXVII) Radiation MMCCCXVI)  CO, HR MMCCCXLII) Treatment: PTU 800-1000mg NG qd;
dexamethasone 2mg IV q6h (decreases hormone
559) Management of the chylous fistula 565) Risk factors for hypothyroidism secretion & peripheral hormone conversion); sodium
MMCCLXXXVIII) When encountered MMCCCXVII) Old age iodide 1g IV (inhibits hormone release)
intraoperatively, ligate it off MMCCCXVIII) Female sex
MMCCLXXXIX) Postoperative management MMCCCXIX) Grave’s disease 570) Thyroiditis
i) Head elevation MMCCCXX) Hashimoto’s disease MMCCCXLIII) Autoimmune (Hashimoto’s): most
ii) Closed suction drainage MMCCCXXI) Other autoimmune disease common, due to anti-TPO (90%) & antithyroglobulin
iii) Pressure dressing MMCCCXXII) Drugs: lithium iodide, amiodarone, iodide (50%) antibodies
iv) Alter diet with MCT’s (directly absorbed into containing drugs MMCCCXLIV) Acute suppurative
portal system, avoids breakdown of LCT’s into MMCCCXXIII) Postthyroidectomy MMCCCXLV) de Quervain’s: viral etiology, most
FFAs & glycerol which are transported in MMCCCXXIV) Euthyroid goiter common cause of painful thyroiditis
chylomicrons) MMCCCXXV) Prior head & neck radiograph MMCCCXLVI) Silent thyrotoxic thyroiditis
MMCCXC) Indication for early surgical intervention management MMCCCXLVII) Riedel’s thyroiditis
i) >600ml in 24 hours MMCCCXXVI) Laryngectomy with/without irradiation MMCCCXLVIII)Lymphocytic thyroiditis
ii) Chylothorax
iii) Cachexia 566) Head & neck signs & symptoms of hypothyroidism 571) Indications for surgery in euthyroid goiter
iv) Persistent for greater than 1 week MMCCCXXVII)Hearing loss: sensorineural, mixed, MMCCCXLIX) Compressive symptoms (airway,
conductive esophagus)
560) What are the symptoms of Horner’s syndrome? MMCCCXXVIII) Vertigo, tinnitus MMCCCL) Recurrent painful hemorrhage
MMCCXCI) Ptosis MMCCCXXIX) Enlarged tongue MMCCCLI) Inability to exclude cancer on FNA
MMCCXCII) Meiosis MMCCCXXX) Hoarseness (mucopolysaccharide MMCCCLII) Cosmetic problems
MMCCXCIII) Anhidrosis infiltration)
MMCCXCIV) Enophthalmos MMCCCXXXI) Blurred vision 572) What are the most common types of thyroid carcinoma?
MMCCCLIII) Papillary 70-80%
561) Histologic features of the primary lesion which may 567) Graves disease triad i) 3rd & 4th decades; F:M 3:1
predict cervical metastasis MMCCCXXXII)Diffuse toxic goiter ii) Multicentric in 80%, high locoregional
MMCCXCV) Thickness of primary: >4mm associated MMCCCXXXIII) Infiltrative ophthalmopathy metastasis to nodes (37-65%), lower rate of
with increased risk MMCCCXXXIV) Infiltrative dermopathy (pretibial distant metastasis (2-17%); size a prognostic
MMCCXCVI) Vascular invasion myxedema) factor
MMCCXCVII) Perineural invasion iii) Histologic subtypes: encapsulated (better
MMCCXCVIII) Grade of differentiation 568) Medical management of Graves disease prognosis); diffuse sclerosing, tall cell,
columnar cell (these 3 have worse prognosis);
oxyphilic, follicular, papillary microcarcinoma
 iv)Lymph node metastasis increases risk of local ii) AGES (Mayo): age, grade, extrathyroidal
recurrence, does not affect mortality 575) FNAB pearls extension, size
v) 5 year survival 70-90% MMCCCLXV) Adequacy of FNAB: >6 properly prepared iii) MACIS: distant metastases, age,
MMCCCLIV) Follicular 10-15% (including Hurthle cell smears with 15-20 groups of well-preserved clumps completeness of resection, extrathyroidal
subtype) of follicular epithelium invasion, size
i) >4th decade, F:M 2-3:1 MMCCCLXVI) 3 diagnostic categories: benign (60-75%),
ii) Encapsulated with varying degrees of suspicious (20%), malignant (5%) 578) Definitions of MEN I, IIA/IIB
extracapsular invasion (required for carcinoma MMCCCLXVII) 20% of suspicious biopsies are from MMCCCLXXIV) Autosomal dominant
diagnosis); multicentricity uncommon malignant tumors MMCCCLXXV)MEN I
iii) Histologic variants: oxyphilic (Hurthle), clear MMCCCLXVIII) Accuracy of biopsy varies with i) Altered tumor suppressor gene (menin) found
cell histology of tumor on chromosome 11
iv) Lower rate of nodal metastasis (20%), higher i) Anaplastic & medullary: 90% ii) Pituitary lesions (prolactinoma)
rate of distant metastasis (65%); size not a ii) Papillary: 80% iii) Parathyroid adenomas/hyperplasia
prognostic factor; angioinvasion a poor iii) Follicular: 40%, cannot diagnose malignancy iv) Pancreatic islet cell tumors (gastrinoma)
prognosis from FNA result; vascular &/or extracapsular MMCCCLXXVI) MEN II: medullary thyroid
v) 5 year survival 70% invasion required on pathology to make this carcinoma, pheochromocytoma (in ~50% of
MMCCCLV) Medullary ~5-7% diagnosis patients) plus:
i) 60-80% sporadic, 10-40% familial (MEN II) i) A: parathyroid adenoma/hyperplasia &
ii) Early lymph node metastasis in 50% of 576) UICC & TNM (2002) staging for thyroid carcinoma (non- hyperparathyroidism (10-30% (KJ) or 85% of
presenting patients anaplastic histology) patients)
iii) Markers: calcitonin, CEA MMCCCLXIX) T: primary tumor ii) B: Marfanoid habitus, multiple mucosal
iv) Total thyroidectomy for MEN IIA by 5-6 years, i) Tx: Primary cannot be assessed neuromas, hyperplastic corneal nerves
for MEN IIB by 6 months of age; 131I not ii) T0: No evidence of primary tumor iii) MEN II syndromes caused by RET mutation on
indicated iii) T1: <2cm, limited to thyroid chromosome 10 (tyrosine kinase), 5 different
v) 5 year survival 88%, 10 year survival 65% iv) T2: 2-4cm, limited to thyroid point mutations identified
MMCCCLVI) Anaplastic ~5% v) T3: >4cm, limited to thyroid or any tumor with
i) >65 years of age minimal extrathyroid extension 579) Histology of medullary thyroid carcinoma
ii) Histology: giant & spindle cells in various vi) T4: Extension beyond thyroid capsule & MMCCCLXXVII) Nests of small round cells with
proportions invades following: subcutaneous soft tissues, abundant granular cytoplasm
iii) 10% survival after 1 year larynx, trachea, esophagus, RLN MMCCCLXXVIII) Presence of amyloid
MMCCCLVII) Lymphoma ~5% vii) T4b: Invades prevertebral fascia, mediastinal MMCCCLXXIX) Dense, irregular areas of
i) More common than anaplastic carcinoma vessels, or encases carotid artery calcification
ii) Hashimoto’s disease increases patients risk MMCCCLXX) N: nodal metastases
70x i) N0: no regional LN metastasis 580) Timing of thyroidectomy in children whose genetic screen
iii) Almost always NHL, immunoblastic most ii) N1a: Level VI metastasis is positive for MEN type 2
common subtype iii) N1b: Metastasis in other unilateral, bilateral or MMCCCLXXX)Risk of developing MCT during lifetime
contralateral cervical or upper/superior >90%
573) Histology of papillary carcinoma mediastinal nodes MMCCCLXXXI) MEN 2A: around 6 years of age
MMCCCLVIII) Multicentricity MMCCCLXXI) M: distant metastases MMCCCLXXXII) MEN 2B: shortly after birth
MMCCCLIX) Papillae formation i) M0: no distant mets
MMCCCLX) Psammoma bodies: laminated calcific ii) M1: distant mets present 581) 3 clinical signs of Marfan’s syndrome
densities, present in ~50% MMCCCLXXXIII) Autosomal dominant
MMCCCLXI) Large nuclei with folded/grooved margins 577) Indicators of worse prognosis for well differentiated thyroid MMCCCLXXXIV) Long spidery fingers, scoliosis,
and intranuclear vacuoles (orphan Annie eyes) cancer, risk profile scales hammer toe, pigeon breast, dolichocephaly, low
MMCCCLXII) Presence of follicles MMCCCLXXII) Risk factors hairline, tall & thin body structure, lens displacement,
i) Older age (men > 40, women >50) has worse aortic root dilatation
574) Name the WHO histologic and architectural subtypes of prognosis MMCCCLXXXV) May have SNHL, CHL or mixed
thyroid follicular adenoma? ii) Size of primary: >5cm worse, <1.5cm improved HL
MMCCCLXIII) Architectural prognosis; thus size >1.5cm consider worse
i) Normofollicular (simple) iii) Unifocal more likely to be malignant versus 582) Pheochromocytoma rule of 10s
ii) Macrofollicular (colloid) multifocal disease; mutifocality increases with MMCCCLXXXVI) 10% bilateral
iii) Microfollicular (fetal) age MMCCCLXXXVII) 10% malignant
iv) Trabecular & solid (embryonal) iv) Extrathyroidal extension MMCCCLXXXVIII) 10% extraadrenal
v) Atypical v) Cervical metastases: does not impact overall
MMCCCLXIV) Cytologic patterns survival but does increase chances of local 583) Lore’s triangle: Identifies location of RLN in the neck
i) Oxyphilic recurrence during thyroidectomy
ii) Clear cell vi) Distant metastases adversely affects prognosis MMCCCLXXXIX) Medial: tracheal sidewall
iii) Mucin-producing MMCCCLXXIII) Risk profiles MMCCCXC) Lateral: carotid sheath
iv) Signet-ring i) AMES (Lahey clinic): age, distant metastasis, MMCCCXCI) Superior: surface of retracted thyroid pole
v) Atypical extrathyroidal extension, size (5cm) inferiorly
 iii)
Kidney effects: ↑ calcium reabsorption, ↓ ii) Digital subtraction angiography: for multiple
584) Branches of the thyrocervical trunk phosphate reabsorption, ↑ 1,25-(OH)2-D3 gland disease in revision cases, 60-70%
MMCCCXCII) Originates off of the 1st portion of the synthesis sensitive
subclavian artery iv) GIT effects: ↑ calcium absorption via vitamin D iii) Selective venous catheterization: same as (ii)
i) Ascending cervical: supplies prevertebral stimulation
muscle region MMCDV) Calcitonin 595) Indications for surgery with asymptomatic primary
ii) Inferior thyroid: to inferior pole of thyroid gland i) ↓ calcium by inhibiting osteoclast function hyperparathyroidism
iii) Transverse cervical MMCDXXIII) Serum calcium >12 mg/dl (>3 mmol/L)
iv) Suprascapular 589) Blood supply to superior & inferior parathyroid glands MMCDXXIV) Hypercalciuria
MMCDVI) Superior and inferior parathyroid arteries, MMCDXXV) Decreased creatinine clearance
585) Management of preoperative hyperthyroidism originating from inferior thyroid artery (86% of time), MMCDXXVI) Age <50 years
MMCCCXCIII) Supressive therapy with thionamides used some contribution from superior thyroid artery MMCDXXVII) Osteoporosis > 2SDs
until patient normothyroid MMCDXXVIII) Any overt manifestations of
i) Propylthiouracil: inhibits peripheral T4 to T3 590) Most common number of parathyroids hypercalcemia: muscle weakness, osteitis fibrosa
conversion (via inhibition of 5’-deiodinase); MMCDVII) ~84% have 4 parathyroids cystica, renal stones
prevents formation of T4 (via inhibition of MMCDVIII) 5-13% have >4
thyroperoxidase) MMCDIX) 3-6% have <4 596) Indications for surgery for hyperparathyroidism
ii) Methimazole, carbimazole: inhibits MIT & DIT MMCDXXIX) Presence of any symptoms
coupling, inhibits iodine oxidation (via inhibition 591) Etiology of hyperparathyroidism MMCDXXX) Less than 50 years
of thyroperoxidase) MMCDX) Primary: adenoma or hyperplasia MMCDXXXI) Perform if surgery desired by patient
MMCCCXCIV) Iodides, lithium used 10-14 days prior to MMCDXI) Secondary: gland hyperplasia due to MMCDXXXII) Any previous episode of life threatening
surgery once normothyroid to inhibit synthesis & malfunction of other organ system hypercalcemia
release of hormone i) Renal failure
MMCCCXCV) Β-blockers used 48-72 hours before ii) Multiple myeloma 597) Management of hypercalcemic crisis
surgery to suppress sympathetic manifestations of iii) Osteogenesis imperfecta MMCDXXXIII) Symptoms: weakness, anorexia, N/V,
thyrotoxicosis iv) Paget’s disease drowsiness, confusion, stupor, coma; serum calcium
v) Carcinoma with bone metastasis (prostate, >15mg/dl
586) Chronic effects of 131I thyroid, lung, breast, kidney) MMCDXXXIV) Causes: malignancy,
MMCCCXCVI) Bladder cancer vi) Pituitary basophlism hyperparathyroidism, increased ingestion of calcium
MMCCCXCVII)Breast cancer MMCDXII) Tertiary: autonomous PTH production in or vitamins D&A
MMCCCXCVIII) AML patients with normal or low calcium levels MMCDXXXV) Therapy
MMCCCXCIX) Chromosomal abnormalities i) Saline hydration & electrolyte correction
MMCD) Hypoparathyroidism/thyroid crisis 592) Normal anatomic locations of the parathyroids ii) Furosemide diuresis
MMCDXIII) Superior pair: usually on deep surface of iii) Organic phosphates: PO, IV, rectal
587) 3 cm tumor in thyroid, 4 risk factors for this to be thyroid within 1cm of RLN entry at cricothyroid joint iv) Mithramycin
malignant, 3 physical findings suggesting malignancy, 3 at Killian-Jamieson triangle v) Adrenal corticosteroids
findings in histopathology in papillary ca, 3 tumors that are MMCDXIV) Inferior pair: usually within 1-2 cm of vi) Calcitonin
hard to dx with even the best FNA of thyroid inferior thyroid artery entry into thyroid gland vii) Dichloromethylene diphosphonate
MMCDI) Risk factors
i) Extremes of age 593) 5 alternative sites for parathyroid adenoma or hyperplasia 598) Epithelium of the nasopharynx
ii) Male gender MMCDXV) Retroesophageal (most common location MMCDXXXVI) Pseudostratified columnar: forms majority
iii) Extent of disease for ectopic superior glands) at birth, slowly replaced over time, by adolescence
iv) Size of lesion MMCDXVI) Superior mediastinal (most common mostly changed to stratified squamous
v) Presence of metastases location for ectopic inferior glands) MMCDXXXVII) Stratified squamous
vi) Previous exposure to radiation MMCDXVII) Intrathymic MMCDXXXVIII) Transitional cell: found at
vii) Family history of thyroid carcinoma MMCDXVIII) Intrathyroidal junction of the two epithelial linings
MMCDII) Physical findings suggesting malignancy MMCDXIX) Carotid sheath
i) Lymphadenopathy MMCDXX) Tracheoesophageal 599) NPC histology and clinical features WHO
ii) Vocal cord paralysis MMCDXXXIX) Keratinizing
iii) Fixation to skin 594) Localization studies for parathyroid adenoma i) Type I: squamous, 25% in nonendemic areas,
MMCDIII) 3 tumors that are hard to diagnose with MMCDXXI) Noninvasive 1-2% in endemic areas; distinct intercellular
the best FNA i) Ultrasonography: 22-82% sensitive bridges, keratin production; 10% 5 year survival
i) Follicular carcinoma ii) CT: 47-76% sensitive MMCDXL) Nonkeratinizing
ii) Medullary carcinoma iii) MRI: 50-80% sensitive i) Type II: squamous (transitional): 12% in
iii) Anaplastic carcinoma iv) Barium swallow nonendemic areas; little/no keratinization
v) Cine esophagoscopy present; papillary morphology; ~50% 5 year
588) Physiology of calcium homeostasis vi) Sestamibi scan: 70-90% sensitive survival
MMCDIV) Parathyroid hormone MMCDXXII) Invasive ii) Type III: undifferentiated/lymphoepithelioma
i) ↑ serum calcium, ↓ serum phosphates i) Arteriography (63% in nonendemic areas, 95% in endemic
ii) Bone effects: ↑ osteoclasts
 areas): clear, enlarged nuclei: ~50% 5 year MMCDLIX) Distant metastasis
survival 611) Indications for radiation therapy for oropharynx cancer
605) Overall survival for NPC postradiotherapy MMCDLXXIX) Primary modality for T1 & T2 lesions with
600) Risk factors for NPC MMCDLX) In general, 5 year survival ~50%, worse equal cure rate as surgery
MMCDXLI) Genetics: HLA-A2, B17, Bw46 (only in for type I and better for types II/III MMCDLXXX) Indications for combined therapy
Orientals) MMCDLXI) Survival continues to decreased past 10 i) Primary lesion: T3/T4, perineural/vascular
MMCDXLII) Geographic: southeast Asia (Kwantung, years invasion, positive margins
Hong Kong, Taiwan) ii) Neck
MMCDXLIII) Environmental: salted preserved foods 606) Boundaries and subsites of the oropharynx (1) N0/N1
MMCDXLIV) Infectious: EBV MMCDLXII) Boundaries (a) 2+ histologically positive nodes
i) Superior: horizontal plane through the hard (b) Histologically positive nodes at
601) What are the top signs & symptoms of NPC? palate multiple sites
MMCDXLV) Neck mass (60%) ii) Inferior: horizontal plane through the hyoid (c) Extracapsular invasion
MMCDXLVI) Ear plugging/fullness (41%) MMCDLXIII) Subsites (d) Perineural or vascular invasion
MMCDXLVII) Conductive hearing loss (37%) i) Base of tongue (2) N2 or N3 neck
MMCDXLVIII) Epistaxis (30%) ii) Soft palate
MMCDXLIX) Nasal obstruction (29%) iii) Tonsillar area (most common location) 612) Boundaries & subsites of the hypopharynx
MMCDL) Cranial nerve palsy (18%), usually V or VI iv) Posterior pharyngeal wall MMCDLXXXI) Boundaries
initially i) Superior: horizontal plane through the hyoid
607) 5 muscles of soft palate ii) Inferior: horizontal plane through inferior margin
602) What three indirect immunofluorescence tests for MMCDLXIV) Palatoglossus of cricoid
antibodies to EBV play a role in NPC diagnosis and MMCDLXV) Palatopharyngeus MMCDLXXXII) Subsites
therapy? MMCDLXVI) Musculus uvulae i) Piriform sinus
MMCDLI) Viral capsid antigen (IgA) & early antigen MMCDLXVII) Levator veli palatini ii) Posterior pharyngeal wall
(IgG): most specific tests for diagnosis, titers ~85% MMCDLXVIII) Tensor veli palatini (innervated by V) iii) Postcricoid region
positive in cases of WHO II & III NPC
MMCDLII) ADCC titers: can be used to predict 608) Nerve ganglia for anterior tongue/base of 613) Staging for hypopharyngeal carcinoma (AJCC 1997)
prognosis of WHO II & III NPC, significant tongue/hypopharynx involved in referred otalgia MMCDLXXXIII)T1: Tumor limited to one subsite of
relationship between lower titers & progression MMCDLXIX) Anterior tongue: V3, from Gasserian hypopharynx and <2cm in greatest dimension
ganglion MMCDLXXXIV) T2: Tumor involves more than
603) TNM Staging for NPC (UICC 6th ed.) MMCDLXX) Posterior tongue: IX, from petrosal one subsite of hypopharynx or an adjacent site, or
MMCDLIII) T staging (superior) ganglion and inferior ganglion measures 2-4cm in greatest dimension without
i) T1: Tumor confined to the nasopharynx MMCDLXXI) Hypopharynx: X, from superior (nodose) hemilarynx fixation
ii) T2: Tumor extends to soft tissues of ganglion and inferior (jugular) ganglion MMCDLXXXV) T3: Tumor >4cm in greatest dimension or
oropharynx or nasal fossa with hemilarynx fixation
(1) T2a: Without parapharyngeal extension 609) Staging for oropharyngeal carcinoma (AJCC 1997) MMCDLXXXVI) T4: Tumor invades adjacent
(2) T2b: With parapharyngeal extension MMCDLXXII) T1: Tumor measuring <2cm in greatest structures (eg. thyroid/cricoid cartilage, carotid
iii) T3: Tumor invades bony structures and/or dimension artery, neck soft tissues, prevertebral
paranasal sinuses MMCDLXXIII) T2: Tumor measuring 2-4cm in greatest fascia/muscles, thyroid and/or esophagus)
iv) T4: Tumor with intracranial extension and/or dimension
involvement of cranial nerves, infratemporal MMCDLXXIV) T3: Tumor measuring >4cm in greatest 614) Management of hypopharyngeal carcinoma
fossa, hypopharynx, orbit, masticator space dimension MMCDLXXXVII) Surgery
MMCDLIV) N staging MMCDLXXV) T4: Tumor invades adjacent structures i) Posterior pharyngeal wall
i) NX: regional nodes cannot be assessed (eg. pterygoids), mandible, hard palate, deep tongue (1) Transhyoid pharyngotomy
ii) N0: no regional lymph node metastases muscle, larynx (2) Lateral pharyngotomy
iii) N1: Unilateral metastasis in lymph node(s), (3) Combined pharyngotomy
<6cm in greatest dimension, above 610) Surgical approaches for management of oropharyngeal ii) Pyriform sinus
supraclavicular fossa carcinoma (1) T1 lesions in high medial area: partial
iv) N2: Bilateral metastasis in lymph node(s), MMCDLXXVI) Transoral laryngopharyngectomy
<6cm in greatest dimension, above i) Visor lip & cheek flap (2) T2 and larger: usually require total
supraclavicular fossa ii) Lateral lip & cheek flap laryngectomy, partial pharyngectomy if
v) N3: Metastasis in lymph node(s) >6cm or in iii) Mandibular lingual release lateral extension present
supraclavicular fossa MMCDLXXVII) Transpharyngeal iii) Postcricoid area
i) Transhyoid pharyngotomy (1) Total laryngectomy, partial pharyngectomy,
604) Ho & Neel’s adverse prognostic indicators for NPC ii) Lateral pharyngotomy cervical esophagectomy
MMCDLV) Length & symptomatology of disease (>2 MMCDLXXVIII)Transmandibular MMCDLXXXVIII) Radiation
months) i) Median translingual pharyngotomy (good only i) Possible to use as primary modality for T1
MMCDLVI) Extension beyond the nasopharynx for small midline BOT lesions) lesions
MMCDLVII) Low neck disease (Levels IV/V) ii) Mandibulotomy: midline or lateral ii) Most commonly used as combination therapy
MMCDLVIII) Keratinizing histology iii) Mandibulectomy with surgery, either preoperative or
 postoperative; usually extensive
micrometastasis or clinically positive cervical
metastases
615) List risk factors for cervical esophageal Ca
MMCDLXXXIX) Smoking: 4.5x increased risk
MMCDXC) ETOH: 11x increased risk, synergistic
with smoking
MMCDXCI) Achalasia
MMCDXCII) Plummer-Vinson syndrome
MMCDXCIII) Prior H&N carcinoma
MMCDXCIV) Caustic burn/scar/stricture
MMCDXCV) Nitrosamines
MMCDXCVI) Tylosis (thickening palms and soles)
MMCDXCVII) Pernicious anemia
MMCDXCVIII) Barrett’s esophagus: distal  5-15%
incrased risk of adenocarcinoma
616) Staging for cervical esophageal carcinoma
MMCDXCIX) T staging
i) T1: <5cm, no circumferential or transmural
involvement, no obstruction
ii) T2: >5cm or circumferential or obstructing; no
transesophageal spread
iii) T3: transesophageal spread (RLN, trachea,
prevertebral fascia)
MMD) N staging
i) N0: no clinically palpable nodes
ii) N1: mobile unilateral nodes
iii) N2: mobile bilateral nodes
iv) N3: fixed nodes
617) 3 methods of reconstructing the cervical esophagus,
advantages & disadvantages
MMDI) Free jejunum
i) Adv: mucosalized tubed structure that
reestablishes conduit
ii) Disadv: requires laparotomy, requires
microvascular anastomosis, often unable to
achieve TE speech
iii) Preferred for total pharyngoesophageal
defects, not ideal if significant base of tongue
resected
MMDII) Gastric pullup/transposition
i) Adv: single anastamotic line, can perform total
esophagectomy for margins
ii) Disadv: morbidity with the pullup
(pneumothorax), postoperative early
satiety/dumping/emesis
iii) Preferred for resections that extend into the
cervical esophagus
MMDIII) Colonic interposition (not a first choice
reconstructive alternative)
i) Adv: mucosalized tube structure that
reestablishes food conduit
ii) Disadv: requires laparotomy, high
morbidity/mortality from postoperative infection
MMDIV) Free microvascular transfer (radial
forearm, lateral thigh)
618) Five categories of early laryngeal squamous malignancy i) Anterior commissure involvement
MMDV) Hyperkeratosis ii) Extension to the vocal process of the arytenoid
MMDVI) Hyperkeratosis with atypia iii) Select superficial transglottic lesions
MMDVII) Carcinoma in-situ iv) Carcinoma recurring after radiotherapy
i) Chance of developing SCC with CIS or severe MMDXXXI) Contraindications
dysplasia ~16% if left untreated i) Fixed vocal cord
MMDVIII) Superficial invasive carcinoma ii) Posterior commissure involvement
MMDIX) Invasive carcinoma iii) Involvement of both arytenoids
iv) Bulky transglottic lesions
619) Histological features of carcinoma in situ v) Thyroid cartilage invasion
MMDX) Increased nuclear:cytoplasmic ratio
MMDXI) Mitotic spindling 625) Criteria for hemilaryngectomy for recurrent cancer after
MMDXII) No penetration through the basement radiotherapy
membrane MMDXXXII) Lesion limited to one cord, may involve
anterior commissure
620) Staging for glottic carcinoma (UICC 2002) MMDXXXIII) Body of arytenoid free of tumor
MMDXIII) T1: Tumor limited to vocal cords (involving MMDXXXIV) Subglottic extension no more than 5mm
anterior or posterior commissure) with normal MMDXXXV) Mobile cord
mobility MMDXXXVI) No cartilage invasion
i) A - Tumor limited to one cord MMDXXXVII) Recurrence correlating with initial tumor
ii) B - Tumor involving both cords
MMDXIV) T2: Tumor extending to supra- or 626) Staging for supraglottic carcinoma (UICC 2002)
subglottis with impaired vocal cord mobility MMDXXXVIII) T1: Tumor limited to one subsite with
MMDXV) T3: Tumor limited to larynx with vocal cord normal vocal cord mobility
fixation and/or invades paraglottic space, and/or with MMDXXXIX) T2: Tumor invading more than one subsite
minor thyroid cartilage invasion of supraglottis or glottis or region outside
MMDXVI) T4a: Tumor invading through thyroid supraglottis (BOT mucosa, vallecula, medial wall of
cartilage, or invades tissues beyond larynx (trachea, pyriform sinus) without vocal cord fixation
soft tissues of neck, deep/extrinsic tongue muscles, MMDXL) T3: Tumor limited to larynx with vocal cord
strap muscles, thyroid, esophagus fixation; may invade postcricoid, paraglottic or
MMDXVII) T4b: Tumor invades prevertebral space, preepiglottic spaces, and/or minor thyroid cartilage
mediastinal structures, encases carotid erosion
MMDXLI) T4a: Tumor invades beyond thyroid
621) 3 treatment modalities for glottic CIN cartilage and/or tissues beyond larynx (soft tissues
MMDXVIII) Suspension laryngoscopy and vocal cord of neck, deep/extrinsic tongue muscles, strap
stripping muscles, thyroid, esophagus)
MMDXIX) Partial laryngectomy for recurrent disease MMDXLII) T4b: Tumor invades prevertebral space,
MMDXX) Radiation therapy for recurrent disease mediastinal structures, or encases carotid
622) Name the (3) treatment modalities for early glottic cancer; 627) Indications for supraglottic laryngectomy
which one has best voice function? MMDXLIII) T1, T2, some T3 lesions (preepiglottic
MMDXXI) Radiation (best voice function, preserves space involvement or minimal medial piriform sinus
normal anatomic relationships) involvement)
MMDXXII) Endoscopic cordectomy MMDXLIV) Mobile vocal cords
i) Cold steel MMDXLV) Anterior commissure uninvolved by
ii) Laser cancer
MMDXXIII) Laryngofissure and cordectomy MMDXLVI) Thyroid cartilage uninvolved by cancer
MMDXXIV) Vertical partial laryngectomy MMDXLVII) Surmountable nodal metastasis
MMDXXV) Hemilaryngectomy MMDXLVIII) General good health
623) Contraindications for laser microlaryngeal excision of early 628) 5 contraindications to supraglottic laryngectomy
glottic carcinoma MMDXLIX) Vocal cord fixation (absolute
MMDXXVI) Anterior commissure involvement contraindication)
MMDXXVII) Posterior commissure involvement MMDL) Bilateral arytenoids cartilage involvement
MMDXXVIII) T3 glottic tumor (absolute contraindication)
MMDXXIX) Subglottic extension MMDLI) Poor medical condition: extreme age, poor
pulmonary function
624) Indications and contraindications for VPL/laryngoplasty in MMDLII) Tumor within 5mm of anterior commissure
early glottic carcinoma MMDLIII) Thyroid cartilage involvement
MMDXXX) Indications MMDLIV) Prior irradiation (relative)
 MMDLXXXII) Inferior: conus elasticus MMDCVIII) Premature failure of prosthesis due to
629) Indications for SCPL-CHP valve degredation with aspiration of liquids through
MMDLV) T2-T3 supraglottic carcinoma 635) Name the histologic barriers to laryngeal carcinoma prosthesis
i) Floor of ventricle involvement spread MMDCIX) Treatment: Nystatin oral suspension
ii) Anterior commissure involvement MMDLXXXIII) Thyroid and cricoid cartilages with
iii) Impaired vocal cord or arytenoids mobility overlying perichondrium 641) Physiologic alterations to the aerodigestive tract with a
iv) Preepiglottic invasion MMDLXXXIV) Conus elasticus tracheostomy tube
v) Paraglottic space invasion below the glottic MMDLXXXV) Quadrangular membrane MMDCX) Inhibits vertical motion of the larynx during
level MMDLXXXVI) Ventricle swallowing
MMDLVI) Selected T4 supraglottic carcinoma MMDLXXXVII) Thyrohyoid membrane MMDCXI) Physiologic obstruction when swallowing
MMDLVII) Transglottic glottic carcinoma MMDLXXXVIII)Hyoepiglottic ligament d/t esophageal compression
MMDLVIII) Radiation failure for glottic and MMDCXII) Tracheomalacia
supraglottic carcinoma 636) Prevention of tracheal stomal stenosis MMDCXIII) Potential for tracheoesophageal fistula in
MMDLXXXIX) Tensionless anastomosis long term
630) Contraindications for SCPL-CHP in supraglottic MMDXC) Cut the medial heads of the SCM MMDCXIV) Reduced subglottic pressure
carcinomas MMDXCI) Bevelled tracheal cuts MMDCXV) Dyscoordination between breathing and
MMDLIX) Hyoid invasion MMDXCII) Use of a laryngectomy tracheostomal tube swallowing
MMDLX) Massive preepiglottic space invasion with MMDXCIII) Infection & radiation predispose to MMDCXVI) Elimination of vocal cord closure reflex
vallecula involvement stenosis while swallowing
MMDLXI) Tongue base invasion
MMDLXII) Arytenoid fixation 637) Methods of voice post-laryngectomy 642) Signs & symptoms of chronic aspiration
MMDLXIII) Subglottic extension to cricoid MMDXCIV) Electrical devices MMDCXVII) Pneumonia
MMDLXIV) Pharyngeal or interarytenoid involvement i) Transcervical (electrolarynx) MMDCXVIII) Bronchorrhea
MMDLXV) Extensive thyroid cartilage invasion ii) Transoral MMDCXIX) Dysphagia
MMDLXVI) Inadequate pulmonary reserve MMDXCV) Esophageal speech MMDCXX) Chronic cough
MMDLXVII) Resectable by supraglottic laryngectomy i) Low fundamental frequency (65Hz), short MMDCXXI) Weight loss
duration (80cc air), effort to produce
631) Staging for subglottic carcinoma (UICC 2002) ii) Injectional technique: air pushed into 643) Therapy for chronic aspiration
MMDLXVIII) T1: Tumor limited to the subglottis esophagus MMDCXXII) Medical
MMDLXIX) T2: Tumor extending to the glottis with or iii) Inhalation technique: air inhaled into esophagus i) NPO
without impaired vocal cord mobility MMDXCVI) Tracheoesophageal puncture ii) Tube feeds, either NG or PEG
MMDLXX) T3: Tumor limited to the larynx with vocal i) Primary (at time of resection) iii) Radiogaphics: MBS, VFSS, FEES
cord fixation ii) Secondary iv) Speech therapy
MMDLXXI) T4a: Tumor invading cricoid or thyroid v) LPR prophylaxis
cartilages and/or invades tissues beyond the larynx 638) Reasons for alaryngeal speech failure MMDCXXIII) Adjunctive procedures
(deep/extrinsic tongue muscles), strap muscles, MMDXCVII) Prosthesis failure: position, size, type, i) Tracheostomy
thyroid, esophagus patency ii) Vocal cord injection (Teflon)
MMDLXXII) T4b: Tumor invades prevertebral space, MMDXCVIII) Reflex pharyngeal constricture spasm: iii) Vocal cord medialization
mediastinal structures, or encases carotid constrictors reflexively contract when dilated iv) Cricopharyngeal myotomy
MMDXCIX) Nonvibrating pharyngoesophageal MMDCXXIV) Reversible surgical procedures
632) Indications for hemithyroidectomy or subtotal segment: postradiation, reconstructed segment i) Airway stenting (eg. Eliachar stent)
thyroidectomy in carcinoma of the larynx/hypopharynx MMDC) Puncture site closure ii) Vertical laryngoplasty
MMDLXXIII) Palpable disease present MMDCI) Inadequate air supply: decreased iii) Laryngotracheal separation or
MMDLXXIV) Glottic or subglottic carcinoma with respiratory support, improper stoma occlusion tracheoesophageal diversion: >90% successful
greater than 1cm subglottic extension iv) Epiglottic flap
MMDLXXV) T4 glottic carcinoma 639) Management of dysfluent speech MMDCXXV) Irreversible surgical procedures
MMDLXXVI) T4 pyriform sinus carcinoma MMDCII) Use correctly sized prosthesis with ideal i) Narrow field laryngectomy
airflow characteristics ii) Subperichondrial cricoidectomy
633) Preepiglottic space boundaries MMDCIII) Pharyngeal constrictor myotomy, iii) Glottic closure
MMDLXXVII) Superior: hyoepiglottic ligament and neurectomy, botox injection iv) Total laryngectomy
vallecular mucosa MMDCIV) Allow edema to subside, provide external
MMDLXXVIII) Anterior: thyrohyoid ligament pressure 644) Pearls on tracheal tumors
MMDLXXIX) Posterior: epiglottis and thyroepiglottic MMDCV) Dilate or repuncture MMDCXXVI) 75% malignant in adults, 90% benign in
ligament MMDCVI) Speech therapy pediatrics
MMDCXXVII) Chondroma most common benign lesion
634) 3 boundaries of paraglottic space 640) Most common cause of TEP failure after successfully in adults
MMDLXXX) Lateral: thyroid cartilage (anterior) and establishing speech MMDCXXVIII) SCC & adenoid cystic most common (70-
mucosa over medial wall of pyriform fossa MMDCVII) Candidal infection of prosthesis 80%) malignant tumors; others adenocarcinoma,
(posteriorly) rhabdomyosarcoma, small cell, melanoma,
MMDLXXXI) Superior: quadrangular membrane chondrosarcoma
 MMDCXXIX) Do not free more than 2cm of trachea
circumferentially if that part remaining
MMDCXXX) Postop radiation for SCC & adenoid cystic
645) Tracheal anatomy & airway lengthening techniques
MMDCXXXI) Anatomy
i) Airway 10-13cm long, 16-20 rings present, can
excise 6.5cm maximum
MMDCXXXII) Lengthening techniques
i) Blunt dissection of larynx & trachea (anterior &
posterior) – 3-5cm
ii) Incision of alternating annular ligaments –
2.5cm
iii) Suprahyoid laryngeal release – 5cm
iv) Infrahyoid laryngeal release (usually causes
dysphagia, risk to SLNs)
v) Release of inferior pulmonary ligament
vi) Reanastomosis of left mainstem bronchus onto
bronchus intermedius – 2.7cm
646) Cavernous sinus contents, draw diagram
647) Structures of the superior orbital fissure and tendon of
Zinn (Left orbit in this example)
MMDCXXXIII) A - Optic nerve, ophthalmic artery
MMDCXXXIV) B - CN IV, lacrimal and frontal divisions of
V1, superior ophthalmic vein
MMDCXXXV) C - CN III (possibly in superior & inferior
divisions), CN VI, nasociliary division of V1
MMDCXXXVI) D - Zygomaticofacial and
zygomaticotemporal divisions of V2, inferior
ophthalmic vein
648) 3 branches of V1, what these pass through, what they
provide autonomics to
MMDCXXXVII) Nasociliary: enters superior orbital fissure
medial to tendon of Zinn, supplies tip of nose
through external branch of anterior ethmoidal nerve,
root of nose through infratrochlear nerve
MMDCXXXVIII) Frontal: enters SOF lateral to
tendon of Zinn, divides into supratrochlear and
supraorbital nerves to supply forehead and scalp
MMDCXXXIX) Lacrimal: enters SOF lateral to tendon of
Zinn, supplies lacrimal gland (postsynaptic
autonomic efferents) and lateral eyelid
649) Contents of jugular foramen
MMDCXL) Anterior: inferior petrosal sinus
MMDCXLI) Middle (pars nervosa): CN IX/X/XI
MMDCXLII) Posterior (pars vasculara)
i) IJV
ii) Meningeal branches from occipital and
ascending pharyngeal arteries
iii) Nodes of Krause
650) Boundaries of the infratemporal fossa
MMDCXLIII) Anterior: posterior surface of the maxilla
MMDCXLIV) Superior: greater wing of the sphenoid
bone, foramen ovale & spinosum
MMDCXLV) Medial: lateral pterygoid plate,
pterygomaxillary fissure
MMDCXLVI) Posterior: articular tubercle of temporalis
bone, spine of sphenoid bone
MMDCXLVII) Lateral: coronoid process and ramus of
the mandible
MMDCXLVIII) Inferior: alveolar border of the maxilla
651) Borders of parapharyngeal space and its connections
MMDCXLIX) Superior: skull base along the sphenoid
MMDCL) Inferior: lesser cornu of hyoid
MMDCLI) Lateral: superficial layer of deep fascia
covering the medial pterygoid, ascending ramus of
the mandible, and deep surface of the parotid
MMDCLII) Medial: superior constrictor fascia
MMDCLIII) Anterior: pterygoid fascia &
pterygomandibular raphe
MMDCLIV) Posterior: prevertebral fascia
MMDCLV) Connects to paralingual, parotid, carotid,
masticator, retropharyngeal, submandibular spaces
652) Contents of the parapharyngeal space
MMDCLVI) Styloid process (Cummings, Janfaza) or
the fascia attaching the TVP to the styloid
(Cummings, Bailey’s) divides space into two
compartments
MMDCLVII) Prestyloid: contains no vital structures
besides fat, variable portions of deep lobe of parotid
(Janfaza, Bailey’s) or the Imax & branches of V3
(lingual, inferior alveolar, auriculotemporal) (KJ Lee)
MMDCLVIII) Poststyloid: contains CN’s XI-XII, IJV,
ICA, sympathetic chain
653) Surgical approaches to the parapharyngeal space and
ancillary procedures which assist in exposing the space
MMDCLIX) Transoral: seldom used, poor access
MMDCLX) Transfacial/transparotid: total
parotidectomy performed
MMDCLXI) Transcervical
MMDCLXII) Transmandibular: midline mandibular
osteotomy with lateral swing
MMDCLXIII) Ancillary procedures
i) Submandibular gland swing or excision
ii) Separation of styloid structures (stylohyoid,
styloglossus, stylopharyngeus, stylomandibular
ligament) provides access to carotid at skull
base
iii) Separation of sphenomandibular ligament
iv) Disarticulation of the TMJ
654) Five tumors of poststyloid parapharyngeal space
MMDCLXIV) Deep lobe parotid tumors (43%)
MMDCLXV) Neurogenic tumors (28%): schwannoma,
neurofibroma, paraganglioma
MMDCLXVI) Lymphoma (25%)
MMDCLXVII) Vascular (3%): hemangiopericytoma,
hemangioendothelioma
MMDCLXVIII) Minor salivary gland tumors: most
frequently malignant, occasionally pleomorphic
adenoma
655) Boundaries of the pterygopalatine fossa
MMDCLXIX) Anterior: posterior wall of the maxilla
MMDCLXX) Posterior: sphenoid bone, base of
pterygoid process, inferior portion of anterior aspect
of greater wing
MMDCLXXI) Medial: perpendicular plate of palatine
bone
MMDCLXXII) Superior: undersurface of sphenoid bone
and orbital process of palatine bone, opens into
inferior orbital fissure
MMDCLXXIII) Lateral: pterygomaxillary fissure
656) Eight openings of the pterygopalatine fossa
MMDCLXXIV) Inferior orbital fissure
MMDCLXXV) Pterygomaxillary fissure
MMDCLXXVI) Sphenopalatine foramen
MMDCLXXVII) Foramen rotundum
MMDCLXXVIII)Pterygoid canal (Vidian)
MMDCLXXIX) Pharyngeal canal
 MMDCLXXX) Greater palatine canal
MMDCLXXXI) Lesser palatine canal

657) 4 connections of pterygopalatine fossa (MCF,

infratemporal fossa, orbit, nose)?
MMDCLXXXII) Middle cranial fossa – foramen rotundum
MMDCLXXXIII)Infratemporal fossa – pterygomaxillary
fissure
MMDCLXXXIV) Orbit – inferior orbital fissure
MMDCLXXXV) Nose – sphenopalatine foramen

