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168 Cards in this Set
- Front
- Back
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Whatis the suspected mechanism of SIDS and how is placement in the supineposition protective?
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A:Laryngeal chemoreflex (LCR) Protective reflex in adults but immature response in kids Bradycardia, apnea, worsened by preexisting hypoxemia A:Decreasing the hypercarbia associated with the prone position whichpotentiates the LCR (bad) |
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Brieflyoutline the Embryology of the Larynx |
A:4 weeks – Formation of the Laryngotracheal Groove in the ventralwall of the primitive pharynx A:5-7 weeks – Elongation of the Laryngotracheal Diverticulum,separated from the dorsal foregut by the Tracheoesophageal Septum A:8-9 weeks – Epithelial proliferation obliterates the laryngeallumenA:10 weeks – Recanalization of the laryngeal lumen is complete |
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Five layers of vocal cord
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A: Mucosal layer – Stratified Nonkeratinizing squamous epithelium
A: Lamina propria, Superficial layer (Reinke’s space) – Few fibroblasts, scant elastic and collagen fibers A: Lamina propria, Intermediate layer – Mainly Elastic fibers, few fibroblasts A: Lamina propria, Deep layer – Collagenous fibers, fibroblasts A: Thyroarytenoid/Vocalis Muscle 3: Addendum: Epithelium types in upper aerodigestive tract: - PSCCE with goblet cells: Nasal cavity beyond limen vestibuli, ET (possibly no PS), Anterior NP, larynx except for TVC and FVC edges - NKSSE: Oral cavity, OP, HP majority of NP (posterior NP to vomer superiorly to ET orifice laterally to palate inferiorly) - Middle ear cleft: ciliated columnar with areas of simple cuboidal epithelium (look up) |
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Six intrinsic muscles of larynx
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A: With conus elasticusThyroarytenoid (vocalis)InterartyenoidLateral cricoarytenoidPosterior cricoarytenoidA: With quadrangular membraneThyroepiglotticAryepiglotticThyroarytenoid (F. Ling)
A: Cricothyroid (disputed) |
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2 motor and 2 sensory innervations of the larynx?
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A: Sensory: internal laryngeal branch of SLN (supraglottis & glottis), RLN (glottis & subglottis) A: Motor: external laryngeal branch of SLN (cricothyroid), RLN (all other intrinsics)A: Nerve of Galen anastomosis btwn SLN and RLN at glottis |
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Superior Laryngeal innervation |
A: Comes off of CN X at lower aspect of Nodose ganglion, ~36 mm from jugular foramen A: Internal branch – Sensory, enters larynx with superior laryngeal artery off of superior thyroid artery through Thyrohyoid membrane, supplies false cord, epiglottis, pyriform sinus, Glottis and partly subglottis (mainly RLN) A: External branch – Motor, supplies Cricothyroid |
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What muscles are the main abductor & adductors of the vocal cord? |
A: Abductor – Posterior cricoarytenoid, supplied by the abductor branch of the recurrent laryngeal nerve A: Adductors (3) – Lateral cricoarytenoid, Thyroarytenoid/vocalis, Interarytenoid |
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Name the four muscles controlling laryngeal elevation |
A: Digastric – Anterior (V) & Posterior (VII) bellies A: Mylohyoid (V) A: Stylohyoid (VII)A: Geniohyoid (C1) |
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Name the four muscles controlling laryngeal depression |
A: SternohyoidA: Sternothyroid A: Thyrohyoid A: Omohyoid3: All innervated by Ansa cervicalis (C1-3) except TH (C1) like GH |
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What five conditions must be met for normal phonation to occur? |
A: Adequate expiratory force A: Approximation of the vocal folds A: Favorable vibratory propertiesA: Control of length and tension A: Favorable vocal fold shape |
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Describe the cover-body theory (Fujimura) and the corresponding vocal cord layers |
A: Cover – Mucosa (nonkeratinized stratified squamous epithelium) and superficial lamina propria (Reinke’s space) A: Transition – Middle & Deep layers of lamina propria A: Body – Vocalis muscle |
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Four primary functions of the larynx |
A: Airway protection A: RespirationA: Phonation A: Valsalva (for heavy lifting) |
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What are the five component processes of speech? |
A: Respiration/Generator – Lungs produce airflow through URT A: Phonation – Sound production by the vocal cords A: Resonance – Modulation of phonatory output by vibration in the chest, pharynx and head with selective amplification of certain component frequencies A: Articulation – Formation of consonants & vowels, controlled by lips, tongue, palate, pharynx A: Prosody – Intonation |
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Six advantages of Rigid endoscopes |
A: Higher resolution A: Brighter, clearer pictures A: Contrast is better A: Large selection of viewing angles A: Image is more accurately magnified than with a flexible endoscope A: The examination is simple and does not usually require topical anesthetic |
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Disadvantages of Rigid endoscopes |
A: Phonation is limited to sustained vowels A: Unnatural positioning with extended neck and protruded tongue A: The size of a glottic gap might appear exaggerated A: Mobility of arytenoids may not be accurately assessed A: Disorders more evident in connected speech rather than sustained vowels are not as well documented (e.g. MTD, SD) 3: A lateral approach to the larynx, or a 90-degree endoscope, to decrease neck extension during the examination, may help improve several of these points |
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Three advantages of Flexible endoscopes |
A: Ability to view the larynx during speech and singing A: Glottic gap can be more accurately described A: Allows the clinician to assess the nasal cavity and velopharyngeal port 3: Preferred when the question is one of movement rather than structure or mucosal health such as in spasmodic dysphonia and vocal-fold motion impairment |
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Six disadvantages of Flexible endoscopes |
A: Light transport is inferior to the rigid endoscope A: Magnification of the image is inferior to the rigid endoscopeA: Distortion of the periphery of the image (wide-angle distortion) A: Trade-off between adequate focus and light fiber mismatch causing a moiré or honeycomb effect that is enhanced by the edge detection software of digital imaging systems A: Many patients find the flexible examination to be more invasive than the rigid A: Risks of nosebleed, adverse reactions to the anesthetic and vasovagal reaction 3: Many of these issues are resolved with newer “chip-tip” scopes |
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Seven points in the assessment of the larynx using Continuous Light (VC SPASM) |
A: Vascularity or risk for hemorrhageA: Vocal Cord Edges A: Laryngeal Structure A: Change in Laryngeal Position or Height A: Arytenoids Movement and Position A: Supraglottic Activity A: Mucous Color and Quantity |
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Five assessment tasks Using Continuous Light |
A: Rest breathing A: Deep breathing A: Easy cough or throat clear A: Laryngeal diadochokinesis (DDK), which consists of rapid repetitions of "ee" or "hee" with glottal stops between productions A: Repetitions of a short "ee" followed by a quick sniff through the nose |