658) Branches of the internal maxillary artery

MMDCLXXXVI) First part: lies medial to the
mandible, all branches go through foramina
i) Anterior tympanic
ii) Deep auricular
iii) Middle meningeal
iv) Accessory meningeal
v) Inferior alveolar
MMDCLXXXVII) Second part: lies lateral to
lateral pterygoid, all branches supply muscles
i) Deep temporal (anterior & posterior)
ii) Medial pterygoid branch
iii) Lateral pterygoid branch
iv) Massseteric artery
v) Buccal artery
MMDCLXXXVIII) Third part lies within
pterygomaxillary fossa
i) Posterior superior alveolar
ii) Infraorbital
iii) Descending palatine
iv) Vidian/pterygoid canal
v) Pharyngeal
vi) Sphenopalatine
vii) Posterior lateral nasal

659) Describe general principles of osseointegration

MMDCLXXXIX) Osseointegration: rehabilitation
of oral/maxillofacial or other head and neck defects
with permanently implanted hardware
MMDCXC) Typically performed after resection &
other therapy (chemo/RT)
MMDCXCI) First surgery: titanium implants placed
into bone and allowed to integrate (form stable
relationship) with bone
MMDCXCII) 2nd surgery: implants exposed and
abutments placed which will connect the impant to
the bone
 Otology & Neurootology iv) 17th week: ossification in medial neck of
malleus
MMDCCXXIII) A connection between the subarachnoid
space near the glossopharyngeal ganglion to the
v) Birth: ossicles are of adult size & shape hypotympanum inferior & anterior to the round
660) External ear embryology (Bailey ch. 128)
MMDCCII) Most common abnormality in middle ear window
MMDCXCIII) 6 hillocks of His, derived from 1st/2nd
atresia: fusion of malleus to a bony atretic plate, MMDCCXXIV) Present in infants, closes off as child
branchial arches during 5th gestational week; reach
incudomalleolar fusion grows
adult form (but not size) by 18th week
MMDCXCIV) 1st arch derivatives
663) Identify the structures formed from the four embryologic 669) Describe the blood supply to the middle ear
i) 1st: Tragus
sacs of the middle ear (Procter) MMDCCXXV) Anterior tympanic artery: from the internal
ii) 2nd: Helical crus
MMDCCIII) Main mucosal sacs of the middle ear, maxillary, 3 branches supply the lateral wall of the
iii) 3rd: Helix
develop between 12th & 28th gestational weeks epitympanum and the ossicles
MMDCXCV) 2nd arch derivatives
i) S. anticus: anterior pouch of von Troltsch MMDCCXXVI) Deep auricular artery: from the internal
i) 4th: Horizontal helix, scapha, antihelix
ii) S. medius: epitympanum and petrous area maxillary, supplies the lateral surface of the TM and
ii) 5th: Descending helix, scapha, antihelix
iii) S. superior: posterior pouch of von Troltsch, the inferior portion of the medial surface
iii) 6th: Antitragus, inferior aspect of helix
part of the mastoid, inferior incudal space MMDCCXXVII)Superior tympanic artery: from the middle
iv) S. posterior: sinus tympani, OW & RW niches meningeal artery, supplies the epitympanum, tensor
661) Embryology of the EAC, TM & middle ear
tympani, posterior portion of stapes
MMDCXCVI) EAC embryology
664) Describe the embryology of the stapes MMDCCXXVIII) Tubal artery: from the
i) 4th gestational week: 1st arch groove invaginates
MMDCCIV) Superstructure & middle ear portion of accessory meningeal artery
over next 4 weeks, ectoderm forms a core of
footplate derived from Reichert’s cartilage (2nd arch) MMDCCXXIX) Inferior tympanic artery: a branch of the
tissue that comes into apposition with
MMDCCV) Otic portion of footplate and annular ascending pharyngeal artery, supplies floor of middle
endoderm of 1st pouch
ligament derived from otic capsule ear, promontory
ii) 28th week epithelial core canalizes from medial
MMDCCVI) Develops from mesenchyme in 6th week MMDCCXXX) Stylomastoid artery: from the posterior
to lateral to form EAC
just before malleus & incus formation; stapedial auricular artery, supplies bone & mucosa of mastoid
MMDCXCVII) TM embryology
artery runs through it region, floor & inferoposterior wall of middle ear,
i) Trilaminar structure comprising 1st arch
MMDCCVII) 8th week IS joint forms facial nerve, stapedius
ectoderm (lateral epidermis), mesoderm
MMDCCVIII) 10th week stapedial artery degenerates, MMDCCXXXI) Posterior tympanic artery: from the
(fibrous layer) & endoderm (medial mucosa)
starts forming its adult shape stylomastoid artery, supplies the chorda tympani
ii) Horizontal position initially, assumes vertical
MMDCCIX) 16th week ossification begins MMDCCXXXII)Superficial petrosal artery: from the
position by 3 years
middle meningeal, supplies the dura & perigeniculate
iii) Tympanic ring starts ossification in 3rd
665) Boundaries of the tympanic cavity facial nerve
gestational month
MMDCCX) Superior: tegmen MMDCCXXXIII) Caroticotympanic arteries: arise
MMDCXCVIII) Middle ear embryology
MMDCCXI) Inferior: jugular wall, styloid prominence from the ICA, extend from the carotid canal to the
i) 4th gestational week: tubotympanic recess
MMDCCXII) Medial: labyrinth middle ear
formed by laterally migrating 1st arch pouch
MMDCCXIII) Lateral: TM, scutum
ii) 5th-6th weeks: mesoderm between branchial
MMDCCXIV) Anterior: carotid wall, Eustachian tube, 670) Blood supply to the incudostapedial joint
cleft & otic capsule condense to form ossicles
tensor tympani MMDCCXXXIV) Incudal artery: terminal branch
iii) Endodermal pouch continues growing by
MMDCCXV) Posterior: mastoid, stapedius, pyramidal of ossicular branch of anterior tympanic artery
surrounding the ossicles & supporting
eminence MMDCCXXXV) Arteries of stapedius tendon:
structures; remains slitlike into the 5th month,
terminal branches of anastomosis of superficial
expands into an open space by the 8th month
666) Describe the anatomy of the tympanic membrane petrosal and stylomastoid arteries supplying facial
iv) Mastoid pneumatization starts in late fetal life,
MMDCCXVI) Four layers nerve
antrum present at birth
i) Squamous epithelium MMDCCXXXVI) Posterior crural artery: terminal
ii) Radiating fibrous layer branch of superficial petrosal artery
662) Describe the embryologic development of the malleus &
iii) Circular fibrous layer MMDCCXXXVII) Anterior crural artery: formed
incus
iv) Mucosal layer from anastomosis of superior & inferior tympanic
MMDCXCIX) Embryologic derivations of the malleus
MMDCCXVII) Average width: 8-9mm arteries
i) Head & neck: Meckel’s cartilage (1st arch)
MMDCCXVIII) Average height: 9-10mm
ii) Manubrium: Reichert’s cartilage (2nd arch)
MMDCCXIX) Average area: 70-80mm2 671) Blood supply to inner ear
iii) Anterior process: process of Folius
MMDCCXX) Average vibrating surface area: 55mm2 MMDCCXXXVIII) Labyrinthine artery branches off
(mesenchyme)
of AICA (80%)
MMDCC) Embryologic derviations of the incus
667) Define Trautmann’s triangle i) Anterior vestibular artery: supplies utricle & part
i) Body & short process: Meckel’s cartilage (1st
MMDCCXXI) Bordered by the bony labyrinth, sigmoid of saccule, horizontal and anterior SCC
arch)
sinus, and superior petrosal sinus or dura ii) Common cochlear artery
ii) Long process: Reichert’s cartilage (2nd arc)
MMDCCXXII) potential weak spot through which (a) Proper cochlear artery/spiral
MMDCCI) Timeline
infections of temporal bone may traverse and affect modiolar artery: supplies cochlea
i) 6th week: appear as a single mass
cerebellum except basal turn
ii) 8 week: separated, with MI joint formed
th
(b) Vestibulocochlear artery
iii) 16th week: ossification in long process of incus
668) What is Hyrtl’s fissure? 1. Cochlear ramus: supplies
basal turn of cochlea
 2. Posterior vestibular artery: MMDCCLX) Inner hair cells MMDCCLXXVI) Low frequency sounds cause
supplies posterior SCC, i) 1 row of IHC’s, flask shaped, few hair cells maximal displacement of the basilar membrane in
saccule ii) 90% of neurons innervating the cochlea the apex
synapse on the IHC’s (type I neurons), 15-20 MMDCCLXXVII) Tonotopic organization
672) 5 Muscles inserting on the mastoid neurons synapse on each IHC preserved in higher brainstem nuclei
MMDCCXXXIX) SCM MMDCCLXI) Outer hair cells
MMDCCXL) Posterior belly of digastric i) 3-4 rows of OHC’s, cylindrical, many hair cells 684) Ewald’s Law
MMDCCXLI) Longissimus capitis ii) 10% of neurons innervating the cochlea MMDCCLXXVIII) The direction of a peripheral
MMDCCXLII) Splenius capitis synapse on the OHC’s (type II neurons), 1 nystagmus is parallel to the semicanal being
MMDCCXLIII) Anterior, superior, posterior auricular neuron innervates ~10 OHC’s stimulated and opposite to the direction of
muscles MMDCCLXII) ~2000 efferent neurons from superior endolymph flow
olive synapse on the hair cells (LSO to IHC’s, MSO MMDCCLXXIX) Horizontal canal utriculopetal
673) Course of a persistent stapedial artery to OHC’s) endolymph flow causes maximal stimulation
MMDCCXLIV) Arises from ICA in hypotympanum MMDCCLXXX)Posterior/superior canal utriculofugal
MMDCCXLV) Runs up between crura of stapes then 679) Describe the endocochlear and hair cell potentials endolymph flow causes maximal stimulation
into fallopian canal MMDCCLXIII) Endocochlear potential: produced by stria
MMDCCXLVI) Continues in fallopian canal to the vascularis, +80-90mV relative to otic capsule bone 685) Alexander’s Law
geniculate ganglion, supplies dura MMDCCLXIV) IHC potentials: -35-40mV MMDCCLXXXI) The intensity of pathologic
MMDCCLXV) OHC potentials: ~ -70mV vestibular nystagmus (slow phase component)
674) Describe the pinna and EAC’s contribution to sound increases during gaze in the direction of the fast
amplification 680) Difference between ossicular stiffness and mass phase (away from the lesion) and decreases during
MMDCCXLVII) Concha’s shape funnels sound into EAC MMDCCLXVI) Resonance frequency of the middle ear gaze in the direction of the slow phase (towards the
MMDCCXLVIII)Resonance frequency of EAC increases ossicles is 800-1200Hz; changes in ossicular lesion)
gain mobility affect low frequency sound transmission,
MMDCCXLIX) Overall 10-15dB increase in gain in 3- whereas changes in mass affect high frequency 686) Seven voluntary muscles of the eye
5kHz range sound transmission MMDCCLXXXII) Superior rectus
MMDCCLXVII) In otosclerosis, early lesions decrease the MMDCCLXXXIII) Inferior rectus
675) Acoustic properties of the head that assist in sound overall mobility of the ossicular chain, and with MMDCCLXXXIV) Lateral rectus
localization subsequent increases in disease will adversely affect MMDCCLXXXV) Medial rectus
MMDCCL) Head shadow effect: head attenuates the ossicular mass and thus spread the hearing loss MMDCCLXXXVI) Superior oblique
sound waves with wavelengths shorter than the into the higher frequencies MMDCCLXXXVII) Inferior oblique
width of the head (>2kHz) by 5-15dB MMDCCLXXXVIII) Levator palpebrae
MMDCCLI) Interaural time difference: maximum 681) dB required to double sound energy
~0.6ms time difference for sound hitting one ear to MMDCCLXVIII) 3dB (IL) or 6dB (SPL) 687) Stimulation of the following SCC causes the activation
reach the other ear and inhibition of which muscles?
682) Origin & ion content of perilymph and endolymph MMDCCLXXXIX) Superior SCC
676) Describe the impedance matching system of the middle MMDCCLXIX) Perilymph i) Activation: ipsilateral SR, contralateral IO
ear i) Thought to be an ultrafiltrate of CSF or blood; ii) Inhibition: ipsilateral IR, contralateral SO
MMDCCLII) Three lever systems similar to extracellular fluid MMDCCXC) Horizontal SCC
i) Catenary lever: TM exerts force upon the ii) Ions: Na 139, K 4, Cl 0, protein 200-400, i) Activation: ipsilateral MR, contralateral LR
malleus handle (minor input) glucose equivalent to serum ii) Inhibition: ipsilateral LR, contralateral MR
ii) Ossicular lever: produced when malleus and MMDCCLXX) Endolymph MMDCCXCI) Posterior SCC
incus rotate as a unit (length ratio 1.3:1) i) Produced by stria vascularis and the dark cells i) Activation: ipsilateral SO, contralateral IR
iii) Hydraulic lever: transmission of sound of the cristae and maculae ii) Inhibition: ipsilateral IO, contralateral SR
pressure collected over TM and transmitted to ii) Similar to CSF
oval window via piston-like stapes movement iii) Ions: Na 13, K 144, Cl 120, protein 126, low 688) Physiologic frequency response of the SCCs
(areal ratio averages 20:1) glucose MMDCCXCII) 0.1-10Hz angular accelerations
MMDCCLIII) Overall catenary-ossicular lever ratio 1:2.3 MMDCCLXXI) Protein content is higher in endolymphatic
MMDCCLIV) Increased gain in SPL from middle ear sac 689) Vestibular nystagmus - definition
and TM ~34 dB (Cummings) or 25-30dB (Baileys) MMDCCXCIII) Nystagmus: the to and fro motion of the
683) What is tonotopic organization? eyes
677) Resonance frequencies of the ear components MMDCCLXXII) Organ of Corti ~35mm long from base to MMDCCXCIV) Vestibular nystagmus: bilateral, conjugate,
MMDCCLV) Concha: 5000Hz apex comprised of a slow phase (image on fovea) and a
MMDCCLVI) External auditory canal: 3000Hz MMDCCLXXIII) Travelling wave from middle ear fast phase (saccade, correction of image)
MMDCCLVII) Middle ear: 800Hz causes simultaneous fluid wave in the perilymph
MMDCCLVIII) Tympanic membrane: 800-1600Hz MMDCCLXXIV) Each place on the basilar 690) 4 types of peripheral nystagmus
MMDCCLIX) Ossicular chain: 500-2000Hz membrane responds best to a specific frequency MMDCCXCV) Positional
MMDCCLXXV)High frequency sounds cause maximal MMDCCXCVI) Induced (calorics)
678) How many rows of OHC’s, IHC’s? Which are more displacement of the basilar membrane in the basal MMDCCXCVII)Gaze
important and why? region MMDCCXCVIII) Spontaneous
 MMDCCCXXIII) BPPV i)Spontaneous or positional nystagmus with
691) 7 types of eye movements MMDCCCXXIV) Recurrent vestibulopathy normal caloric results
MMDCCXCIX) Fixation: holds image of stationary object MMDCCCXXV) Migraine-associated dizziness ii) Direction-changing nystagmus independent of
on fovea stimulus changes
MMDCCC) Vestibular: holds image of seen world 697) Name 7 tests done as part of a normal ENG battery iii) Failure of fixation suppression
steady on retina during brief head rotations MMDCCCXXVI) Calibration at beginning and iv) Bilateral reduced or absent caloric responses
MMDCCCI) Optokinetic: holds images of seen world throughout procedure without a history of labyrinthine or middle ear
steady on retina during sustained head rotations MMDCCCXXVII) Vestibular subtests disease
MMDCCCII) Smooth pursuit: holds image of a moving i) Spontaneous and gaze nystagmus v) Abnormal saccade or pursuit results, especially
target steady on fovea ii) Positional testing with normal caloric results
MMDCCCIII) Nystagmus: resets eyes during prolonged iii) Positioning testing (Dix-Hallpike) vi) Hyperactive caloric responses (loss of
rotation and direct gaze toward oncoming visual iv) Caloric testing cerebellum-generated inhibition)
scene MMDCCCXXVIII) Oculomotor subtests MMDCCCXXXV) Findings suggestive of a
MMDCCCIV) Saccades: Brings images of objects of i) Saccade testing peripheral disorder
interest onto fovea ii) Smooth pursuit testing i) Unilateral caloric weakness
MMDCCCV) Vergence: Moves eyes in opposite iii) Optokinetic testing ii) Bilateral caloric weakness with a history of
directions so that images of a single object are labyrinthine disease or administration of
placed simultaneously on both foveas 698) Factors which may influence the ENG test/subtest ototoxic drugs
outcomes iii) Fatiguing positional nystagmus
692) What is the VOR? MMDCCCXXIX) Recording based on iv) Intact fixation suppression response
MMDCCCVI) Gaze stabilizing system that produces eye corneoretinal potential; can only measure horizontal v) Direction-fixed nystagmus
movement equal in magnitude but opposite in eye movements, not vertical or torsional
direction of a head movement MMDCCCXXX) Test factors 701) Causes of abnormal optokinetic tests on ENG
MMDCCCVII) Maintains binocular fixation and stable i) Changes in skin resistance (sweating) MMDCCCXXXVI) Saccades
binocular foveal images during head movements ii) Interference from eye blinking i) Central pathologic disorder, either cerebellar
iii) Ambient light level can disturb recording lesion (dorsal vermis), brainstem (PPRF and
693) Findings on bilateral internuclear ophthalmoplegia MMDCCCXXXI) Patient factors MLF), or ocular muscles & nerves
MMDCCCVIII) Bilateral failure of adduction i) Age MMDCCCXXXVII) Smooth pursuit system
MMDCCCIX) Impaired vertical VOR ii) Fatigue i) Distributed throughout brainstem and
MMDCCCX) Impaired vertical smooth pursuit iii) Level of attentiveness cerebellum; anatomic localization not possible
MMDCCCXI) Impaired vertical eccentric gaze holding iv) Presence of sedating medications ii) Most common cause of bilateral impaired
v) Congenital nystagmus smooth pursuit: medication side effects
694) 5 clinical signs of acute unilateral vestibular loss (anticonvulsants, sedatives); neurologic
MMDCCCXII) Spontaneous nystagmus (fast phase 699) Jongkee’s formulas and their levels of significance conditions (Parkinson’s, PSNP, Alzheimer’s,
towards contralateral ear) schizophrenia)
MMDCCCXIII) Decreased VOR gain MMDCCCXXXVIII) Optokinetic system
MMDCCCXIV) Increased VOR phase lead at low i) Responsible for optokinetic afternystagmus
frequency (loss of velocity storage) (OKAN), velocity storage mechanisms in the
MMDCCCXV) Ocular tilt reaction (vertical skew cerebellum and brainstem
deviation, head rotated towards weak labyrinth, ii) Absence of asymmetry occurs with peripheral
ocular counterroll) vestibular lesions
MMDCCCXVI) Disturbance of gait (fall towards MMDCCCXXXII) Unilateral weakness
hypoactive labyrinth) i) Comparison of each vestibular organ’s 702) Rotatory chair testing characteristics measured
responsiveness to caloric stimulation MMDCCCXXXIX) Gain: ratio of maximum slow
695) Describe the spontaneous nystagmus of an acute ii) >20% considered significant, a sign of phase eye velocity to maximum chair velocity; ideally
unilateral vestibular loss decreased responsiveness of the HCC or should be equal but opposite (gain of 1)
MMDCCCXVII)Present when head is still, dampened by ampullary nerve MMDCCCXL) Phase: temporal shift between eye
visual fixation, increased or becomes apparent when MMDCCCXXXIII) Directional preponderance velocity relative to chair velocity; normally eye velocity
fixation eliminated i) A comparison of the total right beating leads chair velocity (phase-lead)
MMDCCCXVIII) Horizontal component: fast responses and left beating responses MMDCCCXLI) Symmetry: comparison between peak
phase towards intact ear ii) >25% (Cummings) or >30% (Bailey’s) slow-wave velocity to the left and right; will show
MMDCCCXIX) Torsional component: superior poles beat considered significant, seen in patients with weakness on an affected side
toward intact ear spontaneous nystagmus, also in patients with MMDCCCXLII) Bias velocity: a spontaneous nystagmus,
central asymmetric sensitivities to inhibitory- if present, will add to the rotational response & shift it
696) What conditions may ENG be helpful? excitatory stimuli towards the direction of the slow phase
MMDCCCXX) Unilateral or bilateral vestibular
hypofunction 700) Interpretation of ENG test findings 703) Components of sensory organization test
MMDCCCXXI) Disorders of oculomotor control MMDCCCXXXIV) Findings suggestive of a MMDCCCXLIII) Sensory organization test: tests
MMDCCCXXII)Meniere’s disease or endolymphatic central disorder integration of vestibular, visual and proprioceptive
hydrops balance cues
 i) Condition 1: eyes open, surround stable, MMDCCCLVI) Lermoyez attacks: increasing tinnitus, ear 710) Differential diagnosis of peripheral vertigo
support fixed fullness and hearing loss with all suddenly resolve MMDCCCLXX) Vertigo lasting minutes to hours
ii) Condition 2: eyes closed, surround stable, with the onset of vertigo i) Idiopathic endolymphatic hydrops (Meniere’s
support fixed disease)
iii) Condition 3: eyes open, surround sway, 707) Diagnostic tests in Meniere’s disease ii) Secondary endolymphatic hydrops
support fixed MMDCCCLVII) ENG: 48-74% of patients will have (1) Otic syphilis
iv) Condition 4: eyes open, surround stable, significant caloric reduction; complete loss noted in (2) Delayed endolymphatic hydrops
support sway 6-11% (3) Cogans disease
v) Condition 5: eyes closed, surround stable, MMDCCCLVIII) Glycerol test: 1.5g/kg mixed 1:1 (4) Recurrent vestibulopathy
support sway with juice, serial audiograms over next 3 hours to MMDCCCLXXI) Vertigo lasting seconds (BPPV)
vi) Condition 6: eyes open, surround sway, see if SDS & PTA improves (>16% & 25dB in 3 MMDCCCLXXII) Vertigo lasting days (vestibular
support sway consecutive frequencies a positive test) neuritis)
MMDCCCXLIV) Movement coordination test MMDCCCLIX) ECoG: elevated SP:AP ratio due to MMDCCCLXXIII) Vertigo of variable duration
i) Based on automatic muscle responses thought hydrops causing altered basilar membrane i) Inner ear fistula
to be triggered by proprioceptive changes mechanics ii) Inner ear trauma
(1) Penetrating
708) Medical treatment strategy for Meniere’s disease (2) Nonpenetrating
MMDCCCLX) General principles (3) Barotrauma
i) Salt restriction, avoidance of caffeine, etc. iii) Familial vestibulopathy
MMDCCCLXI) Medications MMDCCCLXXIV) Bilateral vestibular deficit
i) Diuretics: furosemide, acetazolamide (CAI,
theoretic decrease in endolymph production) 711) Nature & 5 characteristics of peripheral nystagmus in
MMDCCCLXII) Vasodilators: betahistine (Serc), histamine BPPV
agonist MMDCCCLXXV) Canalithiasis: loose otoconia in
i) Theorized improvement in strial ischemia & the SCC
bloodflow to labyrinth, also thought to directly MMDCCCLXXVI) Posterior canalithiasis
inhibit neurons in the vestibular nuclei i) Vertical torsional nystagmus (geotropic), due to
ii) Starting dose 16mg po tid activation of the ipsilateral superior oblique and
MMDCCCLXIII) Antihistamines: works against contralateral inferior rectus
acute symptoms ii) Characteristics of the nystagmus
MMDCCCLXIV) Benzodiazapenes: anti-GABA- (1) Latent
ergic (2) Fatigable
MMDCCCLXV) Corticosteroids: anti- (3) Direction does not change with repeated
inflammatory, immunomodulatory stimulation
704) Indications for rotatory chair (4) Reversability
MMDCCCXLV)Monitor changes in vestibular system over 709) Surgical management of Meniere’s disease (5) Brief duration (<1 minute)
time MMDCCCLXVI) For patients who fail medical MMDCCCLXXVII) Horizontal canalithiasis
MMDCCCXLVI) Compensation after injury management (~10%) i) HSCC affected structure in ~17% of cases
MMDCCCXLVII) Residual labyrinthine function MMDCCCLXVII) Hearing preserving nonablative ii) Nystagmus either geotropic or ageotropic, and
in patients with no caloric response procedures of shorter latency, more intense & less fatigable
MMDCCCXLVIII) Pediatrics: postmeningitis, i) Endolymphatic sac decompression: ~50-75% cf. PSCC symptoms
anyone with congenital hearing loss to examine success rate, 1-2% chance of postoperative iii) First, identify whether geotropic (canalolithiasis)
vestibular component hearing loss or ageotropic (cupulolithiasis); Second,
MMDCCCXLIX) Bilateral vestibular hypofunction ii) Cochleosacculotomy (historical) determine side down that is stronger
MMDCCCL) Ototoxicity MMDCCCLXVIII) Hearing preserving ablative (canalolithiasis has affected side strong;
MMDCCCLI) Cerebellar abnormalities procedures opposite for cupulolithiasis)
i) Vestibular neurectomy: complete vertigo MMDCCCLXXVIII) Superior canalithiasis
705) 3 situations of cupula becoming affected by gravity resolution in 95% of patients i) Less common that PSCC & HSCC
MMDCCCLII) Ethanol intoxication (1) Middle fossa ii) Nystagmus is vertical (downward beating) and
MMDCCCLIII) Heavy water poisoning (2) Retrolabyrinthine torsional (ageotropic), due to activation of
MMDCCCLIV) Cupulolithiasis (3) Retrosigmoid ipsilateral superior rectus & contralateral
ii) Chemical vestibular ablation (gentamycin): inferior oblique
706) Two unusual types of attacks seen in Meniere’s ~90% success rate, 6-30% rate of hearing loss
MMDCCCLV) Crisis of Tumarkin: acute utriculosaccular MMDCCCLXIX) Nonhearing conservative
dysfunction, leads to sudden falls without warning vestibular ablative procedures
due to acute vestibular asymmetry & loss of i) Labyrinthectomy: used when serviceable
vestibulospinal efferents; 2-6% of patients hearing absent (>60dB PTA, <50% SDS)
ii) Bilateral Meniere’s disease treatment with
intramuscular streptomycin
 iii) Dimenhydrinate 50mg po q4h ii) Tinnitus, SNHL, vertigo most common
symptoms, vertigo sole complaint in IEDS
718) Classical signs of congenital syphilis (may not present (50%)
until after first 2 years of life), name Hutchinson’s triad iii) Treatment is rapid recompression
MMDCCCXCV) Classical signs
i) SNHL 722) Classes of drugs causing dizziness
ii) Interstitial keratitis MMCMIX) Aminoglycosides, cisplatin: ototoxic
iii) Hutchinson’s teeth MMCMX) Antiepileptics (dilatin, tegretol), alcohol:
iv) Snuffles (nasal septal perforation & saddle cerebellar toxicity
deformity) MMCMXI) Tranquilizers (BZDs, barbiturates, TCA,
v) Frontal bossing alcohol): CNS depression
MMDCCCXCVI) Hutchinson’s triad MMCMXII) Antihypertensives: hypotension,
712) Causes of BPPV (dislodgement of otoconia) i) Interstitial keratitis decreased CBF
MMDCCCLXXIX) Idiopathic (48%) ii) Sensorineural hearing loss MMCMXIII) Anticoagulatns: hemorrhage in inner
MMDCCCLXXX) Closed head injury iii) Notched incisors ear/brain
MMDCCCLXXXI) Vestibular neuritis
MMDCCCLXXXII) Otologic infections postsurgery 719) False positive VDRL is associated with what diseases? 723) Differential diagnosis of central vestibular disorders
& nonpostsurgery MMDCCCXCVII) Malaria MMCMXIV) Vascular
MMDCCCLXXXIII) Prolonged bedrest MMDCCCXCVIII) Measles i) Headache: migraine with/without aura, tension
MMDCCCXCIX) Infectious mononucleosis headache, cluster
713) Characteristics of horizontal canal BPPV MMCM) Smallpox ii) Paroxysmal torticollis
MMDCCCLXXXIV) Dix Hallpike variant maneuver: MMCMI) Collagen vascular diseases: rheumatoid iii) Vertebrobasilar insufficiency
bring patient from sitting to supine with head arthritis, SLE iv) Brainstem infarction: Wallenberg syndrome,
straight, then turn rapidly to test side with ear to the MMCMII) Leprosy lateral pontomedullary syndrome, cerebellar
table MMCMIII) Hepatitis infarction, cerebellar hemorrhage
MMDCCCLXXXV) Nystagmus: horizontal, can be MMCMXV) Neoplastic: brainstem gliomas,
geotropic or ageotropic; shorter latency, increases in 720) What are the two signs associated with otosyphilis? aqueductal/ventricle compressing neoplasms,
magnitude while in test position, slower to fatigue on MMCMIV) Hennebert’s sign: positive fistula test with cerebellar neoplasms
repeat testing an intact tympanic membrane MMCMXVI) Craniovertebral junction disorders
MMCMV) Tullio phenomenon: vertigo & nystagmus i) Basilar impression
714) Treatment of BPPV precipitated by loud noise exposure ii) Assimilation of the atlas
MMDCCCLXXXVI) Medical iii) Atlantoaxial dislocation
i) Habituation exercises 721) Barotrauma iv) Chiari malformation
ii) Brandt-Daroff exercises MMCMVI) Alternobaric trauma MMCMXVII) Multiple sclerosis
iii) Semont liberatory maneuver i) Vertigo, hearing loss & tinnitus of short duration MMCMXVIII) Cerebellar ataxia syndromes
iv) Particle repositioning maneuvers (Epley & (10-15 minutes) with increased (and
Parnes) asymmetric) middle ear pressure 724) Describe Wallenberg syndrome, the vessel affected, the
MMDCCCLXXXVII) Surgical ii) Most prominent in ascent while diving or flying, symptoms/signs seen and the cranial nuclei affected
i) Singular neurectomy decreasing ambient pressure which is relieved MMCMXIX) Lateral medullary syndrome, d/t
ii) Posterior SCC occlusion by equilibration of middle ear & ambient obstruction of vertebral artery or rarely PICA
pressure MMCMXX) Ipsilateral Horner’s syndrome: involves
715) Routes of access for infection into the inner ear MMCMVII) Atmospheric inner ear barotrauma preganglionic sympathetic fibers from the
MMDCCCLXXXVIII) Cochlear aqueduct i) Due to significant sudden pressure changes hypothalamus
MMDCCCLXXXIX) Internal auditory canal placed on the inner ear MMCMXXI) Ipsilateral loss of facial pain &
MMDCCCXC) Spiral modiolar vessels ii) Hearing loss, tinnitus most common temperature sensation: involves nucleus &
complaints, vertigo occurs less frequently; descending tract of CN V
716) Patient with right vestibular neuronitis: 4 characteristics often permanent or long lasting MMCMXXII) Ipsilateral LR weakness and facial
of vertigo, 3 points on pathophysiology iii) Seen either with implosion (RW/OW displaced weakness: involves CN’s VI & VII
MMDCCCXCI) Vertigo: spontaneous, fast phase to into labyrinth) or explosion (increased ICP MMCMXXIII) Spontaneous nystagmus: involvement of
contralateral side, unilateral decreased calorics transmitted to inner ear) vestibular nucleus
MMDCCCXCII) Pathophysiology: vestibular iv) Conservative treatment as spontaneously MMCMXXIV) Ipsilateral paralysis of palate, pharynx,
nerve degeneration, sparing of peripheral receptor resolves most of the time (bedrest, head larynx: involves nucleus ambiguus and exiting fibers
structure; viral etiology suspected elevation), explore for HL progression or failure of CN’s IX & X
of symptom resolution in 3-5 days MMCMXXV) Ipsilateral dysmetria, dysrhythmia,
717) Therapy for acute vertigo MMCMVIII) Inner ear decompression sickness and dysdiadochokinesia: involves cerebellum
MMDCCCXCIII) Severe: dimenhydrinate 50mg isobaric gas counterdiffusion sickness MMCMXXVI) Contralateral loss of pain & temperature
IM q6h i) Formation of gas bubbles in the body due to sensation: involves descending spinothalamic fibers
MMDCCCXCIV) Mild/moderate rapid reduction in atmospheric pressure (IEDS)
i) Valium 2mg po tid & glycopyrrolate 2mg po tid or too rapid an exchange of inspired gas
ii) Antivert 25-50mg po q6h mixtures under isobaric conditions
725) Describe the lateral pontomedullary syndrome, the vessel
affected, the symptoms/signs seen and the cranial nuclei
affected (No horny 6-9 on 10 year olds)
MMCMXXVII) Ischemia in AICA territory
MMCMXXVIII) No CN VI, IX, X, or sympathetics cf.
Wallenberg
MMCMXXIX) Ipsilateral loss of pain & temperature
sensation on the face: involvement of nucleus &
descending tract of CN V
MMCMXXX) Ipsilateral facial weakness: involvement of
CN VII nerve & nucleus
MMCMXXXI) Ipsilateral hearing loss & tinnitus:
infarction of labyrinth & cochlear nerve
MMCMXXXII) Spontaneous vestibular nystagmus:
involvement of labyrinth & vestibular nerve
MMCMXXXIII) Ipsilateral cerebellar dysfunction:
involvement of anteroinferior cerebellum
MMCMXXXIV) Contralateral loss of pain & temperature
sensation: involves descending spinothalamic fibers
726) Basilar impression: diagnosis, etiologies
MMCMXXXV) Chamberlain’s line: line between hard
palate and posterior edge of foramen magnum
MMCMXXXVI) Wackenheim’s clivus-canal line: extension
of clival line through foramen magnum
MMCMXXXVII)Herniation of the odontoid process above
Chamberlain’s line or posterior to Wackenheim’s line
indicates impression exists
MMCMXXXVIII) Etiologies
i) Paget’s disease
ii) Rheumatoid arthritis
iii) Osteomalacia
iv) Osteogenesis imperfecta
v) Cretinism
vi) Rickets
727) Name 6 diseases or syndromes which can cause
cerebellar ataxia
MMCMXXXIX) Spinocerebellar atrophy: cerebellar ataxia
with extrapyramidal signs (bradykinesia, tremor, slow
hesitant gait)
MMCMXL) Cerebellar atrophy: highly localized atropy
of the cerebellum
MMCMXLI) Familial episodic ataxia: recurrent vertigo
and ataxia, triggered by stress or exercise; treatable
with acetazolamide
MMCMXLII) Friedreich’s ataxia: instability of gait,
progressive hearing loss, cardiomyopathy, scoliosis,
pes caus; slowly progressive
MMCMXLIII) Refsum’s disease: retinitis pigmentosa,
polyneuropathy, cerebellar ataxia, SNHL; due to
phytanic acid storage disease, manage with diet
restrictions
MMCMXLIV) Ataxia telangiectasia: autosomal
recessive; slowly progressive cerebellar ataxia with
telangiectasias of skin and conjunctiva, recurrent
URTI
MMCMXLV) Paraneoplastic cerebellar degeneration:
most commonly associated with small cell carcinoma
of the lung, breast, ovary & female genital tract; i) Agreement between PTA and SRT should be
autoimmune mechanism within 5-10dB
MMCMXLVI) Alcoholic cerebellar degeneration: MMCMLXXI) Speech discrimination score (SDS):
selective degeneration of the anterior vermis estimation of a person’s ability to hear and
understand speech a %-age score of correctly
728) Diagnostic clues to the involved labyrinth in repeated words off of a pb word list
uncompensated peripheral vestibular lesion
MMCMXLVII) Unilateral fluctuating or progressive SNHL 734) Define spondees, PBT
MMCMXLVIII) Consistently reproducible UW on calorics MMCMLXXII) Spondee: a two syllable word with equal
(ENG) emphasis on both syllables, used to determine the
MMCMXLIX) Tinnitus SRT
MMCML) Aural fullness MMCMLXXIII) PB word list: phonetically balanced word
MMCMLI) Direction of observed spontaneous or list. 50 words of single syllable words which
positional nystagmus contains the same proportion of phonemes as that
MMCMLII) Rotatory chair asymmetries which occurs in connected American English
discourse; used to determine the SDS
729) Contraindications for surgical intervention for peripheral
vestibular disease 735) Describe the ipsilateral stapedial reflex pathway
MMCMLIII) Only hearing ear MMCMLXXIV) Normally occurs at 70-100dB HL for pure
MMCMLIV) Bilateral disease tones; will be absent with any level of CHL or an
MMCMLV) Central pathology SNHL >65dB HL
MMCMLVI) Suspicion of impaired central MMCMLXXV) Latency of 10ms; will not protect cochlea
compensation following surgery from unanticipated sounds
MMCMLXXVI) Incidence of absent stapedius tendon,
730) Characteristics of the decibel scale muscle & pyramidal eminence: 1%
MMCMLVII) Logarithmic, incorporates a ratio MMCMLXXVII) Reflex pathway
MMCMLVIII) Nonlinear i) Cochlea
MMCMLIX) Relative measure ii) Vestibulocochlear nerve
MMCMLX) Expressed with different reference levels iii) Cochlear nucleus
iv) Trapezoid body (crossover to contralateral side
731) Reference levels for the intensity level (IL) and sound here)
pressure level (SPL) referents v) Superior olivary complex
MMCMLXI) Intensity is equal to the pressure squared vi) Facial motor nucleus
MMCMLXII) Intensity dB = 10log10(Is/Ir) vii) Facial nerve
MMCMLXIII) Sound pressure dB = 20log10(sps/spr) viii) Nerve to stapedius
MMCMLXIV) Intensity level: 10-12watts/m2 or 10-
16
watts/cm2 736) What is the reflex decay test?
MMCMLXV) Sount pressure level: 20 μPa or 0.0002 MMCMLXXVIII) Measured at 500Hz, 10dB
dynes/cm2 above stapedial reflex threshold for ten seconds;
abnormal decay is <50% of original amplitude in 10
732) Describe masking, crossover, and interaural attenuation seconds, indicates probable VIII or brainstem lesion
MMCMLXVI) Crossover: sound energy that exceeds (retrocochlear lesion)
interaural attenuation and can stimulate the nontest
ear 737) Lesions that would cause bilateral stapedial reflex
MMCMLXVII) Interaural attenuation: the reduction in absence
sound energy traveling through the skull (40-65dB MMCMLXXIX) CHL >40dB in reflex-eliciting ear or
for air conduction, 0-10dB for bone conduction) >10dB in probe ear
MMCMLXVIII) Masking: introduction of noise into the MMCMLXXX) Cochlear HL >65-70dB
nontest ear during audiometric testing to eliminate it MMCMLXXXI) CN VIII lesions
from testing MMCMLXXXII) Multiple sclerosis
i) Narrow band noise for pure tones, speech MMCMLXXXIII) Brainstem lesions
noise for speech signals
MMCMLXIX) Used when air conduction of test ear 738) How to audiologically determine whether a lesion is
exceeds bone conduction of nontest ear by 40dB, or cochlear or retrocochlear in origin
when air-bone gap exceeds 10dB in the test ear MMCMLXXXIV) Retrocochlear
i) Asymmetric SNHL on pure tone testing (>15dB
733) Speech audiometry tests in 2f except 6 and 8 KHz or >30 in 1f)
MMCMLXX) Spondee reception threshold (SRT): ii) SDS asymmetry of 12-20% or unusually poor
softest intensity level a patient can repeat back a for PT
spoken word 50% of the time iii) pB rollover >20%
 iv)Positive reflex decay test MMCMXCVIII) Measures far field potentials arising from MMMXV) History inconsistent with that of hearing
v) Carhart tone decay: >30dB above threshold distal auditory pathway (cochlea and auditory nerve) loss recorded on testing
before properly hearing the tone MMCMXCIX) Needle electrode placed either MMMXVI) Referral source is for a compensation
vi) Bekesy types 3 & 4 curves transtympanically onto promontory or transcanal case
MMCMLXXXV) Cochlear (tests of recruitment) MMM) Wide band click most commonly used MMMXVII) Behaviors suspicious for invalid
i) Dynamic range between SRT and discomfort stimulus responding during testing
level with speech: normally 95dB MMMI) Measurable potentials MMMXVIII) Test retest reliability of pure tone
ii) ABLB i) Endocochlear potential: DC response thresholds should be within 5dB
iii) SISI ii) Cochlear microphonic: AC response from hair MMMXIX) Disagreement between SRT and PTA
iv) Metz recruitment test: <60dB between acoustic bearing surface of hair cells, mimics waveform (should be normally within 10dB)
reflex threshold & PTA thresholds; normal is of acoustic signal; not clinically useful MMMXX) Presence of acoustic reflexes with
85dB iii) Summating potential: DC response from hair audiometric air-bone gaps
v) Carhart tone decay 0-25dB above threshold cells, a direct current shift, due to asymmetry in MMMXXI) Absent shadow curve (crossover)
vi) Bekesy type 2 curve basilar membrane movement MMMXXII) Bone conduction thresholds worse than
iv) Compound action potential: averaged response air conduction thresholds
739) Waves of the auditory brainstem response (ABR) of discharge pattern of auditory neurons MMMXXIII) Absence of crossover hearing in unilateral
MMCMLXXXVI) Follows the pathway of the MMMII) Ratio of SP:AP increases over .5 to .7 loss (0 dB bone, 40 dB air)
auditory CNS with hydrops; ~66% of Meniere’s patients will have MMMXXIV) Nonresponse by patient in unmasked air
MMCMLXXXVII) Waves an increased SP:AP ratio; increased ratio also seen conduction stimuli with suspected unilateral hearing
i) I: Distal CN VIII in syphilis loss
ii) II: Proximal CN VIII MMMXXV) Stenger test: based on Stenger effect,
iii) III: Cochlear nucleus 744) What are the clinical applications of ECoG? that when 2 tones of same frequency are presented
iv) IV: Superior olivary complex MMMIII) Threshold testing simultaneously to both ears, the tone is heard by the
v) V: Lateral lemniscus MMMIV) Meniere’s disease better hearing ear
vi) Other waves beyond this: inferior colliculus, MMMV) Acoustic neuroma diagnosis MMMXXVI) Lombard test: based on phenomenon that
medial geniculate ganglion, auditory radiation MMMVI) Intraoperative nerve integrity monitoring one increases the volume of one’s voice in the
(Brodmann’s area 41) (near-field technique) presence of background noise, noise interferes with
self-monitoring
740) Describe the normal intervals on the ABR 745) What are the subclasses of OAEs? MMMXXVII) Doerffler-Stewart test
MMCMLXXXVIII) Absolute latencies MMMVII) Spontaneous OAE: no external stimulus, MMMXXVIII) Delayed auditory feedback
i) Wave I: 2.0ms do not occur where a cochlear HL >40dB exists MMMXXIX) Always check your hardware, reeducate
ii) Wave II: 3.0ms i) Occur in 35-60% of normal ears, usually patient
iii) Wave III: 4.1ms narrow-band signals with SPL 10-30dB
iv) Wave IV: 5.3ms MMMVIII) Evoked OAE’s: Not detectable in patients 748) Describe Austin’s classification of middle ear conductive
v) Wave V: 5.9ms with a hearing loss >55dB apparatus lesions and associated hearing loss
MMCMLXXXIX) Interwave differences i) Transient evoked OAE: evoked by a click or pip MMMXXX) TM perforation: loss proportional to size of
i) Wave I-III interval: <2.0ms (Bailey’s) or <2.3ms ~4-15ms after presentation of acoustic perforation
(Cummings & KJ) stimulus, contains multiple frequencies MMMXXXI) TM perforation with ossicular interruption:
ii) Wave III-V interval: <2.0ms (Bailey’s) or (1) Most sensitive measure of hearing loss in ~38.3dB loss
<2.1ms (Cummings & KJ) children MMMXXXII) Total loss of TM and ossicular chain:
iii) Wave I-V latency: <4.4ms (Cummings) or ii) Stimulus frequency OAE: evoked by a 50dB loss
<4.6ms (KJ) continuous pure tone stimulus, produce a MMMXXXIII) Ossicular interruption with intact TM: 55-
iv) Interaural Wave V latency: <0.2ms (Bailey’s), continuous tonal emission of same frequency 60dB loss
<0.3ms (KJ), <0.4ms (Cummings) iii) Distortion product OAE: evoked by two MMMXXXIV) Ossicular interruption with intact TM and
simultaneous presented pure tones separated closure of oval window: 55-60dB loss
741) What are the clinical applications of ABR? by a few hundred Hz; interaction produces a
MMCMXC) Threshold testing in infants/hard to test frequency that is lower than either of two 749) Degree of CHL with negative Rinne test
individuals frequencies (cubic distortion tone, 2f1-f2), MMMXXXV) 256 Hz: 15dB or more (KJ Lee); 20-30dB
MMCMXCI) Vestibular schwannoma diagnosis sensitive test for cochlear function (Cummings)