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What is a stroboscope? |
A: An instrument for determining the speed of cyclic motion (as rotation or vibration) that causes the motion to appear slowed or stopped. |
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Evaluated criteria on videostroboscopy (remember F-SCAMP) |
A: Fundamental Frequency (Def: component in the vocal fold tone with the lowest frequency) A: Symmetry (in timing of opening and closing and in lateral excursionof VC) A: Glottic Closure (shape of the glottic gap if present)A: Amplitude (lateral excursion of VC from midline, N is 1/3-1/2 width of VC) A: Mucosal wave (moves laterally half the width of the VC) A: Periodicity (regularity of glottal cycles, seen as movement in locked mode)3: Can also comment on Adynamic Segments, Phase Closure, and Vertical Closure Level(Check AG notes for an explanation of each of the above) |
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Nine assessment tasks Using Stroboscopy |
A: Sustained "ee" at normal pitch, normal loudness (NPNL)A: Quiet "ee" A: Loud "ee" A: Pitch glide from mid-range to high A: Sustaining the high note A: Pitch glide from mid-range to lowA: Sustaining the low note A: Phonation on Inhalation A: "ee" at NPNL with locked phase A: Physical manipulation of the larynx or trial therapy (Unloading) also possible 3: Monitor the patient's voice so that all of the necessary information is recorded; Most vibratory parameters are rated from "ee" at NPNL. |
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What is the running and locked phase in stroboscopy? |
A: Running phase is when the light flashes slightly faster or slower than the frequency of VC vibration, creating the illusion of motion. A: Locked phase is when the light flashes at a rate equal to the frequency of VC vibration, creating an illusion that the VC are not moving (if moving→ consider aperiodicity) |
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What are the limitations of stroboscopy? |
A: Does not show every glottis cycle A: Waveform must be relatively periodic to track FF and trigger strobe |
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What is Talbot's law? |
A: Images linger on the retina for 0.2 seconds, and only five distinct images can be viewed per second; if more than five per second are presented, the viewer perceives the images as connected and sees the result as a smooth motion |
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Consensus Auditory Perceptual Evaluation for Voice |
A: “The blue spot is on the key again” – Contains all of the vowel sounds in English A: “How hard did he hit him?” – Emphasizes easy onset A: “We were away a year ago” – Is all-voiced A: “We eat eggs every Easter” – Elicits hard glottal onsetsA: “My mama makes lemon muffins” – Uses nasal sounds A: “Peter will keep at the peak” – Is loaded with voiceless plosive sounds |
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What does the GRBAS scale in voice assessment stand for? |
A: Grade A: Roughness A: Breathiness A: Asthenia (weakness) A: Strain3: Score 0 for normal, and 3 for severe |
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Name 16 Perceptual voice abnormalities |
A: Abnormally High fundamental frequency A: Abnormally Low fundamental frequency A: Abnormally Loud voice A: Abnormally Soft voice A: Decreased Smoothness A: Decreased Intelligibility A: Hypernasality A: Hyponasality A: Hoarseness A: Harshness A: Diplophonia A: Tremorous A: Stridorous A: Breathy A: Arrest of phonation A: Aphonia (Check Fling laryngeal func or AG Voice analysis notes) |
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Six Pathologic conditions that Lower fundamental frequency |
A: NodulesA: Polyps A: Tumors (load-producing) A: Renke’s edemaA: Hypothyroidism A: Aging in women |
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Five Pathologic conditions that Raise fundamental frequency |
A: Tension-producing vocal fold masses (sulcus) A: Muscle tension phenomena A: Aging men A: Parkinson’s disease A: Puberphonia A: anterior glottis web |
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Most common cause of viral laryngitis |
A: Rhinovirus |
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Discuss Laryngeal Diphtheria |
A: Definition – Inflammatory reaction with vascular dilation A: Cause – Corynebacterium diphtheriae, a gram-positive pleomorphic aerobic bacillus A: Clinical – Exudative membranous tonsillitis with fever, dysphonia; Diphtheria exotoxin can cause Myocarditis and Neurologic sequelae A: Treatment –Tracheostomy (not intubation, could dislodge exudate); Antitoxin; High dose Penicillin, Erythromycin or Tetracycline |
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Nine granulomatous diseases of the larynx that can simulate cancer |
A: Pachydermia laryngis A: Coccidiomycosis A: HistoplasmosisA: Blastomycosis A: Rhinoscleroma A: Tuberculosis (most common) A: LeprosyA: Syphilis A: Sarcoidosis A: Wegener’s granulomatosis 3: Remember: “Pachy Cocci Histo Blasto Rhino, TB Lepy, Syphi, Sarcoid, Wegener’s” |
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Five changes to the vocal cord that occur after severing the RLN |
A: Lateral position/Immobile A: Decreased length A: Decreased height A: Atrophy/bowing A: Yellow discoloration |
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Ddx of Unilateral vocal cord Immobility (MINTS, Bailey p.849) |
A: Malignancy (25%, primary pulmonary malignancies and mediastinal adenopathy most commonly) A: Iatrogenic (24%) A: Idiopathic (20%, 70% of which will recover, may take 12 months) A: Infectious – Lyme, Syphilis, TB, EBV, other viralA: Neurologic – Poliomyelitis, Pseudobulbar palsy, MG, MS, ALS, CVA, Wallenberg A: Neurotoxic medications – Cisplatinum, Vincristine, Streptomycin, Quinine, Lead, Arsenic A: Trauma A: Thoracic aneurysm of cadiomegaly (Ortner syndrome) A: Systemic disease – Sarcoid, DM |
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Eight Surgical/Iatrogenic causes of vocal cord paralysis (Bailey p.849) |
A: Thyroidectomy A: Skull base surgeryA: ACDF (R>L) A: CEAA: CABGA: Esophagectomy A: Pulmonary resection A: Mediastinoscopy A: Intubation (pressure-induced neuropraxia from cuff in proximal subglottis) |
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Complete workup for vocal cord paralysis (Bailey p.851) |
A: Complete H&PA: Flexible laryngoscopy +/- videostroboscopy A: Labs (6) – CBCwDiff, Fasting glucose, TFT, FTA-ABS, Lyme titers, Toxin screen (Lead, Arsenic) A: MBS and/or FEES – if suspicion of aspiration A: Ba Swallow – to R/O esophageal mass, vascular compression, or aspiration A: High resolution CT larynx – if suspicion of endolaryngeal pathology A: CT or MRI Skull base to upper chestA: CXR +/- CT chest – to R/O lung mass A: Laryngeal EMG (only useful between 1 and 6 months) – Paralysis vs. fixation, RLN vs. SLN, myopathy vs. neuropathy A: MRI Brain & Neuro consult – if suspicion of central/neurologic cause |
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Eight uses of laryngeal EMG |
A: Intraoperative nerve MonitoringA: Diagnose Neurologic disorders (MG, ALS,…)A: Localization of lesion (RLN vs. SLN or central vs. periphral)A: Establish Prognosis (correlate in 60-70% after 4 weeks)A: BiofeedbackA: Differentiate between paralysis and arytenoid FixationA: Evaluation of synkinesisA: Muscle Localization for Botox injectionA: Help choose VC with worse neuromotor status for destructive procedures in bil. VC palsy3: “Many Nerds form Local Programs use Biofeedback to Fix Sinking Boats” |
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What are the types of electrical activity seen on EMG? |