MMCMXCII) Diagnosis of brainstem lesions/pathology MMMXXXVI) 512 Hz: 25-30dB loss (KJ Lee); 30-45dB
MMCMXCIII) Neonatal/infant hearing screening 746) What is the anatomic pathway of an otoacoustic (Cummings)
MMCMXCIV) Intraoperative brainstem monitoring emission? MMMXXXVII) 1024 Hz: >35dB loss (KJ Lee); 45-60dB
MMMIX) Outer hair cell (Cummings)
742) What drugs can alter the ABR? MMMX) Basilar membrane
MMCMXCV) Lidocaine MMMXI) Cochlear fluids 750) Findings on audiometric testing suggestive of a
MMCMXCVI) Phenytoin MMMXII) Oval window retrocochlear lesion
MMCMXCVII) Diazepam MMMXIII) Ossicles MMMXXXVIII) Asymmetric hearing loss
MMMXIV) Tympanic membrane MMMXXXIX) Abnormally reduced or asymmetric
743) Electrocochleography speech discrimination
747) Evaluation for pseudohypoacusis (malingering) MMMXL) Rollover on SDS testing
 MMMXLI) Abnormal stapedial reflex testing MMMLXIII) Body aid (obsolete) MMMLXXXIII) Multiple programs for different listening
(threshold & decay) MMMLXIV) Eyeglass aid (obsolete) environments
MMMLXV) Behind the ear
751) Adult cochlear implantation criteria MMMLXVI) In the ear 761) Advantages of binaural hearing aid use
MMMXLII) >=18 years of age MMMLXVII) In the canal MMMLXXXIV) Release from masking (binaural squelch):
MMMXLIII) Severe (>70) to profound (>90) SNHL; MMMLXVIII) Completely in the canal improved speech intelligibility in noise due to phase
SDS up to 30% MMMLXIX) CROS (contralateral routing of signal): differences of signal and noise
MMMXLIV) Little or no benefit from amplification trial microphone on deaf side routes signal to MMMLXXXV) Improved sound localization (microphone
(SRS <40-50% correct in best aided condition) of at contralateral side, which has normal hearing placed closely to each middle ear)
least 6 months duration MMMLXX) Bi-CROS: asymmetric bilateral hearing MMMLXXXVI) Elimination of head shadow effect (which
MMMXLV) No medical contraindications loss present, both sides amplified with both signals normally reduces high frequency cues necessary for
MMMXLVI) Psychologically and motivationally suitable going to better hearing ear hearing consonants)
MMMXLVII) No middle ear disease MMMLXXXVII) Increased loudness (binaural summation)
757) Advantages & disadvantages of larger aids; smaller aids
752) Pediatric cochlear implantation criteria MMMLXXI) Larger hearing aids 762) Indications for BAHA
MMMXLVIII) Children 12-24 months i) Advantages MMMLXXXVIII) Congenital malformations of
i) Bilateral profound hearing loss (1) Better power for amplifying severe hearing the external & middle ear
ii) Lack of auditory skills development and minmal losses MMMLXXXIX) Chronic dermatitis of the external ear
hearing aid benefit (documented by parent (2) Better for people with lower dexterity, less MMMXC) Chronic otorrhea from COM or chronic
questionnaire) feedback mastoiditis
iii) No medical contraindications (3) Larger battery means better power supply
iv) Enrollment in a therapy of education program ii) Disadvantages 763) Blood supply to the facial nerve
emphasizing auditory development (1) Poorer cosmesis MMMXCI) Labyrinthine (AICA origin): IAC portion
MMMXLIX) Children 25 months to 17years 11 months (2) Occlusion effect MMMXCII) Superficial petrosal (middle meningeal
i) Bilateral severe to profound hearing loss MMMLXXII) Smaller hearing aids origin): perigeniculate region
ii) Lack of auditory sklls development and minimal i) Advantages MMMXCIII) Stylomastoid (posterior auricular): mastoid
hearing aid benefit (word recognition scores (1) Better cosmesis & tympanic regions
<30% correct) (2) Better for less severe hearing losses MMMXCIV) Rich anastamoses between superficial
iii) No medical contraindications (3) Uses pinna anatomy for natural petrosal and stylomastoid; poor in labyrinthine
iv) Enrollment in a therapy of education program amplification (high frequencies) segments
emphasizing auditory development (4) Decreased occlusion effect
ii) Disadvantages 764) Facial nerve anatomy, lengths of facial nerve segments
753) Contraindications to cochlear implantation (1) Limited to less severe hearing losses MMMXCV) Narrowest portion at fundus of IAC,
MMML) Complete otic capsule aplasia (Michel) (2) Increased feedback 0.68mm
MMMLI) Narrow IAC syndrome (<3mm wide with (3) Requires better dexterity MMMXCVI) Length of segments
normal facial nerve function) (4) More fragile & expensive i) Intracranial 23-24mm
ii) Meatal 8-10 mm
754) Causes of labyrinthitis ossificans 758) Describe the occlusion effect iii) Labyrinthine 3-5mm
MMMLII) Meningitis MMMLXXIII) Occurs with larger hearing aids that block iv) Tympanic 8-11mm
MMMLIII) Labyrinthitis (serous or suppurative) the EAC, shifts the resonance frequency lower, v) Mastoid 10-14mm
MMMLIV) Labyrinthectomy which increases low frequency gain vi) Extratemporal 15-20mm to pes
MMMLV) Cochlear implantation MMMLXXIV) Troublesome in people with normal low
MMMLVI) Autoimmune frequency hearing; improved with smaller hearing 765) Facial muscles supplied by CN VII
MMMLVII) Advanced otosclerosis aids MMMXCVII) Temporal branch
MMMLVIII) Temporal bone trauma i) Occipitofrontalis
MMMLIX) Vascular occlusion 759) 3 things to do to a hearing aid mold to decrease low ii) Orbicularis oculi
frequency gain in patients with HFSNHL iii) Corrugator supercilii
755) Complications of cochlear implantation (mnemonic is MMMLXXV) Open venting of the earmold: allows low iv) Anterior & superior auriculares
CLIT – sorry ladies) frequency sounds to escape MMMXCVIII) Zygomatic branch
MMMLX) Intraoperative complications: partial MMMLXXVI) Shorten the earmold canal i) Zygomaticus major
implant insertion, perilymph gusher, traumatic MMMLXXVII) Enlarge the sound bore ii) Zygomaticus minor
implantation iii) Procerus
MMMLXI) Early postoperative 760) Advantages of digital hearing aids iv) Levator labii superioris
i) Cross stimulation MMMLXXVIII) More flexible programming strategies v) Levator labii superioris alaeque nasi
ii) Leak: CSF, PLF MMMLXXIX) Useful for unusual hearing loss vi) Nasalis
iii) Infection: wound, flap necrosis, meningitis configurations vii) Depressor septi nasi
iv) Tinnitus/vertigo MMMLXXX) Anti-feedback mechanisms viii) Orbicularis oris
MMMLXII) Late: device failure, extrusion MMMLXXXI) Higher fidelity (no internal noise for MMMXCIX) Buccal branch
circuitry) i) Buccinator
756) List different types of wearable hearing aids MMMLXXXII) Improved sound quality ii) Orbicularis oris
 iii) Risorius normal for 10 days, 88% of patients have (1) Temporal bone trauma
MMMC) Marginal mandibular branch complete return (2) Birth trauma
i) Depressor anguli oris iii) Electromyography (>21 days): determines level (3) Barotrauma
ii) Orbicularis oris of muscle activity, does not provide quantitiative iii) Otitis media
iii) Depressor labii inferioris estimate of the state of the nerve (1) Acute bacterial
iv) Mentalis iv) Electroneurography (3-21 days): an objective (2) Chronic bacterial
MMMCI) Cervical branch analysis of extent of muscle electrical (3) Cholesteatoma
i) Platysma response, records facial muscle CMAP’s; iv) Sarcoidosis
>90% degeneration within 14 days is poor v) Melkerson-Rosenthal
766) Facial nerve nitpicky stuff prognosis for immediate/complete restoration of vi) Neurologic
MMMCII) Iter chordae posterior: posterior canal that function (1) HIV
the chorda tympani enters the mesotympanum MMMCXVI) Localization studies (2) Cerebrovascular disorder – central or
through i) Lacrimation (Schirmer’s test): paper strips peripheral
MMMCIII) Iter chordae anterior: anterior canal that placed in conjunctival fornix, unilateral MMMCXXVII) Chronic acquired
the chorda enters the petrotympanic fissure through; difference of >50% or a bilateral total <25mm i) Neoplastic
aka. Canal of Huguier after 5 minutes significant (1) Malignant: primary parotid tumor,
ii) Stapedial reflex metastatic
767) Name and describe four brainstem nuclei associated with iii) Trigeminal (blink) reflex (2) Benign: schwannoma, glomus tumor
CN VII (Schuknecht says there are only 3!) iv) Salivary flow testing: unilateral reduction >25% ii) Cholesteatoma
MMMCIV) Facial motor nucleus: sends SVE abnormal
efferents to muscles of facial expression, stylohyoid, v) Electrogustometry 774) Bell’s palsy
posterior digastric, stapedius vi) Magnetic evoked neuromyography MMMCXXVIII) Etiology: idiopathic disease, attributed to
MMMCV) Nucleus tractus solitarius: receives SSA vasa vasorum failure, viral, ischemic neuropathy, or
taste afferents from oral tongue 771) Electrophysiologic tests in facial nerve palsy autoimmune; viral pathology most likely
MMMCVI) Superior salivatory nucleus: sends GVE MMMCXVII) Not indicated in paretic nerves as integrity MMMCXXIX) Signs/symptoms: complete unilateral
efferents to lacrimal, sublingual, submandibular, not in doubt paralysis of sudden onset (usually over 2 weeks);
nasal glands MMMCXVIII) MST, NET, ENOG not useful in predicting often viral prodrome, hyperacusis, decreased
prognosis until Wallerian degeneration has occurred tearing, numbness or pain of ear/face/neck;
768) Most common areas of facial nerve dehiscence MMMCXIX) ENoG useful in following progression of dysgeusia
MMMCVII) Tympanic segment over oval window palsy in acute period MMMCXXX) Pathology: diffuse demyelination
MMMCVIII) Geniculate ganglion MMMCXX) EMG useful adjunct in evaluating acute throughout intratemporal course, worst at meatal &
MMMCIX) Adjacent to retrofacial air cells in mastoid paralysis & longstanding paralysis, will demonstrate labyrinthine portions
region if voluntary action potentials exist MMMCXXXI) Diagnosis: one of exclusion, rule out any
trauma, infection, neoplasm
769) Describe the Sunderland classification of nerve injuries 772) What four types of potentials are seen on EMG? MMMCXXXII) Prognosis: incomplete paralysis: ~90%
MMMCX) Class I: neuropraxia; conduction block, no MMMCXXI) Normal voluntary action potentials: complete recovery without intervention
disruption of axon continuity, recovery occurs quickly functioning motor axons are connected to and i) Complete paralysis prognosis depends on
MMMCXI) Class II: axonotmesis: wallerian stimulating motor units speed of degeneration; >90% degeneration by
degeneration of nerve from site of injury to motor MMMCXXII) Polyphasic potentials: seen with 14 days will recover to HB Grade I 50% of time
endplate and back to a node of Ranvier, regenerates reinnervation of muscle ~4-6 weeks postevent (Fisch) without intervention
to original destination MMMCXXIII) Denervation/fibrillation potentials: seen in MMMCXXXIII) Management
MMMCXII) Class III: neurotmesis; wallerian denervated muscle ~10-14 days postevent i) Medical
degeneration, disruption of endoneurium, synkinesis MMMCXXIV) Electrical silence: denotes atrophy or (1) Steroids 1mg/kg qd over 7-10 days with
may occur congenital absence of muscle taper
MMMCXIII) Class IV: neurotmesis; perineural (2) Acyclovir 800mg 5x/day x 7 days; reduces
disruption, potential for incomplete/abberant 773) Differential diagnosis of unilateral facial paralysis degeneration and lower incidence of
regeneration is greater MMMCXXV) Congenital unsatisfactory recovery
MMMCXIV) Class V: neurotmesis; epineural i) Congenital unilateral lower lip palsy (CULLP) ii) Surgical
disruption, complete transaction of nerve ii) Mobius syndrome (1) Indications for decompression: >90%
MMMCXXVI) Acute acquired degeneration of motor fibers (on ENoG)
770) Tests of facial nerve function i) Polyneuritis by 14 days
MMMCXV) Electrophysiologic tests (1) Bell’s palsy (idiopathic; 48%) (2) Maximal nerve injury occurs at meatal
i) Nerve excitability test: compare thresholds (2) Herpes zoster oticus/Ramsay Hunt foramen/labyrinthine segment, best
required to cause minimal muscle contraction syndrome (5-9%) approached through middle fossa
on each side of face; >3.5mA difference reliable (3) Guillain-Barre syndrome
sign of progressive degeneration, an indication (4) Autoimmune disease 775) Poor prognostic indicators in Bell’s palsy
for decompression (5) Lyme disease MMMCXXXIV) Complete loss of function
ii) Maximal stimulation test: compare thresholds (6) HIV MMMCXXXV) Hyperacusis
required to cause maximal muscle stimulation (7) Kawasaki disease MMMCXXXVI) Decreased lacrimation
without pain (subjective test); If MST remains ii) Trauma MMMCXXXVII)Severe aural, facial, radicular pain
 MMMCXXXVIII) Age >60 years
MMMCXXXIX) Diabetes mellitus
MMMCXL) Hypertension
MMMCXLI) Recovery time >3 months
776) Herpes zoster oticus/Ramsay Hunt syndrome
MMMCXLII) 2nd most common cause of facial paralysis
(5-9%)
MMMCXLIII) Present with vesicles on pinna,
retroauricular area, face, mouth with acute facial
palsy
MMMCXLIV) 25% of patients will have hyperacusis,
tinnitus, hearing loss, pain, vertigo
MMMCXLV) Severity of paralysis worse, prognosis
poorer; after complete loss, full recovery in 10%;
after incomplete loss, full recovery in 66%
MMMCXLVI) Treatment: corticosteroids (reduces
postherpetic neuralgia, acute pain & vertigo),
acyclovir
777) Differential diagnosis of bilateral facial nerve palsy
MMMCXLVII) Gullain-Barre syndrome
MMMCXLVIII) Bell’s palsy: bilateral in 0.3% of cases
MMMCXLIX) Multiple idiopathic cranial neuropathies
MMMCL) Brainstem encephalitis
MMMCLI) Benign intracranial hypertension
MMMCLII) Syphilis
MMMCLIII) Leukemia
MMMCLIV) Sarcoidosis
MMMCLV) Lyme disease
MMMCLVI) Bacterial meningitis
778) Melkersson-Rosenthal syndrome
MMMCLVII) Triad of symptoms: swollen face (defining
feature), recurrent CN VII paralysis (50-90% of
patients, may be bilateral), fissured tongue (50% of
patients)
MMMCLVIII) Lip biopsy: noncaseating epithelioid cell
granulomas surrounded by histiocytes, plasma cells,
lymphocytes
MMMCLIX) High serum ACE seen on bloodwork in
some cases
779) Mobius syndrome
MMMCLX) Autosomal dominant, possible some
recessive
MMMCLXI) Bilateral facial paralysis (complete)
MMMCLXII) External ear deformities, abducens &
tongue paralysis, other CN palsies, hands/feet
sometimes missing, clubfeet, MR, mixed HL
MMMCLXIII) Poland-Mobius syndrome: congenital
absence of pectoralis muscles
780) Lyme disease
MMMCLXIV) Caused by Borrelia burgdorferi;
transmitted by Ixodes ticks
MMMCLXV) Stage I: acute erythema migrans,
influenzae-like prodrome, lymphadenopathy, malaise
MMMCLXVI) Stage II: seen weeks-months later,
meningitis, cranial & peripheral neuropathies
MMMCLXVII) Stage III: seen months-years later, chronic
arthritis, neurologic deficits, recurrent meningitis,
mental disorders
MMMCLXVIII) Facial nerve palsy seen in 5% of patients,
can be unilateral or bilateral, usually completely
resolves
MMMCLXIX) Treatment: Ceftriaxone x 2 wks
781) What sequences of surgeries are used when considering
facial nerve reanimation?
MMMCLXX) Facial nerve reanastomosis
i) Must be tension free
ii) If within temporal bone, end to end apposition
appropriate
iii) Extratemporally, use 8-0 or smaller nylon for
epineurial repair
MMMCLXXI) Cable grafting
i) Greater auricular nerve (5-10 cm)
(1) Advantages: within surgical field, minimal
morbidity, similar fascicular pattern
(2) Harvest from contralateral neck
ii) Sural nerve (70cm)
(1) Distant from operative field (2 team
approach), minimal donor morbidity; found
between heads of gastrocnemius
iii) Median antebrachial cutaneous nerve (20cm)
(1) Similar branching pattern as facial nerve,
minimal donor morbidity, found in bicipital
groove next to basilic vein
MMMCLXXII) Nerve crossover techniques
i) Requires irreversible facial nerve injury, intact
mimetic function, intact motor endplate
function, intact proximal donor nerve, intact
distal facial nerve
(1) XII-VII transfer
(2) XI-VII transfer
(3) VII-VII transfer
MMMCLXXIII) Dynamic muscle slings
i) Indicated when neural techniques are
unsuitable (no longer an intact facial
neuromuscular system due to absence (Mobius
syndrome), loss of motor endplates from
longstanding facial nerve interruption for at
least 3 years, sacrifice of other cranial nerves)
ii) Steristrips and overcorrection a must
(1) Temporalis muscle transfer (superior
vector forces cf. masseter)
(2) Masseter muscle transfer
(3) Free muscle transfer: 2 stages; 1st is sural
nerve graft, 2nd stage 12 months later,
transfer of gracilis, serratus or pectoralis
major muscle fibers from zygoma to
commissure
MMMCLXXIV) Static slings
i) Goretex
782) Management of unexpected facial weakness post
tympanoplasty
MMMCLXXV) Observation (allow local anesthetic to
wear off)
MMMCLXXVI) Decompression (remove packing)
MMMCLXXVII) Consultation with 2nd surgeon present
MMMCLXXVIII) Reexplore with 2nd surgeon
present
783) Innervation to EAC and auricle
MMMCLXXIX) Lesser occipital (C2.3): mastoid region
MMMCLXXX) Great auricular (C3): majority of inferior
preauricular and medial postauricular area
MMMCLXXXI) Auriculotemporal nerve: superior
preauricular area, tragus, root of helix, anterior
superior EAC
MMMCLXXXII) VII sensory twigs: EAC
MMMCLXXXIII) Jacobsen’s nerve (IX)
MMMCLXXXIV) Arnold’s nerve (X)
784) What is the difference between osteomas and exostoses?
MMMCLXXXV) Osteoma
i) Solitary, pedunculated, related to suture lines
ii) Histo: lamellar bone around trabecular
cancellous bone with marrow and fibrovascular
tissue
MMMCLXXXVI) Exostosis
i) Multiple/bilateral, broad based, medial EAC
ii) Cold water exposure correlation
iii) Histo: parallel layers of subperiosteal bone, no
or poorly developed trabeculated fibrovascular
channels
785) Differential diagnosis of painful nodule on the ear
MMMCLXXXVII) Chondrodermatitis helicis: can
simulate BCC or SCC
MMMCLXXXVIII) Gout: purine metabolic
disorder, uric acid deposited in tissues
i) Acute pain treated with colchicines; allopurinol
(overproducers) or probenecid (underexcretors)
MMMCLXXXIX) Furuncle
MMMCXC) Ochronosis: alkaptonuria, homogentisic
acid metabolic disorder; turns black when oxidized,
deposited in cartilage
786) Bacteriology of external otitis media
MMMCXCI) Acute: Pseudomonas aeruginosa,
Peptostreptococcus, Staphylococci, Streptococci
MMMCXCII) Chronic: Proteus vulgaris, fungi
787) What are the fissures of Santorini
MMMCXCIII) Fissures present in the auricular cartilage
which allows passage of infection of neoplasm from
the EAC into the preauricular or parotid tissues
788) Management of OE: four basic principles
MMMCXCIV) Thorough cleaning & debridement
MMMCXCV) Antibiotic treatment (topical +/- oral
depending on severity)
MMMCXCVI) Analgesia (depending on severity)
MMMCXCVII) Instruction of the patient: avoid
instrumentation
789) Most common cranial nerves involved in malignant OE
 MMMCXCVIII) Four cardinal features of MOE i) Epithelial invasion: main modality of secondary MMMCCXXXVII) Extradural or perisinus abscess
i) Otalgia >1 month acquired cholesteatoma, due to meatal MMMCCXXXVIII) Labyrinthitis: serous or
ii) Otorrhea/granulation tissue epithelium invading middle ear through a suppurative
iii) Advanced age, diabetes or immune marginal or attic perforation (contact inhibition) MMMCCXXXIX) Facial nerve paralysis: acute
suppression ii) Squamous metaplasia theory (infection) or chronic (slow expansion)
iv) Cranial neuropathy iii) Implantation: iatrogenic implantation into middle MMMCCXL) Meningitis secondary to tegmen erosion
MMMCXCIX) Nerves involved ear or eardrum from surgery, foreign body, blast MMMCCXLI) Sigmoid sinus thrombosis/phlebitis
i) Facial (75%) injury MMMCCXLII) Subperiosteal abscess/Bezold’s abscess
ii) Vagus (70%) due to erosion of mastoid cortex
iii) Accessory (56%) 795) Causes of bony resorption in cholesteatoma MMMCCXLIII) Recurrent cholesteatoma
MMMCCXVII) Cellular: osteoclasts play major role
790) An elderly diabetic is being treated for a malignant otitis MMMCCXVIII) Biochemical: bacterial endotoxins, 801) Advantages & disadvantages of the modified radial
externa. Which radionucleotide tests do you use to granulation tissue products, substances related to mastoidectomy (CWD mastoidectomy)
monitor the disease process? cholesteatoma itself MMMCCXLIV) Advantages
MMMCC) Technetium99 scan: used to identify MMMCCXIX) Mechanical i) Ability to deal with the disease in one setting
presence of acute or chronic osteomyelitis, identifies ii) Ability to see recurrent disease more easily
increased osteogenic activity; stays positive for 796) Chemical mediators in cholesteatoma iii) Lower incidence of recurrent disease
prolonged period & lags behind gallium for months MMMCCXX) Osteoclasts: acid phosphatase, iv) Cost effective
MMMCCI) Gallium67 scan: incorporated into proteins collagenase, acid proteases MMMCCXLV) Disadvantages
& leukocytes during acute inflammatory process, MMMCCXXI) Macrophages: IL’s 1, 6, 11; TNF-α, CSF- i) Altered anatomy
used to follow resolution of the disease, will fade as 1, OPF, TGF-α, prostaglandins, leukotrienes, PTH- ii) Necessity to clean mastoid bowl for rest of
disease process settles rP patient’s life
MMMCCXXII) Osteocytes: BMP-2, TGF beta iii) More frequent episodes of postoperative
791) Person with otomycosis, 6 classes of topical agents used discharge
(first 6 from KJ Lee) 797) Boundaries of Prussak’s space iv) Greater difficulty achieving hearing
MMMCCII) Merthiolate MMMCCXXIII) Anterior, posterior and superior: lateral improvement
MMMCCIII) 1.5% acetic acid malleal fold
MMMCCIV) 79-95% isopropyl alcohol MMMCCXXIV) Inferior: lateral process of malleus 802) Advantages & disadvantages of ICW mastoidectomy
MMMCCV) Methyl cresyl-acetate MMMCCXXV) Medial: neck of malleus MMMCCXLVI) Advantages
MMMCCVI) Nystatin MMMCCXXVI) Lateral: Shrapnell’s membrane i) Physiologic TM position
MMMCCVII) Clotrimazole ii) Deep middle ear
MMMCCVIII) Gentian violet 798) Most common locations of origin of primary acquired iii) No mastoid bowl
MMMCCIX) Locacortin vioform cholesteatoma MMMCCXLVII) Disadvantages
MMMCCX) Drying agents: boric acid, hydrogen MMMCCXXVII) Posterior epitympanum: i) Residual cholesteatoma may be occult
peroxide originates in Prussak’s space, breaks out by either ii) Recurrent cholesteatoma may occur in attic
penetrating posterior into superior incudal space and iii) Delayed canal breakdown
792) Agents used for otitis externa into aditus and mastoid, or inferiorly into posterior iv) Incomplete exteriorization of facial recess
MMMCCXI) Neomycin: aminoglycoside, 6-8% pouch of von Troltsch v) Second stage often required
hypersensitivity to topical application MMMCCXXVIII) Posterior mesotympanum: pars
MMMCCXII) Polymyxin B tensa retracts into sinus tympani and facial recess 803) Indications for CWD mastoidectomy
MMMCCXIII) Colistin (polymyxin E) MMMCCXXIX) Anterior epitympanum: retraction pocket MMMCCXLVIII) Only hearing ear
anterior to malleus head, follows anterior pouch of MMMCCXLIX) Labyrinthine fistula
793) What is the theory of origin of congenital cholesteatoma? von Troltsch into supratubal area MMMCCL) Sclerotic mastoid
MMMCCXIV) Continued growth of the epidermoid MMMCCLI) Posterior canal wall involved by disease
formation, derived from 1st branchial groove 799) What are the bugs most commonly seen in COM?
ectoderm, found at junction of Eustachian tube MMMCCXXX) Pseudomonas aeruginosa 804) Rates of cholesteatoma recurrence after ICW and CWD
orifice and middle ear near anterior tympanic MMMCCXXXI) Staphylococcus aureus mastoidectomy
annulus; normally disappears in 33rd week of MMMCCXXXII) Cornybacterium MMMCCLII) ICW: residual 20-35%, recurrence 5-20%
gestation MMMCCXXXIII) Klebsiella pneumoniae MMMCCLIII) CWD: residual 2-17%, recurrence 0-10%
MMMCCXXXIV) In presence of cholesteatoma,
794) 4 theories of acquired cholesteatoma formation B. fragilis, Peptococcus, Peptostreptococcus, 805) Most common causes of malleus head fixation
MMMCCXV) Primary acquired Proprionibacterium anaerobes seen more commonly MMMCCLIV) Otosclerosis
i) Invagination theory: main modality of primary cf. COM’ MMMCCLV) Tympanosclerosis
acquired cholesteatoma; infection has not given MMMCCLVI) Postinfectious
rise to the cholesteatoma 800) What are the complications of COM with cholesteatoma MMMCCLVII) Congenital fixation
ii) Basal cell hyperplasia theory in order of frequency?
iii) Epithelial invasion theory MMMCCXXXV) CHL: ossicular chain disruption 806) Surgical landmarks of CN VII through the middle ear
iv) Otitis media with effusion theory in up to 30% MMMCCLVIII) Fossa incudis
MMMCCXVI) Secondary acquired MMMCCXXXVI) Inner ear fistula: 10% of cases, MMMCCLIX) Horizontal and posterior SCCs
mainly HSCC, rarely cochlea MMMCCLX) Cochleariform process
 MMMCCLXI) Digastric ridge MMMCCXCIII) Abscess results from petrositis with 818) What is auditory neuropathy?
MMMCCLXII) Chorda tympani inflammation of Dorello’s canal between petrous tip MMMCCCXIV) A pattern of hearing loss suggesting loss
MMMCCLXIII) Oval window and petroclinoid ligament of cochlear nerve function
MMMCCLXIV) Cog MMMCCXCIV) Contains CN VI and the inferior petrosal MMMCCCXV) Audiogram shows SNHL pattern of
MMMCCLXV) Pyramidal process sinus hearing loss with significantly depressed SDS out of
keeping with HL
807) 5 things to do in surgery during modified radical 813) Surgical pathways to petrous apex for drainage of MMMCCCXVI) Normal OAE & ECoG testing, abnormal
mastoidectomy to ensure dry ear infection ABR testing
MMMCCLXVI) Complete saucerization of mastoid bowl MMMCCXCV) Petrous apex divided into
MMMCCLXVII)Lower the facial ridge to remove any anterior/posterior by plane running through IAC or 819) Sudden SNHL definition & etiology, what percentage will
dependent spaces cochlea get some recovery
MMMCCLXVIII) Take down the mastoid tip MMMCCXCVI) Posterior petrous apex pneumatized in MMMCCCXVII) Definition of idiopathic SSNHL:
MMMCCLXIX) Cavity obliteration with fat or muscle 30%, anterior petrous apex pneumatized in 10% loss of at least 30dB of hearing in 3 contiguous
(Palva flap) MMMCCXCVII) Posterior approaches frequencies in fewer than 3 days
MMMCCLXX) Temporalis muscle obliteration i) Subarcuate MMMCCCXVIII) ~33% recover without therapy
MMMCCLXXI) Wide meatoplasty ii) Sinodural MMMCCCXIX) Etiology
iii) Retrofacial i) Idiopathic: viral, vascular, membrane breaks,
808) Bacteria most common in chronic otomastoiditis MMMCCXCVIII) Anterior autoimmune etiologies suspected
MMMCCLXXII)Pseudomonas aeruginosa i) Peritubal ii) Defined causes
MMMCCLXXIII) Proteus sp. ii) Infralabyrinthine
MMMCCLXXIV) Klebsiella iii) Infracochlear 820) Treatment for SSNHL: general categories
MMMCCLXXV) Staphylococcus MMMCCCXX) Vasodilators: histamine, nicotinic acid,
814) 4 stages of intracranial abscess formation papaverine, procaine, niacin, carbogen
809) Sade & Berco’s stages of middle ear atelectasis MMMCCXCIX) Invasion: fever, malaise, drowsiness, MMMCCCXXI) Rheologics: dextran, pentoxiphylline,
MMMCCLXXVI) I: retraction headache heparin, warfarin
MMMCCLXXVII) II: severe retraction MMMCCC) Localization: clinically silent MMMCCCXXII) Antiinflammatories: steroids
MMMCCLXXVIII) III: atelectasis MMMCCCI) Enlargement: mass effect, seizures, LOC MMMCCCXXIII) Antivirals: acyclovir, amantidine
MMMCCLXXIX) IV: adhesive otitis seen MMMCCCXXIV) Diuretics
MMMCCCII) Termination: rupture into ventricle or MMMCCCXXV) Triiodobenzoic acid: assists
810) Name the intratemporal complications of otitis media subarachnoid, usually fatal stria in maintaining endocochlear potential
MMMCCLXXX) Mastoiditis with or without MMMCCCXXVI) Surgery: PLF closure if
abscess (postauricular, Bezold’s, zygomatic, 815) CT findings in temporal bone infection complications suspected
parapharyngeal, retropharyngeal) contraindicating lumbar puncture
MMMCCLXXXI) Facial paralysis MMMCCCIII) Lateral shift of midline structures 821) Poor prognostic indicators for SSNHL
MMMCCLXXXII) Labyrinthine fistula MMMCCCIV) Loss of basal cisterns (suprachiasmal & MMMCCCXXVII) Age of patient (advanced age
MMMCCLXXXIII) Labyrinthitis: serous or basal) poorer)
suppurative MMMCCCV) 4th ventricle obstruction MMMCCCXXVIII) Severity of hearing loss (total
MMMCCLXXXIV) Petrositis MMMCCCVI) Obliteration of superior cerebellar, deafness worse)
quadrigeminal plate cisterns MMMCCCXXIX) Audiogram shape
811) Name 6 intracranial complications of otitis media (flat/downsloping worse)
MMMCCLXXXV) Meningitis 816) Treatment of ottitic hydrocephalus secondary to middle MMMCCCXXX) Presence of vertigo
MMMCCLXXXVI) Extradural abscess ear/mastoid infection MMMCCCXXXI) Other vascular risk factors
MMMCCLXXXVII) Subdural abscess MMMCCCVII) Increased intracranial pressure secondary MMMCCCXXXII) Delay in initiation of treatment
MMMCCLXXXVIII) Brain abscess to acute or chronic middle ear disease without MMMCCCXXXIII) Elevation of ESR on bloodwork
MMMCCLXXXIX) Lateral sinus thrombophlebitis evidence of meningitis or abscess
MMMCCXC) Otitic hydrocephalus MMMCCCVIII) Surgical: mastoidectomy, expose 822) Good prognostic indicators for SSNHL
diseased dura, debride granulations MMMCCCXXXIV) Minimal hearing loss
812) Gradenigo syndrome (aka. petrous apex syndrome) MMMCCCIX) Medical: initially acetazolamide, steroids, MMMCCCXXXV) Low frequency loss (upsloping
MMMCCXCI) Triad of symptoms repeated LP’s; next furosemide & mannitol if not shape)
i) Deep facial pain/retroorbital pain (CN V) controlled; VP shunt MMMCCCXXXVI) Absence of vestibular
ii) Aural discharge symptoms
iii) CN VI palsy (diplopia) 817) Indications for mastoidectomy in facial nerve palsy MMMCCCXXXVII) Early treatment (within 3 days)
iv) Others: fever, headache, CN VII, VIII, IX secondary to otitis media complication MMMCCCXXXVIII) No changes in N1 latency on
involvement MMMCCCX) Onset of paralysis >2 weeks after onset of ECoG
MMMCCXCII) Originally due to extradural abscess OM
involving petrous bone, more commonly caused MMMCCCXI) History of COM 823) Most common sources of temporal bone metastases
today by tumor at the petrous apex (cholesteatoma, MMMCCCXII) Failure of paralysis to resolve after MMMCCCXXXIX) Breast
meningioma, etc) appropriate medical management MMMCCCXL) Lung
MMMCCCXIII) ENOG: >90% degeneration after 6 days MMMCCCXLI) Kidney
MMMCCCXLII)GI tract
 MMMCCCXLIII) Larynx MMMCCCLXXXVI) Subluxed stapes
MMMCCCXLIV) Prostate 829) Patients who may benefit from early surgical intervention
MMMCCCXLV) Thyroid in facial nerve injury & other indications 835) Treatment options for CSF leak
MMMCCCLXIV) Immediate paralysis with no MMMCCCLXXXVII) Bedrest with head elevation,
824) Discuss temporal bone fractures return of function & absent responses >1 week avoid increased ICP
MMMCCCXLVI) Longitudinal: ~75-85% MMMCCCLXV) Immediate paralysis with MMMCCCLXXXVIII) Compression dressing
i) Due to lateral impacts; often with tearing of TM progressive decline on ENoG to <10% (postmastoidectomy)
and hemotympanum MMMCCCLXVI) Immediate paralysis with CT MMMCCCLXXXIX) Lumbar drain if conservative
ii) Present with CHL; vestibular involvement mild evidence of significant temporal bone disruption or measures fail
(concussive); CSF leak; ~20% CN VII paralysis bony impingement on fallopian canal MMMCCCXC) Open exploration indications
of delayed onset, if fallopian canal damaged will MMMCCCLXVII) Exploration at time of surgery i) Persistent leak despite medical mgmt (10-14
usually be in tympanic segment for other reasons days)
iii) TB course: through EAC & tympanic ring, ii) Recurrent meningitis
fractures tegmen, avoids otic capsule, runs 830) Pathway of crocodile tears (Bogorad’s syndrome) when iii) Brain/meningeal herniation
through foramen lacerum, foramen ovale, due to temporal bone fracture iv) Persistent pneumocephalus
and/or Eustachian tube Fibers crossinnervate from the LSPN to the GSPN after v) Brain penetration by bony spicule
MMMCCCXLVII) Transverse: ~15-25% trauma to the superior surface of the temporal bone vi) Large defect
i) Due to occipitomastoid trauma, usually of high MMMCCCLXVIII) Inferior salivatory nucleus
energy MMMCCCLXIX) Jacobsen’s nerve 836) Discuss the types of osteogenesis imperfecta
ii) Present with significant SNHL and vestibular MMMCCCLXX) Lesser superficial petrosal MMMCCCXCI) Type I (van der Hoeve syndrome): AD,
dysfunction; ~50% CN VII paralysis of nerve mildest form; nondeforming pediatric fractures,
immediate onset MMMCCCLXXI) Greater superficial petrosal normal stature, blue sclerae, CHL
iii) TB course: through jugular foramen & foramen nerve MMMCCCXCII) Type II: AR, most severe; lethal
magnum, courses through otic capsule through MMMCCCLXXII) Sphenopalatine ganglion in utero or shortly thereafter; shortened long bones,
vestibule or medial IAC, then through foramen MMMCCCLXXIII) Zygomaticotemporal branch of beaded ribs, platyspondylisis, calvarial
spinosum & lacerum V2 demineralization
MMMCCCLXXIV) Lacrimal gland MMMCCCXCIII) Type III: variable inheritance;
825) Name 5 otologic complications of temporal bone trauma progressive growth failure, frequent fractures, severe
MMMCCCXLVIII) Conductive hearing loss 831) Etiology of CSF otorhinorrhea deformity, dentinogenesis imperfecta, grey sclerae,
MMMCCCXLIX) Sensorineural hearing loss MMMCCCLXXV) Traumatic CHL or SNHL
MMMCCCL) CSF leak i) Accidental (80%); 90% will close MMMCCCXCIV) Type IV: AD; intermediate
MMMCCCLI) Facial nerve injury spontaneously severity between types I and III, grey sclerae
MMMCCCLII) Transient or prolonged vertigo ii) Surgical/iatrogenic (16%) MMMCCCXCV) CHL associated with blue
MMMCCCLXXVI) Nontraumatic (4%) sclerae, SNHL associated with grey sclerae
826) 4 most common ossicular injuries in temporal trauma i) High pressure: tumors, hydrocephalus
(ENT Secrets) ii) Normal pressure: congenital, spontaneous, 837) Discuss fibrous dysplasia
MMMCCCLIII) Incudostapedial joint dislocation (most osteitis or osteomyelitis MMMCCCXCVI) Replacement of normal
common) medullary bone with fibroosseous tissue
MMMCCCLIV) Complete incus dislocation 832) Tests to identify CSF fluid i) Presents before age 30; 25% occurs in H&N
MMMCCCLV) Stapedial crural fracture MMMCCCLXXVII) Clinical: clear nonsticky (mainly maxilla)
MMMCCCLVI) Malleus fracture nasal/aural discharge with head tilting, straining ii) Lesions typically present as painless enlarging
MMMCCCLVII)Epitympanic ossicular fixation MMMCCCLXXVIII) Halo sign bony swelling
MMMCCCLXXIX) Test for glucose content MMMCCCXCVII) 3 clinical presentations
827) Most common site of CN VII damage from temporal bone MMMCCCLXXX) B2 transferrin: disilated form of i) Monoostotic (80%)
trauma and the reasons for it transferrin, almost exclusively found in CSF; also ii) Polyostotic (17%)
MMMCCCLVIII) Distal labyrinthine segment and found in perilymph, aqueous & vitreous humor iii) McCune-Albright syndrome (3%): polyostotic
geniculate ganglion i) Most sensitive measure of identifying CSF, disease associated with triad of
MMMCCCLIX) Reasons for trauma controversial because of small volumes of fluid hyperpigmentation, precocious puberty &
i) Small size & lack of fibrous supporting tissue used for testing endocrinopathy
ii) Traction between GSPN and geniculate MMMCCCXCVIII) Treatment is surgical
ganglion 833) Most common sites of middle ear CSF leak recontouring
iii) Watershed areas of vascularization MMMCCCLXXXI) Oval window
MMMCCCLXXXII) Round window 838) Differences between fibrous dysplasia & Paget’s disease
828) 4 poor prognostic indicators in traumatic CN VII MMMCCCLXXXIII) Hyrtl’s fissure MMMCCCXCIX) Fibrous dysplasia: age of onset
paralysis? <30, monostotic most common, occurs in ribs or
MMMCCCLX) Transverse temporal bone fracture 834) Most common locations of a spontaneous perilymph femur, in H&N maxilla often involved, treated by
MMMCCCLXI) Immediate onset of paralysis fistula curettage or excision
MMMCCCLXII)Complete paralysis cf. paresis MMMCCCLXXXIV) Fissula ante fenestram MMMCD) Paget’s disease: age of onset >40,
MMMCCCLXIII) Penetrating mechanism of MMMCCCLXXXV) Fissure of round window niche polyostotic most common, occurs in lumbar spine, in
injury connected to PSCC ampulla H&N skull often involved, treated with calcitonin
 i) Negative on/off effect: a diphasic stapedial i) Anaesthesia
839) Differential diagnosis of CHL reflex MMMCDXLI) Intraoperative
MMMCDI) Fixed ii) Carhart’s notch: BC (sensorineural) notch seen i) TM perforation
i) Ossicular chain fixation NOS at 2000Hz, resolves after stapedectomy ii) Flap tear
ii) Pagets iii) Low frequency conductive hearing loss iii) Overhanging CN VII
iii) Osteogenesis imperfecta (stiffness effect) iv) Chorda tympani injury
iv) Congenital stapes fixation MMMCDXXII) Late findings v) Floating footplate
MMMCDII) Variable i) Maximal CHL (flat audiogram, mass effect) vi) Depressed footplate
i) EAC collapse ii) Absent stapedial reflex vii) Perilymph gusher
ii) Increased perilymph pressure iii) Type As tympanogram (from tympanosclerosis, viii) Persistent stapedial artery
iii) Inner ear conductive hearing loss scarred TM) ix) High riding IJV causing bleeding
iv) Ossicular chain discontinuity x) Malleus fixation
845) Etiology of SNHL in otosclerosis xi) Incus fracture
840) Genetics & epidemiology of otosclerosis MMMCDXXIII) Toxic metabolites in endolymph causing xii) Malleoincudal dislocation
MMMCDIII) Autosomal dominant with incomplete neuroepithelial damage MMMCDXLII) Postoperative
(40%) penetrance MMMCDXXIV) Vascular compromise from narrowing and i) Bleeding
MMMCDIV) 8-10% of Caucasians have histologic sclerosis of vascular channels ii) Infection: otitis media, labyrinthitis, meningitis
changes, only 12% of these people are symptomatic MMMCDXXV) Direct extension of lesion into inner ear, iii) Postoperative vertigo/disequilibrium: usually
MMMCDV) Contralateral ear affected in 80% of cases affecting basilar membrane biomechanics and subsides after a few days; persistent causes
MMMCDVI) 60% of people report family history electrolyte concentrations include depressed footplate, prosthesis too
deep into oval window, perilymph fistula, oval
841) What anatomic locations does otosclerosis occur most 846) Management of otosclerosis window granuloma
often? MMMCDXXVI) Trial of amplification iv) Fluctuating CHL: due to loose prosthesis
MMMCDVII) Fissula ante fenestram MMMCDXXVII) Medical v) Incus necrosis
MMMCDVIII) Round window niche i) Sodium fluoride 20-120mg/d creates vi) Persistent TM perforation
MMMCDIX) Medial wall of cochlear apex fluoroapatite bone which is resistant to vii) Delayed facial palsy
MMMCDX) Area posterior to cochlear aqueduct absorption; taken with vitamin D and calcium viii) Dysgeusia (10%)
MMMCDXI) Region adjacent to SCC’s gluconate ix) Tinnitus
MMMCDXII) Stapes footplate ii) Indications: presence of SNHL or vertigo; x) Delayed SNHL (1%)
patients who are unfit or refuse surgery fixation
842) Histopathologic stages of otosclerosis iii) Contraindications: pregnancy 850) Standard results for stapedectomy, virgin & revision
MMMCDXIII) Otospongiosis MMMCDXXVIII) Surgery MMMCDXLIII) Initial stapedectomy: 90% have closure of
i) Histiocytes, osteoclasts, osteoblasts involved; i) An elective surgery, should have negative ABG <10dB, 10% no change, 1-2% profound SNHL
bone around blood vessels resorbed, vessels Rinne with 512Hz fork MMMCDXLIV) Revision stapedectomy: 65% have
dilate ii) Procedures successful result, 7x increased risk of profound
ii) Osteocytes lay down rich amourphous ground (1) Stapes mobilization SNHL in revision setting
substance that lacks collagen, rich blue color (2) Stapedotomy (better high frequency)
under H&E (mantles of Manasse) (3) Stapedectomy (better low frequency) 851) Reasons for stapedectomy failure
MMMCDXIV) Otosclerosis MMMCDXLV) Prosthesis displacement
i) Formation of dense bone in areas of previous 847) Indications for LSCC fenestration MMMCDXLVI) Incus tip erosion
bony resorption, vascular channels narrowed MMMCDXXIX) Footplate refixation after stapedotomy MMMCDXLVII) Footplate refixation
due to bone deposition MMMCDXXX) Facial nerve overhang MMMCDXLVIII) Perilymph fistula
MMMCDXV) Schwartze’s sign: reddish/vascular tinge MMMCDXXXI) Persistent stapedial artery MMMCDXLIX) Otosclerotic regrowth
to promontory seen through TM in otosclerosis MMMCDXXXII) Absent oval window (?)
852) Name 4 conditions associated with perilymph gusher
843) Differences between Paget’s disease vs. otosclerosis 848) Contraindications for stapedectomy/stapedotomy MMMCDL) X-linked stapes gusher syndrome
MMMCDXVI) Paget’s involves all bones of the skull & MMMCDXXXIII) Active Meniere’s disease MMMCDLI) Congenital fixed footplate
often see enlarged calvaria, vs. temporal bone MMMCDXXXIV) Only hearing ear MMMCDLII) Mondini deformity
involvement only, MMMCDXXXV) Avoid otospongiosis phase of MMMCDLIII) Enlarged vestibular aqueduct
MMMCDXVII) Paget’s onset is 6th decade, otosclerosis otosclerosis
onset usually 3rd MMMCDXXXVI) Otitis externa/otitis media of 853) Discuss X-linked stapes gusher imaging abnormalities
MMMCDXVIII) Pagets initially periosteal but eventually chronic nature MMMCDLIV) Cochlear modiolus deficient
involves endosteal and endochondral layers, vs. only MMMCDXXXVII) Tympanic membrane MMMCDLV) Lateral portion of IAC bulbous
endochondral involvement in otosclerosis perforation MMMCDLVI) Labyrinthine portion of fallopian canal
MMMCDXIX) Paget’s rarely involves stapes footplate or MMMCDXXXVIII) Extremes of age dilated
ossicles MMMCDXXXIX) Any uncompensated vestibular MMMCDLVII) PSCC dysplasia
MMMCDXX) Greater degree of SNHL seen in Pagets disorder MMMCDLVIII) VA enlargement

844) 3 early 3 late findings audio/impedance in otosclerosis? 849) Complications of stapedectomy 854) 8 viruses involved in SNHL
MMMCDXXI) Early findings MMMCDXL) Preoperative
 MMMCDLIX) CMV (most common cause of congenital MMMCDLXXXV) 15-20% of patients experience MMMDIV) Earmuffs: more effective protectors,
viral deafness) persistent SNHL reduces noise by 30-40dB, works best in 500-
MMMCDLX) Mumps (most common cause of acquired MMMCDLXXXVI) Incidence varies with strain: 1000Hz range
unilateral SNHL) Pneumococcus 31%, N. meningitides 11%, H. MMMDV) Must be worn at all times; removal even
MMMCDLXI) Rubella influenzae 6% for short periods severely reduces their effective
MMMCDLXII) HSV I & II cumulative attenuation capability (eg. 30dB effective
MMMCDLXIII) Varicella 859) Why do all noise induced HL have 4000 Hz notch? attenuation reduced to 13-15dB if earmuffs removed
MMMCDLXIV) Variola (smallpox) MMMCDLXXXVII) 4000Hz is the natural for 5% of an 8 hour day)
MMMCDLXV) EBV resonance frequency of external canal
MMMCDLXVI) Polio MMMCDLXXXVIII) 3000Hz as natural resonance 864) Pathologies in non-organ specific AIED
MMMCDLXVII)Influenza frequency of external canal but routine audio only MMMDVI) Polyarteritis nodosa
MMMCDLXVIII) Adenovirus tests 4000Hz MMMDVII) Cogan’s syndrome
MMMCDLXIX) Measles (rubeola): Warthin-Finkleday MMMCDLXXXIX) Hair cells at the basal turn are MMMDVIII) Wegener’s granulomatosis
cells (multinucleated giant cells) most susceptible to oxidative stress MMMDIX) Behcet’s syndrome
MMMCDLXX) Hepatitis MMMCDXC) Greatest sensitivity of human ear is to MMMDX) Relapsing polychondritis
frequencies between 1-5kHz, protective effect of MMMDXI) Systemic lupus erythematosis
855) Neonatal CMV infection and SNHL acoustic reflex is <2kHz MMMDXII) Rheumatoid arthritis
MMMCDLXXI) Most common cause of viral congenital MMMCDXCI) Intermittent loud sounds are more
deafness protective for the lower frequencies 865) Antigen specific tests for AIED
MMMCDLXXII)Unusual for CMV infection acquired after MMMDXIII) Lymphocyte transformation test (LTT)
birth to cause hearing loss 860) Describe the TTS and PTS i) Targets type II collagen, predictive value 70%,
MMMCDLXXIII) 1% of all children born; 95% MMMCDXCII) Temporary threshold shift sensitivity 70-80% & specificity 93% in
clinically silent infection, 1-5% symptomatic with CID i) From exposures to moderately intense sounds detecting organ specific AIED
MMMCDLXXIV) Cytomegalic inclusion disease ii) Elevated thresholds, esp. 3-6kHz, with tinnitus, MMMDXIV) Lymphocyte migration inhibition test
i) Hemolytic anemia, hepatosplenomegaly, loudness recruitment, diplacusis (LMIT)
jaundice, purpura, intracerebral calcifications & iii) Recovery occurs over minutes, hours & days i) Sensitivity & specificity of test results
microcephaly MMMCDXCIII) Permanent threshold shift questionable
ii) 30-65% of surviving neonates will have severe, i) Permanent cochlear damage, specifically to the MMMDXV) Western blot testing
symmetric SNHL mostly in high frequencies OHCs i) Detection of autoantibodies against inner-ear
MMMCDLXXV) Asymptomatic CMV infection ii) Two main causes antigen epitope with a 68kD molecular weight;
i) Remainder of CMV infected children; 8-15% (1) Acoustic trauma: single, short lasting possibly best evidence of organ-specific AIED
will have mild-moderate SNHL exposure to a very intense sound; causes ii) 68kD antigen either a heat shock protein (HSP-
MMMCDLXXVI) Treatment: acyclovir, sudden, painful loss of hearing 70) or an antigen bound to it
gangcyclovir used; no real clinical improvements (2) NIHL: chronic exposure to more moderate
seen sound levels 866) Describe the characteristics of Cogan’s syndrome
MMMDXVI) Interstitial keratitis (90% of patients with
856) Differential of false positive heterophil antibody test for 861) Symptoms of NIHL typical syndrome; atypical syndrome patients have
infectious mononucleosis (B RASH2) MMMCDXCIV) SNHL (bilateral) scleritis, episcleritis, papilledema, retinal
MMMCDLXXVII) Brucella MMMCDXCV) Tinnitus detachment)
MMMCDLXXVIII) Rheumatoid arthritis MMMCDXCVI) Recruitment MMMDXVII) Meniere-like hearing loss: peak shaped
MMMCDLXXIX) Serum sickness MMMCDXCVII) Diplacusis initially, but bilateral and progressive and can
MMMCDLXXX) Hodgkin’s lymphoma MMMCDXCVIII) Distortion become profound
MMMCDLXXXI) Hepatitis MMMCDXCIX) Nonauditory (anxiety, etc.) MMMDXVIII) Vestibular symptoms: sudden true vertigo,
ataxia, vegetative symptoms
857) What are the components of the classical rubella triad 862) AAO-HNS hearing handicap MMMDXIX) Systemic inflammatory involvement: heart
MMMCDLXXXII) Classic triad MMMD) Assumptions and lungs involved in typical form, more systemic
i) Deafness: SNHL typically in a cookiebite i) Hearing loss does not begin handicapping until involvement seen in atypical form
configuration the PTA HTL at 0.5, 1, 2, 3 kHz exceeds 25dB MMMDXX) Patients typically have URTI within 7-10
ii) Cataracts (also glaucoma, microphthalmia) ii) Handicap grows at rate of 1.5% per dB of HL days of initial onset
iii) Heart defects (PDA, pulmonary artery stenosis) beyond 25dB MMMDXXI) Untreated may lead to profound SNHL
MMMCDLXXXIII) Expanded syndrome includes iii) Unilateral deafness only a mild handicap, two and loss of vestibular function
microcephaly, mental retardation, ears should not be equally weighted MMMDXXII) Therapy: corticosteroids (systemic &
hepatosplenomegaly at birth, thrombocytopenia, MMMDI) Monoaural impairment topical), cyclophosphamide
radiolucencies in the long bones, interstitial i) MI = 1.5(PTA – 25)
pneumonitis, encephalitis, low birth weight MMMDII) Hearing handicap 867) Therapy for AIED
i) HH = [5(MIbetter) – (MIworse)]/6 MMMDXXIII) Steroids: prednisone 60mg po qd for 4
858) SNHL postmeningitis weeks
MMMCDLXXXIV) Responsible for ~33% of all 863) General advice on hearing protection MMMDXXIV) Add MTX 7.5-20mg po qweekly with folic
hearing deficits acquired after birth MMMDIII) Earplugs: reduce noise by 15-30dB, work acid for people who relapse during steroid taper
best in 2-5kHz range
 MMMDXXV) Add cyclophosphamide 1-2mg/kg/d for 871) Differential diagnosis of a soft tissue mass overlying the MMMDLXXIII) If unilateral, work up same as asymmetric
nonresponders to steroids and methotrexate promontory HL
MMMDXLVIII) Glomus tympanicum MMMDLXXIV) Management strategy for tinnitus
868) List the sites of action for the following ototoxic drugs MMMDXLIX) Congenital cholesteatoma i) Stop caffeine, stop smoking
MMMDXXVI) Aminoglycosides MMMDL) Schwannoma ii) Discontinue drugs, especially aspirin
i) Affects OHCs from base to apex MMMDLI) Adenoma iii) Needs: emotional support, realistic
ii) Effects usually irreversible MMMDLII) Aberrant carotid artery understanding of tinnitus, attitude to pursue
iii) Streptomycin & gentamycin more MMMDLIII) Persistent stapedial artery helpful activities, battery of tactics & strategies
vestibulotoxic; tinnitus common MMMDLIV) High riding jugular bulb (defined so if iv) Tell the patient: tinnitus is real, has a physical
iv) Neomycin, amikacin, kanamycin, tobramycin superior limit above the floor of the IAC) basis; may be permanent, reaction to tinnitus
more cochleotoxic not tinnitus itself creates a problem, reaction is
MMMDXXVII) Macrolides 872) Course of an abberant internal carotid artery manageable & can be modified
i) Erythromycin, azithromycin MMMDLV) Cervical portion of ICA fails to develop v) Surgery: when associated with a condition
ii) Reversible flat SNHL, thought to affect strial MMMDLVI) Inferior tympanic artery enters ME through (otosclerosis, Meniere’s, acoustic neuroma,
function but no definite mechanism known inferior tympanic canaliculus, joins caroticotympanic glomus), tinnitus improves in ~50%; auditory
MMMDXXVIII) Vancomycin artery and forms horizontal petrous portion of the nerve section specifically for tinnitus will make
i) Ototoxicity disputed, no firm mechanism ICA it worse in 50%
MMMDXXIX) Cisplatin MMMDLVII) Commonly associated with persistent MMMDLXXV) Prognosis
i) Bilateral symmetric high frequency SNHL & stapedial artery i) 25% better
tinnitus, usually permanent loss ii) 50% slight improvement
ii) Affects OHC’s at basal turn, degeneration of 873) Paraauditory/objective causes of tinnitus iii) 25% unchanged
stria and ganglion cells also noted; possibly MMMDLVIII) Vascular
due to oxygen free radicals i) Aberrant carotid 876) Residual inhibition phenomenon
MMMDXXX) Loop diuretics ii) High riding jugular bulb MMMDLXXVI) Tinnitus will subside for periods after
i) Reversible (furosemide) or permanent MMMDLIX) AVM’s masking exposure
(ethacrynic acid) cochleotoxicity, with tinnitus i) Congenital causes
and vertigo (1) Occipital artery to transverse sinus 877) MRI characteristics of CPA and petrous apex tumors
ii) Affects stria vascularis by altering potassium (2) Internal carotid to vertebral vessels MMMDLXXVII) Vestibular schwannoma: T1
ion transport, alters endocochleal potential (3) Middle meningeal to greater superficial iso/hypointense, T2 iso/hypointense, strong Gad
MMMDXXXI) Antiinflammatories petrosal artery enhancement
i) Aspirin, NSAIDs, quinine ii) Acquired MMMDLXXVIII) Meningioma: T1
ii) All cause reversible high frequency tinnitus and (1) Paraganglioma iso/hypointense, T2 variable, moderate Gad
mild-moderate flat/high frequency hearing loss (2) Carotid-cavernous sinus fistula enhancement
iii) OHC main site of toxicity, salicylates can also (posttraumatic, spontaneous, or Ehlers- MMMDLXXIX) Epidermoid: T1 hypointense, T2
affect cochlear blood flow Danlos syndrome) iso/hyperintense, nonenhancing on Gadolinium
MMMDLX) Venous abnormalities MMMDLXXX) Paraganglioma: salt & pepper mixture of
869) Name 6 preexisting conditions which increase i) Hypertension (venous hum) intensities on T1 & T2, strong Gad enhancement
susceptibility to ototoxicity ii) Dehiscent jugular bulb MMMDLXXXI) Cholesterol granuloma: Hyperintense on
MMMDXXXII) Renal failure iii) Transverse sinus obstruction T1 & T2
MMMDXXXIII) Liver failure MMMDLXI) Muscle contraction tinnitus MMMDLXXXII) Arachnoid cyst: appear as well defined
MMMDXXXIV) Immunocompromise i) Palatal myoclonus: associated with MS, CVA, rounded cyst, low intensity on T1, high intensity on
MMMDXXXV) Advanced age intracranial neoplasms, psychogenic T2 (same as CSF density)
MMMDXXXVI) Prior ototoxicity MMMDLXXXIII) Dermoid/lipoma: T1
MMMDXXXVII)Concurrent use of other known ototoxic 874) Etiologies of subjective tinnitus hyperintense, T2 hyopintense, Gad nonenhancing
agents MMMDLXII) Otologic: SNHL, NIHL, Meniere’s MMMDLXXXIV) Chordoma & chondrosarcoma:
MMMDXXXVIII) Preexisting SNHL MMMDLXIII) Metabolic: hyperthyroidism, T1 isointense, T2 hyperintense, strong Gad
MMMDXXXIX) Collagen vascular disorders hypothyroidism, hyperlipidemia, decreased zinc, enhancement
hypovitaminosis
870) Indications of high risk in patients taking ototoxic meds MMMDLXIV) Neurologic: skull trauma, whiplash, MS, 878) What IAC lesions light up with gadolinium?
MMMDXL) Impaired renal function meningitis MMMDLXXXV) Acoustic neuromas
MMMDXLI) Elevated peak and trough drug levels MMMDLXV) Drugs MMMDLXXXVI) Facial nerve neuromas
MMMDXLII) Preexisting SNHL MMMDLXVI) Dental: TMJ disorders MMMDLXXXVII) Petrous bone metastasis
MMMDXLIII) More than one ototoxic drug administered; MMMDLXVII) Psychiatric: depression, anxiety MMMDLXXXVIII) Inflammatory nerve lsions
previous history of ototoxic drug MMMDLXXXIX) AVM’s
MMMDXLIV) Treatment course >14 days 875) Evaluation & management of tinnitus, prognosis MMMDXC) Vascular loops
MMMDXLV) Cochlear or vestibular symptoms MMMDLXVIII) Audiometry
MMMDXLVI) Advanced age (>65 years) MMMDLXIX) Thyroid function tests 879) Differences between vagal schwannoma and carotid body
MMMDXLVII) Coadministration of loop diuretics & MMMDLXX) Cholesterol tests tumor on angio
aminoglycosides MMMDLXXI) BP check MMMDXCI) Schwannoma will push vessels anterior &
MMMDLXXII) FTA-ABS lateral
 MMMDXCII) Carotid body tumor will splay ECA and
ICA apart (Lyre sign)
MMMDXCIII) Filling effect from vessel ingrowth seen in
carotid body tumors
880) Assessment of cerebral blood flow in skull base surgery
MMMDXCIV) Unselected ICA interruption: 26% rate of
cerebral infarction
MMMDXCV) 4 vessel arteriography with venous phase
MMMDXCVI) Functional cerebral blood flow evaluation
i) 50ml/100g/min normal CBF; <20ml/100g/min
produces failure of brain function
ii) Indications: en bloc resection requiring ICA
resection; tumor encases ICA on imaging;
contour irregularities of ICA on angio
iii) Xenon-CBF study: 15 minute balloon occlusion
(1) Group I: No CBF side difference
(2) Group II: mild symmetric CBF decrease
(3) Group III (10-15%): marked decrease in
CBF (<30ml/100g/min)
(4) Group IV (5%): neurologic deficit, CBF
<20ml/100g/min
iv) Preop permanent balloon occlusion for groups I
& II
v) Prophylactic or intraoperative revascularization
for group III, or for groups I & II if patient young
or if contralateral disease present
vi) No surgery, or prophylactic revascularization for
group IV patients
881) What is the anastamotic vein of Labbe?
MMMDXCVII) Drains the temporal lobe, communicates
the superficial middle cerebral vein with the
transverse sinus medial to superior petrosal sinus
MMMDXCVIII) Occlusion will cause temporal lobe edema
882) Surgical approaches to the lateral temporal bone
MMMDXCIX) Sleeve resection
i) Removes cartilaginous EAC & some or all of
the bony canal wall skin circumferentially
without bone removal; for malignancies
localized to the cartilaginous EAC
MMMDC) Lateral temporal bone resection
i) Removes en bloc the entire osseous &
cartilaginous EAC with the tympanic
membrane; for malignancies localized to
osseous EAC with no encroachment on medial
mesotympanum
MMMDCI) Subtotal temporal bone resection
i) For en bloc resection of the medial surfaces of
the mesotympanum, leaves air cells of petrous
apex & portions of bony labyrinth; for tumors
involving the middle ear
MMMDCII) Total temporal bone resection
i) For en bloc resection of the temporal bone,
including petrous apex & sigmoid sinus
883) Primary indication for a Fisch A approach? 7 steps in
order of procedure
MMMDCIII) Main indication is for paragangliomas of MMMDCXVI) Neuroendocrine origin, nonchromaffin
the temporal bone refers to no staining from chromium containing
MMMDCIV) Fisch A approach provides access to stains
jugular bulb, vertical petrous carotid, posterior MMMDCXVII) Cell types
infratemporal fossa i) Chief cells: granule storing
i) Neck dissection to expose CN IX-XII, ICA, IJV ii) Satellite cells: Schwann-like cells
ii) Wide field mastoidectomy: removal of mastoid iii) Zelballen pattern – chief cell clusters enclosed
tip, entire EAC, middle ear contents in fibrous septa & supporting cells within
iii) Identification of CN VII, removal from canal and vascular network
anterior translocation
iv) Exposure of posterior and middle cranial fossa 887) Most common sites of paraganglioma occurrence
dura for intracranial extension MMMDCXVIII) Carotid body (65%)
v) Removal of disease MMMDCXIX) Jugulotympanic
vi) Obliteration of cavity with abdominal fat, rotated MMMDCXX) Intravagal
temporalis muscle, tensor fascia lata flap MMMDCXXI) Laryngeal
vii) Layered closure and compression dressing MMMDCXXII) Nasal
application MMMDCXXIII) Nasopharyngeal
MMMDCV) Fisch B approach provides access to MMMDCXXIV) Orbital
petrous apex, clivus, superior infratemporal fossa
MMMDCVI) Fisch C approach provides access to 888) Paraganglioma pearls
nasopharynx, peritubal space, rostral clivus, MMMDCXXV) 5-10% of patients have multiple lesions
parasellar area, pterygopalatine fossa, MMMDCXXVI) 1-3% active secretors
anterosuperior infratemporal fossa MMMDCXXVII) 10% familial, with multiple
lesions in 26%
884) Describe the major types of jugular foramen syndromes MMMDCXXVIII) Malignant in 3-5%, clinically will
MMMDCVII) Vernet syndrome: CN IX, X, XI palsies; have signs of invasion of surrounding structures &
due to jugular foramen neoplasm (most commonly distant metastasis
lymphadenopathy of Krause’s nodes) MMMDCXXIX) Symptoms in secretors: flushing,
MMMDCVIII) Collet-Sicard syndrome: CN IX, X, XI, XII diarrhea, palpitations, headache, hypertension,
palsies; most commonly due to extradural tumor of perspiration, orthostasis
posterior fossa or retroparotid space MMMDCXXX) Clinical signs
MMMDCIX) Villaret syndrome: CN IX, X, XI, XII i) Brown’s sign: seen in glomus typmanicum
palsies, sympathetic chain involvement leads to tumors; a reddish blush seen behind an intact
Horner’s; suggests lesion distal to jugular foramen, tympanic membrane which blanches upon
usually retrostyloid area introducing pneumatic pressure that exceeds
MMMDCX) Hughlings-Jackson: CN X, XI, XII palsies the systolic BP
MMMDCXI) Tapia syndrome: Lesion in neck (usually ii) Aquino’s sign: seen in paragangliomas,
traumatic) involving CN X & XII below level of inferior pulsation of paraganglioma decreases with
ganglion of X (vocal palsy seen, palate intact) carotid artery compression
MMMDCXII) Schmidt syndrome (vagal-accessory): CN MMMDCXXXI) Tests: serum catecholamines, urine VMA,
X & XI; lesion of nucleus ambiguous & bulbar spinal metanephrines, 5-HIAA; treated with α & ß blockade
nuclei of accessory; paralysis of soft palate, pharynx MMMDCXXXII) Radiography: CT shows
& larynx, flaccid weakness & atrophy of irregular destruction of jugular foramen & temporal
SCM/trapezius bone; MRI shows salt & pepper mix on T1 & T2
MMMDCXXXIII) Treatment primarily surgical
885) Management of air embolism during surgery MMMDCXXXIV) Radiotherapy indicated for high
MMMDCXIII) Usually through diploic veins in skull into risk patients, incompletely excised or recurrent
jugular system & sigmoid sinus lesions, bilateral lesions, metastases
MMMDCXIV) 30cc of air will cause signs & symptoms:
hypotension, churning precordial sounds 889) What is the Glasscock-Jackson classification for glomus
MMMDCXV) Management tympanicum?
i) Pack surgical wound with wet sponges MMMDCXXXV) Type I: small mass limited to
ii) Trendelenburg prevents further leaks the promontory
iii) Left lateral decubitus position traps air in right MMMDCXXXVI) Type II: mass completely filling
heart and prevents lung embolism middle ear space
iv) Wait until patient stabilizes (air absorbed) or MMMDCXXXVII) Type III: Tumor filling middle
aspirate air via venous catheter ear and extending to mastoid
v) Fix source of air leak MMMDCXXXVIII) Type IV: Tumor filling middle
ear, extending to mastoid, or through TM to fill EAC;
886) 2 cell types present in normal paraganglia may also extend anterior to ICA

890) What is the Glasscock-Jackson classification for glomus
jugulare?
MMMDCXXXIX) Type I: Tumor involves jugular
bulb, middle ear, and mastoid
MMMDCXL) Type II: Tumor extends under IAC, may
have intracranial involvement
MMMDCXLI) Type III: Tumor extends into petrous apex;
may have intracranial extension
MMMDCXLII) Type IV: Tumor extending beyond petrous
apex into clivus or infratemporal fossa; may have
intracranial involvement
891) Surgical approaches for gloumus jugulare & tympanicum
MMMDCXLIII) Tympanicum
i) Type I: endaural resection
ii) Type II, III, IV: extended facial recess approach
MMMDCXLIV) Jugulare: Fisch type A infratemporal fossa
approach
MMMDCXLV) Efficacy of preoperative embolization
disputed
892) Radiotherapy and paragangliomas
MMMDCXLVI) Chief cells unaffected, but causes
obliterative endarteritis of tumor vessels, controls
rate of tumor growth in 90%
MMMDCXLVII) Overall, not the management of choice,
can reduce tumor mass; useful for management of
recurrences & unresectable lesions
893) Anatomy of internal acoustic canal
MMMDCXLVIII) Anterior superior: facial nerve
MMMDCXLIX) Posterior superior: superior vestibular
nerve
MMMDCL) Posterior inferior: inferior vestibular nerve
MMMDCLI) Anterior inferior: cochlear nerve
MMMDCLII) Bill’s bar (crista verticalis): superior ridge
MMMDCLIII) Falciform crest (crista falciformis): divides
upper and lower halves
894) What is the differential diagnosis of a posterior fossa
lesion?
MMMDCLIV) Common CPA lesions
i) Acoustic neuroma (78-80%, most common
adult lesion)
ii) Meningioma (3%, 2nd most common adult
lesion)
iii) Epidermoid (2.5%, 3rd most common adult
lesion)
iv) Nonacoustic neuroma (facial schwannoma
most common, 1%)
v) Paraganglioma
vi) Arachnoid cyst
vii) Hemangioma
MMMDCLV) Uncommon CPA lesions
i) Metastatic malignant tumor
ii) Lipoma
iii) Dermoid
iv) Teratoma
v) Chordoma
vi) Chondrosarcoma
vii) Giant cell tumor
MMMDCLVI) Petrous apex lesions
i) Cholesterol granuloma (20x more frequent than
epidermoids in the petrous apex)
ii) Epidermoid
iii) Asymmetric pneumatization
iv) Retained mucus/mucocele
v) Petrous ICA aneurysm
MMMDCLVII) Intraaxial tumors
i) Hemangioblastoma
ii) Medulloblastoma
iii) Brainstem glioma (most common pediatric CPA
lesion)
iv) Malignant choroids plexus papilloma &
ependymomas
895) Pearls for working up acoustic neuromas
MMMDCLVIII) Things to remember
i) Originate at schwann cell-glial junction
(Obersteiner-Redlich zone)
MMMDCLIX) Clinical
i) Hitselberger’s sign: numbness of EAC from
compression of sensory branches of facial
nerve
MMMDCLX) Audiometrics
i) PTA: 65% will have HFSNHL; 5% have normal
hearing; 10% of patients with AN present with
SSNHL
ii) SDS: scores not proportional to PTA
suspicious; rollover present
iii) Stapedial reflex: 88% will have absent reflex or
positive reflex decay
MMMDCLXI) Electrophysiologic tests
i) ABR: ILDV >0.2msec in 40-60%, absent
waveforms in 20-30%, wave I only wave
present 10-20%, normal ABR in 10-15%
(1) 18-30% false positive rate for small
intracanalicular tumors
MMMDCLXII) Vestibular testing
i) ENG abnormal in 70-90%, usually unilateral
weakness; tumors arising from inferior
vestibular nerve will be missed
896) Management strategy for acoustic neuroma
MMMDCLXIII) Observation: 3 categories of growth
i) Slow/no growth (40%): <0.2cm per year
ii) Limited growth: ~0.2cm per year
iii) More rapid growth: ~1cm per year
MMMDCLXIV) Surgery
i) Criteria for hearing preservation: 30dB PTA,
70% SDS, <2cm extension into CPA
ii) Complications: SNHL, CN VII palsy,
hemorrhage, meningitis, air embolism, CSF
leak, cerebellar ataxia, headache
897) Stereotactic radiosurgery: limitations
MMMDCLXV) Tumor is not excised, stops tumor growth
MMMDCLXVI) Delayed facial weakness
MMMDCLXVII)Only small tumors can be radiated
MMMDCLXVIII) Not hearing preserving
MMMDCLXIX) Trigeminal neuropathy
MMMDCLXX) Postradiation scarring makes salvage
surgery more difficult
898) Name 3 common approaches with advantages &
disadvantages for acoustic neuroma excision
MMMDCLXXI) Translabyrinthine
i) Advantages: safest approach for CN VII
function preservation; direct approach to IAC;
wide exposure not limited by tumor size;
minimal cerebellar retraction
ii) Disadvantanges: total hearing eradication
MMMDCLXXII)Middle fossa
i) Adv: CN VIII nerve preservation possible; ideal
for small intracanalicular tumors
ii) Dis: contraindicated if >1cm extension into
CPA; increased risk to CN VII cf. TL approach,
requires significant temporal lobe retraction
MMMDCLXXIII) Retrosigmoid
i) Adv: excellent for hearing preservation; useful
for tumors <2cm with limited IAC involvement
ii) Dis: contraindicated if tumor extends to fundus;
increased risk to CN VII cf. TL approach; 10%
postoperative headaches; need for cerebellar
retraction
899) Name other approaches used for approaching skull base
lesions requiring drainage or sectioning
MMMDCLXXIV) Retrolabyrinthine
i) Main indication is vestibular nerve section, can
be used for resection of selected arachnoid
cysts, meningiomas, metastatic CPA lesions;
minimal cerebellar retraction; hearing
preservation
MMMDCLXXV) Transcochlear
i) Extension of translabyrinthine approach,
removal of cochlea & displacement of facial
nerve for access to petrous tip and clivus
MMMDCLXXVI) Transotic
i) Similar to transcochlear, but facial nerve is
skeletonized and left in the fallopian canal
MMMDCLXXVII) Extended middle fossa
i) Extended by removal of petrous ridge and
posterior aspects of temporal bone up to
labyrinth
900) Approaches for skull base lesions requiring drainage
MMMDCLXXVIII) Translabyrinthine: most direct
route if hearing and vestibular function are absent
MMMDCLXXIX) Middle fossa approach: permits
hearing preservation but requires increased temporal
lobe retraction, no readily available space for
drainage or aeration
MMMDCLXXX) Infralabyrinthine: after
mastoidectomy, sigmoid sinus decompressed & air
cell tracts followed into petrous apex; might be
impossible with a high jugular bulb
MMMDCLXXXI) Transcanal infracochlear: air
cell tract between IJV and ICA is followed into apex,
 permits dependent drainage, but requires EAC MMMDCCXI) Inflammation and hemorrhage,
transection which heals over prolonged period, also subsequent breakdown of RBC’s & foreign body
requires exposure of petrous carotid artery reaction to cholesterol crystals
MMMDCCXII) Incites more inflammation and a vicious
901) 6 histological types of meningioma circle
MMMDCLXXXII) Meningotheliomatous (most
common) 907) Skull base lesions associated with facial twitching/tics
MMMDCLXXXIII) Transitional MMMDCCXIII) Epidermoid
MMMDCLXXXIV) Psammomatous MMMDCCXIV) Facial nerve schwannoma
MMMDCLXXXV) Fibroblastic MMMDCCXV) Facial nerve hemangioma
MMMDCLXXXVI) Angioblastic
MMMDCLXXXVII) Malignant 908) Surgical approaches to the anterior cranial fossa
MMMDCCXVI) Anterior craniofacial resection: bifrontal
902) In order, what sites do meningiomas commonly occur? craniotomy combined with a transfacial exposure of
MMMDCLXXXVIII) Parasagittal nasal cavity, ethmoid, maxillary & orbital areas
MMMDCLXXXIX) Falx MMMDCCXVII) Basal subfrontal approach:
MMMDCXC) Convexity similar to craniofacial approach; less extensive
MMMDCXCI) Olfactory groove transfacial exposure; target area is sphenoid & clivus
MMMDCXCII) Tuberculum sellae
MMMDCXCIII) Sphenoid ridge 909) Surgical approaches to the middle cranial fossa
MMMDCXCIV) CPA (petrous face) MMMDCCXVIII) Central compartment (line
MMMDCXCV) Tentorium through medial pterygoid plate and occipital condyle
MMMDCXCVI) Lateral ventricle on both sides)
MMMDCXCVII) Clivus i) Transseptal sphenoid
ii) Transethmoidal sphenoid
903) Pearls of meningioma management iii) Lateral rhinotomy
MMMDCXCVIII) Arise from cap cells around iv) Transantral
tips of arachnoid villi v) Midfacial degloving
MMMDCXCIX) Histology: lobulated groups of cells vi) LeFort I osteotomy
reminiscent of normal arachnoid granulations; vii) Transpalatal
psammoma bodies often present viii) Transoral
MMMDCC) Hyperostosis of surrounding bone in 25% ix) Mandibulotomy
x) Extended maxillotomy
904) Radiographic differences between meningiomas and xi) Midfacial split
acoustic neuromas xii) Infratemporal fossa
MMMDCCI) Meningiomas more dense & homogenous xiii) Facial translocation
MMMDCCII) Meningiomas cause more hyperostosis of MMMDCCXIX) Lateral compartment
surrounding bone i) Transtemporal: lateral, mainly extradural;
MMMDCCIII) Meningiomas sessile, broad base, not anterior limit is intrapetrous ICA; adjuncts used
centric over IAC in combination with other MCF approaches
MMMDCCIV) Dural tail can be present ii) Infratemporal
iii) Transfacial: facial translocation
905) Temporal bone epidermoids iv) Intracranial: temporal craniotomy
MMMDCCV) 1% of all intracranial tumors, 3-4% of CPA
lesions
910) Describe chordoma
MMMDCCVI) Four anatomic groups: middle ear,
MMMDCCXX) Rare slow growing skull base malignancy
perigeniculate, petrous apex (most common),
derived from notochord remnant
cerebellopontine angle
MMMDCCXXI) Histology: physaliferous cells (soap
MMMDCCVII) Entrapped epithelial rests; slow growing,
bubble appearance)
infiltrative & expanding, local inflammatory reaction
MMMDCCXXII) Treatment: surgery,
MMMDCCVIII) Symptoms: imbalance & hearing loss;
radiotherapy for incomplete excision; 20% 5 year
facial weakness & spasm; trigeminal numbness &
survival
pain; very gradual onset
MMMDCCIX) Complete excision nearly impossible, 30%
recurrence