A: InsertionalA: SpontaneousA: Voluntary |
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Lateral (cadaveric or intermediate) cord position in vocal cord palsy suggests |
A: SLN & RLN injury, loss of cricothyroid with SLN injury causes increased abductionA: Treated with types I & IV thyroplasty |
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Paramedian position in vocal cord palsy suggests |
A: RLN injury only, implies a lesion below the nodose ganglionA: Treated with type I thyroplasty3: Wagner and Grossman theory |
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Three Symptoms of SLN injury |
A: Unstable pitchA: Difficult with high pitchA: Dysphagia/aspiration (loss of sensation) |
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Three findings with SLN injury |
A: Asymmetric VC Tension – Bowed cordA: Asymmetric VC Height – Inferior displacement (superior on phonation?)A: Ipsilateral rotation of posterior glottis3: PPP rule = Posterior commissure Points to Paralyzed side in unilateral SLN paralysis3: Poling of secretions on ipsilateral side |
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Therapeutic options for unilateral vocal cord paralysis |
A: Observation A: Voice therapy A: Injection techniques (percutaneous, transoral,laryngoscopically) A: Type I Isshiki thyroplasty (medialization thyroplasty) A: Type I Isshiki + Arytenoid adductionA: Laryngeal reinnervation (ansa cervicalis transfer) Pic: Arytenoid adduction |
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Factors in the choice of procedure/treatment for unilateral vocal cord paralysis (Bailey p.856) |
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Seven injectable materials for vocal cord medialization (Bailey, p.857) |
A: Gelfoam –If VC recovery expected, lasts 4-6 weeks, saline resorption so overinject 30% A: Zyplast – Bovine collagen, lasts 4-6mo, Risk of host reaction→must get allergy testing A: Alloderm – Acellular dermis, lasts 2-4 mo, no allergy testing needed, expensive A: Perlane – Hyaluronic acid, no antigenic properties, lasts 6-10 months. A: Radiesse – Ca Hydroxyapatite, longer lasting 2 yr+A: Fat – ≥6 months, 50% resorption so overinject 40%, morbidity of harvest site A: Polytef – Teflon; permanent, if no recovery expected; discontinued due to granuloma formation, irreversibility, risks of migration, stiffening of mucosal wave |
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Ddx of Bilateral vocal cord Immobility |
A: Iatrogenic A: Malignancy A: Neurologic A: Endotracheal intubation A: Idiopathic/Infectious 3: “I M Not En Idiot!”3: Important to differentiate bilateral VC paralysis from posterior glottic stenosis |
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Seven Therapeutic options for Bilateral vocal cord paralysis |
A: Tracheostomy A: Laser cordotomy – Transverse cut between vocal process and vocal fold A: Laser cordectomy A: Arytenoidectomy – Endolaryngeal (unilat or bilat, laser partial or total), Extralaryngeal (Woodman lateral approach, or Anterior thyrotomy approach) A: Arytenoidopexy – Plicating vocal process to external laryngeal framework (Woodman lateral approach, or Anterior thyrotomy approach) A: Reinnervation with Neuromuscular pedicle transposition to PCA A: Type II Isshiki thyroplasty (lateralization thyroplasty) |
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List long term changes in the paralyzed cord? |
A: Muscle atrophy, anterior arytenoid displacement, shortened cord, lower position, pooling of secretions |
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Classification of laryngeal framework (Isshiki) procedures |
A: Type I – Vocal cord Medialization A: Type II – Vocal cord Lateralization A: Type III – Vocal cord Shortening, Relaxing = Decreasing pitch A: Type IV – Vocal cord Lengthening, Tensing = Increasing pitch |
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Five indications for Type I Isshiki medialization thyroplasty |
A: Paralysis – Glottic incompetence with dysphonia, poor cough, and aspiration A: Skull base surgery – High vagal paralysis A: Atrophy – Presbyphonia A: Sulcus (difficult to treat) A: Scarring |
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Six contraindications for Type I Isshiki medialization thyroplasty |
A: Immunodeficiency A: Coagulopathy A: Neoplasm A: Previous Teflon A: Previous surgery or trauma A: Previous XRT |
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Six complications of vocal cord medialization by injection |
A: Underinjection – requires multiple procedures A: Overinjection – airway compromise A: Improper placement A: Migration of injection material A: Intrachordal injection – impairs vibratory ability A: Granuloma formation (polytef) |
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Five implant options for Type I Isshiki medicalization thyroplasty |
A: Silastic A: Goretex A: Hydroxyapatite A: Titanium A: Prefabricated implants |
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Top 3 reasons for failure of Type I Isshiki medialization thyroplasty |
A: Implant too High A: Implant too Anterior A: Undercorrection of the glottic gap posteriorly 3: Others include Extrusion, Infection, Hematoma |
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What is Ortner’s syndrome? |
A: Vocal cord paralysis caused by severe cardiomegaly, enlarged left atrium caused by mitral stenosis, thoracic aortic aneurysms, or dilated pulmonary arteries with pulmonary hypertension 3: AKA cardiovocal syndrome |
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Describe the Guttman’s test |
A: A test for SLN paralysis (Cricothyroid paralysis) A: Normally, anterior thyroid cartilage pressure decreases pitch, lateral thyroid cartilage pressure increased pitch; with cricothyroid paralysis this reverses |
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Define the Reflux Symptom Index (RSI) |
A: Hoarseness A: Clearing A: Excess mucus/ Postnasal drip A: Dysphagia A: Cough after eating/lying down A: Dyspnea/Choking spells A: Troublesome cough A: Globus sensation A: Heart burn, indigestion, pain3: Nine symptoms worth up to 5 points each = Max 45; >13 is abnormal |
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Reflux Finding Score |
A: Pseudosulcus – Subglottic edema (/2) A: Vocal fold edema (/4) A: Ventricular obliteration (/4) A: Diffuse laryngeal edema (/4) A: Posterior commissure hypertrophy (/4) A: Erythema/Hyperemia (/4) A: Granulation/Granuloma (/2) A: Thick endolaryngeal Mucus (/2) 3: Eight signs, Max score = 26; >7 is significant |
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Name 10 associations of laryngopharyngeal reflux (LPR) |
A: Laryngotracheal stenosis (SGS most common association = 92%, Bailey p.833) A: Laryngomalacia A: Laryngospasm/Cough/Asthma/Recurrent Croup/SIDS A: Vocal cord Nodules A: Vocal cord Polyps A: Otitis media A: Vocal process (contact) ulcers/Granulation/Granulomas A: Carcinoma A: Chronic laryngitis/Mucosal thickening/Pachyderma laryngis A: Dental caries and erosion |
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What constitutes an abnormal 24 hour pH probe result |
A: Hypopharyngeal probe pH <4 anytime A: Proximal esophageal pH <4 >1% of the time A: Distal probe pH <4 >4% of the time |
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Name 5 classes of drugs used to treat LPR, and give an example of each |
A: Proton pump inhibitors – Pantoprazole A: H2-Blocker – Ranitidine A: Pro-kinetics – Metaclopramide, cisapride A: Cytoprotectants – Sucralfate A: Buffer – CaCO3 |
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Tests for GERD |