906) Pathogenesis of cholesterol granulomas

MMMDCCX) Obstruction of air cell drainage pathways
Pediatric Otolaryngology MMMDCCXXXI) Most common type of branchial
anomaly, present as either cyst, sinus or fistula
MMMDCCXLVII) Associated with a syndrome in
50-80% of cases, most commonly Stickler & VCF
MMMDCCXXXII) Pathway syndromes
911) Discuss the nerve, muscle, cartilage and artery
i) External opening along anterior border of SCM MMMDCCXLVIII) Airway interventions (a
derivatives of the branchial arches
in lower third of neck progressive sequence)
MMMDCCXXIII) 1st arch structures
ii) Internal opening found in tonsillar fossa, i) Prone positioning
i) Nerve: trigeminal
associated with posterior pillar ii) Nasopharyngeal airway
ii) Muscle: muscles of mastication, TVP,
iii) Penetrates through platysma muscle iii) Endotracheal intubation
mylohyoid, anterior digastric, tensor tympani;
iv) Runs between ECA and ICA iv) Tracheostomy (preferred especially if cleft
sphenomandibular ligament, anterior mallear
v) Runs lateral to CN IX and XII on ascent into palate present)
ligament
oropharynx
iii) Cartilage: malleus, incus, mandible
vi) Exits into the tonsillar fossa 918) Describe the clinical features of Stickler syndrome
iv) Artery: maxillary
MMMDCCXLIX) Autosomal dominant, mutation
MMMDCCXXIV) 2nd arch structures
914) Discuss 3rd branchial anomalies and its associations of COL2A1 gene on chromosome 12, responsible
i) Nerve: facial
MMMDCCXXXIII) Rare abnormalities for type II collagen gene
ii) Muscle: muscles of facial expression,
MMMDCCXXXIV) Also present lower in neck MMMDCCL) Small jaw with Robin sequence & cleft
auricularis, stapedius, posterior digastric,
anterior to SCM palate
stylohyoid
MMMDCCXXXV) Deep to 3rd arch structures – MMMDCCLI) Myopia with retinal detachment &
iii) Cartilage: stapes, lesser cornu and upper body
CN IX, internal carotid cataracts
of hyoid
MMMDCCXXXVI) Superficial to 4th arch MMMDCCLII) Hypermobility & enlarged joints, early
iv) Artery: stapedial
structures – vagus nerve onset arthritis, occ. spondyloepiphyseal dysplasia
MMMDCCXXV) 3rd arch structures
MMMDCCXXXVII) Enters pharynx at thyrohyoid MMMDCCLIII) SNHL or mixed HL in 80%, educationally
i) Nerve: glossopharyngeal
membrane or piriform sinus significant in 15%
ii) Muscle: stylopharyngeus
iii) Cartilage: greater cornu & lower body of hyoid
915) Which skull bones are formed from intramembranous or 919) Discuss achondroplasia
iv) Artery: common and internal carotid
endochondral ossification? MMMDCCLIV) Most common cause of short limb
MMMDCCXXVI) 4th arch structures
MMMDCCXXXVIII) Intramembranous dwarfism
i) Nerve: superior laryngeal nerve
i) Calvarial portions of occipital, temporal, MMMDCCLV) Autosomal dominant, most cases
ii) Muscle: constrictors of pharynx, cricothyroid
parietal, frontal, sphenoid bones spontaneous; due to mutation of FGFR-3 gene
iii) Cartilage: laryngeal cartilages
ii) Ethmoid & anterior concha (4p16.3)
iv) Artery: subclavian on right, arch of aorta on left
iii) Nasomaxillary: nasal, lacrimal, maxillary, MMMDCCLVI) Short stature, shortened limbs, long
MMMDCCXXVII) 6th arch structures
zygomatic, pterygoid, vomer narrow trunk, frontal bossing, midface hypoplasia,
i) Nerve: recurrent laryngeal nerve
iv) Mandible: mandible forms from membranous lumbar lordosis, limited elbow extension, genu
ii) Muscle: intrinsics laryngeal muscles
bone laid down lateral to Meckel’s cartilage, varum, trident hand
iii) Cartilage: laryngeal cartilages
Meckel’s then disappears MMMDCCLVII)Normal cognitive function
iv) Artery: pulmonary artery on right, ductus
MMMDCCXXXIX) Endochondral
arteriosus on left
i) Skull base portions of occipital, temporal, 920) Craniofacial features of Down syndrome
sphenoid & ethmoid bones MMMDCCLVIII) Brachycephaly
912) Discuss the 1st branchial arch cysts
MMMDCCLIX) Flat occiput
MMMDCCXXVIII) Comprise ~1% of all branchial
916) Synchondroses of the pediatric skull base MMMDCCLX) Abnormal small ears
cleft anomalies
MMMDCCXL) Sphenooccipital synchondrosis: principal MMMDCCLXI) Upslanting palpebral fissures
MMMDCCXXIX) Type I
growth center; flexion of flat neonatal skull base into MMMDCCLXII)Epicanthic folds
i) Epidermoid elements only (no cartilage or
a more curved form occurs here as nasomaxillary MMMDCCLXIII) Short small nose
adnexal structures)
complex grows under anterior skull base; fusion MMMDCCLXIV) Midface hypoplasia
ii) Duplication anomaly of the EAC
occurs in midadolescence MMMDCCLXV) Large fissured lips
iii) Medial to concha, extends to postauricular
MMMDCCXLI) Sphenoethmoidal MMMDCCLXVI) Large fissured tongue
crease
MMMDCCXLII)Sphenofrontal MMMDCCLXVII) Dental abnormalities
iv) Lateral to facial nerve, parallel to EAC
MMMDCCXLIII) Intersphenoidal MMMDCCLXVIII) Short neck
v) Cyst, sinus or fistula
MMMDCCXLIV) Frontoethmoidal MMMDCCLXIX) Atlantoaxial subluxation &
MMMDCCXXX) Type II
instability
i) More common than type I
917) Describe the classic triad and pathology of Robin
ii) Ectodermal & mesodermal elements
sequence and airway interventions for it 921) Treacher-Collins syndrome (mandibulofacial dysostosis)
iii) May present in neck, typically at angle of
MMMDCCXLV) Triad of: MMMDCCLXX) Autosomal dominant, 40% will
mandible
i) Retrognathia have family history, other 60% new mutations
iv) Variable relationship to the facial nerve
ii) Glossoptosis MMMDCCLXXI) TCOF1 gene found on
v) End inferior to EAC or into bony/cartilaginous
iii) Cleft palate chromosome 5q (TREACLE gene)
junction
MMMDCCXLVI) Pathology: due to retrognathia MMMDCCLXXII) Malformation of 1st (& 2nd)
which prevents descent of the tongue into the oral branchial arches
913) 7 anatomic relationships of a 2nd branchial arch anomaly
cavity; prevents secondary palate fusion
 MMMDCCLXXIII) Otologic: Malformed ossicles, MMMDCCLXXXVII) Hemifacial macrosomia often MMMDCCXCV) Management of subglottic
auricular deformity, aural atresia, CHL present 30% placed in this category hemangioma
of time, occasional SNHL MMMDCCLXXXVIII) Most cases sporadic, some i) 50% will have a cutaneous hemangioma
i) 50% will have hearing impairment from EAC autosomal dominant transmission reported ii) Depends on size and extent of airway
and/or middle ear malformations compromise; usually present with biphasic
MMMDCCLXXIV) Preauricular fistulas, 926) Clinical differences between hemangiomas and vascular stridor, lesion left posterolateral subglottis
mandibular and malar hypoplasia, antimongoloid malformations iii) Systemic steroids to prevent progression of
palpebral fissures, coloboma of the lower eyelids, MMMDCCLXXXIX) Hemangioma lesion and reduce airway obstruction
may have cleft lip and palate, normal IQ i) Usually not present at birth, appear during first iv) Continuing airway compromise despite
6 weeks of life systemic steroids: intralesional steroids,
922) Apert (acrocephalosyndactyly) and Crouzon (craniofacial ii) Proliferates in first year of life then involutes; interferon-α2a, surgery; safest surgical option
dysostosis) syndromes growth due to endothelial cell hyperplasia is tracheostomy
MMMDCCLXXV) Both autosomal dominant, most iii) 80% isolated lesions, 20% multiple
cases of Apert due to spontaneous mutation iv) 50% involute by 5 years, 70% by 7 years 928) Discuss Kasabach-Merritt syndrome
MMMDCCLXXVI) Both due to mutation of FGFR- v) Appearance depends on depth: superficial MMMDCCXCVI) Up till recently associated with
2 gene (10q26) lesions raised & bright red, deeper lesions hemangioma; skin lesion with red/brown
MMMDCCLXXVII) Common findings more bluish in appearance discoloration that suddenly enlarges into a
i) Craniosynostosis vi) MRI: hyperintense on T2, flow voids present on violaceous plaque
ii) Hypertelorism T1 & T2 MMMDCCXCVII) Characterized by platelet
iii) Exophthalmos vii) Infrequent mass effect on bone, rare sequestration, ecchymosis, no female predominance
iv) Midface hypoplasia hypertrophy MMMDCCXCVIII) Histologic lesion a tufted
v) Mandibular prognathism viii) Complications: ulceration, airway obstruction, angioma or kaposiform hemangioendothelioma
vi) Parrot-beaked nose high output cardiac failure, psychologic MMMDCCXCIX) Management supportive;
vii) Syndactyly and cervical fusion seen in Aperts consequences heparin contraindicated, use of blood products
viii) Cognitive function normal to severe mental MMMDCCXC) Vascular malformation avoided because of increased trapping within lesion;
retardation i) Present at birth and grow with child; growth anemia treated with PRBC’s
due to endothelial hypertrophy; do not involute
923) Pfeiffer’s syndrome ii) Sudden growth seen, due to trauma, infection, 929) Management of vascular malformations
MMMDCCLXXVIII) Similar to Apert’s syndrome but hormonal changes MMMDCCC) Capillary malformations
have digital broadening rather than syndactyly iii) Divided into high flow (AV malformation) and i) Laser therapy the management of choice
low flow (venous, capillary, lymphatic) (argon, pulsed tunable dye)
924) Describe the clinical features of branchiootorenal iv) Low flow lesions can cause bony distortion, ii) Surgical excision possible; watch for
syndrome (Melnick-Fraser syndrome) hypertrophy or hypoplasia; high flow lesions hypertrophy or unpredictable pigmentation
MMMDCCLXXIX) Autosomal dominant, involves can cause destruction, distortion or hypertrophy MMMDCCCI) Venous malformations
8q between D8S87 and D8S165 (EYA1 gene) i) Reassurance the best thing
MMMDCCLXXX) Branchial cleft anomalies 927) Management of hemangiomas ii) Symptomatic lesions: sclerotherapy only or
(63%): cysts or fistulae MMMDCCXCI) 90% observed; other 10% intervention surgery
MMMDCCLXXXI) Otologic malformations: taken because of complications (ulcer/bleeds), MMMDCCCII) Lymphatic malformations
hearing loss (89%), preauricular pits (77%), auricle ophthalmic changes, psychological considerations, i) Nomenclature divided into macrocystic (>1cm)
abnormalities (41%), ossicular & cochlear airway impingement or microcystic (<1cm), correlates with
malformations, lacrimal duct stenosis MMMDCCXCII) Oral corticosteroids mainstay of supramylohyoid (microcystic) or inframylohyoid
i) 2% of children with severe/profound SNHL management; 30-60% will respond, if effective (macrocystic) disease
MMMDCCLXXXII) Renal dysplasia (66%): continue for 8-10 months until involution well ii) Sudden increases in size occur with bleeding
agenesis, polycystic kidneys, duplicated ureters; established or infection of cystic spaces
renal abnormalities identifiable on IVP or renal U/S MMMDCCXCIII) Management of oral iii) MRI findings: septated masses with low
corticosteroid resistant lesions intensity on T1, high intensity on T2 without
925) Describe Goldenhar syndrome (oculoauriculovertebral i) Intralesional corticosteroid: used in small flow voids
spectrum) localized lesions every 6 weeks iv) Surgical resection mainstay of therapy, cold
MMMDCCLXXXIII) Characterized by unilateral ii) Interferon-α2a: inhibits angiogenesis by knife or laser (CO2, Nd:YAG) if oral cavity &
facial asymmetry, unilateral external & middle ear blocking fibroblast growth factor; daily use for tongue; sclerotherapy, I&D, aspiration, radiation
changes, vertebral malformations 9-14 months to prevent relapse, watch for unsuccessful
MMMDCCLXXXIV) Ocular findings: upper lid complications (worst is spastic diplegia) v) OK-432: lyophilized low virulence S. pyogenes
colobomata iii) Surgery: cold knife; CO2 laser the therapeutic used successfully for macrocystic
MMMDCCLXXXV) Otologic findings: mildly option for patients who fail to respond to malformations
deformed ears to anotia, EAC atresia, ossicular corticosteroids MMMDCCCIII) AV malformations
abnormalities MMMDCCXCIV) Photocoagulation: ideal for i) Abnormal communications between arteries &
MMMDCCLXXXVI) Underdevelopment of superficial hemangioma, flashlamp pumped pulsed veins, bypass capillary bed
mandible, orbit, facial muscles, also may have dye laser (585nm) well absorbed by superficial ii) Characteristically a pulsatile mass with an
hemivertebrae of vertebral column lesion associated thrill or bruit, confirmed by present
of a bruit found at auscultation or Dopler
 iii) Complications: skin necrosis, ulceration, MMMDCCCXVIII) Surgical repair approaches MMMDCCCXXXIV) Encephalocele: always has a
bleeding, heart failure i) Transnasal (higher incidence of restenosis and dural connection, transilluminates, positive
iv) MRI: no enhancement on T2, flow voids dilatation) Furstenburg test, associated with meningitis,
present on both T1 & T2 ii) Transpalatal (reserved for older children d/t histologically an ependymal lined sac the
v) Treatment: nothing required for asymptomatic orthodontic growth) communicates with the CSF spaces
lesions; symptomatic lesions require surgery iii) Transantral MMMDCCCXXXV) Dermoid: rare dural connection,
with preoperative embolization and total iv) Transseptal rarely transilluminate, negative Furstenburg test,
resection rarely associated with meningitis
934) What syndromes are associated with choanal atresia? i) Found in midline as a fluctuating cyst with a
930) Describe Sturge-Weber syndrome (AC-ACT TV) sinus tract leading to the skin; epithelium lined,
MMMDCCCIV) Capillary malformation of the ophthalmic MMMDCCCXIX) 50% of all cases associated contains skin appendages
division of the trigeminal associated with vascular with a syndrome ii) 50% penetrate deep to the nasal bones
malformations of the leptomeninges, leads to i) Apert syndrome iii) 33% may connect to the dura
ischemic atrophy and cortical calcification ii) Crouzon disease iv) Treatment: manage any intracranial portion
MMMDCCCV) Clinically causes seizures, focal iii) Treacher-Collins syndrome first; surgical excision through vertical midline
neurologic deficits, developmental delay iv) Trisomy 18 dorsal excision, external rhinoplasty, or
v) Velocardiofacial syndrome bicoronal approach
931) Describe Maffucci syndrome
MMMDCCCVI) Multiple cavernous hemangiomas with 935) Describe the CHARGE syndrome 939) Define the classification of congenital nasal
dyschondroplasia & shortening and deformity of MMMDCCCXX) Coloboma encephaloceles
involved bones MMMDCCCXXI) Heart disease or hearing defect MMMDCCCXXXVI) Encephaloceles 5x more
MMMDCCCVII) Occasional visceral vascular MMMDCCCXXII) Atresia (choanal) common in lumbosacral area
lesions; 25% incidence of chondrosarcoma MMMDCCCXXIII) Retardation of growth MMMDCCCXXXVII) Occipital: most common, ~75%
MMMDCCCXXIV) Genital defects (in males) of cases
932) von Hippel Lindau syndrome MMMDCCCXXV) Endocardial cushion defect or MMMDCCCXXXVIII) Sincipital (frontonasal): ~15%
MMMDCCCVIII) Autosomal dominant ear anomalies & deafness of cases, external lesions, seen over nose, glabella,
MMMDCCCIX) Hemangioblastomas of CNS & retinas, medial canthus, lower forehead; nasofrontal (most
renal cysts/carcinoma, pheochromocytoma, 936) Embryologic spaces & structures of note in glioma & common subtype), nasoethmoidal, nasoorbital
pancreatic cysts, papillary cystademonata of encephalocele formation MMMDCCCXXXIX) Basal (~10%): intranasal
epididymis MMMDCCCXXVI) Anterior neuropore: most distal masses, often not discovered until later in life;
MMMDCCCX) Endolymphatic sac tumors in 11% end of the ectoderm derived neural tube, vulnerable transethmoidal (most common subtype),
to developmental errors sphenoethmoidal, transsphenoidal, sphenoorbital
933) Describe choanal atresia and the parts of the anatomic MMMDCCCXXVII) Foramen cecum: pathway
deformity between frontal and ethmoid bones that usually 940) What is Furstenburg’s sign?
MMMDCCCXI) Incidence 1:5000-8000 births, F:M 2:1 obliterates itself, continuous with the prenasal space MMMDCCCXL) Expansion of a nasal mass with
MMMDCCCXII) 50% have other congenital MMMDCCCXXVIII) Fonticulus nasofrontalis: compression of the IJV’s, usually associated with
abnormalities (75% of bilateral cases associated embryonic space between the frontal and nasal sincipital and basal encephalocele (but not glioma)
with other anomalies) bones
MMMDCCCXIII) 30% bony, 70% mixed bony- MMMDCCCXXIX) Prenasal space: potential 941) Parson’s major criteria for chronic pediatric sinusitis
membranous space during development between the nasal bones MMMDCCCXLI) Chonic nasal obstruction
MMMDCCCXIV) 65-75% unilateral, rest are and the cartilaginous precursors of the septum MMMDCCCXLII) Nasal discharge
bilateral MMMDCCCXLIII) Headache
MMMDCCCXV) Severity of presentation 937) A young child presents with a midline nasal mass. What MMMDCCCXLIV) Chronic cough
depends on whether unilateral or bilateral; bilateral is the differential? MMMDCCCXLV) Behavioral change
atresia presents with immediate cyclical cyanosis MMMDCCCXXX) Dermoid cyst (most common) MMMDCCCXLVI) Halitosis
(cyanosis interrupted by crying spells); unilateral MMMDCCCXXXI) Neurogenic: glioma, MMMDCCCXLVII) Postnasal drainage
atresia can remain hidden for years encephalocele, neurofibroma
MMMDCCCXVI) Four parts to the anatomic MMMDCCCXXXII) Hemangioma 942) What are the most reliable and consistent symptoms of
deformity pediatric sinusitis?
i) Narrow nasal cavity 938) What are the three types of congenital nasal masses of MMMDCCCXLVIII) Nasal airway obstruction
ii) Lateral bony obstruction from pterygoid plate neuroectodermal origin? MMMDCCCXLIX) Purulent nasal discharge
iii) Medial bony obstruction from vomer MMMDCCCXXXIII) Glioma: no dural connection, MMMDCCCL) Headaches
iv) Membraneous obstruction do not transilluminate, negative Furstenburg test, not MMMDCCCLI) Irritability
MMMDCCCXVII) General management approach associated with meningitis, a solid mass of glial MMMDCCCLII) Daytime cough with nighttime
i) Unilateral atresia: nonurgent repair, can wait tissue with a fibrous stalk exacerbation
until ~1 year of age i) 60% external, 30% internal, 10% combined
ii) Bilateral atresia: establish airway & feeding ii) Usually found at the glabella, can present as 943) Indications for CT scanning for pediatric rhinosinusitis
pathway (McGovern nipple, oropharyngeal lateral nasal mass also MMMDCCCLIII) Severe illness or toxic condition
airway; intubation not necessary unless iii) 15% connect with the dura MMMDCCCLIV) Acute RS that does not
mechanical ventilation required) improve with medical therapy in 48-72 hours
 MMMDCCCLV) Immunocompromised host i) Schweckendiek: closure of soft palate only epithelium proportion and decreases respiratory
MMMDCCCLVI) Presence of a suppurative ii) Von Langenbeck proportion
complication other than orbital cellulitis iii) Bardach two flap palatoplasty (for complete CP
repair) 955) Blood supply to the tonsil
944) Viruses most commonly associated with acute iv) Furlow double Z-plasty (for secondary CP MMMDCCCXCV) Facial artery (tonsillar branch,
rhinosinusitis repair) ascending palatine branch)
MMMDCCCLVII) Rhinovirus v) V-Y pushback technique (for secondary CP MMMDCCCXCVI) Dorsal lingual branch of lingual
MMMDCCCLVIII) Influenzae repair) artery
MMMDCCCLIX) Parainfluenza MMMDCCCXCVII) Internal maxillary artery
MMMDCCCLX) Adenovirus 951) Four patterns of velopharyngeal closure (descending palatine, greater palatine artery)
MMMDCCCLXXIX) Coronal (55%, most common) MMMDCCCXCVIII) Ascending pharyngeal artery
945) Bacteriology of acute pediatric sinusitis MMMDCCCLXXX) Sagittal (10-15%, least
MMMDCCCLXI) Aerobes: Pneumococcus, M. common) 956) Four zones of antigen processing in adenotonsillar tissue
catarrhalis, H. influenzae, S. aureus, α-hemolytic MMMDCCCLXXXI) Circular (10-20%) MMMDCCCXCIX) Specialized squamous
Strep, Pseudomonas MMMDCCCLXXXII) Circular with Passavant’s ridge epithelium (dendritic cells)
MMMDCCCLXII) Anaerobes: Peptococcus, (15-20%) MMMCM) Extrafollicular area (T-cells)
Peptostreptococcus, Bacteroides MMMCMI) Mantle zone of lymphoid follicle (mature
952) Describe velocardiofacial syndrome lymphocytes)
946) Bacteriology of chronic pediatric sinusitis MMMDCCCLXXXIII) Autosomal dominant disease, MMMCMII) Germinal center of follicle (B-cells)
MMMDCCCLXIII) Aerobes: S. aureus, S. characterized by abnormal facies, VPI, CLP, and
pneumoniae, H. influenzae cardiac anomalies 957) Definitions of adenotonsillar infectious states
MMMDCCCLXIV) Anaerobes: Prevotella, MMMDCCCLXXXIV) Deletion of 22q11 MMMCMIII) Acute adenoiditis: purulent rhinorrhea,
Porphyromonas, Fusobacterium MMMDCCCLXXXV) Almond shaped palpebral nasal obstruction, fever and otitis media; difficult to
fissures, deficient nasal alae, tubuar nose with differentiate from acute sinusitis
947) Most common bacteria seen in pediatric acute sialadenitis bulbous tip, small mouth MMMCMIV) Recurrent acute adenoiditis: 4+ episodes
MMMDCCCLXV) S. aureus MMMDCCCLXXXVI) Long face with vertical maxillary in a 6-month period
MMMDCCCLXVI) Streptococcus viridans excess, malar flatness, mandibular retrusion MMMCMV) Chronic adenoiditis: persistent nasal
MMMDCCCLXVII) Streptococcus pneumoniae MMMDCCCLXXXVII) Palatal clefting ranges from discharge, malodorous breath, postnasal drip,
MMMDCCCLXVIII) Esherichia coli submucus clefting to overt wide cleft palate with chronic congestion; difficult to differentiate from
MMMDCCCLXIX) Bacteroides melaninogenicus hypernasality chronic sinusitis
MMMDCCCLXX) Streptococcus micros MMMDCCCLXXXVIII) Cardiac anomalies in 80%, MMMCMVI) Obstructive adenoid hyperplasia: triad of
most commonly VSD; other anomalies include right obligate mouth breathing, snoring, hyponasal
948) 3 diagnostic signs of submucous cleft palate sided aortic arch, tetralogy of Fallot, aortic valve speech; rhinorrhea, postnasal drip, nocturnal chronic
MMMDCCCLXXI) Bifid uvula disease cough common but nonspecific
MMMDCCCLXXII) Zona pellucida MMMDCCCLXXXIX) Medial displacement of ICA’s MMMCMVII) Acute tonsillitis: sore throat, fever,
MMMDCCCLXXIII) Notched hard palate present in up to 25% of patients dysphagia, tender cervical adenopathy with
erythematous exudative tonsils
949) Environmental factors contributing to cleft palate 953) Management of velopharyngeal insufficiency (VPI) MMMCMVIII) Recurrent acute tonsillitis: 7 infections in
MMMDCCCLXXIV) Drugs: phenytoin, vitamin A MMMDCCCXC) Medical a year, 5 infections for 2 consecutive years, or 3
derivatives, folic acid antagonists i) Speech therapy infections for 3 consecutive years
MMMDCCCLXXV) Smoking & alcohol use in 1st ii) Prosthetics: palatal lift or obturator MMMCMIX) Chronic tonsillitis: chronic sore throat,
trimester iii) Biofeedback with nasometry malodorous breath, tonsilloliths, peritonsillar
MMMDCCCXCI) Surgical erythema and persistent tender cervical adenopathy
950) Surgical repair of cleft lip & palate i) Pharyngoplasty MMMCMX) Obstructive tonsillar hyperplasia: snoring,
MMMDCCCLXXVI) Lip adhesion: if done, ii) Pharyngeal flaps obstructive disturbances, dysphagia and voice
performed @ 2-4 weeks of age with definitive repair iii) Posterior pharyngeal wall augmentation changes with enlarged tonsils
at 4-6 months of age
MMMDCCCLXXVII) Cleft lip repair: if no 954) Adenoid anatomy 958) Etiology of pseudomembranous tonsillitis
contraindications and no previous lip adhesion, MMMDCCCXCII) Blood supply MMMCMXI) Epstein-Barr virus (mononucleosis)
repair performed at 10-12 weeks; rule of 10’s i) Pharyngeal branch of the internal maxillary MMMCMXII) Candidiasis
i) Straight line closure (rarely used anymore) (major supply) MMMCMXIII) Vincent’s angina
ii) Millard rotation advancement technique ii) Ascending palatine branch of the facial artery MMMCMXIV) Neisseria gonnorheae
iii) Tennison-Randall (single) triangular flap iii) Ascending cervical branch of thyrocervical MMMCMXV) Syphilis
interdigitation trunk MMMCMXVI) Corynebacterium diphtheriae
iv) Bardach (double) triangular flap interdigitation iv) Ascending pharyngeal artery MMMCMXVII) Group A ß-hemolytic Streptococcus
v) Bilateral cleft repair (Millard) MMMDCCCXCIII) Innervation: CNs IX & X
MMMDCCCLXXVIII) Cleft palate repair: performed MMMDCCCXCIV) Histology: ciliated 959) Indications for tonsillectomy
9-12 months up to 18 months of age if child is pseudostratified columnar, stratified squamous and MMMCMXVIII) Infection
growing & gaining weight; restoration of soft palate transitional epithelia present; presence of i) Recurrent acute infections >7 in 1 year, > 5 in 2
sling incorporating tensor and levator palate inflammation increases specialized squamous years, >3 in 3 or more years
 ii)Recurrent acute infections with complications MMMCMXXXIV) Atlantoaxial subluxation MMMCMXLIX) Hypertrophied lymphoid tissue
(cardiac valve disease, febrile seizures) (Grisel’s syndrome): deep calcification of anterior MMMCML) Compliance & elasticity of pharyngeal soft
iii) Chronic tonsillitis associated with halitosis, arch of atlas, laxity of anterior transverse ligament; tissues
persistent sore throat, tender cervical adenitis, Down syndrome children more prone to this MMMCMLI) Facial morphology
unresponsive to medical therapy MMMCMXXXV) Eagle syndrome MMMCMLII) Physiologic changes of pharyngeal
iv) Streptococcus carrier MMMCMXXXVI) Malodorous breath (most dilators during sleep (neuromuscular control)
v) Peritonsillar abscess common complaint)
vi) Tonsillitis with cervical abscess 968) High risk groups for pediatric OSAS
vii) Mononucleosis with obstructing tonsils 963) Risk factors for VPI after adenoidectomy MMMCMLIII) Obesity
unresponsive to therapy MMMCMXXXVII) Occult submucus cleft MMMCMLIV) Craniofacial abnormalities:
MMMCMXIX) Obstruction MMMCMXXXVIII) Family history of clefts achondroplasia
i) Excessive snoring or mouth breathing MMMCMXXXIX) Neuromuscular problems MMMCMLV) Neuromuscular disease: cerebral palsy,
ii) OSA (CNS) Down syndrome
iii) Cor pulmonale MMMCMXL) History of nasal fluid regurgitation MMMCMLVI) Mucopolysaccharidoses: Hunter or Hurler
iv) Failure to thrive & dysphagia syndromes
v) Speech abnormalities 964) Parents of a child with chronic nasal obstruction, purulent
vi) Craniofacial growth abnormalities rhinorrhea, otitis media with effusion, malodorous breath 969) Differences in adult and pediatric OSAS
vii) Occlusion abnormalities and hyponasal speech want surgery. What’s the MMMCMLVII) Snoring uncommon in adults, common in
MMMCMXX) Other diagnosis and what surgery? pediatrics
i) Suspicion of malignancy MMMCMXLI) Hard to tell clinically whether its sinusitis MMMCMLVIII) Mouth breathing more common in
or adenoiditis; perform adenoidectomy first, ~67% of pediatrics
960) Criteria which should suggest an overnight stay children will have resolution MMMCMLIX) Obesity a more common factor in adults
posttonsillectomy MMMCMLX) Failure to thrive & enuresis seen in
MMMCMXXI) OSA or other craniofacial abnormalities 965) Long question on peritonsillar abscess with initial mgmt pediatrics
MMMCMXXII) Emesis or hemorrhage (which fails), subsequent mgmt, complications if MMMCMLXI) Daytime somnolence more often seen in
MMMCMXXIII) Under 3 years of age untreated 5 adults, behavior changes seen in pediatrics
MMMCMXXIV) Patient lives greater than 60 minutes away MMMCMXLII) Thought to be secondary to an infection of (hyperactivity, attention deficit, aggression)
from hospital a peritonsillar salivary gland (Weber gland) MMMCMLXII) Nighttime arousals uncommon in
MMMCMXXV) Poor socioeconomic class which may MMMCMXLIII) Symptoms: severe sore throat, pediatrics
predispose to neglect odynophagia, drooling, muffled voice, trismus,
MMMCMXXVI) Any other medical comorbidity which referred otalgia 970) Criteria for abnormal polysomnogram in pediatric OSAS
requires attention postoperatively (diabetes, MMMCMXLIV) Initial management of peritonsillar MMMCMLXIII) Apnea index >1 (a significant apnea
seizures, Down syndrome, asthma, cardiac disease, abscess defined as one lasting longer than two consecutive
etc) i) Hydration breaths)
ii) Analgesia MMMCMLXIV) Oxygen desaturation to less than 92%
961) Indications for adenoidectomy iii) Incision & drainage or needle aspiration (75% MMMCMLXV) Oxygen desaturation greater than 4%
MMMCMXXVII) Infection effective) more than 3 times an hour, or associated with a
i) Recurrent/chronic adenoiditis iv) Antibiotics, either parenteral, enteral, or change in heart rate >25%
ii) Chronic otitis media with or without effusion combined MMMCMLXVI) Elevated end tidal CO2 >50mmHg >8% of
(kids >4 years) MMMCMXLV) Subsequent management total sleep time, or >45mmHg >60% of total sleep
MMMCMXXVIII) Obstruction i) CT scan time
i) Adenioid hyperplasia with chronic nasal ii) Reincision & drainage
obstruction or obligate mouth breathing iii) Quinsy tonsillectomy 971) Indications for PSG postsurgery for pediatric OSAS
ii) OSA or sleep disturbances MMMCMXLVI) Complications MMMCMLXVII) Persistent snoring
iii) Associated with cor pulmonale, FTT i) Airway obstruction MMMCMLXVIII) Preoperative FTT or cor
iv) Craniofacial growth abnormalities ii) Dehydration pulmonale
v) Occlusion abnormalities iii) Sepsis MMMCMLXIX) Age <1 year
vi) Speech abnormalities iv) Spread to other spaces
vii) Swallowing abnormalities v) Carotid artery erosion 972) Identify the transmission, defect and symptoms of
MMMCMXXIX) Other vi) IJV thrombophlebitis (Lemierre’s syndrome) Hurler’s syndrome
i) Suspected neoplasm MMMCMLXX) Autosomal recessive, deficiency of α-1-
ii) Chronic sinusitis 966) Causes of unilateral tonsillar hyperplasia iduronidase which breaks down heparan-, dermatan-
MMMCMXLVII)Neoplastic: lymphoma and keratan-sulfates; visceromegaly, macroglossia,
962) Complications of adenotonsillectomy MMMCMXLVIII) Infectious macrocephaly, progressive neurologic dysfunction;
MMMCMXXX) Postoperative hemorrhage: 0.5-10% i) Mycobacterium tuberculosis death in 1st decade
MMMCMXXXI) Postoperative pulmonary edema & ii) Atypical mycobacteria
hypoxemia: loss of auto-PEEP from chronic iii) Actinomycosis 973) Hunter’s syndrome
obstruction, loss of hypercapneic respiratory drive iv) Fungal MMMCMLXXI) X-linked disorder
MMMCMXXXII) Velopharyngeal insufficiency MMMCMLXXII) A mucopolysaccharidosis,
MMMCMXXXIII) Nasopharyngeal stenosis 967) Factors influencing pediatric OSAS involving lack of beta-galactosidase
 MMMCMLXXIII) Facies: macroceophaly, broad ii) Diffuse, small cleaved ii) Bone
face, low nasal bridge iii) Diffuse, mixed iii) Bone marrow
MMMCMLXXIV) Death usually occurs from iv) Diffuse large cell (most common in H&N)
infiltrative CMO & valvular disease leading to CHF MMMCMXCV) High grade 984) Rhabdomyosarcoma histolopathology
i) Small noncleaved MMMMXIV) Embryonal (75%): most common in
974) Differential diagnosis of small blue cell malignancies of ii) Immunoblastic infants and children; spindle shaped cells with
childhood iii) Lymphoblastic eosinophilic cytoplasm; best prognosis of all the
MMMCMLXXV) Neuroblastoma histologic subtypes
MMMCMLXXVI) Lymphoma 980) Staging of non-Hodgkin’s disease i) Botryoid variant: forms condensed layer
MMMCMLXXVII) PNET MMMCMXCVI)Single LN region or ES site with exclusion beneath mucosa, produces polypoid lesion
of mediastinum and abdomen MMMMXV) Alveolar (20%): most common in
975) Differential diagnosis of aural polyp in pediatrics MMMCMXCVII) Single ES site with regional adolescents; small round cells separated by fibrous
MMMCMLXXVIII) Cholesteatoma node involvement; 2+ LN regions or ES sites on septae into alveolar groups
MMMCMLXXIX) Eosinophilic granuloma same side of diaphragm MMMMXVI) Pleomorphic: most common in adults
MMMCMLXXX) Rhabdomyosarcoma MMMCMXCVIII) Nodal regions or ES sites on
both sides of diaphragm; any intrathoracic, 985) TNM pretreatment staging for rhabdomyosarcoma from
976) Rye classification of Hodgkin’s lymphoma paraspinal, epidural tumor IRS-IV
MMMCMLXXXI) Lymphocyte predominant (2- MMMCMXCIX)Disseminated disease or any of above MMMMXVII) T staging
10%): rare Reed-Sternberg cells, favorable with initial involvement of CNS, bone marrow, or both i) T1: confined to anatomic site of origin
prognosis ii) T2: extension
MMMCMLXXXII) Mixed cellularity (20-40%): 981) Describe the high-grade NHL lesions iii) A: =<5cm in diameter
pleomorphic lymphocytes, more numerous RS cells MMMM) >90% of children have high grade lesions iv) B: >5cm in diameter
MMMCMLXXXIII) Nodular sclerosis (40-80%): MMMMI) Burkitt lymphoma (small noncleaved): MMMMXVIII) N staging
nodules of lymphoid infiltrates, lacunar variants of diffuse B-cell malignancy, classic starry sky pattern i) N0: not clinically involved
RS cells of phagocytic histiocytes and tumor cells ii) N1: clinically involved
MMMCMLXXXIV) Lymphocyte depleted (2-15%): MMMMII) Lymphoblastic: immature T-cell origin, iii) Nx: clinical status unknown
paucity of lymphocytes, diffuse fibrosis and bizarre small lymphoblasts with round/convoluted nuclei, MMMMXIX) M staging
RS cells; worse prognosis distinct nuclear membranes, basophilic cytoplasm i) M0: no distant metastases
MMMMIII) Large cell: heterogeneous group of ii) M1: distant metastasis
977) Ann Arbor staging of Hodgkin’s lymphoma lymphocytic & histiocytic tumors; 80% of adults are MMMMXX) Stage
MMMCMLXXXV) Single LN region or B-cell in origin; in children equal numbers originate i) I: Head and neck; T1 or T2, a or b; any N; M0
extralymphatic site (IE) from T-cell, B-cell or indeterminate origin ii) II: Parameningeal; T1 or T2, a; N0 or Nx; M0
MMMCMLXXXVI) 2+ LN regions or EL sites (IIE) iii) III: Parameningeal; T1 or T2, b; N0, N1, or Nx;
on same side of diaphragm 982) Discuss the clinical assessment for non-Hodgkin’s M0
MMMCMLXXXVII) Nodal regions, EL sites (IIIE), lymphoma iv) IV: All sites; T1 or T2, a or b; N0 or N1; M1
or spleen involvement (IIIS) on both sides of MMMMIV) History
diaphragm MMMMV) Physical exam with direct laryngoscopy 986) 4 commonest congenital midline masses
MMMCMLXXXVIII) Disseminated disease MMMMVI) CBCD and LFT’s MMMMXXI) Thyroglossal cyst
MMMCMLXXXIX) A (absence) or B (presence) of: MMMMVII) CT chest MMMMXXII) Hemangioma
unexplained weight loss >10% of total body weight, MMMMVIII) Barium swallow (3-11% of patients with MMMMXXIII) Dermoid cyst
unexplained fever >38, night sweats Waldeyer ring lymphoma will have an associated GI MMMMXXIV) Thymic cyst
lesion) MMMMXXV) Cystic hygroma
978) Treatment of Hodgkin’s lymphoma MMMMIX) Bone marrow biopsy (18% of patients with MMMMXXVI) Plunging ranula
MMMCMXC) Early disease (stage I & IIA): external extranodal H&N lymphoma will have involvement) MMMMXXVII) Teratoma
beam radiation, 10-year survival 90%, 10-year MMMMX) Lumbar puncture (for patients at risk of
relapse free survival 75-80% CNS involvement: high grade lymphoma, 987) Sistrunk procedure
MMMCMXCI) Advanced disease: combination intermediate grade lymphoma of the paranasal MMMMXXVIII) For thyroglossal duct cyst excision;
chemotherapy; complete response rate 44-87%, sinuses, bone marrow, testes, paraspinal areas) excision of cyst, surrounding tissue, central portion
long term disease free survival rate 50% of hyoid given variability of tract pathway
MMMCMXCII) Children: combined modality therapy 983) Most common primary sites in the head and neck for
equally effective while causing less growth rhabdomyosarcoma, most common metastatic sites 988) Atypical mycobacterial infection
impairment MMMMXI) 35-40% of all cases occur in the head and MMMMXXIX) Childhood disease
neck MMMMXXX) No pulmonary involvement
979) Working classification of non-Hodgkin’s MMMMXII) Sites in descending order MMMMXXXI) Drug therapy ineffective (Biaxin may be
MMMCMXCIII) Low grade i) Orbit effective)
i) Small lymphocytic ii) Nasopharynx MMMMXXXII) Incision and drainage may cause
ii) Follicular small cleaved iii) Middle ear/mastoid fistulization
iii) Follicular mixed iv) Sinonasal cavity MMMMXXXIII) Nontender, slowly enlarging
MMMCMXCIV)Intermediate grade MMMMXIII) Metastatic sites MMMMXXXIV) Skin fixation common
i) Follicular large i) Lungs MMMMXXXV) Few systemic effects
 MMMMXXXVI) Curretage treatment for neck masses i) Severe stridor with FTT
996) Location of stridor by its pattern ii) Obstructive apnea
989) Differences between the pediatric & adult larynx MMMMLXIV) Inspiratory: dynamic supraglottis and iii) Weight loss
MMMMXXXVII) Pediatric larynx higher in neck glottis iv) Severe chest deformity
(C2 vs C6) MMMMLXV) Biphasic: subglottis and cervical trachea v) Cyanotic attacks
MMMMXXXVIII) Epiglottis curved/omega MMMMLXVI) Expiratory: fixed intrathoracic trachea vi) Pulmonary hypertension
shaped, in contact with soft palate vii) Cor pulmonale
MMMMXXXIX) Thyroid cartilage oblique, no defining 997) Stridor history mnemonic viii) Desaturation documeted by hospital studies
angle MMMMLXVII) S: parents’ subjective impression MMMMXCII) Interventions
MMMMXL) Infant vocal cords 4-4.5mm long at birth, MMMMLXVIII) P: progression of obstruction over time i) Division of aryepiglottic fold
adults 14-23mm MMMMLXIX) E: eating/feeding difficulties ii) Partial epiglottis amputation
MMMMXLI) Infant true vocal cord 50% composed of MMMMLXX) C: cyanotic spells iii) Epiglottopexy with glossoepiglottic adhesion
vocal process of arytenoid, in adults 25-33% MMMMLXXI) S: sleep disordered breathing iv) Removal of redundant supraarytenoid mucosa
MMMMXLII) Infant subglottis narrowest portion of MMMMLXXII) R: radiographics that detect a specific and lateral borders of epiglottis
infant airway, 4.5-7mm in a full term infant abnormality v) Removal of cuneiform & corniculate cartilages
MMMMXLIII) Circumferential mucosal edema in an vi) Tracheostomy
infant narrows the subglottis by >60% 998) When is endoscopic examination indicated in pediatric
stridor? 1004) Describe Beckwith-Wiedemann syndrome
990) Radiographic clues to glottic obstruction on inspiratory MMMMLXXIII) Severe stridor MMMMXCIII) Macroglossia, omphalocele,
films MMMMLXXIV) Progressive stridor visceromegaly, cytomegaly of adrenal cortex
MMMMXLIV) Dilated hypopharynx MMMMLXXV) Stridor associated with unusual features: MMMMXCIV) “Overall growth syndrome”, sporadic
MMMMXLV) Indistinct vocal cords (in infectious cyanotic attacks, apneic attacks, dysphagia, occurrence
processes) aspiration, failure to thrive, radiologic abnormality MMMMXCV) Macroglossia may cause airway
MMMMXLVI) Collapse of subglottis on insipiration, MMMMLXXVI) Stridor causing undue parental anxiety obstruction or chronic alveolar hypoventilation
dilation on expiration
MMMMXLVII) Steeple sign (in infectious processes) 999) What pediatric airway abnormalities are improved in the 1005) Describe the classification of the cleft larynx
prone position? MMMMXCVI) Seen in patients with VATER and G
991) Embryology of tracheoesophageal formation MMMMLXXVII)Laryngomalacia syndromes
MMMMXLVIII) Day 20: appearance of median pharyngeal MMMMLXXVIII) Pierre-Robin sequence i) Type I: supraglottic interarytenoid cleft above
groove MMMMLXXIX) Vascular compression level of vocal cords
MMMMXLIX) Day 21: esophagus appears as a distinct MMMMLXXX) Mediastinal mass ii) Type II: partial cricoid cleft, extends below level
entity of vocal cords and partially through the cricoid
MMMML) Day 22: pharynx, laryngotracheal sulcus, 1000) Clinical characteristics of laryngomalacia lamina
pulmonary primordium appear as distinct entities MMMMLXXXI) Variable inspiratory stridor: begins in first iii) Type III: total cricoid cleft with/without extension
MMMMLI) Day 24: right & left lungs divide few days/weeks after birth, worse with crying, into cervical tracheoesophageal wall
MMMMLII) Day 26: digestive & respiratory tubes feeding, or supine position with H&N flexed, better iv) Type IV: laryngotracheoesophageal cleft
pursue independent courses when prone or with H&N extended
MMMMLIII) Day 28: trachea identifiable MMMMLXXXII)Signs of intermittent upper airway 1006) Describe cri-du-chat syndrome
obstruction MMMMXCVII) Partial deletion of 5p
992) Differential diagnosis of a pediatric base of tongue mass MMMMLXXXIII) Normal cry MMMMXCVIII) Congenital high-pitched stridor with
MMMMLIV) Thyroglossal duct cyst MMMMLXXXIV) Normal general health and elongated endolarynx with floppy epiglottis, triangular
MMMMLV) Lingual thyroid gland development shaped posterior larynx on phonation
MMMMLVI) Vallecular cyst MMMMXCIX) Microcephaly, hypertelorism, generalized
1001) Pathology of laryngomalacia hypotonia, severe MR, low slung ears
993) Pediatric patient with a base of tongue mass. What three MMMMLXXXV) Not known with certainty
tests would you perform and why? MMMMLXXXVI) Abnormal flaccidity of laryngeal 1007) Differential diagnosis of unilateral & bilateral vocal
MMMMLVII) CT scan to define margins of the mass tissues and incoordination of the supraglottic cord palsy in pediatrics
MMMMLVIII) FNAB for tissue diagnosis cartilage and mucosa of the arytenoids, aryepiglottic MMMMC) >50% of pediatric palsies will be bilateral
MMMMLIX) TSH, T3/T4: establish thyroid function folds, epiglottis MMMMCI) Differential
MMMMLX) 131
I scan: to rule out lingual thyroid, i) Idiopathic (36%)
identify other foci of functioning thyroid tissue 1002) Factors influencing development of laryngomalacia ii) Birth trauma (19%)
MMMMLXXXVII) Shortened aryepiglottic folds iii) Neurologic disease (18%)
994) 9 wk baby with biphasic stridor x 2 weeks, level of MMMMLXXXVIII) Anterior cuneiform cartilage (1) Meningomyelocele with Arnold-Chiari
obstruction and most likely dx collapse malformation & hydrocephalus (14%)
MMMMLXI) Glottis or subglottis MMMMLXXXIX) Immature neuromuscular (2) Hydrocephalus
MMMMLXII) Most likely diagnosis is hemangioma control (3) Cerebral palsy
MMMMXC) GERD (4) Hypoxic encephalopathy
995) Baby inspiratory stridor worse with crying and supine 6 (5) Leukodystrophy
wks old 1003) Indications & surgeries for severe laryngomalacia (6) Generalized benign hypotonia
MMMMLXIII) Laryngomalacia, subglottic stenosis MMMMXCI) Indications (7) Arthrogryposis multiplex congenita
 iv) Other trauma (11%) distal multisite spread of disease, rapid regrowth i) Normal shape
v) Malignant disease (1%) with airway compromise (1) Small for infant’s size
(1) Brainstem lesions i) Interferon therapy: most common, exact ii) Abnormal shape
vi) Familial disease (1%) mechanism unknown (1) Large anterior lamina
vii) Other reasons: Mobius syndrome, Charcot- ii) Autogenous vaccine (2) Large posterior lamina
Marie Tooth iii) Photodynamic therapy (3) Generalized thickening
viii) Drugs: vinca alkaloids (neurotoxicity) iv) Indole-3-carbamol diet supplementation: found (4) Elliptical shape
in cruciferous vegetables (5) Submucus cleft (incomplete laryngeal
1008) 2-year-old, Arnold-Chiari malformation with v) Antivirals cleft)
respiratory distress and poor feeding, 3 ENT causes (1) Ribavirin: used in RSV pneumonia, some (6) Other congenital cricoid stenosis
MMMMCII) Herniation of the cerebellum through the promise for RRP treatment iii) Trapped first tracheal ring
foramen magnum (2) Acyclovir MMMMCXXVII) Combined stenosis
MMMMCIII) Stages (3) Cidofovir
i) Type I: protrusion of cerebellar tonsils vi) Mitomycin C 1016) Classification systems of subglottic stenosis
ii) Type II: protrusion of inferior cerebellar vermis vii) Mumps vaccine MMMMCXXVIII) Myer-Cotton original article
iii) Type III: bony occipital defect with descent of i) I - <50%
entire cerebellum 1011) Neonatal tracheostomy safety factors intraoperatively ii) II – 51-70%
iv) Type IV: cerebellar hypoplasia and postoperatively iii) III – 71-99%
MMMMCIV) ENT manifestations (CN IX-XII difficulties) MMMMCXIII) Stay sutures in tracheal incision iv) IV – complete obliteration
i) Bilateral vocal cord paralysis MMMMCXIV) Placement of ETT before performing MMMMCXXIX) Cummings
ii) Poor feeding tracheotomy i) I - <70%
iii) Aspiration MMMMCXV) Keep NG tube in situ to prevent mistaking ii) II – 70-90%
esophagus for trachea iii) III - >90%, visible lumen
1009) Etiology, symptoms, and common sites of lesion for MMMMCXVI) Postoperative observation in PICU iv) IV - Obliterated lumen
recurrent respiratory papillomatosis MMMMCXVII) Tracheostomy set at the bedside
MMMMCV) Etiology: HPV infection (6 & 11) MMMMCXVIII) Extension of neck while applying ties 1017) Pediatric bronchoscope sizes
MMMMCVI) Vertical transmission from mother during MMMMCXIX) Do not tack skin edges together to avoid Size Length ID OD Age
parturition (risk 1:80-1:500) subcutaneous emphysema 2.5 20 3.5 4.2 Preemie
MMMMCVII) Types 3.0 20/26 4.3 5.0 0-3mo.
i) Juvenille onset (<12 years): more common & 1012) What are the dimensions of the normal full term
3.5 20/26/30 5.0 5.7 3-18mo.
more aggressive, typically diagnosed by 2-4 neonatal subglottis? What is the definition of a narrowed
3.7 26/30 5.7 6.4 1-3yr
years subglottis in a full-term neonate?
ii) Adult onset (>12 years): peaks between 20-40 MMMMCXX) 4.5-5.5mm; premature infants normally 4.0 26/30 6.0 6.7 3-5yr
years ~3.5mm 5.0 30 7.1 4.8 5-10yr
MMMMCVIII) Symptoms: triad of progressive MMMMCXXI) Anything less than 4mm in a full-term 6.0 30/40 7.5 8.2 >10 yrs
hoarseness, stridor & respiratory distress; dysphonia neonate or 3.5mm in a preemie is narrowed 6.5 43 8.5 9.2 Adult
MMMMCIX) Preferential sites of lesion: junction of
squamous epithelium with respiratory epithelium 1013) What percentage reduction of area occurs when the 1018) Surgical treatment of subglottic stenosis
i) Limen vestibuli subglottic airway diameter of a full-term neonate is MMMMCXXX) Endoscopic: for grade I/II lesions without
ii) Nasopharyngeal surface of soft palate reduced by 1mm? factors predisposing to failure
iii) Midline of laryngeal surface of epiglottis MMMMCXXII) Airway area drops ~40% or to 60% of its i) Laser: success rates 66-80%
iv) Upper & lower ventricle margins original area ii) Dilation
v) Undersurface of the vocal cords iii) Cryosurgery
vi) Carina 1014) What are the causes of subglottic stenosis? iv) Division
vii) Bronchial spurs MMMMCXXIII) Congenital v) Micro trapdoor flap
MMMMCXXIV) Acquired vi) Cold knife
1010) Treatment modalities for RRP i) Trauma: external (clothesline, MVA) vs. internal MMMMCXXXI) Failed extubation stenosis
MMMMCX) Tracheostomy associated with increased (>90%, most commonly due to intubation) i) Cricoid split
risk of distal spread, avoid unless absolutely ii) Chronic infection ii) Tracheostomy
necessary iii) Chronic inflammatory disease: Wegener’s, MMMMCXXXII) Grade III/IV lesions
MMMMCXI) Surgical debulking the standard of care: SLE, relapsing polychondritis, etc. i) Laryngotracheal reconstruction
remove as much disease as possible, preserve iv) Neoplastic disease (1) Anterior +/- posterior split with stenting
normal structures (2) Anterior +/- posterior split with
i) Laser laryngoscopy 1015) Histopathologic classification of congenital subglottic augmentation
ii) Microlaryngoscopy with cold knife or stenosis ii) Cricotracheal resection: limited to patients with
microdebrider MMMMCXXV) Soft tissue purely subglottic/tracheal lesions with a normal
iii) Cryosurgery i) Granulation tissue lumen of at least 10mm below glottis
MMMMCXII) Adjuvant therapy: 10% of patients will ii) Submucosal gland hyperplasia
require some form; criteria include >4 surgeries/year, iii) Submucosal fibrosis 1019) Factors likely to indicate open subglottic stenosis
MMMMCXXVI) Cricoid cartilage deformity repair vs. endoscopic approach
 MMMMCXXXIII) Circumferential cicatricial MMMMCLX) Keloid formation 1029) Indications for surgical treatment for compression
scarring MMMMCLXI) Severely altered anatomy by stenosis or due to vascular anomalies
MMMMCXXXIV) Abundant scar greater than 1 surgery MMMMCLXXXVIII) Absolute
cm in height MMMMCLXII) Unstable cartilage grafts i) Reflex apnea: reflex respiratory arrest from
MMMMCXXXV) Significant loss of cartilaginous MMMMCLXIII) Lack of airway wall rigidity vagal stimulation
framework MMMMCLXIV) Posterior cricoid split without cartilage ii) Failure of medical management of severe
MMMMCXXXVI) Previous history of severe grafting respiratory distress after 48 hours
bacterial infection associated with tracheostomy iii) Prolonged intubation
MMMMCXXXVII) Posterior glottic stenosis with 1025) Name the various stents used in pediatric airway MMMMCLXXXIX) Relative
arytenoid fixation reconstruction i) Repeated URTI episodes
MMMMCXXXVIII) Failure of previous endoscopic MMMMCLXV) Finger cot ii) Exercise intolerance
procedures MMMMCLXVI) Endotracheal tube iii) Significant failure to thrive & dysphagia
MMMMCXXXIX) Combined laryngotracheal MMMMCLXVII) Montgomery laryngeal stent or iv) Coexisting pathology: subglottic stenosis,
stenosis T-tube asthma, CF, or previous TEF repair
MMMMCXL) Exposure of cartilage or perichondrium MMMMCLXVIII) Polymeric silicone sheet rolls
during CO2 laser excision predisposing to MMMMCLXIX) Aboulker prosthesis 1030) Symptoms, signs, management of postobstructive
perichondritis and chondritis MMMMCLXX) Cotton-Lorenz stent pulmonary edema
MMMMCXC) Clinical: hypoxemia, pink frothy
1020) Bogdasarian classification of adult posterior glottic 1026) Name the most common GER related laryngeal secretions, bilateral end expiratory wheezing with
stenosis disorders in pediatrics rales, radiographic findings consistent with
MMMMCXLI) Interarytenoid adhesion with posterior MMMMCLXXI) Recurrent croup increased pulmonary markings & fluid overload
sinus tract MMMMCLXXII) Laryngospasm MMMMCXCI) Treatment: fluid restriction, diuretics,
MMMMCXLII) Posterior commisure stenosis MMMMCLXXIII) Laryngomalacia continuous positive airway pressure
MMMMCXLIII) Posterior commissure stenosis with MMMMCLXXIV) Hoarseness
unilateral cricoarytenoid ankylosis MMMMCLXXV) Subglottic stenosis 1031) Discuss TEF types, presentation, investigations,
MMMMCXLIV) Posterior commissure stenosis with MMMMCLXXVI) Aspiration interventions
bilateral cricoarytenoid ankylosis MMMMCLXXVII) Chronic cough MMMMCXCII) Present with immediate feeding problems
and aspiration
1021) Indications for pediatric/neonatal cricoid split 1027) What anatomic structures routinely cause MMMMCXCIII) Investigations: inability to pass a feeding
MMMMCXLV) 2 or more failed extubations secondary to compression of the esophagus? tube; x-rays reveal a curled tube in the pharynx and
laryngeal pathology MMMMCLXXVIII) Cricopharyngeus an air bubble in the stomach; fluoroscopy;
MMMMCXLVI) Weight > 1500g MMMMCLXXIX) Aortic arch endoscopy the mainstay
MMMMCXLVII)No assisted ventilation for 10 days before MMMMCLXXX) Left mainstem bronchus MMMMCXCIV)Types
evaluation MMMMCLXXXI) Lower esophageal sphincter i) Esophageal atresia (EA) & distal TEF (85%)
MMMMCXLVIII) Supplemental oxygen ii) Isolated EA (10%)
requirements <30% 1028) What are the most common congenital vascular iii) Isolated true TEF (H-type, 4%)
MMMMCXLIX) No CHF for 1 month prior to evaluation anomalies that can cause tracheomalacia? iv) EA with proximal TEF (0.5-1%)
MMMMCL) No acute URTI/LRTI MMMMCLXXXII) Inominate artery compression v) EA with double TEF (0.5)
MMMMCLI) No antihypertensive medications for 10 i) Most common vascular anomaly causing MMMMCXCV) Management: surgical correction, dilation
days before evaluation compression of strictures
ii) Arises more medially than normal and causes
1022) Indications for laryngotracheal reconstruction with anterior compression of the trachea 1032) Describe the components of VATER syndrome?
division of the posterior cricoid lamina MMMMCLXXXIII) Double aortic arch MMMMCXCVI)V: Vertebral/vascular anomalies
MMMMCLII) Combined posterior glottic and subglottic i) Most common true symptomatic vascular ring MMMMCXCVII) A: Anal atresia
stenosis MMMMCLXXXIV) Right aortic arch with left MMMMCXCVIII) T: Tracheal anomalies: TE
MMMMCLIII) Moderate subglottic and upper tracheal ligamentum arteriosum fistula
stenosis when there is loss of cartilaginous support MMMMCLXXXV) Anomalous right subclavian MMMMCXCIX)E: Esophageal anomalies: distal stenosis
MMMMCLIV) Complete glottic stenosis artery or agenesis
MMMMCLV) Complete subglottic stenosis i) Dysphagia lusoria; artery arises from left MMMMCC) R: Renal/radial bone anomalies
descending aorta MMMMCCI) VACTERL: C indicates cardiac anomalies
1023) Indications for cartilage grafting in the posterior ii) Passes between trachea & esophagus (15%) (PDA, valve problems); L indicates limb anomalies
glottis and subglottis or behind the esophagus (85%) (extra digits, shortened limbs)
MMMMCLVI) Posterior glottic or subglottic stenosis MMMMCLXXXVI) Pulmonary artery sling
MMMMCLVII) Isolated subglottic shelves i) Left 6th arch resorbs, left pulmonary artery 1033) Tracheal causes of stridor
MMMMCLVIII) Circumferential subglottic stenosis arises as a collateral off the right pulmonary MMMMCCII) Tracheomalacia
MMMMCLIX) Total or near total obstruction at the glottic artery and passes between esophagus & MMMMCCIII) Vascular compression
or subglottic level trachea MMMMCCIV) TE fistula
MMMMCLXXXVII) Pulmonary artery dilation MMMMCCV) Stenosis
1024) Indications for long term stenting in pediatric airway MMMMCCVI) Hemangioma
reconstruction MMMMCCVII) Tracheal cyst
 MMMMCCVIII) Tracheal agenesis MMMMCCXXVI) If evaluation starts >48 hours ii) URI prodrome in children usually <6, fever,
MMMMCCIX) Tracheal bronchus postingestion, barium swallow as initial evaluation as sore throat, progressive dysphagia, drooling
esophagoscopy may cause iatrogenic perforation; iii) Diagnosed on lateral soft tissue x-ray:
1034) Surgical management of tracheal stenosis: most useful role is to verify perforation or identify subcutaneous gas, widening of prevertebral
procedures, complications stricture formation tissues (>2x diameter of C2 body 90%
MMMMCCX) Endoscopic approach MMMMCCXXVII) Definitive management sensitive); CT scan
i) Cold knife/laser excision i) Observation for grade 1 & 2 lesions iv) Management: secure airway, IV antibiotics,
ii) Stents ii) Stenting with NGT if risk of stricture possible OR drainage (transoral vs.
MMMMCCXI) Open approaches iii) Thoracotomy for mural exam if difficult to transcervical)
i) Tracheoplasty: rib cartilage, pericardium determine transmural injury
ii) Wedge resection iv) Esophagectomy (blunt vs. thoracotomy) 1038) Pediatric otologic development
iii) Segmental resection MMMMCCXXXII) Pinna
iv) Slide tracheoplasty 1037) What is the differential diagnosis of pediatric upper i) Adult configuration and location at birth; near
MMMMCCXII) Complications airway infections? adult size at 4-5 years, full size by 9 years
i) Granulation tissue MMMMCCXXVIII) Laryngotracheitis (croup) MMMMCCXXXIII) Tympanic membrane
ii) Anastomotic dehiscence i) Caused by parainfluenza; also influenza, RSV, i) Adult sized at birth but horizontal because of
iii) RLN damage measles, adenovirus, varicella, HSV I incomplete ossification of EAC; vertical position
iv) Infection ii) URI prodrome, slow onset, affects 6 months – reached by 2 years
v) Fistulization 3 years, variable/minimal fever, hoarse with MMMMCCXXXIV) Eustachian tube
barking cough, can develop respiratory difficulty i) -~50% adult length at birth, almost horizontal
1035) Agents responsible for caustic ingestion and their with inspiratory stridor (10 degrees), enters nasopharynx @ hard
damage pattern iii) Diagnosis: clinical; radiographic “steeple sign” palate
MMMMCCXIII) Corrosives or acids: pH <7, cause on AP views ii) -by 5-7 years lateral portion rises, tube
coagulative necrosis, forms a superficial coagulum iv) Treatment: expectant lengthens & widens, enters nasopharynx at
and prevents deeper damage (1) Humidification inferior turbinate level
MMMMCCXIV)Caustics or bases: pH >7, cause (2) Racemic epinephrine, 0.5ml of 2.25% MMMMCCXXXV) Ossicles & petrous temporal
liquefactive necrosis, causes early disintegration of solution diluted in 3ml saline bone adult sized at birth
tissues with deep penetration into tissues (3) Steroids: controversial MMMMCCXXXVI) Mastoid
MMMMCCXV) Bleaches: ph ~7, eg. sodium hypochlorite, (4) Intubation if medical therapy fails, use i) Antrum present at birth, increases in size
esophageal irritants tube 0.5mm smaller than estimated, during 1 year, pneumatization continues into
st