A: Dual pH probe – Short term or Long term (gold standard) A: Barium swallow A: Radionuclide Reflux scan A: Esophagoscopy & biopsy A: Manometry (although 30% will be normal) A: Lipid laden macrophage test – BAL A: Acidification tests – Rarely used; Bernstein test instills N/S for 15 minutes via NGT, then 0.1M HCl @ 6cc/min until symptomatic or for 45 minutes; Tuttle test in children is similar, uses age depedent HCl instillation, pH <3 x 2 occasions is positive |
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Six Indications for Tracheotomy |
A: Bypass upper airway Obstruction (including Severe OSA) A: Prolonged intubation A: Protection from Aspiration (Inability of patient to handle own secretions) A: Assist with tracheo-bronchial suctioning (pulmonary toilet) A: Adjunct to H&N surgery with possible airway compromise A: Adjunct to management of severe facial fractures |
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Complications of tracheotomy |
A: Intraoperative Great vessel injury Laryngeal damage (improper placement) Injury to tracheoesophageal partition Pneumothorax Pneumomediastinum Thymus injury (in children) Death A: Early postoperative Tracheostomy tube obstruction (mucus plug) Tracheostomy tube displacement Infection Pulmonary edema A: Late postoperative Tracheal stenosis Granulation tissue Subglottic stenosis Tracheal-inominate fistula Tracheoesophageal fistula |
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Endotracheal tube pearls & complications |
A: Most commonly made of polyvinyl chloride A: Cuff pressure >25 cm H2O will compromise mucosal capillary blood flow and cause necrosis |
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Eight local factors that increase risk for laryngeal damage from ETT |
A: Cuff pressure too high A: Too large an ETT for the larynxA: Tube movement A: Length of intubation greater than 7 days in adults, ~3-4 weeks in pediatrics A: Blind intubation/poor visualization A: Preexisting laryngeal anatomic abnormality A: Presence of GERDA: Presence of local Infection |
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What is the cause of post-extubation stridor occurring after short-term, uneventful intubation? |
A: Acquired subglottic cyst A: laryngospasm |
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Risk factors for cardiorespiratory complications in patients with airway obstruction (OSA?) |
A: Craniofacial malformation A: Abnormal pharyngeal musculature A: Congenital heart disease A: Susceptibility of pulmonary vasculature A: Obesity A: Concurrent URTI |
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Most common causes of stridor in children Infants? |
A: Laryngeal (60%) = Laryngomalacia (60%), Subglottic stenosis (20%), VC palsy (13%), Others (7%) A: Tracheal (15%) = Tracheomalacia (45%), Vascular compression (45%), Stenosis (5%) A: Bronchial & tracheal infections 5% each; miscellaneous 15% 3: Croup most common in children? |
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Discuss Laryngoceles? |
A: Definition – Laryngocele = Air-filled dilatation of the appendix of the ventricle; Laryngopyocele = Infected pus-filled laryngocele; A: Causes – Congenital or acquired expansion of the laryngeal saccule (in ventricle) from increased intraglottic pressure (trumpet players, glass blowers), obstruction of ventricle by neoplasm A: Types – Internal (remains within the thyroid cartilage, less common), External (protrudes through the thyrohyoid membrane, presenting as a mass in the neck), or Combined (most common) A: Clinical – Lateral compressible neck mass, increases in size with intralaryngeal pressure (external); Dysphonia and cough (internal), BRYCE’S SIGN: borborygmi on auscultation while palpating neck (ddx Zenker’s) A: Diagnosis – Flexible laryngoscopy, CT neck A: Complications – Secondary infection, rare malignancy, airway obstruction A: Treatment – Marsupialization, complete endoscopic (laser) removal for internal, open approach for external, Bx to r/o Ca as a cause |
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Discuss laryngeal cysts? |
A: Types: Epithelial (Ductal 75% & Saccular 25%), Tonsillar, Oncocytic A: Ductal: Arise from obstruction of glandular ducts, they can occur at any site, <1cm majority of the time A: Saccular cyst: Fluid-filled dilatation of the saccule without communication with the laryngeal lumen, subclassified as Anterior (60%): cyst tends to bulge medially; obscures anterior portion of VF Lateral (40%): larger; extends superiorly and laterally; can bulge through thyrohyoid membraneCommonly seen in infants; can be congenitalDiagnosis: Flex scope, xray, CTMGT: Control airway, Endoscopic marsupialization with aspiration vs external approaches for large lateral cysts; may need intubation for couple of days post op Pic: A, Normal anatomy. B, Anterior saccular cyst. C, Lateral saccular cyst. D, Laryngocele types. |
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Differences between laryngoceles and saccular cysts? |
A: Air filled sacs in laryngoceles compared to the fluid filled saccular cysts A: Laryngoceles maintain an open communication with the larynx which is not seen in saccular cysts A: Laryngoceles occur more in older population compared to saccular cysts in children |
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Ddx of benign vocal cord lesions (8) |
A: Polyp (most common) – Mucoid or AngiomatousA: Nodules (bilateral) A: Cyst – Mucus retention or Epithelial inclusion A: Pseudocyst (no capsule)/Fibrous Mass? A: Polypoid degeneration/Reinke’s edema A: Granuloma A: Sulcus vocalis A: Papillomas A: Lymphatic/vascular malformations A: Granular cell tumor A: Schwannoma A: Chondroma – Posterior cricoid A: Sarcoid A: Amyloid |
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Discuss Vocal Cord NodulesA: Causes – Vocal abuse/misuse +/- LPR |
A: Clinical – ALWAYS bilateral, mid to anterior 1/3 of vocal fold, mid-membranous, affect primarily the epithelial basement membrane and superficial lamina propria, minimal effect on mucosal wave A: Treatment – SLP, PPI, rarely surgery; avoid operating on singers -> correct underlying problem |
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Discuss Vocal Cord Polyps |
A: Causes – Vocal abuse/misuse A: Clinical – Usually unilateral, but can have a reactive lesion on the opposite cord, may occur anywhere on the vocal fold, stems from inflammation in superficial lamina propria space; variably affect the mucosal wave, more with larger polyps A: Types – Mucoid or Angiomatous A: Treatment – SLP, PPI, surgery (nearly all) |
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Discuss Vocal Cord Cysts |
A: Causes – Vocal abuse/misuse A: Clinical – Usually unilateral, but can have a reactive lesion on the opposite cord; may occur anywhere on the vocal fold, usually deeper in the lamina propria/vocal ligament; variably affect the mucosal wave A: Types – Mucous retention or Epidermoid inclusion (keratin filled, more often associated with abuse) A: Treatment – SLP (more useful for Epidermoid inclusion cysts), PPI, surgery (nearly all) |
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Discuss Vocal Cord Pseudocyst/Fibrous Mass |
A: Causes – Vocal abuse/misuse, previous trauma A: Clinical – Usually unilateral, but can have a reactive lesion on the opposite cord; may occur anywhere on the vocal fold, usually deeper in the lamina propria/vocal ligament; reduced mucosal wave A: Treatment – SLP, PPI, surgery (nearly all) |
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Discuss Polypoid Degeneration of the Vocal Cords |
A: Definition – AKA Reinke’s edema; accumulation of gelatinous mucoid material in the superficial lamina propria A: Cause – Women>Men, Tobacco, Vocal abuse, LPRA: Clinical – Marked edema of the superficial layer of the VC, may prolapse inward during inspiratory phonation; may have marked decrease in fundamental frequency A: Smoking cessation, PPI, SLP, but do not usually go away without Surgery |