extubate when air leak detected childhood

1036) Initial management strategy for caustic ingestions MMMMCCXXIX) Supraglottitis (epiglottitis) ii) Fully developed mastoid & styloid by 3 years
MMMMCCXVI)Presence of oral injury cannot accurately i) Caused by HIB, also GABHS, Staph,
predict presence or absence of more distal pneumococcus, klebsiella, H. parainfluenzae 1039) Relevant eustachian tube anatomy
involvement ii) Mild URI prodrome, rapid onset of high fever, MMMMCCXXXVII) 31-38mm long in adults,
MMMMCCXVII) Do not induce vomiting or give toxic symptoms, drooling, dysphagia; affects ~18mm long in infants
neutralizing agents children 1-8 years MMMMCCXXXVIII) 1/3 bony, 2/3 cartilaginous
MMMMCCXVIII) Judicious dilution with water or iii) Diagnosis: history, clinical presentation, do not MMMMCCXXXIX) Wide at both ends, narrow in
milk up to 15ml/kg agitate child; radiographics only if diagnosis is midportion at the isthmus (1x2mm wide)
MMMMCCXIX)NPO in question MMMMCCXL) Lateral end 4mm above floor of
MMMMCCXX) IV fluids iv) Management: OR intubation, rigid/flexible epitympanum; relatively horizontal, meets
MMMMCCXXI)Steroids: most useful for grade 2 injuries bronchoscopy; IV antibiotics (ceftiraxone, cartilaginous portion at a 160 degree angle;
MMMMCCXXII) Antibiotics: controversial usage cefotaxime, ampicillin/sulbactam); extubation cartilaginous portion then descends at a 40-45
empirically usually within 48 hours once swelling down and degree angle, 45 degrees off saggital, into the
MMMMCCXXIII) Antireflux medications air leak present nasopharynx
MMMMCCXXIV) Lathyrogens: reduce collagen MMMMCCXXX) Bacterial tracheitis MMMMCCXLI) Torus tubarius: formed by soft tissue
cross binding, used to decrease esophageal i) Caused by S. aureus, also S. pyogenes, H. overlying the medial cartilaginous end of the tube
stricture; penicillamine, ß-aminoproprionitrile, influenzae, M. catarrhalis MMMMCCXLII) Rosenmuller’s fossa:
acetylcysteine; unproven benefit ii) URI prodrome, rapid onset in children 6 nasopharyngeal mucosal fold found posterior to
MMMMCCXXV) Esophagoscopy – timing months – 8 years; high fever, hoarseness with torus
controversial: <24 vs. 24-48 vs. 48-72 hrs; insertion cough, dysphagia, toxic symptoms
of NG tube at time of esophagoscopy; identifies iii) Management: OR intubation, bronchoscopic 1040) Muscles related to the eustachian tube
amount of damage and whether injury is suction and cultures of airway exudates; MMMMCCXLIII) Tensor veli palatini/dilator tubae
circumferential or not extubation when normothermic, decreased MMMMCCXLIV) Levator veli palatini
i) Grade 1: mucosal erythema secretions, air leak present MMMMCCXLV) Salpingopharyngeus: originates
ii) Grade 2: mucosal erythema with MMMMCCXXXI) Retropharyngeal abscess off torus tubarius, interdigitates with
noncircumferential exudate i) Caused by mixed bacteriae: Streptococci, S. palatopharyngeus
iii) Grade 3: circumferential exudates aureus, H. influenzae, Bacteroides, MMMMCCXLVI) Tensor tympani
iv) Grave 4: circumferential exudates with peptostreptococci, fusobacteria
perforation 1041) Tensor veli palatini anatomy
 MMMMCCXLVII) Lateral head: origin from MMMMCCLXXII) Sensitivity 90-100%, specificity 1051) Describe classification and pathology for congenital
scaphoid fossa & greater sphenoid wing, swings 82-84% inner ear malformations
anterior, lateral & inferior, tendon around hamulus, MMMMCCLXXIII) Factors influencing success: MMMMCCLXXXVI) Membranous inner ear
inserts onto posterior hard palate and palatine noise level in test environment, vernix in the EAC, malformations (~80%)
aponeurosis middle ear dysfunction, decreased responses in low i) Bing-Siebenmann: complete membranous
i) Posterosuperior fibers arise from lateral head, birth weight infants & preemies labyrinthine dysplasia
forms tendon, inserts on manubrium of malleus ii) Scheibe: most common histopathologic plasia,
MMMMCCXLVIII) Medial head: origin from 1047) Behavioral auditory testing limited membranous cochleosaccular dysplasia
posterior half of lateral membranous wall of ETT, MMMMCCLXXIV) For infants/children from 5-6 iii) Alexander: partial aplasia of cochlear duct at
insertion blends into fibers of lateral head months to 5 years in age basal turn; patients have high frequency HL
MMMMCCLXXV) Behavioral observation MMMMCCLXXXVII) Bony & membranous
1042) Functions of the eustachian tube audiometry (BOA) malformations (~20%)
MMMMCCXLIX) Pressure regulation/ventilation i) For infants from 0 to 6 months of age, based i) Michel aplasia: complete labyrinthine aplasia;
MMMMCCL) Protection from nasopharyngeal pressure on reflex responses & state changes arrest occurs at end of 3rd week prior to otic
MMMMCCLI) Drainage of middle ear secretion ii) Unconditioned responses, variable & capsule formation
imprecise, habituate rapidly ii) Cochlear anomalies
1043) JCIH Position Statement 1994 for neonatal hearing MMMMCCLXXVI) Visual reinforcement (1) Common cavity (4th week)
screening audiometry (VRA) (2) Cochlear aplasia (5th week)
MMMMCCLII) Any history of hereditary childhood SNHL i) For toddlers 6 months – 2 years (3) Cochlear hypoplasia (6th week)
MMMMCCLIII) STORCH ii) Operant conditioning: child trained to look for (4) Mondini: incomplete partition/development
MMMMCCLIV) Craniofacial abnormalities and/or external auditory stimuli (lights, motion) of bony and membranous labyrinth;
ear malformations MMMMCCLXXVII) Conditioned play audiometry cochlea may be present as a curved tube;
MMMMCCLV) Birth weight under 1500g (CPA) arrest at 7th week of gestation
MMMMCCLVI) Hyperbilirubinemia requiring exchange i) For children 2-5 years iii) Labyrinthine anomalies (40% of radiologically
transfusion ii) Child performs a task in response to an abnormal cochleas will have SCC abnormality)
MMMMCCLVII) Ototoxic medications auditory stimulus (1) SCC dysplasia, 4x as common as SCC
MMMMCCLVIII) Bacterial meningitis iii) Play activity changes to keep the childs interest aplasia
MMMMCCLIX) APGAR 0-4 at 1 minute or 0-6 at 5 (2) SCC aplasia: lateral canal affected most
minutes 1048) Indications for bone conducting hearing aids often (last to develop)
MMMMCCLX) Mechanical ventilation >5 days MMMMCCLXXVIII) For situations where air iv) Aqueductal anomalies: normally 0.4-1mm in
MMMMCCLXI) Findings associated with syndrome conducting hearing aides do not fulfill the diameter when measured halfway between
involving HL amplification needs for CHL common crus and external aperture
MMMMCCLXXIX) Atresia/microtia, chronic (1) Enlarged VA: >1.5mm in diameter,
1044) JCIH Position Statement 1994 for infant (29d-2y) otorrhea, abnormally small EACs measured at halfway mark between
hearing screening common crus & external aperture; ~40%
MMMMCCLXII) Parent/caregiver concern 1049) Central auditory processing disorders with enlarged VA eventually develop
regarding hearing, speech, language, or MMMMCCLXXX) A disorder in how the brain profound SNHL
developmental delay processes auditory signals (2) Enlarged CA: usually 3-4mm in diameter,
MMMMCCLXIII) Bacterial meningitis & other MMMMCCLXXXI) Signs ranges from 1-10mm
infections associated with SNHL i) Easy distraction v) IAC abnormalities
MMMMCCLXIV) Head trauma with associated ii) Delayed responses (1) Narrow IAC: <3mm (Cummings), if facial
LOC or skull fracture iii) Frequent requests for repetition function present then CN VIII most likely
MMMMCCLXV) Stigmata or other findings iv) Symptoms of hearing loss absent
associated with a syndrome known to include SNHL v) Frequent reversals (2) Widened IAC: >10mm (Cummings),
MMMMCCLXVI) Ototoxic medications vi) Difficulty following directions associated with stapes gusher
MMMMCCLXVII) Recurrent or persistent OME vii) Inconsistent academic performance
for at least 3 months viii) Unexpalined behavior difficulties 1052) Classification of microtia
MMMMCCLXXXVIII) Class I: mild, auricle decreased
1045) ABR for hearing screens 1050) Indications for imaging in pediatric hearing loss in size
MMMMCCLXVIII) Sensitivity 98%, specificity 96% MMMMCCLXXXII) Evaluation for cochlear MMMMCCLXXXIX) Class II: curving vertical ridge
MMMMCCLXIX) Click stimuli from 30-40 dB implantation of tissue, all major structures present but with
nHL, estimates hearing in 1-4kHz range; requires MMMMCCLXXXIII) Children with recurrent absolute deficiency of tissue
natural sleep or conscious sedation meningitis MMMMCCXC) Class III: rudimentary soft tissue structure
MMMMCCLXX) ABR reaches adult levels by 18 MMMMCCLXXXIV) History of sudden or
months to 3 years; newborn ABR composed of progressive SNHL (especially associated with head 1053) Classification of EAC/ME deformity (de la Cruz)
waves I, III, V trauma) MMMMCCXCI) Major: EAC & TM usually
MMMMCCLXXXV) Patients with hearing loss absent, decreased or absent middle ear space,
1046) OAE’s for hearing screens whose imaging results will have an impact on ossicles rudimentary or absent, fused or fixed to
MMMMCCLXXI) TEOAE used most often, counselling atretic plate
DPOAE being used more
 MMMMCCXCII) Minor: EAC may be mildly MMMMCCCXV) Chronic infection MMMMCCCXLVII) Unsatisfactory response to
stenoitic, ME space & TM normal or slightly small, MMMMCCCXVI) EAC stenosis empiric antibiotics
conductive hearing loss secondary to ossicle MMMMCCCXLVIII) AOM in a child already
absence or fixation 1060) Risk factors for pediatric AOM receiving antibiotics
MMMMCCCXVII) Male gender MMMMCCCXLIX) Suppurative complications of
1054) Describe Jahrsdoerfer’s grading system for MMMMCCCXVIII) Bottle feeding AOM
congenital aural atresia MMMMCCCXIX) Sibling(s) with OM MMMMCCCL) AOME in the newborn or immune
MMMMCCXCIII) 10 point system based on high MMMMCCCXX) Early occurrence of OM deficient patient
resolution CT findings MMMMCCCXXI) Daycare attendance
i) Mastoid pneumatization MMMMCCCXXII) Lower socioeconomic status 1065) Indications for myringotomy
ii) Oval window status MMMMCCCXXIII) Smoking by the mother MMMMCCCLI)AOM with facial paralysis
iii) Round window status MMMMCCCXXIV) Parental history of OM MMMMCCCLII) AOM with meningitis or other
iv) Status of the malleus MMMMCCCXXV) Allergies (disputed) CNS event
v) Status of the incus MMMMCCCXXVI) Craniofacial abnormalities MMMMCCCLIII) AOM not responding to
vi) Facial nerve course through the middle ear MMMMCCCXXVII) Congenital/acquired antimicrobial therapy
vii) Status of the mesotympanum immunodeficiency MMMMCCCLIV) AOM in immunosuppressed
viii) External ear appearance patients
ix) Presence of the stapes (worth 2 points) 1061) Most common etiologic agents in pediatric acute OM
MMMMCCCXXVIII) S. pneumoniae 1066) Bacteriology of acute mastoiditis not due to
1055) Syndromes associated with microtia/aural atresia MMMMCCCXXIX) H. influenzae cholesteatoma
MMMMCCXCIV) CHARGE MMMMCCCXXX) Moraxella catarhallis MMMMCCCLV) Pneumococcus
MMMMCCXCV) Crouzon’s disease MMMMCCCXXXI) Group A Strep MMMMCCCLVI) H. influenzae
MMMMCCXCVI) Goldenhar’s MMMMCCCLVII) Streptococcus pyogenes
MMMMCCXCVII) Hemifacial macrosomia 1062) 8 sequelae of otitis media MMMMCCCLVIII) Staphylococcus aureus
MMMMCCXCVIII) Pierre-Robin sequence MMMMCCCXXXII) Adhesive otitis media
MMMMCCXCIX) Treacher-Collins MMMMCCCXXXIII) Chronic suppurative OM 1067) Complications of tympanostomy tubes
MMMMCCC) VATER MMMMCCCXXXIV) Permanent TM perforation MMMMCCCLIX) Otorrhea: ~3.5% rate of
MMMMCCCXXXV) Tympanosclerosis persistent drainage
1056) General management approach for EAC/ME atresia MMMMCCCXXXVI) TM retraction pocket MMMMCCCLX) Granulation tissue formation
MMMMCCCI) Uniateral microtia & aural atresia: do not MMMMCCCXXXVII) Cholesteatoma MMMMCCCLXI) Myringosclerosis
reconstruct canal, as speech & learning will develop MMMMCCCXXXVIII) Ossicular necrosis MMMMCCCLXII) TM perforation
normally MMMMCCCXXXIX) Sensorineural hearing loss MMMMCCCLXIII) TM atrophy, retraction,
MMMMCCCII) Defer surgery to 5-8 years, allows growth atelectasis
of contralateral ear (template) and rib cage (cartilage 1063) Indications for tympanostomy tube placement MMMMCCCLXIV) Cholesteatoma
graft source) (Bluestone’s controversies chapter in Baileys) MMMMCCCLXV) Loss of tube in the middle ear
MMMMCCCIII) Bone conduction hearing aids for bilateral MMMMCCCXL) Recurrent AOM with failed MMMMCCCLXVI) Early extrusion
cases medical management, >3 episodes in 6 months or MMMMCCCLXVII) Plugged tube
>4 episodes in 12 months with one being recent
1057) Indications for surgery in EAC/ME atresia MMMMCCCXLI) COME unresponsive to 1068) What percentage of pediatric hearing loss is due to
MMMMCCCIV) Normal sensorineural function medical management for >3 months bilaterally or >6 genetic factors?
MMMMCCCV) Ossicles at least present months unilaterally; earlier when significant hearing MMMMCCCLXVIII) 50% due to genetic causes;
MMMMCCCVI) Middle ear space at least 50% loss (>25dB), speech/language delay, severe 50% due to a genetic component as part of an
normal size retraction pocket, disequilibrium/vertigo, or tinnitus identifiable syndrome; AR accounts for ~75%, AD
MMMMCCCVII) Presence of cholesteatoma present ~20%, sex-linked defects ~3-4%, mitochondrial
(emergent indication) MMMMCCCXLII) Recurrent MEE not meeting defects <1%
criteria for chronic disease but cumulative duration MMMMCCCLXIX) 20-25% due to pre-, peri-,
1058) Facial nerve findings in middle ear atresia excessive (6-12 months) postnatal environmental causes
MMMMCCCVIII) Tympanic segment dehiscence MMMMCCCXLIII) Eustachian tube dysfunction MMMMCCCLXX) 25-30% sporadic cases of
MMMMCCCIX) Inferior displacement of the when persistent or recurrent signs & symptoms, unknown etiology
tympanic segment disequilibrium or vertigo, tinnitus, or severe retraction
MMMMCCCX) Anterior/lateral displacement of the pocket, unrelieved by medical management; 1069) Discuss connexin 26 (CX26)
mastoid segment patulous eustachian tube; hyperbaric oxygen therapy MMMMCCCLXXI) Gene GJB2 product
MMMMCCCXI) More acute angle taken at 2nd MMMMCCCXLIV) Tympanoplasty when MMMMCCCLXXII) Most common association with
genu eustachian tube function poor genetic nonsyndromic hearing loss
MMMMCCCXLV) Suppurative complication, MMMMCCCLXXIII) Present in 30% of
1059) Complications in atresia surgery present or suspected nonsyndromic sporadic HL, and >50% of cases
MMMMCCCXII) Recurrent/persistent hearing where there is an affected sibling
conductive hearing loss 1064) Indications for tympanocentesis
MMMMCCCXIII) SNHL MMMMCCCXLVI) AOM in a seriously ill or toxic 1070) Mondini malformation is associated with which
MMMMCCCXIV) Facial nerve injury child syndromes?
 MMMMCCCLXXIV) Pendred iii)Pseudoarthrosis, scoliosis, or thinning of the MMMMCDXIII) Profound bilateral congenital SNHL (high
MMMMCCCLXXV) Waardenburg tibia; sphenoid wing dysplasia frequencies worse)
MMMMCCCLXXVI) Branchiootorenal iv) Lisch nodules (iris hamartomas) MMMMCDXIV)Heart disease: prolonged QT, large T
MMMMCCCLXXVII) Treacher-Collins v) Optic gliomas waves, Stokes-Adams attacks
MMMMCCCLXXVIII) Wildervanck (Klippel Feil) vi) Axillary or inguinal freckling MMMMCDXV) Recurrent syncope, usually terminates
MMMMCCCLXXIX) Mobius syndrome vii) 1st degree relative with confirmed NF fatally with sudden death; treated with ß-blockade
viii) Family history of NF
1071) Scheibe malformation is associated with which MMMMCCCXCIX) Acoustic neuromas present in 1079) Pendred syndrome
syndromes? 5% of all patients MMMMCDXVI)Autosomal recessive
MMMMCCCLXXX) Jervell-Lange Nielsen MMMMCD) CNS involvement may lead to MR, MMMMCDXVII) SNHL associated with iodine
MMMMCCCLXXXI) Refsum blindness, SNHL metabolism defect leading to euthyroid goiter
MMMMCCCLXXXII) Usher MMMMCDXVIII) Thyroid abnormality detected
MMMMCCCLXXXIII) Waardenburg 1075) Discuss neufibromatosis type II with a perchlorate discharge test (shows abnormal
MMMMCDI) Mutation of tumor suppressor gene organification of nonorganic iodine)
1072) Name some autosomal dominant syndromes (merlin) on chromosome 22 MMMMCDXIX)Temporal bones of Pendreds patients
associated with SNHL (WANTCBS) MMMMCDII) Autosomal dominant, but 50% of cases often show Mondini or enlarged VA’s
MMMMCCCLXXXIV) Waardenburg syndrome due to spontaneous mutations
MMMMCCCLXXXV) Apert MMMMCDIII) Fewer café au lait spots & cutaneous 1080) Name some X-linked recessive syndromes
MMMMCCCLXXXVI) Neurofibromatosis nodules cf. type I, but 95% incidence of bilateral associated with SNHL
MMMMCCCLXXXVII) Treacher-Collins syndrome acoustic neuromas often before age 21; also have MMMMCDXX) Alport syndrome
MMMMCCCLXXXVIII) Crouzan central meningiomas, gliomas, schwannomas, early MMMMCDXXI)Norrie syndrome
MMMMCCCLXXXIX) Branchiootorenal syndrome lens opacifications i) Congenital/rapidly progressive blindness due to
(Melnick-Fraser) MMMMCDIV) Subtypes pseudoglioma, exudative vitreoretinopathy,
MMMMCCCXC) Stickler syndrome i) Wishart: early onset & rapid growth, other opacification, ocular degeneration
MMMMCCCXCI) Osteogenesis imperfecta tumors than acoustic neuromas ii) Ear findings: progressive SNHL with onset in
ii) Gardner type: slower rate of growth & onset, 2nd/3rd decade, occasional progressive mental
1073) Describe the types of Waardenburg’s syndrome usually only bilateral acoustic neuromas deterioration
MMMMCCCXCII) Defined by the presence (type iii) Mutation of NDP gene on Xp11.4, produces
I) or absence (type II) of dystopia canthorum; SNHL 1076) Name some autosomal recessive syndromes norrin protein, structurally similar to TGF-ß
occurs in 20% in Type I, 50% in Type II associated with SNHL (PUGJAR) MMMMCDXXII) Otopalatodigital syndrome
MMMMCCCXCIII) Autosomal dominant MMMMCDV) Pendred’s syndrome i) Hypertelorism, craniofacial deformities
i) Type I gene locus PAX3 on chromosome 2 MMMMCDVI) Usher syndrome (supraorbital deformity, flat midface, small
ii) Type II gene locus MITF (microphthalmia MMMMCDVII) Jervell-Lange Nielsen syndrome nose, cleft palate), short stature, wide space
transcription factor) on chromosome 3 (20% of between 1st & 2nd toe
cases) 1077) Usher syndrome ii) CHL due to ossicular malformation
MMMMCCCXCIV) Clinical findings MMMMCDVIII) Autosomal recessive, 10% of hereditary iii) Mutation localized to Xq28
i) Pigment abnormalities: white forelock, deafness MMMMCDXXIII) Wildervaank syndrome
premature graying, vitiligo, heterochromia iridis MMMMCDIX) Retinitis pigmentosa causing progressive i) Klippel-Feil malformation
ii) Craniofacial abnormalities (dystopia canthorum, visual loss; patients born deaf secondary to atrophy ii) SNHL or mixed loss, due to bony inner ear
broad nasal root, synophrys) of organ of Corti; ataxia and vestibular dysfunction malformation
iii) Unilateral or bilateral SNHL common iii) CN VI paralysis with eye retraction on lateral
MMMMCCCXCV) Klein-Waardenburg (Type III): MMMMCDX) Eye changes detected on gaze (Duane retraction syndrome)
features of WS1 plus blue eyes, hearing impairment, electroretinography even before funduscopic
upper limb skeletal dysplasias, muscular hypotonia changes identified; ophthalmology consult essential 1081) Alport syndrome
MMMMCCCXCVI) Waardenburg-Shah (Type IV): MMMMCDXI) Four main types MMMMCDXXIV) 6 subtypes, 3 AR, 3 X-linked
phenotype similar to WS2 plus Hirschprung i) Type I: profound congenital deafness, RP onset MMMMCDXXV) Progressive SNHL (usually 2nd
megacolon; AR by age 10, no vestibular response; 90% of decade) with varying degrees of renal disease (renal
Ushers agenesis to mild renal dysplasia identifiable on
1074) Describe neurofibromatosis Type I (von ii) Type II: moderate/severe congenital deafness, ultrasound)
Recklinghausen’s disease) onset of RP in teens/twenties, normal or MMMMCDXXVI) Renal disease can be severe in
MMMMCCCXCVII) Mutation of nerve growth factor decreased vestibular response, 10% of all men/boys; dialysis/renal transplant important
(neurofibromin) on chromosome 17 cases therapies
MMMMCCCXCVIII) Diagnosis made by confirming iii) Type III: progressive HL, RP begins in puberty,
2 of the following: <1% of cases 1082) Revision stapedectomy – Patient has recurrent CHL
i) 6 or more café au lait spots >15mm in adults, iv) Type IV: X-linked inheritance, similar to type II on the previously operated side that is slightly worse than
>10mm in children the CHL on the other side. Treatment options, why do
ii) 2 or more cutaneous neurofibromas, or a single 1078) Jervell Lange-Nielsen disease they fail in late period? Bailey Chap 143
plexiform neurofibromas (larger, more swollen MMMMCDXII) Autosomal recessive; one form linked to a MMMMCDXXVII) Amplification, serial
looking) potassium channel gene (KVLQT 1) on 11p15.5 audiograms
 MMMMCDXXVIII) Medical Management (not 1089) Indications for ORIF for mandible # (5) (Bailey’s MMMMCDLXXVII) Type IV – graft onto mobile
really indicated in a revision case, as limited to non- chap 65) stapes footplate
surgical candidates or those with exclusive SNHL or MMMMCDLIV) Unable to reduce with closed fixation MMMMCDLXXVIII) Type Va – HSSC fenestration
vestibular symptoms due to otosclerosis). Treatment MMMMCDLV) Displaced and unstable MMMMCDLXXIX) Type Vb – Stapes footplate
includes: Sodium fluoride (and possibly Vit D and MMMMCDLVI) Associated midface fractures fenestration
CaCarbonate) MMMMCDLVII) Need to avoid MMF (epilepsy,
MMMMCDXXIX) Surgical Management on alcoholics, psychiatric, diabetics or severe disability) 1094) MRI characteristics of CPA tumors compared to
previously operated ear - MOST COMMON CAUSE MMMMCDLVIII) Angle of mandible fracture if brain (T1/T2/gad) (Dr Quinn)
OF SURGICAL FAILURE IS PROSTHESIS unfavourable MMMMCDLXXX) AN – iso/hyper/enhancing on
DISPLACEMENT WITH OR WITHOUT INCUS TIP MMMMCDLIX) Symphysis/parasymphysis if vertically T1
EROSION. unfavourable MMMMCDLXXXI) Meningioma – iso/hyper/less
MMMMCDXXX) Surgical Management of the MMMMCDLX) Condylar Neck fractures enhancing than AN on T1
non operated ear – clearly wrong answer here as i) Absolute MMMMCDLXXXII) Epidermiod – hypo/very hyper/
general rule of thumb is to operate on the worse ear (1) Displacement into middle cranial fossa (ie same as CSF)
(although the complication rate would be higher on (2) Impossibility of normal occlusion with MMMMCDLXXXIII) Arachnoid cyst – hypo/very
the operated ear). closed reduction hyper/ (ie identical to Epidermoid as need special
(3) Lateral extracapsular displacement of protocols to differentiate); hypointense on DWI
1083) Signs of cavernous sinus thrombosis (Bailey pg 96, condyle
956) (4) Invasion by foreign body (GSW) 1095) AN vs meningioma
MMMMCDXXXI) Proptosis ii) Relative MMMMCDLXXXIV) AN…
MMMMCDXXXII) Chemosis (1) Bilateral in edentulous when splinting not i) No dural tail
MMMMCDXXXIII) Edematous eyelid possible ii) Acute angle to petrous bone
MMMMCDXXXIV) Red Eye (2) Uni or bilateral when splinting (medical iii) Intracanulicular component
MMMMCDXXXV) CN III, IV, VI dysfunction reasons) or physio not possible iv) Generally homogenous
(opthalmoplegia) (3) Bilateral condylar # when also MMMMCDLXXXV) Meningioma
comminuted midface # i) Dural tail
1084) Advantage of local flap in closing infraorbital cheek (4) Bilateral condylar # with marked preinjury ii) Flow voids at periphery
defect (Bailey Chap 161) malocclusion iii) No intracanulicular component
MMMMCDXXXVI) Superior tissue match iv) Obtuse angles to petrous bone
MMMMCDXXXVII) Single stage procedure 1090) Indications for closed reduction of mandible v) Not necessarily centered on porous
MMMMCDXXXVIII) No disruption of underlying fractures vi) Less homogenous (area of central
nerves and muscles MMMMCDLXI) Nondisplaced and favourable fractures hypointensity)
MMMMCDXXXIX) Low donor site morbidity MMMMCDLXII) Severely comminuted with
unlikely stabilization 1096) Classic shape of Epidermoid
1085) Non-surgical treatment of laryngeal papillomata MMMMCDLXIII) Severely atrophic edentulous MMMMCDLXXXVI) Dumbbell (into MCF)
(Bailey chap 85) mandible MMMMCDLXXXVII) Can also extend into
MMMMCDXL) Alpha interferon MMMMCDLXIV) Pediatric fractures with contralateral cistern
MMMMCDXLI) Indole 3 carbinol developing dentition
MMMMCDXLII) Photodynamic therapy 1097) Definition of functional hearing
MMMMCDXLIII) Cidofovir 1091) RF for vocal cord polyps (4 of them) MMMMCDLXXXVIII) Speech reception threshold of
MMMMCDXLIV) Acyclovir MMMMCDLXV) Smoking less than 50 dB
MMMMCDXLV) Ribavirin MMMMCDLXVI) Vocal abuse MMMMCDLXXXIX) Speech discrimination
MMMMCDXLVI) Retinoic acid MMMMCDLXVII) ?Chronic laryngitis threshold of greater than 50 percent
MMMMCDXLVII) Mumps vaccine MMMMCDLXVIII) ?GERD
MMMMCDXLVIII) Methotrexate 1098) Give examples of pre-treatment, very superficial,
1092) Picture of bullous myringitis – infectious cause (KJ superficial, medium and deep peels
1086) 4 findings on endoscopy in aged larynx (Dr Quinn) page 473 – infections of ear) MMMMCDXC) Pre-treatment – tretinoin
MMMMCDXLIX) Bowed vocal cords MMMMCDLXIX) H. flu MMMMCDXCI) Very superficial – TCA 10% (1
MMMMCDL) Edema of vocal cords MMMMCDLXX) S. pneumo coat)
MMMMCDLI) Vocal cord atrophy MMMMCDLXXI) M. catarrhalis MMMMCDXCII) Superficial – TCA 10-35% (1
MMMMCDLXXII) Parainfluenza virus coat)
1087) Main muscle in pitch control (ie the main tensor) MMMMCDLXXIII) Mycoplasma (this was the right MMMMCDXCIII) Medium – TCA 35% modified
MMMMCDLII) cricothyroid (Dr Quinn lecture series answer) with Jessner’s solution
2004) MMMMCDXCIV) Deep – Baker-Gordon Phenol
1093) Tympanoplasty classification formula
1088) 70 y.o. women w/ vertigo, get ENG – technician MMMMCDLXXIV) Type I – myringoplasty
report: calculate excitability difference, down beating MMMMCDLXXV) Type II – ossicular 1099) Indications for Pediatric maxillary sinus aspirate
nystagmus – meaning? reconstruction MMMMCDXCV) Unresolving symptoms after 72
MMMMCDLIII) Excitability difference – MMMMCDLXXVI) Type III – myringostapediopexy hours
MMMMCDXCVI) Immunocomprimise
 MMMMCDXCVII) Work up for fever of unknown MMMMDXXV) Single MMMMDXLV) Hyperemia over the lateral rectus muscle
origin MMMMDXXVI) Immature
MMMMCDXCVIII) Severe toxic child MMMMDXXVII) Male 1116) Two conditions with congenitally shallow orbits
MMMMCDXCIX) Suppurative complications MMMMDXXVIII) Overly expectant MMMMDXLVI) Crouzons
MMMMDXXIX) Narcisstic MMMMDXLVII)Aperts
1100) Immune workup for recurrent sinusitis
MMMMD) IgG subclasses 1110) Dedo classification of neck and chin relationship 1117) Definition and significance of Zero Degree Meridian
MMMMDI) IgM MMMMDXXX) Class I - youthful, normal neck of Gonzales-Ulloa
MMMMDII) IgA MMMMDXXXI) Class II – skin laxity of midline neck MMMMDXLVIII) Line drawn perpendicular to the
MMMMDIII) IgE MMMMDXXXII) Class III – fat accumulation Frankfort horizontial line through the nasion.
MMMMDIV) Ability to respond to polysaccharide MMMMDXXXIII) Class IV – muscle i) Pogonion should be within 5 mm of this line
antigens of S. pneumoniae, and H. flu accentuation, platsymal banding ii) 1st Degree retraction - Up to 1 cm
MMMMDXXXIV) Class V – aquired or congential iii) 2nd degree retraction – 1-2 cm
1101) Lab finding with common variable hypoglobulinemia? retrognathia iv) 3rd degree retraction – more than two cm
MMMMDV) Consistently low total immunoglobulins MMMMDXXXV) Class VI – low set hyoid bone MMMMDXLIX) 1st and 2 nd degree retractions can be
treated with chin implants whereas 3rd degree should
1102) How is pediatric allergic fungal sinusitis different 1111)What creates endolymph? How absorbed? be treated with orthognathic surgery
from adult? MMMMDXXXVI) Marginal cells of stria
MMMMDVI) Peds – more likely to facial skeleton vascularis (cochlea) 1118) Hinderer facial analysis for malar implants
abnormalities MMMMDXXXVII) Dark cells of the macula and MMMMDL) Line from oral commissure to lateral
MMMMDVII) Peds – more likely unilateral cristae (Utricle and Saccule, and SCC) canthus
MMMMDXXXVIII) Absorbed in endolymphatic sac MMMMDLI) Line from tragion to inferior margin of
1103) Define phase delay and glottal puff nasal ala
MMMMDVIII) Glottal puff is the release of air as the 1112) Innervation blood supply of Vestibular organs MMMMDLII) mallar eminence should fall superior to the
upper margins of the vocal cords separate MMMMDXXXIX) Innervation intersection of these two lines
MMMMDIX) Phase delay is the time difference i) Inferior vestibular n – PSCC (via singular
between closure of the upper margin of the vocal nerve) and Saccule 1119) Two theories of BPPV
cords compared with the lower. ii) Superior vestibular n – HSCC, SSCC, and MMMMDLIII) cupulolithiasis theory proposes that
utricle calcium deposits become embedded on the cupula,
1104) Three physical properties that alter frequency of MMMMDXL) Blood supply rendering the PSCC dependent on gravity
vocal cord vibration i) Labyrinthine artery (from AICA (45%, Superior MMMMDLIV) canalithiasis theory, calcium debris
MMMMDX) Mass cerebellar artery, basilar artery) (displaced otoconia) are found within the PSCC but
MMMMDXI) Stiffness (1) Anterior vestibular artery does not adhere to the cupula
MMMMDXII) Viscosity (a) Utricle, SSCC, HSCC, small portion
of saccule 1120) Six types of melanoma
1105) Three findings on laryngeal EMG and significance (2) Posterior vestibular artery MMMMDLV) Superficial spreading
MMMMDXIII) Normal – joint fixation (a) PSCC, most of saccule, and part of MMMMDLVI) Nodular
MMMMDXIV) Fibrillation – denervation utricle, SSCC, HSCC MMMMDLVII) Acral lentiginous
MMMMDXV) Polyphasic potentials – synkinesis and MMMMDLVIII) Desmoplastic
reinnervation 1113) Compare two types of hair cells found in the MMMMDLIX) Lentigo Maligna melanoma (Lentigo
ampullae (containing neuroepithelium known as the maligna is the premalignant state)
1106) Properties seen on stroboscopy cristae ampullaris) MMMMDLX) Mucosal
MMMMDXVI) Glottic closure configuration (mucosal MMMMDXLI) Type I hair cells – flask shaped and have
wave form) chalice shaped nerve ending. One chalyx nerve 1121) Define tip defining point
MMMMDXVII) Amplitude (horizontial excursion) ending can synapse with 1-4 hair cells MMMMDLXI) Highest, medial and cephalic portion of
MMMMDXVIII) Symmetry MMMMDXLII) Type II hair cells – cylinder shaped nerve the lateral crus that corresponds to the light reflex
MMMMDXIX) Periodicity cells with both efferent and afferent nerve fibers externally
synapsing on a single hair cell. 1122) Nasal tip incisions, approaches
1107) Two indications for arytenoid adduction MMMMDLXII) Incisions: Intercartilaginous,
MMMMDXX) Posterior glottic gap not corrected with 1114) Otolith organs – name of neuroepithelial compenent Transcartilaginous (Intracartilaginous), Marginal
type I thryoplasty and significance of striola MMMMDLXIII) Approaches: Delivery, Non-Delivery
MMMMDXXI) Vocal processes at different levels in the MMMMDXLIII) Macula (either cartilage splitting or retrograde), and Open
caudal/rostral level MMMMDXLIV) Striola – central line through otolith
membrane 1123) Techniques of Tip Volume Reduction
1108) Three methods of vocal cord lateralization i) Cilia movement towards striola for utricle MMMMDLXIV) Complete strip
MMMMDXXII) Aryteniodopexy causes excitation MMMMDLXV) Weakened complete strip
MMMMDXXIII) Arytenoidectomy ii) Cilia movement away striola for saccular MMMMDLXVI) Suture modification of complete strip
MMMMDXXIV) Cordectomy causes excitation MMMMDLXVII) Interrupted (Incomplete) strip