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Discuss Sulcus Vocalis |
A: Definition – Epithelium-lined pocket, whose lips parallel the free edge of the folds, may represent an epidermoid cyst that has spontaneously emptied. A: Causes – Emptied cyst, History of voice overuse, iatrogenic, LPR A: Clinical – Chronic hoarseness, diplophonia, aphonia at certain frequencies A: Types – Congenital or Acquired, see classification in pic below (type IIb is type III) A: Treatment – Voice Tx, LPR Rx, Surgical options include intracordal HA/collagen injection, medialization thyroplasty, fat implant via microflap or Gray’s minithyrotomy, mucosal slicing technique of pontes, Bipedicle flap with submucosal division of scar |
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Discuss the pathophysiology of Varices/Capillary Ectasias |
A: Repeated microtrauma A: Capillary angiogenesis A: Dilated capillaries (proceeds from anterior to posterior, may look like capillary lake) making cord even more susceptible to trauma A: Vocal cord swelling A: Hemorrhagic polyp formation |
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Management of vocal cord Varices/Capillary Ectasias |
A: Behavioural – Reduce voice training duration period, avoid sudden explosive vocals A: Medical – Hydration, stop anticoagulants/antiplatelet agents, PPI A: Surgical – Spot coagulation with CO2 laser to interrupt blood supply; visible spots should involute spontaneously |
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Discuss Vocal Cord Hemorrhage |
A: Causes – Following acute vocal trauma; predisposing factors are laryngitis, anticoagulants, varicosities/capillary ectasias A: Clinical – Arise from a varicosity on the medial vibrating edge of the vocal fold; Deeper bleeds may cause a blood blister (may stiffen the cord, lead to hemorrhagic polyp); On biopsy, may have hyalinization, Polyp may lose its vascular appearance and be pedunculated fall in and out of the airway A: Treatment – Voice rest, +/- steroids, +/- surgical evacuation |
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Five predisposing factors for Intracordal Hematoma |
A: Voice abuse; extreme vocal effort (sporting event, forceful singing, sneezing) A: Usually Men A: Anticoagulants A: Laryngitis A: Capillary ectasia is a precursor, rupture of submucosal capillaries/vessels |
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Surgical Treatment for Intracordal Hematoma |
A: Microlaryngoscopy and evacuation of hematoma |
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What 2 systemic diseases should be considered in the differential of a vocal cord lesion? |
A: Hypothyroidism A: Acromegaly |
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What do you want to R/O in a patient with laryngeal amyloidosis |
A: Multiple myeloma (very low percentage) A: Need bone marrow biopsy to rule this out, SPEP and UPEP for M protein, CXR |
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Histopathologic origin of Vocal cord granuloma |
A: Repetitive contact trauma leads to mucosal ulceration over the vocal processes of the arytenoids, cartilage exposure and inflammation leads to granuloma formation |
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Four risk factors for Vocal cord granuloma |
A: Vocal abuse (chronic cough, throat clearing) A: Traumatic intubation A: GERDA: Male sex |
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Five treatment options for Vocal cord granuloma |
A: Dietary and lifestyle modifications – Cut out coffee A: Vocal hygiene A: Voice therapy A: Antireflux medications – longterm, PPIs bid A: Botox injection – 12 U on side of lesion, 3-5 units contralaterally to prevent overcompensation A: Intralesional vs. systemic corticosteroids (controversial) A: Microlaryngeal Surgery – Cold steel vs. Endoscopic CO2 excision; rarely indicated, only if very symptomatic, may recur |
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Three benign tumors arising from Schwann cells |
A: Schwannoma – Benign, encapsulated, slow growing, rare malignant sarcomatous degeneration A: Neurofibroma – Proliferation of sheath cells & fibers, nonencapsulated, nodular & diffuse A: Granular cell tumor – Slow, painless growth, well circumscribed |
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Describe Granular cell tumors |
A: Definition – Large polygonal cells in nests/strands/sheets; infiltrative, no distinct capsule; defining characteristic are abundant eosinophilic cytoplasm filled with granules of varying sizes (lysosomes in varying stages of fragmentation); keratin pearl formation in some cases (pseudoepitheliomatous hyperplasia), S-100 positive A: Diagnosis – Endoscopy with biopsy A: Causes – Arise from Schwann cells A: Clinical – Slow, painless growth; well circumscribed; Typically solitary, polypoid, sessile, papillary or cystic; Commonly found at the posterior aspect of the true VC, but Tongue is most common site of origin A: Complications – Recurrence (8%), malignant transformation(5%)A: Types (3) – Congenital, Mucosal, Gingival A: Tests – Biopsy stain positive for S-100 and PAS A: Treatment – Complete excision (endoscopic or open via laryngofissure or conservative resection) |
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Six pseudoepitheliomatous lesions of the larynx |
A: Granular cell tumor A: Rhinoscleroma A: Necrotizing sialometaplasia A: Pachydermia laryngis A: Histoplasmosis A: Blastomycosis A: Aspergillus/Candida |
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Travelling wave theory in Voice production |
A: VC vibration occurs in lateral & vertical planes A: Sequence – Lower margin separates, elliptical volume of air formed in subglottal vault (“glottal puff”), which is released as upper margin separates; lower margin returns to midline, then upper margin does also. Anterior before posterior also A: Phase delay (vertical phase difference)= Delay between closure of upper and lower vocal cord margins; phase closure should normally be ~1/3-1/2 of the vibratory cycle |
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Define Phase delay |
A: The time difference between closure of the upper margin of the vocal cords compared with the lower |
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Describe the 2 Theories of Vocal Cord vibration |
A: Myoelastic Aerodynamic theory When the vocal cords are brought together and breath pressure is applied to them, the cords remain closed until the subglottic pressure is sufficient to push them apart, allowing air to escape and reducing the pressure enough for the muscle tension recoil to pull the folds back together again. Pressure builds up once again until the cords are pushed apart, and the whole cycle keeps repeating itself. A: Neurochronaxic theory (old & invalid): Each vibratory cycle is initiated by nerve impulse to vocalis muscle via recurrent/vagus nerve |
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What is the human vocal fundamental frequency? |
A: Men ~125 Hz; increases with age A: Women ~225 Hz; decreases with age |
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What 4 mechanisms alter vocal pitch? |
A: Changes in vocal cord length A: Changes in vocal cord tension A: Changes in vocal cord mass A: Changes in subglottic air pressure 3: Speed of vibration of the vocal folds (Pasha?) |
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Define Diplophonia |
A: Phonation with two simultaneous fundamental frequencies A: Occurs with divergent travelling wave velocities due to asymmetric stiffness |
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Four objective voice measures |
A: Glottography – Photo or Electroglottography A: Videostroboscopy A: Airflow measures A: Acoustic measures |
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Describe two types of Glottography |
A: Photoglottography – Change in light transillumination measures degree of glottic opening A: Electroglottography – Change in electrical conduction measures degree of glottic contact A: Speed quotient – Ratio of duration of glottic opening to duration of glottic closure A: Shift quotient – Ratio of time to peak glottic opening over the duration of glottic opening A: Open quotient – Ratio of duration of open folds to length of the glottic cycle A: Closed quotient – Proportion of the glottic cycle during which the glottis is closed |
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Describe Videostroboscopy |
A: Examines vibratory nature of vocal cords during phonation A: Strobe controlled by pitch of phonation or a frequency generator |
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Describe Airflow voice measures |
A: Airflow through glottis & subglottic pressure measured, which determines the glottic resistance (Ohms law) A: Vocal efficiency = Acoustic power/subglottic power (pressure) A: Maximum phonation time A: Phonation threshold pressure (minimum pressure to drive the VC to vibrate) |
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In Speech Aerodynamic (Airflow) studies, give the normal values for Transglottal airflow rate, Glottal resistance, and Subglottal pressure |
A: Transglottal airflow rate = 100 cc/sec A: Glottal resistance = 30-50 cmH2O/lps A: Subglottal pressure = 6-8 cmH2O |
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Describe Acoustic voice measures |
A: Frequency: average and range A: Intensity: average, minimum and max A: Variability: Quantitate vocal harshness, measures perturbation in the peak to peak timing of each glottal pulse Jitter = Cycle to cycle Frequency fluctuations (normal ≤0.4%) REMEMBER JF Kennedy Shimmer = Cycle to cycle Amplitude fluctuations (normal ≤0.5 dB) A: Harmonic-to-Noise Ratio (normal ≤11 dB) A: Time domain measures – Timing relationships in the acoustic signal (Jitter and shimmer) A: Others: Fundamental period, spectral tilt |
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Definition of Maximum phonation time |
A: Maximum period a subject can maintain audible phonation of a vowel at comfortable pitch and loudness A: Women = 16-25 secA: Men = 22-34 sec |
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Definition of Phonation quotient |
A: MPT/VC 3: Maximum phonation time divided by patient’s vital capacity |
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Two essential parameters of normal vocal cord vibration and voice production |
A: Glottal gap – Interarytenoid & lateral cricoarytenoid muscles both close and appose the vocal cords A: Normal vocal cord stiffness – Thyroarytenoid controls stiffness, which increases pitch and resistance; Cricothyroid antagonizes thyroarytenoid, thins & lengthens vocal cord which increases tension and pitch while decreasing the area of contact |
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Three characteristics of Normal phonatory posture |
A: Posterior commissure closure A: Symmetric thyroarytenoid stiffness A: Equal vertical position |
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Four clinical Signs & Symptoms of Presbylaryngeus |
A: Hoarse, breathy voice A: High pitch voice ? (men) A: Vocal fatigue A: Tremor A: Aspiration |
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Five clinical laryngeal findings in Presbylaryngeus |
A: Yellow/dark gray discoloration of vocal fold (fibrofatty accumulation) A: Vocal fold atrophy, bowing and incomplete glottic closure A: Arrowhead configuration of glottis (from atrophy) A: Visibility of ventriclesA: Prominent vocal process A: Mucosal dryness |
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Subclassify Hypokinetic Neurologic disorders of the larynx (4) |
A: CNS – Arnold-Chiari, MS, Parkinsons, Parkinson plus (Global atrophy, Shy-Drager, Diffuse Lewy-Body disease) A: Anterior Horn cells – ALS A: Neuromuscular junction – MG A: Myopathic |
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Subclassify Hyperkinetic Neurologic disorders of the larynx (7) |
A: Muscular tension dysphonia A: Spasmodic dysphonias A: Essential tremor A: Tic (Tourette) A: Myoclonus A: Functional dysphonia/aphonia A: Paradoxical movement of the vocal cords |
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Three goals of voice therapy |
A: Vocal Hygiene A: Decrease Phonotrauma A: Increase Coordinated voice production |
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Seven strategies for voice therapy (ABPR4) |
A: Attack A: Behavior A: Pitch A: Rest A: Relax A: Respiration A: Rate |
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Five concepts of Lee-Silverman voice training (MAISE) |
A: Quantify with a Sound Meter A: Increase the Amplitude of vocal output A: Administer in Intensive fashion A: Increase Sensory perception A: Administer in High Effort style 3: Three problems in Parkinsons are 1) Decreased vocal drive, 2) Poor self-perception, and 3) Inability to regulate output |
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Define dystonia? |
A: syndrome dominated by sustained or intermittent contractions of skeletal muscles which causes twisting, repetitive movement or abnormal posture A: Can be primary when action induced and normal at rest or secondary which has a fixed dystonic posture frequently A: AD inheritance in most cases of childhood onset idiopathic dystonia |
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Name 4 common dystonias in the head and neck |
A: Spasmodic dysphonia A: Blepharospasm A: Torticollis A: Oromandibular dystonia |
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Define Meige’s syndrome |
A: Blepharospasm & Oromandibular dystonia syndrome |
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Three clinical indicators of a hyperfunctional laryngeal dysphonia on indirect laryngoscopy |
A: Anteroposterior compression of the larynx A: Aryepiglottic fold contraction A: False vocal cord compression (lateral compression?) |
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Describe Spasmodic Dysphonia and 4 types |
A: An action induced laryngeal motion disorder; a focal dystonia, which may have an associated family history of other dystonias in 12% A: Adductor dysphonia (80%) Hyperactivity of Thyroaryteniod/vocalis muscle complex; Choked, strained or strangled voice with abrupt initiation & termination causing short phonation breaks; vocal tremor, slow speech rate & decreased speech smoothness, reduced loudness, reduced speech intelligibility, normal whispering, singing or laughing can all be present; Botox – initial dose 1-1.25U to TA (range below) A: Abductor dysphonia (15%) More difficult to treat; Hyperactivity of posterior cricoarytenoid muscle; Breathy, effortful voice quality with abrupt termination, causes aphonic segments of speech; vocal tremor often seen, reduced loudness, reduced speech intelligibility, abnormal whispering; Botox – initial dose 3.75U to PCA (range below) A: Mixed spasmodic dysphonia A: Adductor breathing disorder (paradoxical VC motion) Rare disorder, patients adduct their vocal cords while inspiring causing stridor and dyspnea, they DO NOT become hypoxic and DO NOT need trachs Characteristic posterior glottic chink while adducting VC abduct with sniffing Can have organic causes (brainstem compression, upper motor neuron or LMN injury, irritant exposure, LPR) or non-organic (malinger, conversion) In young females, type A personality, asthma in 60%, anxiety PFT: Produces blunting/flattening of inspiratory loop if symptomatic compared to asthma which impairs the expiratory loop Tx: acute with heliox, PPV, reassurance and anxiolytics, long term with speech & psych Tx +/- bil TA botox inj in severe casesCheck http://www.fauquierent.net/voicesd.htm for voice samples Posteriorglottic chink in PVCM |