1109) Red flag for cosmo patients 1115) Pathognomic for Graves orbitopathy on PE 1124) Indications for open rhinoplasty
 MMMMDLXVIII) Cleft lip nose deformity 1129) Definition of Vestibular Neuritis MMMMDCV) To record a wave I
MMMMDLXIX) Severe tip asymmetry MMMMDLXXXVI) Acute, peripheral and unilateral
MMMMDLXX) Marked overprojection vestibular disorder not associated with hearing loss 1137) Normal interear latency difference for ABR waves
MMMMDLXXI) Significant underprojection MMMMDLXXXVII) Typically occurs in middle age MMMMDCVI) 0.4 ms
MMMMDLXXII) Eccentric anatomy MMMMDLXXXVIII) Single episode of severe
MMMMDLXXIII) Difficult tip revisions prolonged vertigo 1138) Abnormal SP/AP ratios
MMMMDLXXIV) Teaching MMMMDLXXXIX) Decreased caloric response in MMMMDCVII) More than 50% for EAC probe
affected ear MMMMDCVIII) More than 40% tympanic mb
1125) Tip projection I) preservation and II) enhancement MMMMDXC) Complete resolution of symptoms within 6 MMMMDCIX) More than 30% for transtympanic
MMMMDLXXV) Preservation – maintain tip months
support mechanisms 1139) Spontaneous OAE absence
i) Complete strip (as compared to incomplete) 1130) Define dB SPL, dB HL, dB SL MMMMDCX) Normal variant
ii) Avoid septal transfixion incision MMMMDXCI) dB – 10log (output intensity/reference MMMMDCXI) More than a 25 dB hearing loss
MMMMDLXXVI) Enchancement intensity)
i) Cartilage strut placed below or between the MMMMDXCII) SPL – sound pressure level: actual 1140) OAE come from …
medial crura amount of sound pressure (eg 6.5 dB SPL at MMMMDCXII) Outer Hair cells
ii) Strut can be combined with plumping grafts 1000Hz)
(greater strut platform) MMMMDXCIII) HL – hearing level: accounts for human 1141) TEOAE are found when hearing is better than…
iii) Suturing of medial crura together, with ear having different sensitivities at different MMMMDCXIII) 35dB, but not effective for evaluating
resection of intercrural soft tissue frequencies. (eg 6.5 dB SPL at 1000Hz, 45 dB SPL higher frequency hearing loss
iv) Tip onlay grafts for a 125 Hz, and both of these are 0 dB HL)
v) Transdomal suturing MMMMDXCIV)SL – sensation level: intensity of the 1142) DPOAE are found when hearing is better than…
vi) Interrupted strip: lateral crural recruitment stimulus in decibels above an individual’s hearing MMMMDCXIV)50 dB, and are effective up to 6000 Hz
vii) Illusionary threshold. (a person has a hearing loss of 30 dB HL
(1) Plumping grafts and if a test is to be given at 40 dB SL, then this 1143) What are central auditory processing disorders 4
(2) Reduction of cartilaginous dorsum would translate to 70 dB HL) categories
MMMMDCXV) Decoding - impairment of breakdown of
1126) Increasing tip rotation techniques 1131) Define SRT, Word recognition score auditory processing at the phonemic level.
MMMMDLXXVII) Volume reduction of alar MMMMDXCV) SRT - the softest intensity level at which a MMMMDCXVI)Tolerance fading memory - poor auditory
cartilages with complete strip or incomplete strip patient can correctly repeat 50% of the words memory or difficulty understanding speech under
(more pronounced with incomplete. Can control (spondees) adverse conditions
complete strip resection with base up triangle MMMMDXCVI)Word recognition score – phonems MMMMDCXVII) Integration - difficulty
resection laterally). If using complete strip, use presented at 30 dB above threshold integrating auditory information with other functions,
adjuctive procedures to augment. such as visual and nonverbal aspects of speech
MMMMDLXXVIII) Illusionary 1132) EAC volume normals MMMMDCXVIII) Organization - reversals and
i) Cartilage grafts in the infratip lobule, columella, MMMMDXCVII) Children: 0.5ml – 1ml sequencing errors
nasolabial angle (plumping grafts) MMMMDXCVIII) Adults 0.6ml -2ml
MMMMDLXXIX) Adjuctive 1144) Diagnostic criteria of Sjogrens
i) Shortening of caudal septum 1133) Type A vs Type C tympanogram peak division MMMMDCXIX)Dry eyes more than 3/12 or recurrent or
ii) Shortening of caudal upper lateral cartilage (Baileys) persistent swelling of salivary glands
iii) Septal shortening with high transfixion incision MMMMDXCIX)-100 mmH2O MMMMDCXX) Dry mouth more than 3/12
iv) Reduction of convex caudal medial crura MMMMDCXXI)Schrimer test (< 5mm in 5 min)
v) Resection of membranous columellar skin 1134) Stapes reflex threshold MMMMDCXXII) More than 50 lymphocytes in 4
vi) Minor MMMMDC) Up to 50-55 dbHL – normal stapes reflex mm2 of glandular tissue
(1) Resection of excess vestibular skin threshold MMMMDCXXIII) Abnormal salivary scintigraphy,
(2) Proper taping MMMMDCI) 50-80 dbHL – elevated stapes reflex abnormal parotid sialography, or unstimulated flow of
(3) Cutting of depressor septi muscle threshold <1.5 mL in 15min
MMMMDCII) Greater than 80 db HL – likely no reflex MMMMDCXXIV) Presence of anti Ro(SS-A) or
1127) Four stages of Supparative Labyrinthitis MMMMDCIII) I-III represent cochlear hearing losses, for anti La(SS-B) antibodies, RF+, or ANA+
MMMMDLXXX) Serous or irritative phase VIII nerve losses (despite the degree of loss, there is
MMMMDLXXXI) Acute or purulent stage likely an absent reflex). Also VIII losses are 1145) Relapsing polychondritis criteria
MMMMDLXXXII) Fiberous or latent stage associated with reflex decay. MMMMDCXXV) Defined features of the disease
MMMMDLXXXIII) Osseous stage include
1135) Stapes reflex threshold – pure tones vs broadband i) recurrent chondritis of the auricles,
1128) Most common cause of bacterial meningitis, and noise ii) nonerosive inflammatory polyarthritis,
incidence of hearing loss MMMMDCIV) Broadband noise has 20-25 dB lower iii) chondritis of the nasal cartilages,
MMMMDLXXXIV) S. pneumo (H.flu prevous to thresholds compared to pure tones. This difference iv) ocular inflammation,
Hib vaccine) lessens as hearing worsens. v) chondritis of laryngeal or tracheal cartilage, and
MMMMDLXXXV) 10-20% vi) cochlear (SNHL or tinnitus) or vestibular
1136) Main goal of ABR damage (vertigo).
 MMMMDCXXVI) Diagnosis requires three of MMMMDCLV) Spindle-Pleomorphic MMMMDCLXXVII) Combined orbital floor and
these features in the absence of histologic MMMMDCLVI) Adenoid Squamous medial wall defects with soft tissue displacement
confirmation, two of these features with response to noted radiologically on CT scans
steroids or dapsone, or any one of these features 1154) Histologic risk factors for aggressive behavior in MMMMDCLXXVIII) Radiological evidence of a
with histologic confirmation. SCC fracture or comminution of the body of the zygoma
MMMMDCLVII) Undifferentiated histologic itself as determined by CT
1146) Polyarteritis nodosa head and neck features pattern, MMMMDCLXXIX) Physical or radiological
MMMMDCXXVII) Bilateral SSNHL or vestiblar MMMMDCLVIII) Depth into and beyond the evidence of exopthalmos or orbital content
dysfunction subcutaneous fat, impingement caused by displaced periorbital
MMMMDCXXVIII) CN palsy (VII most common) MMMMDCLIX) perineural invasion, and fractures.
MMMMDCLX) lymphatic invasion
1147) Churg-Strauss 1159) What are the 4 R’s of radiation therapy?
MMMMDCXXIX) Seen in patients with known 1155) Merkels Cell carcinoma characteristics MMMMDCLXXX) Theraputic advantage gained
asthma or allergic rhinitis MMMMDCLXI) High recurrence rate, high lymphatic met by one of the 4 following mechanisms
MMMMDCXXX) Vasculitis includes… rate i) Repair of cellular damage
i) systemic small-vessel vasculitis, MMMMDCLXII) Poorly differentiated histiology (1) Sublethal exposure of normal tissue
ii) extravascular granulomas and MMMMDCLXIII) Requires post op XRT after (reason for fractionation)
iii) hypereosinophilia. wide resection ii) Reoxygenation of the tumor
MMMMDCLXIV) Need to treat lymphatics (1) Another reason for fractionation
1148) Hallmark pathologic lesion of Wegeners iii) Redistribution within the cell cycle
MMMMDCXXXI) Necrotizing granulomatous 1156) Indications for XRT in cutaneous malignancy (1) S phase (DNA synthesis) is most
vasculitis MMMMDCLXV) Advanced tumors (invade bone, susceptible, vs G2 phase delay
muscle, cartilage, and nerve) (radioresistant)
1149) Kawasaki’s disease MMMMDCLXVI) Merkels\ cell (2) Rapdily dividing cells more susceptible
MMMMDCXXXII) fever, MMMMDCLXVII) Larger SCCa (>2 cm), (3) Another reason for fractionation
MMMMDCXXXIII) conjunctivitis, MMMMDCLXVIII) recurrent tumors iv) Repopulation of tumor cells
MMMMDCXXXIV) red dry lips, MMMMDCLXIX) Marjolin’s ulcer (1) Determines length of course
MMMMDCXXXV) erythema of the oral mucosa, MMMMDCLXX) To the neck: Multiple positive (2) Reason for accelerated treatment
MMMMDCXXXVI) polymorphous truncal rash, nodes, extracapsular spread and lymphovascular schedules
MMMMDCXXXVII) desquamation of the fingers invasion. (3) Reason against treatment delay,
and toes, and protracted couse of XRT, split course of
MMMMDCXXXVIII) cervical lymphadenopathy. 1157) Name the three vertical and four horizontial XRT
buttresses of the midface
1150) Define nevoid basal cell carcinoma syndrome MMMMDCLXXI) Vertical 1160) Typical radiation dose
(Gorlin's syndrome) i) Nasomaxillary MMMMDCLXXXI) 1.8 – 2.0 Gy given 5x/week for
MMMMDCXXXIX) rare autosomal dominant ii) Zygomaticomaxillary 6-8 weeks
condition iii) Pterygomaxillary
MMMMDCXL) multiple basal cell carcinomas, MMMMDCLXXII) Horizontial 1161) Toxic dose to serous cells of salivary glands
MMMMDCXLI) pitting of the palms and the soles of the i) Frontal bar MMMMDCLXXXII) 35 Gy in 3.5 weeks
feet, ii) Infraorbital rim
MMMMDCXLII) jaw cysts, iii) Zygomatic arch 1162) Toxic CNS doses
MMMMDCXLIII) spine and rib anomalies, iv) Palate/Alveolus MMMMDCLXXXIII) Myelopathy – 30Gy in 25
MMMMDCXLIV) calcification of the falx cerebri, fractions
and 1158) Indications for orbital exploration with MMMMDCLXXXIV) Transverse myelitis – 50-60Gy
MMMMDCXLV) cataracts. zygomaticomaxillary fractures MMMMDCLXXXV) Somnolence syndrome
MMMMDCLXXIII) 1) Persistent diplopia which MMMMDCLXXXVI) Brain necrosis – 65-70 Gy
1151) Basal cell carcinoma clinical subtypes failed to improve in 7 or more days, positive forced
MMMMDCXLVI) Nodular duction testing, and radiologic evidence of 1163) Dose limiting for intensity and total dose
MMMMDCXLVII) Pigmented perimuscular tissue entrapment MMMMDCLXXXVII) Intensity – acute toxicity –
MMMMDCXLVIII) Superficial MMMMDCLXXIV) Cosmetically significant and mucositis
MMMMDCXLIX) Morpheaform clinically apparent enopthalmos associated with MMMMDCLXXXVIII) Total dose – late toxicity – soft
radiological findings tissue fibrosis
1152) Basal cell carcinoma histiological subtypes (SCAK) MMMMDCLXXV) Radiological evidence of
MMMMDCL) Solid significant comminution and/or displacement of the 1164) 3 neural systems of nose
MMMMDCLI) Cystic orbital rim MMMMDCLXXXIX) CN I
MMMMDCLII) Adenoid MMMMDCLXXVI) Radiological evidence of MMMMDCXC) CN V
MMMMDCLIII) Keratotic significant displacement or comminution of greater MMMMDCXCI) CN 0 (nervus terminalis)
than 50% of the orbital floor with herniation of soft
1153) Histiologic subtypes of SCC tissue into the maxillary sinus 1165) Olfactory neuroepithelium histology
MMMMDCLIV) Verrucous
 MMMMDCXCII) Pseudostratified columnar MMMMDCCXIX) Antibodies to Thryoid MMMMDCCXLIV) Chronic nasal obstruction with
epithelium peroxidase (key enzyme in organification) or rhinorrhea or recurrent sinusitis,
thyroglobulin TBG (therefore can measure anti-TPO MMMMDCCXLV) recurrent otitis media with
1166) Six distinct cells seen in Neuroepithelium or anti-TBG) effusion,
MMMMDCXCIII) Bipolar sensory receptor MMMMDCCXLVI) recurrent and chronic
neurons 1176) NIH guidelines for parathyroidectomy (1991) adenoiditis,
MMMMDCXCIV) Microvillar cells MMMMDCCXX) Serum calcium > 12mg/dl MMMMDCCXLVII) speech and swallowing
MMMMDCXCV) Supporting cells MMMMDCCXXI) Hypercalciuria > 400 mg/day abnormalities
MMMMDCXCVI) Globose basal cells MMMMDCCXXII) Classic presentation with renal MMMMDCCXLVIII) suspected neoplasia.
MMMMDCXCVII) Horizontial basal cells stones, osteitis fibrosa, or neuromuscular disease MMMMDCCXLIX) children older than 4
MMMMDCXCVIII) Cells lining Bowmans glands MMMMDCCXXIII) Cortical bone loss greater than experiencing recurrent otitis media have shown to
2 standard deviations below the mean benefit from adenoidectomy with the second set of
1167) Classification of olfactory problems MMMMDCCXXIV) Reduced creatinine clearance tympanostomy tubes
MMMMDCXCIX) Conductive MMMMDCCXXV) age less than 50. MMMMDCCL) chronic otitis media with effusion, initial
MMMMDCC) Sensorineural impairment tympanostomy tube placement without
MMMMDCCI) Central impairment 1177) Surgical Strategies to increase support for dental adenoidectomy is associated with a higher rate of
prosthesis repeat surgeries.
1168) Most common vascular malformation causing MMMMDCCXXVI) Remove tooth and cut through
tracheal compression with stidor a socket 1183) Absolute indications for tonsillectomy
MMMMDCCII) Double aortic arch MMMMDCCXXVII) Preserve anatomy MMMMDCCLI)severe dysphagia,
i) mandible – Alveolus, retromolar pad, buccal MMMMDCCLII) failure to thrive,
1169) 7 steps in thyroid metabolism shelf MMMMDCCLIII) cor pulmonale.
MMMMDCCIII) Uptake of Iodine by thyroid ii) maxilla - tuberosity, alveolus, hard palate
MMMMDCCIV) Coupling of Iodine to MMMMDCCXXVIII) preservation of strip of mucosa 1184) Relative indications for tonsillitis
Thryroglobulin (organification) MMMMDCCXXIX) avoid true hemimaxillectomy (ie MMMMDCCLIV) recurrent acute tonsillitis,
MMMMDCCV) Storage of MIT/DIT in follicular space save medial and lateral incisor) – tripod effect MMMMDCCLV) chronic tonsillitis,
MMMMDCCVI) Re-absorption of MIT/DIT MMMMDCCXXX) skin grafting of cheek flap, and MMMMDCCLVI) obstructive sleep apnea,
MMMMDCCVII) Formation of T3 and T4 form areas of the obturator contact MMMMDCCLVII) peritonsillar abscess,
MIT/DIT MMMMDCCXXXI) skin grafting of the maxillary MMMMDCCLVIII) suspected neoplasia
MMMMDCCVIII) Release of T3 and T4 into sinus MMMMDCCLIX) halitosis
serum MMMMDCCXXXII) resection of inferior turbinate
MMMMDCCIX) Breakdown of T3 and T4 to 1185) Indications for twenty-three hour inpatient monitoring
release Iodine 1178) Classification of obturators include the following:
MMMMDCCXXXIII) Surgical MMMMDCCLX) Age younger than 3.
1170) Percentage of thyroid hormone as T4 MMMMDCCXXXIV) Postsurgical MMMMDCCLXI) Those with obstructive sleep
MMMMDCCX) 98% MMMMDCCXXXV) Definitive apnea or craniofacial syndromes involving the
airway.
1171) Homostatic control of thyroid function (hypothalamus 1179) Symptoms typical of tonsillitis (2 or more for dx) MMMMDCCLXII) Systemic disorders which
and pituitary) and more metabolically active thyroid MMMMDCCXXXVI) fever greater than 38.5, would put the patient at increased perioperative risk.
hormone MMMMDCCXXXVII) positive GABHS culture, MMMMDCCLXIII) Poor socioeconomic situation
MMMMDCCXI) T3 MMMMDCCXXXVIII) tender cervical MMMMDCCLXIV) Situation which would limit the
lymphadenopathy > 2cm, patient’s ability to return quickly to the hospital.
1172) Wolff-Chiakoff effect MMMMDCCXXXIX) erythematous or exudative MMMMDCCLXV) When the procedure is done
MMMMDCCXII) Large iodine load causes tonsils for a peritonsillar abscess.
transient inhibition of thyroid hormone production MMMMDCCLXVI) Those experiencing vomiting or
MMMMDCCXIII) Autoimmune thyroiditis may go 1180) Adult PSG results (3 categories) hemorrhage.
hypothyroid due to this effect MMMMDCCXL) Obstructive Sleep Apnea is
diagnosed as an RDI >5, SpO2 <90%. 1186) Most common cause of chronic benign pediatric
1173) Jod-Basedow phenomenon MMMMDCCXLI) Upper airway resistance lymphadenopathy, and easiest way to diagnose,
MMMMDCCXIV) Large iodine load in overactive syndrome is diagnosed as a RDI <5, and SpO2 treatmennt
states such as Grave’s or multinodular goiter >90%, MMMMDCCLXVII) Cat Scratch Disease
induces hyperthyroidism MMMMDCCXLII) Primary snoring when RDI <1 MMMMDCCLXVIII) Serologic testing
and SpO2 >90%. MMMMDCCLXIX) Azithromycin (or self limiting)
1174) Classification of hypothyroidism MMMMDCCLXX) Avoid I+D (draining tract)
MMMMDCCXV) Primary (gland) 1181) Only absolute indication for adenoidectomy
MMMMDCCXVI) Secondary (pituitary) MMMMDCCXLIII) airway obstruction with 1187) Condition in immunocomprimized patients with B.
MMMMDCCXVII) Tertiary (Hypothalamus) secondary cardiopulmonary complications and henselae infection
MMMMDCCXVIII) Peripheral resistence failure to thrive MMMMDCCLXXI) Bacillary angiomatosis