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Differences between asthma and PVCM in flow-volume loops? |
A: See below UAO extrathoracic PFT = what you see in PVCM, Obstructive PFT = asthma A: Normal, B: PVCM |
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Descibe the Koufman and Blalock classification system for muscular tension dysphonia |
A: Class I – Increase in muscular tension manifested by an enlarged posterior glottal chink, an elevated larynx, and palpable neck tension or tenderness; may produce a breathy or strident voice and commonly occurs with vocal nodules A: Class II – Lateral to medial constriction with the false vocal folds adducted; in its most severe form, the false folds are used for phonation (plica ventricularis) A: Class III – Anterior to posterior constriction of the supraglottis when the epiglottis and the arytenoids obscure at least 50% of the laryngeal aditus A: Class IV – Epiglottis and arytenoids contact one another, lateral constriction is often seen |
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Describe Functional dysphonia |
A: AKA Psychogenic dysphonia; related to psychologic issues: severe decrease in voice output A: Women > men A: Ddx = Spasmodic dysphonia, secondary MTD, Tremor A: Treatment = THERAPY! – Speech, Psycho, Pharmaco |
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Approaches to PCA muscle for Botox injection in Abductor spasmodic dysphonia |
A: Anterior/transcricoid approach – via Cricothyroid membrane, then thru posterior cricoid ring A: Lateral/retrocricoid approach – through inferior constrictor 3: Confirmation of PCA location by EMG with sniffing |
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Alternative treatment to Botox for spasmodic dysphonia |
A: Speech therapy but generally ineffective alone A: Geste antagoniste (sensory trick): certain actions that temporarily interrupt dystonias (e.g. pulling on ear) but not really a treatment modality A: Medical: anticholinergics or muscle relaxants, limited benefit A: Surgical Denervation of RLN +/– Reinnervation to ansa (crush, neurolysis) A: Abductor SD: Type I thyroplasty, PCA myoplasty (limited evidence) A: Adductor SD: Type 2 lateralization thyroplasty, Bil TA +/- LCA myectomy |
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Two methods to help differentiate Spasmodic Dysphonia from Functional Dysphonia |
A: SD will not respond to speech therapy, although functional will A: SD may be improved with whispering, singing or laughing |
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Describe voice changes in Essential Tremor |
A: Altered Pitch & Loudness A: Phonation Stoppages A: Decreased Intelligibility A: Tremor Absent at rest, attenuated at end of movement, maximal during posturing 3: Treatment – Proplanolol, primidone, Botox, inject muscles with most tremor (in many cases sternohyoid and sternothyroid) 3: Essential Tremor def: Involuntary, action induced purposeless rhythmic movement of a body part around 6-8 Hz, affects all laryngophayngeal muscles compared to SD which affects intralaryngeal muscles only |
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What is oculopalatolaryngopharyngeal myoclonus? |
A: uncommon d/o consisting of rhythmic contraction of the soft palate, pharynx and larynx at a rate of 1-2 / second A: Lesion in the central tegmental tract → need MRI A: slow rhythmic adduction and abduction of VC at the same time as the palatal and pharyngeal contractions → choppy voice and intermittent hypernasality A: Tx: baclofen, carbamazepine, clonazepam, serotonin, botox inj |
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Describe mechanism of action of botulinum toxin (Botox), how does its effect wear off, and what doses are given in hyperfunctional laryngeal disorders |
A: Causes irreversible blockage of receptors controlling presynaptic release of acetylcholine A: Wears off through regeneration of fresh synaptic terminals A: Dose in ADductor SD = 1 to 3.75 units A: Dose in ABductor SD = 0.5 to 5 units 3: Can say between 1 and 5 units in general |
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Botox – how long until onset of paralysis and how long overall effect |
A: 48 hours (presynaptic vesicles depleted) A: 90 days (although new axons begin sprouting at 28 days) |
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Number of Botox exotoxins, and most clinically useful |
A: 7 (A to G) exotoxins; A – longest lasting A: Active form has a heavy chain for binding, and a light chain for intracellular toxicity |
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Three steps in Botox toxin mediated paralysis |
A: Binding A: Internalization (endocytosis) A: Inhibition of neurotransmitter release |
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Eleven indications for Botox for laryngopharyngeal pathology |
A: Adductor Spasmodic dysphonia (into TA) A: Abductor Spasmodic dysphonia (into PCA) A: Stuttering (into TA) A: Vocal Tic (into TA) A: Mutational dysphonia (Puberophonia) (into Cricothyoid) A: Ventricular dysphonia/Dysphonia plica ventricularis (injection into false cord/aryepiglottic muscle) A: Dysphagia due to cricopharygeal dysfunction (into cricopharygeus) A: TEP speech failure due to cricopharygeal spasm (into cricopharygeus) A: Vocal fold granuloma and prevention of posterior glottis stenosis (into TA- decreases strength of vocal cord closure, tends to take a more abducted position at rest) A: Arytenoid rebalancing (post-dislocation, into adductor muscles on that side) A: Bilateral true vocal fold paralysis (into adductors) |
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Name 4 other clinical uses for Botox in the head and neck |
A: Facial dystonias (eg. blepharospasm, torticollis) A: Forehead rhytids A: Ptyalism (drooling) A: Frey’s syndrome |
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Name 5 side effects of Botox injection |
A: Dysphagia (most common) A: Aspiration A: Weak breathy voice A: Sore throat A: Blood tinged sputum A: Hyperventilation and dizziness A: Airway obstruction |
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Contraindications to Botox |
A: Prior allergic reaction A: Injection into areas of infection or inflammation A: Pregnancy (category C), or breastfeeding A: Myasthenia Gravis, Eaton Lambert Sx, motor neuron disease A: Medications that decrease NM transmission (can have botulism like effects at high doses) – Aminoglycoside, Penicillamine, Quinine, Calcium channel blockers |
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What is the lethal dose of Botox A? |
A: 2500- 3000 units (emedicine) |
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Four Conditions that steroid are indicated for the professional voice user |
A: Allergic vocal fold edema A: Edema from episodic abuse A: Mild to moderate laryngitis A: Vocal fold hemorrhage 3: Do not give for first time on night of performance |
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Five indications for the professional voice user to cancel a concert |
A: Submucosal Hemorrhage A: Enlarging vocal cord Varix A: Break in vocal fold mucosa A: Significant systemic Illlengthness A: Severe laryngitis |
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Define glottal puff |
A: The release of air as the upper margins of the vocal cords separate |
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Three physical properties that alter frequency of vocal cord vibration (what is the difference with the pitch question?) |
A: Mass A: Stiffness A: Viscosity (what about length and tension?) |
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Three findings (normal, fibrillation, and polyphasic potentials) on laryngeal EMG and significance with clinical setting of vocal cord immobility |
A: Normal – Joint fixation A: Fibrillation – Denervation A: Polyphasic potentials – Reinnervation and Synkinesis |
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Three elements of EMG analysis |
A: Spontaneous activity – Present or absent A: Recruitment – Normal, reduced, or absent A: Motor unit morphology – Normal/bi/triphasic, low amplitude, polyphasic, fibillation |
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Good prognostic EMG findings |
A: No Spontaneous activity A: Some RecruitmentA: Normal/bi/triphasic, or low amplitude polyphasic motor unit potentials |
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Poor prognostic EMG findings |
A: Presence of Spontaneous activity A: No RecruitmentA: Fibrillations A: Electrical silence |
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Optimal timing for LEMG? |
A: Early use (<3 mo) has debatable prognostic benefit A: 4-6 mo: most helpful for prognostication of nerve injury recovery |
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Two indications for arytenoid adduction procedure |
A: Posterior glottic gap not corrected with type I thyroplasty A: Vocal processes at different levels in the caudal/rostral axis 3: Usually necessary with posterior glottic gap ≥4 mm |
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Five effects resulting from an arytenoid adduction |
A: Increased stiffness at the vocal process A: Medializes and stabilizes the vocal process A: Increased length of the vocal cord A: Decreased difference in height between the 2 vocal cords (lowers vocal process) A: Decreased malrotation of the arytenoid 3: Always admit patient postop due to risk of hematoma, or airway obstruction |
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Seven Physiologic alterations to the aerodigestive tract with a tracheostomy tube |
A: Inhibits vertical motion of the larynx during swallowing A: Reduced subglottic pressure A: Dyscoordination between breathing and swallowing A: Elimination of vocal cord closure reflex while swallowing A: Physiologic obstruction when swallowing d/t esophageal compression by cuffA: TracheomalaciaA: Interferes with Ciliary function 3: Potential for Tracheoesophageal fistula in long term |
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What are the most common causes of Severe Aspiration? |
A: Neuromuscular – MS, ALS, PD, CVA A: Head injury |
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When can aspiration occur in regards to the pharyngeal phase of swallowing and why? |
A: Before – reduced tongue control or delayed pharyngeal swallow A: During – incompetence of airway sphincters A: After – reduced laryngeal elevation, tongue base control, delayed pharyngeal constriction, CP dysfunction |
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Five signs & symptoms of chronic aspiration |
A: Bronchorrhea (>100cc watery sputum, secondary to chronic bronchitis) A: Pneumonia A: Chronic cough A: Dysphagia A: Weight loss |
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Name 4 swallowing investigations? |
A: MBS (tests all phases) A: Manometry A: FEES / FEEST (tests only pharyngeal phase but can test sensation) A: Scintigraphy |
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Name 4 uses of a MBS? |
A: To define an oral or pharyngeal motility d/o A: to identify aspiration.A; to assess the speed of a swallow A: to assess effects of therapy strategies |
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Four therapeutic approaches for Chronic Aspiration |
A: Medical management A: Adjunctive procedures A: Reversible surgical procedures A: Irreversible surgical procedures |
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Seven Medical management options for Chronic Aspiration |
A: NPOA: Tube feeds, either NG or PEG A: Oral hygiene A: Speech therapy – Swallowing retraining, PosturalCompensatory manoeuvers, Head position manoeuvers, Oral motor exercises A: Optimization of pulmonary status A: LPR prophylaxisA: Anti-sialogogues |
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5 methods of voluntary control of swallowing to decrease aspiration? |
A: Supraglottic swallow: inhale and hold breath, swallow, cough then swallow A: Super-supraglottic swallow: same as above but bearing down as holding breath A: Mendelsohn maneuver: voluntary elevation of the larynx A: Effortful swallow: muscle effort used during oral & pharyngeal phases A: Shaker exercise: This exercise is used to strengthen the suprahyoid muscles |
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5 postural effects on swallowing to decrease aspiration? |
A: Head rotation to side of palsy closes off that pyriform sinus to the bolus A: Chin tucking brings anterior wall of pharynx posterior, airway entrance narrowed A: Head tilt to one side directs food down that side of the oral cavity & pharynx A: Lifting chin decreases oral transit time via gravity A: Supine position causes residual to stick to pharyngeal walls rather than fall down airway |
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Six Adjunctive procedures for Chronic Aspiration |
A: Vocal cord Medialization – Injection, Thyroplasty, Arytenoid adduction A: Laryngeal Suspension A: Cricopharyngeal Myotomy or Botox injection A: Posterior cricoid resection A: Elevation of the Interarytenoid area A: Tracheostomy |
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Four Reversible surgical procedures for Chronic Aspiration |
A: Airway stenting (eg. Eliachar stent) A: Vertical laryngoplasty A: Supraglottic closure – Epiglottic flap A: Laryngotracheal separation or tracheoesophageal diversion, >90% successful |
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Four Irreversible surgical procedures for Chronic Aspiration |
A: Subperichondrial cricoidectomy A: Glottic closure A: Narrow field laryngectomy A: Total laryngectomyCheck http://www.nature.com/gimo/contents/pt1/full/gimo51.html for pics on above |
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Opera singer with VC edema, wants to sing, what to suggest (2) |
A: Hygiene – Voice rest and Hydration A: Meds – Steroid and PPI |
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Opera singer with Intracordal Hematoma and performing in 8 days; what are your recommendations? |
A: Stop any anticoagulants A: Humidity & Hydration A: Voice rest A: Antireflux A: Reassess in a week prior to next performance |
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Opera singer with good vocal hygiene and Acute Laryngitis; 4 Options |
A: Vocal rest until day of performance A: Increase amplification A: Alter repertoire for the upcoming performance A: Offer steroids for short term |
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Opera singer with good vocal hygiene and Acute Laryngitis; 6 Recommendations |
A: Antitussive agent (if cough is a problem) A: Use feel of singing rather than sound quality A: Sing in normal, unforced voice without whispering A: Educate about increased risk of vocal cord hemorrhage that could cause permanent damage A: Follow-up after performance, and counsel as to when normal activities can be restarted |
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Seven Ancillary tests for subglottic stenosis |
A: Plain film A: Fluoroscopy A: Angiogram (R/O vascular ring) A: Flow-volume loops A: pH probe A: cANCA A: Biopsy (R/O TB, WG, scleroma) |
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What two forces bring the vocal folds to midline? |
A: Elastic Recoil. A: Bernoulli’s forces. |