1175) Cause of Hashimoto’s 1182) Relative indications for adenoidectomy

1188) Typical presentation of child with mycobacterium 1192) Indications for Mohs surgery (Clinics of 1199) Describe SMAS connections from superior to
lymphadenitis and most common organism, and treatment Otolaryngology) inferior
MMMMDCCLXXII) Submandibular MMMMDCCLXXXVI) Recurrent skin cancer MMMMDCCCIX) SMAS equivalent to galea
lymphadenopathy, most common in under 12 MMMMDCCLXXXVII) Skin cancer in a “high risk MMMMDCCCX) Becomes temporoparietal
MMMMDCCLXXIII) Draining sinus from area if anatomic area” – ears, periauricular region, temporal fascia (same as superficial temporal fascia)
untreated, later calcifies region, periocular region, nasal tip ala, melolabial MMMMDCCCXI) Thins over zygomatic arch
MMMMDCCLXXIV) M.scrofulaceum sulcus, upper lip. MMMMDCCCXII) Superficial to parotid fascia
MMMMDCCLXXV) Surgical excision MMMMDCCLXXXVIII) Histologically aggressive skin MMMMDCCCXIII) Envelopes zygomaticus major
cancer – morpheaform, infiltrative type, sclerosing (which has cutaneous attachments at nasolabial
1189) Electron microscopy finding of Histiocytosis X and keratinizing (basosquamous or metatypical) fold)
MMMMDCCLXXVI) Birbeck granules MMMMDCCLXXXIX) Large skin cancer – defined by MMMMDCCCXIV) Neck – becomes platsma,
the location of tumor excision dehiscent medially and lateral to angle of mandible
1190) Ddx of granulomatous diseases of H+N MMMMDCCXC) Skin cancer with ill-defined
MMMMDCCLXXVII) Infectious clinical margins 1200) Two facial nerves most at risk in face lift, and most
i) Bacterial MMMMDCCXCI) Skin cancer in irradiated skin common nerve injury
(1) Cat scratch disease/Bacillary MMMMDCCXCII) Skin cancer in a cosmetically MMMMDCCCXV) Frontal (most common, and
angiomatosis important area least likely to recover) and marginal
(2) Rhinoscleroma MMMMDCCXCIII) Dermatofibrosarcoma MMMMDCCCXVI) Greater Auricular N
(3) TB protuberans
(4) Non-tuberculous mycobacterium MMMMDCCXCIV) Selected mucosal squamous 1201) Where does frontal branch cross the arch of the
(5) Leprosy cell carcinomas zygoma
(6) Syphilis MMMMDCCCXVII) 2 cm posterior to lateral
(7) Actinomycosis 1193) Mohs reconstructive options canthus
ii) Fungal MMMMDCCXCV) Secondary intention
(1) Histoplasmosis i) Medial canthus, forehead, temporal, concave 1202) Marginal mandibular is protected by platysma except
(a) Fibrosing mediastinitis areas (nasolabial), and perioricular for…
(b) Mediastinal granulomatosis MMMMDCCXCVI) Primary MMMMDCCCXVIII) Area 2 cm from oral
(2) Blastomycosis MMMMDCCXCVII) Skin Graft commissure
(3) Coccidiomycosis MMMMDCCXCVIII) Locoregional flap
(4) Candidiasis 1203) Plane of frontal bar above zygoma
(5) Rhinosporidious 1194) Two general types of locoregional flaps MMMMDCCCXIX) Between SMAS and superficial
(6) Aspirgillus/Mucorales MMMMDCCXCIX) Random Pattern – Subdermal layer of the deep temporal fascia
iii) Parasites plexus which arise from musculocutaneous plexus
(1) Leishmaniasis MMMMDCCC) Axial Pattern – direct cutaneous arteries 1204) Safe dissection plane at level of Zygoma and above
MMMMDCCLXXVIII) Trauma zygoma
i) Intubation 1195) Melolabial flap (superiorly based nasolabial) blood MMMMDCCCXX) Zygoma – subperiosteal
ii) Teflon granuloma supply MMMMDCCCXXI) Above – between deep and
MMMMDCCLXXIX) Neoplastic MMMMDCCCI) Perforators of levator labii superficial layers of the deep temporal fascia (sub-
i) Histiocytosis X (Langerhans Cell superioris muscle follicular plane)
Granulomatous)
ii) Pyogenic granuloma (Lobular capillary 1196) Nasal tip defect of less than 1.5 cm – alternative to 1205) Zygomatic and buccal branches – safe dissection
hemangioma) paramedian forehead plane
iii) Necrotizing Sialometaplasia MMMMDCCCII) Dorsal nasal flap – MMMMDCCCXXII) Supramuscular (innervates
iv) T-Cell lymphoma advancement flap of dorsal nasal skin based on the muscle on deep surface)
MMMMDCCLXXX) Idiopathic angular artery
i) Sarcoidosis 1206) Five planes of skin in neck
MMMMDCCLXXXI) Autoimmune/vasculitis 1197) 4 options for auricular reconstruction MMMMDCCCXXIII) Superficial Subcutaneous
i) Wegeners Granulomatous MMMMDCCCIII) Secondary intention (lobule and MMMMDCCCXXIV) Mid-subcutaneous
ii) Relapsing Polychondritis helix do the worst) MMMMDCCCXXV) Supraplatysma (ie
iii) Systemic lupus Erythematous MMMMDCCCIV) FTSG (post-auricular) SupraSMAS)
iv) Sjorgrens Syndrome MMMMDCCCV) Primary closure (helical defects MMMMDCCCXXVI) Subplatysma (ie SubSMAS)
v) Churg-Strauss syndrome <1.5cm) MMMMDCCCXXVII) Subperiosteal
MMMMDCCCVI) Composite graft from opposite
1191) 4 parts to pilosebaceous unit ear half of the width of defect 1207) Three layers of blood vessels in neck (from deep to
MMMMDCCLXXXII) hair follicle, superficial)
MMMMDCCLXXXIII) apocrine sweat gland, 1198) Borders of vermilion MMMMDCCCXXVIII) Musculocutaneous perforator
MMMMDCCLXXXIV) sebaceous gland MMMMDCCCVII) Made up of modified mucosa MMMMDCCCXXIX) Septocutaneous perforator
MMMMDCCLXXXV) errector pili muscle MMMMDCCCVIII) Vermilion border to innermost MMMMDCCCXXX) Subdermal plexus
point of mucosa where lips contact
1208) Ideal facelift patient
 MMMMDCCCXXXI) Elastic skin MMMMDCCCLVI) Prophylactic Cesarean section MMMMDCCCLXXX) Group II – edema and
MMMMDCCCXXXII) Little subcutaneous fat is not routinely recommended, hematoma, nondisplaced fracture, minor mucosal
MMMMDCCCXXXIII) Distinct bony landmarks (High MMMMDCCCLVII) should be strongly considered ingury, no exposed cartilage,
cheek bones and strong jaw line) in young, primiparous mothers with recent HPV MMMMDCCCLXXXI) Group III – massive edema,
MMMMDCCCXXXIV) High hyoid bone infection and genital warts mucosa tears, exposed cartilage, vocal cord
immobility,
1209) Preauricular incision difference in males and females 1219) Risk factor for increased spread of RRP MMMMDCCCLXXXII) Group IV – see group III, more
MMMMDCCCXXXV) Male pre-auricular crease MMMMDCCCLVIII) Juvenile, than two fractures, anterior commissure damage,
MMMMDCCCXXXVI) Female can go behind tragus MMMMDCCCLIX) young age, skeletal insufficiency,
MMMMDCCCLX) HPV type 11 MMMMDCCCLXXXIII) Group V – Laryngotracheal
1210) Four types of rhytidectomies separation
MMMMDCCCXXXVII) Subcutaneous 1220) Extralaryngeal spread in %age of adults and children
MMMMDCCCXXXVIII) Subcutaneous with SMAS MMMMDCCCLXI) 15% adult 1227) Indications for surgery for laryngeal trauma, such as
suspension MMMMDCCCLXII) 30% children MMMMDCCCLXXXIV) active bleeding,
MMMMDCCCXXXIX) Deep plane MMMMDCCCLXXXV) hemoptysis,
MMMMDCCCXL) Composite 1221) Where do RRP lesions occur MMMMDCCCLXXXVI) need for emergent surgical
MMMMDCCCXLI) Minimal access MMMMDCCCLXIII) Junction of respiratory and airway,
squamous epithelium MMMMDCCCLXXXVII) exposed cartilage and
1211) Two techniques of SMAS suspension i) limen vestibuli (junction of the nasal vestibule significant lacerations on laryngoscopy,
MMMMDCCCXLII) Plication and nasal cavity proper), MMMMDCCCLXXXVIII) air escaping through the neck
MMMMDCCCXLIII) Imbrication ii) nasopharyngeal surface of the soft palate, wound.
iii) midline laryngeal surface of the epiglottis, MMMMDCCCLXXXIX) multiple or displaced
1212) Deep facelift difference and purpose iv) upper and lower margins of the ventricle, cartilaginous fractures (especially if located median
MMMMDCCCXLIV) Areas of subSMAS dissection v) undersurface of the true vocal cords, or paramedian thyroid cartilage),
(superficial to zygomaticus major and minor) vi) carina, and MMMMDCCCXC) vocal cord immobility,
MMMMDCCCXLV) Improvement of nasolabial fold vii) bronchial spurs. MMMMDCCCXCI) fractured cricoid,
viii) tracheostomy site (iatrogenic junction) MMMMDCCCXCII) disruption of the cricoarytenoid
1213) Composite facelift purpose ix) GERD (causing squamous metaplasia) joint,
MMMMDCCCXLVI) Dissection continues to the MMMMDCCCXCIII) lacerations involving the free
bleph incision 1222) Hallmark triad of Juvenile RRP margin of the vocal cord or anterior commisure.
MMMMDCCCXLVII) Addresses all three zones of MMMMDCCCLXIV) relentlessly progressive MMMMDCCCXCIV) Group II-V often require
face hoarseness (most common symptom), surgery
MMMMDCCCLXV) stridor (non-positional), and
1214) Zones in facelift surgery MMMMDCCCLXVI) respiratory distress 1228) Medical management for laryngeal trauma (indicated
MMMMDCCCXLVIII) Zone 1 – cheek and lower face for Grade I)
MMMMDCCCXLIX) Zone 2 – periorbital area 1223) RRP: most common criteria for adjuvant treatment MMMMDCCCXCV) observation x 24h,
(inferior) include MMMMDCCCXCVI) HOB elevated,
MMMMDCCCL) Zone 3- forehead MMMMDCCCLXVII) more than 4 surgical MMMMDCCCXCVII) Systemic steroids,
procedures required per year, MMMMDCCCXCVIII) antibiotics (especially if
1215) Classify Recurrent Laryngeal Papillomatosis MMMMDCCCLXVIII) distal multisite spread, mucosal disruption),
MMMMDCCCLI) Adult onset (20-40 most MMMMDCCCLXIX) rapid regrowth of disease with MMMMDCCCXCIX) Voice rest,
commonly) airway compromise. MMMMCM) humidification,
MMMMDCCCLII) Junvenile onset (diagnosis MMMMCMI) Reflux precautions,
before age 12, most commonly dx 2-4 years old) 1224) Adjunctive therapies in RRP MMMMCMII) possible NG if mucosal damage
MMMMDCCCLXX) Alpha interferon
1216) Most common benign neoplasm of larynx in children MMMMDCCCLXXI) Photodynamic therapy 1229) Indications for endolaryngeal stenting
MMMMDCCCLIII) RRP MMMMDCCCLXXII) Indole-3-Carbinol MMMMCMIII) reserved for wounds involving disruption
MMMMDCCCLXXIII) Retinoic acid of the anterior commissure,
1217) What is the triad of Juvenile Onset Risk factors and MMMMDCCCLXXIV) Ribavirin MMMMCMIV) massive mucosal injuries
adult onset risk factors MMMMDCCCLXXV) Cidofovir (iv/intralesional) MMMMCMV) comminuted fractures of the laryngeal
MMMMDCCCLIV) Juvenile MMMMDCCCLXXVI) Acyclovir (co-infections skeleton. (2-3 weeks)
i) First born (75% of cases) treatment only)
ii) Vaginal delivery 1230) Surgical treatment of laryngeal trauma (3
iii) Teenage mother 1225) Natural history of RRP possibilites)
MMMMDCCCLV) Adult MMMMDCCCLXXVII) Spontaneous regression, MMMMCMVI) endoscopy,
i) Frequent oral sex MMMMDCCCLXXVIII) not associated with puberty MMMMCMVII) exploration, or
ii) multiple sex partners MMMMCMVIII)exploration with stenting
1226) Laryngotracheal Injury classification
1218) RRP C-section recommedations: MMMMDCCCLXXIX) Group I – minor hematoma, 1231) Gell and Coombs Type Hypersensitivity Reactions
edema or laceration with no fracture,
 MMMMCMIX) Type I – IgE immediate (Allergic rhinitis, MMMMCMXXX) Trees – spring iii)
Vascular dilation due to surrounding bone
anaphylaxis, asthma) MMMMCMXXXI) Grass - summer resorption
MMMMCMX) Type II – cytotoxic IgG or IgM MMMMCMXXXII) Weeds – fall (1) Schwartze sign
MMMMCMXI) Type III – Immune complex MMMMCMLIV)Mature (sclerotic phase)
MMMMCMXII) Type IV – Delayed type hypersensitivity 1239) List types of perennial allergens i) Deposition of new bone (sclerotic and less
MMMMCMXXXIII) Mold dense than normal bone)
1232) Describe 3 phases of allergic rhinitis MMMMCMXXXIV) Danders
MMMMCMXIII)Acute – due to histamine and other MMMMCMXXXV) Cockroach allergens 1246) Pathognomic histiologic sign in Otosclerosis
preformed/newly synthesized mediators Causes MMMMCMXXXVI) Dust mite MMMMCMLV) Blue Mantles of Manasseh
sneezing, itchy eyes, nose and throat, nasal
discharge. 1240) Most common pollen allergen and most common 1247) Layers of bone involved with otosclerosis
MMMMCMXIV) Intermediate or transitional – mold allergen and most common perennial allergens MMMMCMLVI) Always begins in endochondral bone, but
asymptomatic, due to recruitment and activation of MMMMCMXXXVII) Pollen – short ragweed later can involve endosteal or periosteal layers of
leukocytes into nasal tissue MMMMCMXXXVIII) Mold – Alternaria bone
MMMMCMXV) Late phase – 4-6 hours post exposure, MMMMCMXXXIX) Perennial – house dust mite
due to leukocytes in nasal tissue. Main symptom in (Dermatophagoides spp) 1248) Percentage of otosclerosis which is bilateral
nasal congestion MMMMCMLVII) 80%
1241) Indications for use of in-vitro allergy testing include
1233) Two cytologic findings with Allergic Rhinitis (from MMMMCMXL) impracticality of skin testing due to skin 1249) Percentage of otosclerosis with vestibular symptoms
inferior turbinate) disorder, drug inhibition or uncooperative patients, (most commonly disequilibrium)
MMMMCMXVI) Increased ratio of columnar MMMMCMXLI)clarification of skin test results from MMMMCMLVIII) 25%
epithelium to goblet cells (4:1 instead of 5:1) bizarre or borderline results,
MMMMCMXVII) Increased number of MMMMCMXLII) prevention of systemic 1250) What is the paracusis of Willis
eosinophils (>20% of granulocytes is suggestive of reactions in patients with a prior history of or MMMMCMLIX)Ability to hear better in the presence of
inhalant allergy) suspected anaphylactic reactions, asthma, or when background noise (seen with CHL)
testing for stinging hypersensitivity,
1234) Skin endpoint titration – technique and results MMMMCMXLIII) convenience of in vitro testing 1251) Ddx of otosclerosis
MMMMCMXVIII) 0.01 mL injected – wheel MMMMCMLX) Ossicular discontinuity
respose of 5 mm normal with control 1242) Treatment of Inhaled allergy i) Greater than 60 dB HL and type Ad
MMMMCMXIX) Induration (not erythema) is MMMMCMXLIV) Enviromental tympanogram
measured, serial increase by 2 mm is the endpoint MMMMCMXLV) Pharmacological MMMMCMLXI)Congenital Stapes fixation
titration. Recall that need a confirmatory wheel of i) Systemic decongestants i) Usually diagnosed in first decade of life
greater than 2 mm to confirm previous wheel which ii) Cromolyn ii) Only 10% (vs 66% with Otosclerosis) fmhx
also grew by at least 2 mm) iii) Antihistamines iii) Non-progressive hearing loss
iv) Leukotriene inhibitors MMMMCMLXII) Malleus head fixation
1235) Condition of positive skin endpoint titration with v) Inhaled steroids (mainly inhibits delayed i) If congenital – high incidence of aural atresia
control solution only reacation) ii) Type As tympanogram (only seen in the most
MMMMCMXX) Dermatographia vi) Systemic steroids advanced otosclerosis)
MMMMCMXLVI) Immunotherpy iii) Presense of tympanosclerosis
1236) Three abnormal wheeling patterns on SET MMMMCMLXIII) Pagets disease
MMMMCMXXI) Flash 1243) Most common sites of involvement in otosclerosis i) Increased alk phos
i) Day 1: 5-5-5-13-18-21 MMMMCMXLVII) fissula ante fenestrum (at the ii) CT findings seen on bilateral petrous bones
ii) Day 2: 5-5-5-5-7-9-11 anterior oval window) (demineralization)
MMMMCMXXII) Plateau MMMMCMXLVIII) round window niche (30-50% iii) Typically causes crowding of the ossicles in the
i) 7-7-9-9-11-11 of cases) epitympanium
ii) Confirmatory here is fifth injection with fourth MMMMCMXLIX) Anterior wall of IAC MMMMCMLXIV) Osteogenesis imperfecta
injection the SET i) Blue sclera
MMMMCMXXIII) Hourglass 1244) Define bipolar involvement, biscut footplate, and ii) History of multiple bone fractures
i) 9-7-5-5-7-9-11 obliterative otosclerosis
MMMMCML) Bipolar – both anterior and posterior ends 1252) Acoustic reflexs seen in otosclerosis as disease
1237) Factors influencing SET of footplate involved progresses
MMMMCMXXIV) Volume injected MMMMCMLI) Biscut footplate – involvement limited to MMMMCMLXV) early otosclerosis (even before
MMMMCMXXV) Skin reactivity (eg to trauma) the footplate any conductive hearing loss is detected) is a
MMMMCMXXVI) Increased Allergen exposure MMMMCMLII) Obliterative otosclerosis – entire footplate diphasic reflex pattern (ie increase compliance at the
(greater response during allergic season) and annular ligament involved onset and cessation of the sound stimulus).
MMMMCMXXVII) Food allergens MMMMCMLXVI) Acoustic reflex amplitudes are
MMMMCMXXVIII) Antihistamines 1245) Describe two histiologic phases of otosclerosis reduced,
MMMMCMXXIX) Age MMMMCMLIII) Active (otospongiosis phase) MMMMCMLXVII) Elevation of ipsilateral side
i) Osteocytes, osteoblasts and histiocytes thresholds, then
1238) Pollen season for seasonal allergens ii) Active bone resorption
 MMMMCMLXVIII) Contralateral thresholds, and MMMMCMXCIV) associated musculature, 1264) Classification of Benign Thyroid Disease
finally, MMMMCMXCV) superior laryngeal nerve and MMMMMXXVI) Benign Nontoxic
MMMMCMLXIX) Disappearance of the reflexes MMMMCMXCVI) recurrent laryngeal nerve for i) Diffuse and Nodular Goiter
that unit MMMMMXXVII) Benign Toxic
1253) Audiogram pattern i) Toxic multinodular goiter
MMMMCMLXX) Early – low frequency loss due 1259) Contraindications to supraglottic laryngectomy ii) Toxic adenoma
to stiffness effect MMMMCMXCVII) Involvement at the glottic level iii) Graves Disease
MMMMCMLXXI) Late – flattening of air line due MMMMCMXCVIII) Invasion of the cricoid or MMMMMXXVIII) Inflammatory
to mass effect thyroid cartilage i) Chronic (Hashimoto’s) thyroiditis
MMMMCMLXXII) Later – may see involvement of MMMMCMXCIX) Involvement of the tongue base ii) Subacute (de Quervain’s) thyroiditis
cochlea with high frequency sensioneural loss (ie to within 1 cm of the circumvallate papillae. iii) Riedel’s Thyroiditis
basal turn most commonly afftected) MMMMM) Patient medical factors
MMMMCMLXXIII) If primarily cochlear 1265) Treatment possibilities for goiter
otosclerosis, “cookie bite pattern” with a mixed 1260) Contraindications to Vertical Partial Laryngectomy MMMMMXXIX) Suppression therapy
hearing loss pattern (indicated for T1 or T2 glottic Ca with or without extension MMMMMXXX) Medical therapy
MMMMCMLXXIV) Carhart notch to supraglottis) MMMMMXXXI) I131
MMMMCMLXXV) Typical max CHL 50 dB MMMMMI) A fixed true vocal cord MMMMMXXXII) Surgical
MMMMMII) Involvement of the posterior commissure
1254) Criteria for diagnosis of pure sensioneural MMMMMIII) Invasion of bilateral arytenoids 1266) Approaches to oropharynx
otosclerosis MMMMMIV) Bulky transglottic lesions MMMMMXXXIII) Transoral
MMMMCMLXXVI) A positive Schwartze’s sign MMMMMV) Thyroid cartilage invasion i) True transoral
MMMMCMLXXVII) Family history of surgically MMMMMVI) More than 15 mm of subglottic extension ii) Pull down
confirmed stapedial otosclerosis anteriorly and 5 mm posteriorly MMMMMXXXIV) Mandibulotomy
MMMMCMLXXVIII) Symmetric progressive MMMMMVII) Lesion extending above the free edge of i) Lip split (mandibular swing)
sensorineural loss, with stapes fixation in one ear the false vocal cords superiorly. ii) Lateral mandibulotomy
MMMMCMLXXIX) Unusually good speech MMMMMVIII) More than 5 mm of contralateral true vocal iii) Mandibulectomy
discrimination for a pure sensorineural loss cord involvement MMMMMXXXV) Transcervical
MMMMCMLXXX) Onset of hearing loss at usual MMMMMIX) Pulmonary reserve i) Anterior
age for stapes fixation and progressing without other (1) Suprahyoid
known etiology 1261) List factors for treatment of glottic Ca with VPL (2) Subhyoid
MMMMCMLXXXI) CT scan in patient with one or compared to XRT ii) Lateral
more of above criteria that shows cochlear capsule MMMMMX) Radioresistant tumors (eg verrucous (1) High
demineralization (a negative scan does not preclude carcinoma) (2) Low
diagnosis because mature disease resemble normal MMMMMXI) Salivary gland malignancies
bone on CT) MMMMMXII) Benign laryngeal tumors 1267) Define epipericardial ridge
MMMMCMLXXXII) On-Off effect of impedance MMMMMXIII) Patients deemed unreliable for 6 weeks of MMMMMXXXVI) Collection of mesoderm forms
tympanometry XRT SCM, trap, lingual and infrahyoid musculature
MMMMMXIV) Young patients (due to the theoretical MMMMMXXXVII) Nerves present include XI and
1255) Contraindications to stapes surgery increased risk of late radiation-induced sarcoma) XII
MMMMCMLXXXIII) Menieres MMMMMXV) Neck nodes >2 cm in size favors primary
MMMMCMLXXXIV) TM perf surgery for both neck and primary. 1268) Proper surgical management of Type II first
MMMMCMLXXXV) AOM MMMMMXVI) Obese branchial arch abnormality
MMMMCMLXXXVI) Employment requiring excellent MMMMMXVII) T1 extending to anterior commisure MMMMMXXXVIII) Superficial parotidectomy, VII
balance identification, trace track back to origin (typically at
MMMMCMLXXXVII) Downsloping SNHL loss (often 1262) Factors that allow VPL for salvage after XRT the bony/cartilaginous junction of EAC) with cartilage
hearing will deteriorate postop) MMMMMXVIII) Limited to one TVC (anterior commissure resection. Relation to VII variable.
involvement is acceptable)
1256) Indications for fluoride therapy MMMMMXIX) Body of the arytenoid must be free of 1269) 3 and 4th Branchial abnormalites can manifest as
MMMMCMLXXXVIII) Non-surgical candidates tumor what condition in children
MMMMCMLXXXIX) Positive Schwartze’s sign pre- MMMMMXX) Subglottic extension must be <5-10 mm MMMMMXXXIX) Acute suppurative thyroiditis
op (Rx for 6 months prior to surgery) MMMMMXXI) The TVC must be mobile
MMMMCMXC) Otospongiosis type bone seen intraop MMMMMXXII) Thyroid cartilage must NOT be invaded 1270) What is CHAOS and two example of lesions that
MMMMMXXIII) The entire area of pre-XRT tumor can cause conditions
1257) Contraindication to any organ preserving laryngeal involvement must be encompassed in the resection MMMMMXL) Congenital High Airway Obstruction
surgery MMMMMXXIV) The lesion must extend no Syndrome
MMMMCMXCI) Cricoarytenoid joint involvement higher than the lateral wall of the ventricle MMMMMXLI) Lymphangiomas and teratomas located in
the anterior compartment.
1258) Define Cricoarytenoid unit 1263) Most common reconstruction after VPL
MMMMCMXCII) arytenoid cartilage, MMMMMXXV) Bipedicled Strap muscle flap 1271) Most common infectious organism in pediatric
MMMMCMXCIII) cricoid cartilage, bacterial cervical lymphadenitis
 MMMMMXLII) Strep Group A and S. Aureus 1282) TNM staging of Rhabdomyosarcoma ii)submental artery island flap, (submental
MMMMMLXVIII) T1 – tumor confined to branch of facial art)
1272) Bacterial cause of Lemierre’s Syndrome anatomic site of orgin iii) facial artery musculomucosal flap (FAMM)
MMMMMXLIII) Fusobacterium necroforium MMMMMLXIX) T2 – tumor spread to surrounding sites (includes some buccinator, and buccal fat)
i) a<5cm iv) Platysma flap
1273) Non-tuberculous vs tuberculous lymphadenopathy in ii) b>5cm v) deltopectoral flap (historical)
Pediatrics MMMMMLXX) N0 – no LN/ N1 - +LN MMMMMXCI) Free tissue transfer
MMMMMXLIV) Clinical – TB: single large node with MMMMMLXXI) M0- no mets/ M1 - + mets i) Free radial forearm
fevers and malaise, NTB: rarely systemic symptoms
MMMMMXLV) PPD –strongly positive in TB, weak or neg 1283) Discuss staging of Rhabdomyosarcoma of Head 1288) Options for reconstruction of Anterior Tongue
in NTB and neck in Peds MMMMMXCII) Up to 50% resection, no reconstruction or
MMMMMXLVI) Lung disease – often in TB, rare in NTB MMMMMLXXII) All head and neck (aside from STSG only
MMMMMXLVII) Violaceous skin changes in parameningeal site) M0 or better is stage 1 MMMMMXCIII)Larger or composite resection – Free
NTB MMMMMLXXIII) Parameningeal less than 5 cm radial forearm or Lateral arm flap for increased bulk
MMMMMXLVIII) Treatment – medical in TB, is stage 2 and greater than 5 cm is Stage 3 (based on posterior radial collateral artery).
NTB often resistant to medical, therefore often MMMMMLXXIV) M1 stage 4
require surgical excision 1289) Options for reconstruction of Buccal mucosa
1284) Ddx of small blue round cell tumors (Peds): MMMMMXCIV) Small – primary closure or
1274) Most sensitive tests for Mononucleosis MMMMMLXXV) Neuroblastoma, STSG
MMMMMXLIX) IgM and IgG for EBV (monospot MMMMMLXXVI) Ewing’s sarcoma, MMMMMXCV) Moderate – temporoparietal fascia flap
(heterophile Ab) negative in early disease) MMMMMLXXVII) NHL, (with STSG)
MMMMMLXXVIII) primitive neuroectodermal MMMMMXCVI) Larger/full thickness
1275) Most common pediatric Hand N malignancy tumors, i) Regional
MMMMML) Lymphoma (60% NHL and 40% HL) MMMMMLXXIX) undifferentiated soft-tissue ii) Distant – Pectoralis major or lat dorsi
sarcomas and iii) Free flap
1276) Pediatric NHL - %age that are high grade MMMMMLXXX) esthesioneuroblastoma
MMMMMLI) 90% 1290) Mandible reconstruction
1285) WHO classification of NPC MMMMMXCVII) Anterior
1277) Histo classification of NHL MMMMMLXXXI) Type I –Keratinizing Squamous i) Free fibular – minimal soft tissue defect
MMMMMLII) Low cell carcinoma ii) Scapula – circumflex scapular artery for large
MMMMMLIII) intermediate MMMMMLXXXII) Type II – Non-Keratinizing SCC tissue defect
MMMMMLIV) high MMMMMLXXXIII) Type III – Undifferentiated MMMMMXCVIII) Lateral
carcinoma (lymphoepithelioma) i) No reconstruction of mandible (soft tissue only)
1278) Classification of high-grade NHL ii) Low profile plate
MMMMMLV) Lymphoblastic 1286) flap physiology: Define stress, strain, creep, and iii) Iliac crest (Descending Circumflex iliac artery)
MMMMMLVI) Small cell noncleaved (Burkitts) stress relaxation. or scapula
MMMMMLVII) Large cell MMMMMLXXXIV) Stress: force applied per
cross-sectional area. 1291) Total glossectomy
1279) Staging of HL and NHL (Ann Arbor) MMMMMLXXXV) Strain: change in length divided MMMMMXCIX) Rectus abdominus
MMMMMLVIII) Stage I – single lymph node region or by the original length of the given tissue to which a MMMMMC) Lat dorsi
extralymphatic site force is applied.
MMMMMLIX) Stage II – multiple LN regions or one LN MMMMMLXXXVI) Creep: increase in strain seen 1292) Approach to Drooling
and one extralymphatic site on same side of when skin is under constant stress. This occurs MMMMMCI) Acute
diaphragm over a matter of minutes and is due to an extrusion MMMMMCII) Chronic
MMMMMLX) Stage III – LN on both sides of the of fluid from the dermis and a breakdown of the i) Medications
diaphram, and possible splenic involvement dermal framework. ii) Neurologic
MMMMMLXI) Stage IV – diffuse involvement of an MMMMMLXXXVII) stress relaxation: decrease in iii) Indirect (Nasal obstn, head position
extralymphatic organ stress when skin is held in tension at a constant malocclusion, tongue size, sitting position, and
MMMMMLXII) A or B subtypes (fever, night sweats, wt strain for a given time. This occurs over a matter of emotional state.)
loss more than 10%) days to weeks and is due to an increase in skin
cellularity and the permanent stretching of skin 1293) Treatment Options for drooling
1280) Classification of Hodgkin’s Lymphoma components. MMMMMCIII) Speech therapy
MMMMMLXIII) Lymphocyte predominate MMMMMCIV) Behavior therapy
MMMMMLXIV) mixed cellularity 1287) Options for reconstruction of floor of mouth MMMMMCV) Dental Appliance
MMMMMLXV) nodular sclerosing MMMMMLXXXVIII) STSG (small defect) MMMMMCVI) Drugs (glycopyorolate, trihexaphenydl,
MMMMMLXVI) lymphocyte deplete MMMMMLXXXIX) Local flaps Scopolamine Botox)
i) Nasolabial flap (moderate defect) MMMMMCVII) Radiation
1281) Pathognomic cell in HL MMMMMXC) Regional flaps (moderate defects) MMMMMCVIII)Surgery
MMMMMLXVII) Reed Sternberg cell i) forehead flap, (superficial temporal artery) i) Submandibular gland excision or duct re-
routing,
 ii) Parotid Duct ligation, 1299) Initial management of Unilateral and bilateral aural MMMMMCLII) Type IV – graft laid on stapes footplate
iii) trans-tympanic neurectomy, atresia MMMMMCLIII) Type Va – LSSC fenestration
iv) Intraductal laser photocoagulation MMMMMCXXXI) ABR for both - unilateral to MMMMMCLIV)Type Vb – Stapes fenestration
confirm other ear is normal, and evaluate cochlear
1294) Ddx of objective pulsatile tinnitus function for bilateral. 1309) Define marginal reflex distance
MMMMMCIX) AV malformation MMMMMCXXXII) Unilateral and bilateral need CT MMMMMCLV) Distance from corneal light reflex to the
MMMMMCX) Vascular tumors (paraganglioma) at age 5-6 margin of the lids.
MMMMMCXI) Venous Hum (high flow states such as MMMMMCXXXIII) Bilateral need bone conduction MMMMMCLVI) Normal upper lid distance is 4-5 mm and
thyrotoxicosis, pregnancy, anemia, or Benign hearing aids lower lid is 5 mm. (corresponds to upper lid just
intracranial hypertension), below limbus and lower lid at limbus).
MMMMMCXII) Dehiscent jugular bulb, 1300) Surgical correction of aural atresia absolute MMMMMCLVII) Reflex to limbus is 2.5 mm
MMMMMCXIII)aberrent carotid artery, contraindications above and below.
MMMMMCXIV) persistent stapedial artery, MMMMMCXXXIV) abnormal inner ear morphology MMMMMCLVIII) Palpebral fissure width is 10
MMMMMCXV) Paget’s Disease, demonstrated on CT scan mm.
MMMMMCXVI) atherosclerosis, MMMMMCXXXV) abnormal cochlear function
MMMMMCXVII) cardiac murmur, demonstrated by audiologic testing. 1310) Protractor and Retractors of upper lid
MMMMMCXVIII) vascular loops MMMMMCXXXVI) score of 5/10 is also a MMMMMCLIX)Protractor – orbicularis
contraindication MMMMMCLX) Retractor – levator and Mullers muscle
1295) Ddx of objective non-pulsatile tinnitus 1311) Which muscle is important in the lacrimal extretory
MMMMMCXIX) Palatal myoclonus, 1301) Two approaches to aural atesia repair pump
MMMMMCXX) Idiopathic stapedius muscle contraction, MMMMMCXXXVII) transmastoid approach MMMMMCLXI)Horner’s muscle (Deep head of pretarsal
MMMMMCXXI) Patulous eustachian tube MMMMMCXXXVIII) anterior approach orbicularis)

1296) Classification of Congential Aural Atresia 1302) Describe the typical facial n course abnormalities 1312) Options for lower lid reconstruction
MMMMMCXXII) Group I atresia is characterized seen in Aural atresia MMMMMCLXII) Primary closure (30% loss in
by a small EAC, hypoplastic temporal bone and MMMMMCXXXIX) More anterolateral than usual young and 45% loss in elderly)
tympanic membrane (TM), a normal or small middle MMMMMCXL) angle at the second genu is about 60 MMMMMCLXIII) Lateral Cantholysis
ear cleft and normal or mildly deformed ossicles. degrees vs 90-120 normally, MMMMMCLXIV) Tenzel rotational flap
MMMMMCXXIII) Group II includes those cases MMMMMCXLI)nerve moves more lateral as it crosses MMMMMCLXV) Hughes procedure
with an absent EAC, an atretic plate, a small middle middle ear. (nerve may be lateral to middle ear MMMMMCLXVI) Free tarsal grafts
ear space and fixed and malformed ossicles. encased in atretic bone at position of round window MMMMMCLXVII) Mustarde (cheek rotational) flap
MMMMMCXXIV) Group III is characterized by an
absent EAC, a severely contracted or absent middle 1303) blood supply to tympanic membrane 1313) Options for upper lid reconstruction
ear space, and absent or severely malformed MMMMMCXLII) Lateral surface – deep auricular MMMMMCLXVIII) Primary closure
ossicles. art MMMMMCLXIX) Lateral cantholysis
MMMMMCXLIII) Medial surface – anterior MMMMMCLXX) Tenzel flap
1297) Major and Minor classification of aural atresia tympanic artery MMMMMCLXXI) Sliding tarso-conjunctival flap
MMMMMCXXV) The minor category is MMMMMCXLIV) Both from Imax MMMMMCLXXII) Posterior lamellar graft with
characterized by normal mastoid pneumatization, myocutaneous flap
normal oval window, reasonable oval window-facial 1304) Dividing line between the pars flaccida and tensa MMMMMCLXXIII) Cutler-Beard (bridge) flap
nerve relationship and a normal inner ear. MMMMMCXLV) Anterior and posterior mallear MMMMMCLXXIV) Pedicled flap from lower lid
MMMMMCXXVI) The major category is folds
comprised of cases with poor pneumatization, 1314) normal of subglottic diameter (at level of cricoid) at
abnormal or absent oval window, abnormal course of 1305) Number of dB gained by middle ear mechanism birth:
the horizontal facial nerve and inner ear anomalies MMMMMCXLVI) 25dB MMMMMCLXXV) 4.5 – 5.5 mm

1298) Jahrsdoerfer classification of aural atresia. 1306) Small perforations selectively reduce which 1315) Diagnosis of subglottic stenosis:
MMMMMCXXVII) score (up to 10) based upon frequencies MMMMMCLXXVI) less than or equal to 4mm full
findings of high-resolution CT scans of the temporal MMMMMCXLVII) Lower increasingly more term 3.5 mm premature
bone. affected
MMMMMCXXVIII) 1 point - open oval window, 1316) Biped epiglottis – what other test required
width of the middle ear cleft, facial nerve course, 1307) New perforation of TM – how long wait until repair Thyroid function
malleus-incus complex, mastoid pneumatization, MMMMMCXLVIII) 3 months
incudostapedial continuity, round window patency 1317) Classification of laryngeal (saccule) cysts
and auricle appearance – 1308) Classification of tympanoplasty MMMMMCLXXVII) Superior (extending into
MMMMMCXXIX) 2 points - presence of a stapes. MMMMMCXLIX) Type I – myringoplasty (no ventricle) and
MMMMMCXXX) Less than or equal 5 – not ossicular reconstruction) MMMMMCLXXVIII) posterior (extending into the AE
surgical candidates. 8 or better – 80% success MMMMMCL) Type II – malleus eroded, grafted on to folds and false cord)
malleus remnant or incus
MMMMMCLI) Type III – myringostapedopexy or PORP 1318) Ddx of congenital supraglottic abnormalities
 MMMMMCLXXIX) Laryngomalacia, 1324) Standard of care for subglottic hemangioma, and MMMMMCCXXVI) exposure of cartilage during
MMMMMCLXXX) Hemangioma, other treatment options laser excision leading to chondritis,
MMMMMCLXXXI) lymphatic malformation, MMMMMCCII) Standard of care = Tracheostomy and MMMMMCCXXVII) severe bacterial infection,
MMMMMCLXXXII) Laryngocele, wait for involution MMMMMCCXXVIII) posterior inlet scarring with
MMMMMCLXXXIII) Saccular cyst, MMMMMCCIII)Medical – steroids (intralesional or arytenoid fixation,
MMMMMCLXXXIV) anomalous cuneiform cartilage, systemic) MMMMMCCXXIX) combined laryngeal or tracheal
MMMMMCLXXXV) Bifed epiglottis, MMMMMCCIV) Cryotherapy stenosis or
MMMMMCLXXXVI) supraglottic web MMMMMCCV) Sclerosing therapy MMMMMCCXXX) vertical scar length >1cm.
MMMMMCCVI) Radiation therapy
1319) Techniques for improving airway in bilateral vocal (brachytherapy or external beam) 1332) Indications for anterior cricoid split
cord paralysis: MMMMMCCVII) CO2 or KTP laser procedure MMMMMCCXXXI) extubation failure on two
MMMMMCLXXXVII) CO2 laser cordotomy MMMMMCCVIII) Open procedure (resection) occasions or more due to laryngeal pathology,
MMMMMCLXXXVIII) open arytenoidectomy, MMMMMCCXXXII) weight >1500g,
MMMMMCLXXXIX) artenoidpexy, 1325) Define Pallister-Hall syndrome MMMMMCCXXXIII) no assisted ventilation for 10
MMMMMCXC) arytenoid separation with cartilage grafting MMMMMCCIX) Hypothalamus abnormalities days prior to evaluation,
MMMMMCXCI) laser arytenoidectomy and MMMMMCCX) polydactly MMMMMCCXXXIV) O2 requirements <30%,
cordectomy MMMMMCCXI) laryngeal (clefts or biped MMMMMCCXXXV) no CHF for one month prior to
MMMMMCXCII) laryngeal reanimation epiglottis) evaluation,
techniques (phrenic to RLN, phrenic to PCA, or MMMMMCCXXXVI) no acute respiratory tract
omohyoid muscle pedicle) 1326) Best imaging study for laryngeal cleft infection,
MMMMMCCXII) Ba swallow MMMMMCCXXXVII) no antihypertensive
1320) Classification of glottic webs medications ten days prior to evaluation
MMMMMCXCIII) Type I – less than 35% of 1327) Classification of laryngeal clefts
glottic opening, true cords visable, little or no MMMMMCCXIII) type I clefts as a supraglottic, 1333) How much distraction of the cricoid is required for a
subglottic extension, airway not a problem, mildly interarytenoid clefts. cartilage graft to be placed in the anterior split
abnormal cry MMMMMCCXIV) Type II clefts are a partial MMMMMCCXXXVIII) 3mm
MMMMMCXCIV) Type II - anterior webbing cricoid cleft.
involving 35-50% of glottis, thickened web that MMMMMCCXV) Type III clefts are a complete 1334) Indications for Laryngofissure with division of
extends into subglottis, cricoid normal, airway a cricoid cleft with or without extension into the posterior cricoid lamina
problem only with URTI or post intubation, weak esophagus and MMMMMCCXXXIX) patients with posterior
voice MMMMMCCXVI) type IV cleft are full subglottic stenosis,
MMMMMCXCV) Type III – 50-75% obstruction, laryngotrachealesophageal clefts. MMMMMCCXL) posterior glottic stenosis that
thick web with vocal cords not visable, cricoid extends to the glottis,
abnormalites, marked airway and voice problems 1328) Age 1 and recurrent croup – what investigation MMMMMCCXLI) complete or circumferential
MMMMMCXCVI) Type IV – 75-90%, web thick MMMMMCCXVII) Endoscopy – R/O subglottic stenosis, or
and vocal cords not visible, immediate airway stenosis MMMMMCCXLII) if there is significant cricoid
management needed at birth deformity
1329) McCaffrey system classifies laryngotracheal
1321) Treatment of glottic webs stenosis 1335) Indication for two step procedure with LTR:
MMMMMCXCVII) Type I – divide with laser/cold MMMMMCCXVIII) stage I lesions are confined to MMMMMCCXLIII) severe stenosis,
at age 3-4 the subglottis or trachea and are less than 1cm long, MMMMMCCXLIV) history of reactive airway, or
MMMMMCXCVIII) Type II – incise along one cord MMMMMCCXIX) stage II lesions are isolated to MMMMMCCXLV) poor pulmonary function,
then serial dilations or incise along other cord two the subglottis and are greater then 1 cm long, MMMMMCCXLVI) institutions with inadequate
weeks later. If keel required, trach needed MMMMMCCXX) stage III are subglottic/tracheal intensive care facilities
MMMMMCXCIX) Type III/IV – trach, corrective lesions not involving the glottis, and
procedure at age 3-4… laryngotomy, with keel MMMMMCCXXI) stage IV lesions involve the 1336) Define tubercles of Zuckerkandl
incison or LTR glottis MMMMMCCXLVII) posterior extensions of each
thyroid lobe
1322) CHOAS – how diagnosed and findings 1330) Which has worse symptoms and prognosis:
MMMMMCC) Ultrasound findings in utero for diagnosis Congenital or aquired Subglottic stenosis 1337) Advantages of free flap
i) Large echogenic lungs MMMMMCCXXII) Aquired, Congenital tends to MMMMMCCXLVIII) Two team approach
ii) flattened diaphrams improve with growth of the child MMMMMCCXLIX) Improved vascularity and
iii) Dilated airways below the level of the upper wound healing
airway obstruction 1331) Failure of endoscopic techniques are associated MMMMMCCL) Low rate of resorption
iv) fetal ascites with… MMMMMCCLI) Defect size of little
MMMMMCCXXIII) previous attempts at consequence
1323) EXIT procedure endoscopic repair, MMMMMCCLII) Potential for sensory and motor
MMMMMCCI) Ex-utero intrapartum delivery MMMMMCCXXIV) circumferential scarring, innervation
MMMMMCCXXV) loss of cartilaginous support, MMMMMCCLIII) Permits use of osseointegrated
implants
 MMMMMCCLIV) Two team approach MMMMMCCLXXIII) Associated with sinusitis and iii) Gad – intense lesion (but less than AN)
MMMMMCCLV) Improved vascularity and bronchiectasis MMMMMCCLXXXVIII) General features
wound healing MMMMMCCLXXIV) Patients with KO (vs i) Obtuse angles to temporal bone
MMMMMCCLVI) Low rate of resorption Cholesteatoma) are ii) Dural tail present (50-75%)
MMMMMCCLVII) Defect size of little i) Younger iii) May herniated into MCF (50%)
consequence ii) Less or no draining ear iv) May show calcification (25%)
MMMMMCCLVIII) Potential for sensory and motor iii) More generalized in position (compared to v) Pial blood vessels with flow voids
innervation Choles. which is just localized to lateral to vi) No widening of porus acousticus
MMMMMCCLIX) Permits use of osseointegrated annulus)
implants iv) Widens EAC (but doesn’t destroy bone) 1349) Radiographic features of epidermoid
MMMMMCCLXXXIX) CT
1338) End to side anastamosis – maximum angle of 1344) Most common feeding vessels of paragangliomas i) Hypodense to CSF
anastamotic vessels MMMMMCCLXXV) Ascending pharyngeal (most MMMMMCCXC) MRI
MMMMMCCLX) Less than 60 degrees common) i) T1 – isointense to CSF (dark –low signal
MMMMMCCLXXVI) Postauricular intensity)
MMMMMCCLXXVII) Occipitial ii) T2- isointense to CSF (“v. bright”)
MMMMMCCLXXVIII) Imax iii) FLAIR – heterogeneous with hyperintense foci
MMMMMCCLXXIX) Ipsi or contra ICA iv) CISS, diffusion weighted
MMMMMCCXCI) General
1339) Techniques for vessels mismatch 1345) MRI – labyrinthine enhancement before and after i) May dumbbell into MCF or contralateral cistern
MMMMMCCLXI) Less than 2:1 – uneven stiches contrast ii) Cauliflower surface appearance
end to end, dilation MMMMMCCLXXX) Before – blood (ie trauma) iii) Similar to arachnoid cyst (CISS, DW useful)
MMMMMCCLXII) 2:1 – 3:1 – beveled or spulation MMMMMCCLXXXI) After – inflammation (ie iv) T1 being low signal intensity differentiates from
(max angle of beveling is 30 degrees) labyrinthitis) cholesterol granuloma in petrous apex lesions
MMMMMCCLXIII) More than 3:1 – end to side
1346) Most useful imaging for treatment progress of MOE 1350) Radiographic features of Arachnoid Cyst
1340) Greatest period of flap failure and most common site MMMMMCCLXXXII) Iridium 111 WBC scan or MMMMMCCXCII) CT
MMMMMCCLXIV) 15-20 post anastamosis, then SPECT scan i) Isointense to CSF
the first 3 days MMMMMCCXCIII) MRI
MMMMMCCLXV) Venous anastamosis 1347) Radiographic features of Acoustic Neuroma i) T1 and T2– isointense to CSF homogeneous
MMMMMCCLXXXIII) CT – lesion
1341) No re-flow phenonmenon i) Non contrast: usually isodense to brain, MMMMMCCXCIV) General
MMMMMCCLXVI) Failure to establish re-perfusion calcifications and central necrosis rare. Larger i) Smooth surface
of blood supply after blood vessel repair to an lesions central necrosis
ischemic organ is known as the no-reflow ii) Contrast: 90% of non treated and not large 1351) Radiographic findings of Cholesterol granuloma
phenomenon tumors enhance homogenously MMMMMCCXCV) CT – soft tissue mass
MMMMMCCLXVII) Occurs after 12 hours MMMMMCCLXXXIV) MRI MMMMMCCXCVI) MRI T1 and T2 – both intense,
MMMMMCCLXVIII) Ischemia-induced no-reflow i) T1 – isointense to brain, hyperintense to CSF may show central hypointensity
phenomenon is caused by endothelial injury, cellular ii) T2 – hyperintense to brain, iso/hypointense to
swelling, intravascular (platelet) aggregation, and the CSF 1352) List 5 dysplasias affecting the temporal bone
leakage of intravascular fluid into the interstitial iii) Gad – intense enhancement on T1 MMMMMCCXCVII) Fibrous dysplasia
space MMMMMCCLXXXV) General features MMMMMCCXCVIII) Pagets disease
MMMMMCCLXIX) Severity of this effect is i) Centered on porus acousticus MMMMMCCXCIX) Hyperparathyroidism
correlated with ischemia time ii) Acute angles to temporal bone MMMMMCCC)Osteogenesis imperfecti
iii) Homogeneous enhancement MMMMMCCCI) McCune-Albright Syndrome
1342) Exostosis vs Osteomas iv) No dural tail
MMMMMCCLXX) Exostosis… v) Rare calcifications 1353) Most common primary lesion of petrous apex
i) More common vi) Enlarged IAC (>2 mm compared to MMMMMCCCII) Cholesterol granuloma
ii) Found in medial portion of the canal contralateral side)
iii) Found along tympanomastoid suture line and vii) Rare extension anteriorly and superiorly 1354) Classification of microtia
tympanosquamous suture line viii) Almost never dumbbell into MCF MMMMMCCCIII) Grade 1 – pinna with all
iv) Multiple in number subunits present but misshapen
v) Sessile, broad base 1348) Radiographic features of Meningoma MMMMMCCCIV) Grade II – anatomic subunits
vi) Associated with cold water exposure MMMMMCCLXXXVI) CT either deficient or absent
MMMMMCCLXXI) Osteoma…the opposite i) Isodense to brain, may see calcifications MMMMMCCCV) Grade III – “peanut ear”
MMMMMCCLXXII) Radiographically…both show MMMMMCCLXXXVII) MRI (nubbin of cartilage in the superior remnant and
an intact cortex i) T1 – isointense to brain, not homogeneous with inferior lobule) or anotia
central hypointensity if larger
1343) Keratitis Obturans – seen with which conditions and ii) T2 – hyperintense to brain, and hypointense to 1355) Describe the Brent technique of microtia repair
contrast to Cholesteatoma CSF
 MMMMMCCCVI) Stage 1 – auricular framework (c) Anterior and Posterior Cricoid split
fabrication with rib cartilage 1361) Most important factor for ETT as causing SGS, and (with cartilage graft)
MMMMMCCCVII) Stage 2 - Lobule transposition list others (d) Four quadrant LTR
MMMMMCCCVIII) Stage 3 - Auricular framework MMMMMCCCXXI) Duration intubation (2) Segmental resection (Cricotracheal
elevation MMMMMCCCXXII) Other include resection)
MMMMMCCCIX) Stage 4 - Tragus reconstruction i) Size of ETT (a) Primary
1356) Describe the Nagata technique of microtia repair ii) Movement of ETT (b) Salvage
MMMMMCCCX) Stage 1 - Fabrication of the iii) Traumatic intubation (c) Extended CTR (CTR with expansion
auricular framework, tragus reconstruction and iv) Number of reintubations procedure, arytenoid lateralization or
lobule transposition v) Presence of an infection while intubated arytenoidectomy)
MMMMMCCCXI) Stage 2 – Framework elevation
1362) Ddx of laryngotracheal stenosis 1364) Contraindications to airway surgery
1357) Indication for prosthetic reconstruction MMMMMCCCXXIII) Congenital MMMMMCCCXXX) Absolute
MMMMMCCCXII) Failed autogenous i) Tracheomalacia i) Tracheotomy dependent (aspiration, severe
reconstruction ii) Laryngomalacia BPD)
MMMMMCCCXIII) Significant soft tissue/skeleton iii) VC paralysis ii) Severe GER refractive to surgical and medical
hypoplasia iv) Laryngeal cleft therapy
MMMMMCCCXIV) Low hairline v) Congenital cysts iii) Unable for GA
MMMMMCCCXV) Aquired total or subtotal defect vi) Extrinsic compression for congenital lesion MMMMMCCCXXXI) Relative
usually in adults (1) Vascular compression i) Diabetes
(a) Innominate artery ii) Steroid use
1358) Classification of Subglottic stenosis (b) Right sided aortic arch iii) Cardiac, renal or pulmonary disease
MMMMMCCCXVI) Congenital SGS (c) Aberrant left pulmonary artery
i) Membranous (2) Mass 1365) Risk factors for failure of Endoscopic procedure
ii) Cartilaginous (a) Teratoma MMMMMCCCXXXII) previous attempts at
(1) Cricoid cartilage deformity (b) Lymphatic malformation endoscopic repair,
(a) Small cricoid (c) Hemangioma MMMMMCCCXXXIII) circumferential scarring,
(b) Elliptical cricoid MMMMMCCCXXIV) Infectious/inflammatory MMMMMCCCXXXIV) loss of cartilaginous support,
(c) Large anterior lamina i) Croup MMMMMCCCXXXV) exposure of cartilage during
(d) Large posterior lamina ii) Retropharyngeal abscess laser excision leading to chondritis,
(e) Generalized thickening iii) GER MMMMMCCCXXXVI) severe bacterial infection,
(f) Submucous cleft iv) Tracheitis MMMMMCCCXXXVII) posterior inlet scarring with
(2) Trapped first ring MMMMMCCCXXV) Neoplastic arytenoid fixation,
MMMMMCCCXVII) Aquired SGS i) Subglottic hemangioma MMMMMCCCXXXVIII) combined laryngeal or tracheal
i) Intubation ii) RRP stenosis or
ii) Laryngeal Trauma MMMMMCCCXXVI) Traumatic MMMMMCCCXXXIX) vertical scar length >1cm
(1) Previous airway surgery i) External compression
(a) High tracheostomy ii) Foreign body 1366) Indications for Anterior cricoid split
(b) Cricothryoidotomy MMMMMCCCXL) extubation failure on two
(c) Prior respiratory papillomatosis 1363) Treatment of SGS occasions or more due to laryngeal pathology, w
(d) Prior laser surgery for hemangioma MMMMMCCCXXVII) Medical (Reflux) MMMMMCCCXLI) eight >1500g,
(2) Accidential MMMMMCCCXXVIII) Observation MMMMMCCCXLII) no assisted ventilation for 10
(a) Inhalational i) Grade I and mild Grade II with minimal days prior to evaluation,
(b) trauma symptoms and reliable follow up (repeat bronch MMMMMCCCXLIII) O2 requirements <30%,
iii) Autoimmune q3-6 months) MMMMMCCCXLIV) no CHF for one month prior to
iv) Infection ii) Especially usuful for congenital evaluation,
v) GER MMMMMCCCXXIX) Surgical MMMMMCCCXLV) no acute respiratory tract
vi) Inflammatory disease i) Tracheostomy infection,
(1) Wegeners ii) Endoscopic MMMMMCCCXLVI) no antihypertensive
(2) Sarcoidosis (1) Dilation medications ten days prior to evaluation
(3) SLE (2) Laser
vii) Neoplasm iii) Open procedure (laryngotracheoplasty, 1367) Ideal ET tube size for adult and child
MMMMMCCCXVIII) Idiopathic SGS Laryngotracheal reconstruction) MMMMMCCCXLVII) Adult: cuff leak at 20-25 cm
(1) Expansion procedure (one stage or with water
1359) Definition of Congenital SGS (vs Aquired SGS) trach and stent) MMMMMCCCXLVIII) Child: cuff leak at 20cm water
MMMMMCCCXIX) No hx of ETT or laryngeal (a) Anterior cricoid split (with or without
trauma cartilage graft) 1368) Safe length of time for intubation in adults and
(b) Posterior cricoid split (with or without children
1360) Most common cause of aquired SGS cartilage graft) MMMMMCCCXLIX) Adults: 5-10 days
MMMMMCCCXX) ETT (90%) MMMMMCCCL) Children: ? Up to 50 days
 iv) Temporal fascia sling repair of ectropion
1369) How long to wait if recovery potential of VII before v) Tarsorrhaphy
reanimation and what is maximum length of time post vi) Formal brow lift
injury for restoration of neural input. (1) Direct incision
MMMMMCCCLI) 1 year for recovery (2) Mid forehead incision
MMMMMCCCLII) 3 years is max length (3) Pretricheal incision
vii) Rhytidectomy with SMAS placation
1370) Rank best procedures for outcome of facial nerve viii) Lower lip wedge resection with transposition of
reanimation orbicularis oris
MMMMMCCCLIII) Best: One which restores ix) Botox injection for synkinesis or hypertonia
neural input (ie distal facial nerve available)
MMMMMCCCLIV) 2nd: Replace nonfunctional 1374) Indications for muscle transfer techniques
facial neuromuscular units (regional or free muscle MMMMMCCCLXVII) long-standing paralysis (greater
transfer) than 3-4 years) with a small chance of recovery
MMMMMCCCLV) 3rd: Statically resuspend facial using nerve grafting procedures,
tissues MMMMMCCCLXVIII) lack of intact facial
neuromuscular units due to fibrosis, a
MMMMMCCCLXIX) trophy or congenital absence
1371) Functional defects of facial nerve paralysis and
MMMMMCCCLVI) Lagopthalmos and ectropion MMMMMCCCLXX) patient contraindications to
MMMMMCCCLVII) Oral incompetence nerve crossover techniques
MMMMMCCCLVIII) Nasal obstruction
MMMMMCCCLIX) Mastication difficulties 1375) Treatment algorithm for facial nerve paralysis
MMMMMCCCLX) Articulation difficulties reamination
MMMMMCCCLXXI) Duration since facial n injury
1372) Goals of surgery i) Greater than 3 years
MMMMMCCCLXI) Functional (1) Healthy patient
i) Eye protection (a) Regional/free muscle transfer
ii) Oral competence (2) Unhealthy patient, poor prognosis
MMMMMCCCLXII) Cosmo (a) Static resuspension
i) Symmetry ii) Less than 3 years
ii) Volitional facial expressions (1) Unhealthy patient, poor prognosis
(a) Static resuspension
1373) Classification of facial N rehabilitation procedures (2) Healthy patient, good prognosis
MMMMMCCCLXIII) Restore neural input (Dynamic) (a) Facial N present, and disease free
i) Direct reanastamosis (i) No
ii) Cable graft 1. regional/free muscle
iii) Nerve cross over technique (XI, XII) transfer
iv) Cross facial Nerve grafting technique (ii) Yes
MMMMMCCCLXIV) Replace nonfunctional facial 1. proximal n available
muscles (dynamic) a. Yes
i) Regional i. End-to end
(1) Temporalis anastamosis or
(2) Masseter interposition
ii) Microvascular (with facial nerve crossover) graft
(1) Extensor digitorum brevis b. No
(2) Gracilis i. Cross over or
(3) Lat dorsi cross facial
(4) Pec major graft
MMMMMCCCLXV) Static resuspension facial
tissues
i) Elevation of oral commissure
ii) Elevation of ptotic brow
iii) Materials include tensa fascia lata, goretex, or
alloderm
MMMMMCCCLXVI) Specific defects
i) Gold weight implant
ii) Palpebral spring
iii) Wedge resection and lateral canthopexy (for
ectropion)