Voice, laryngeal function, airway and sleep
Laryngology questions hinge on history and laryngoscopy. Persistent dysphonia requires visualization according to the actual presentation. The AAO-HNS framework recommends assessment when it fails to improve within four weeks, or earlier whenever a serious cause is suspected. Distinguish organic causes (vocal fold nodules, polyps, cysts, papilloma, carcinoma, paralysis) from functional causes (muscle tension dysphonia, spasmodic dysphonia).
Know the benign mucosal lesions: nodules are bilateral, at the junction of the anterior and middle thirds (phonotrauma); polyps are typically unilateral and related to vocal abuse or smoking; Reinke edema is smoking-related and bilateral. Recurrent respiratory papillomatosis (HPV 6/11) causes hoarseness and airway obstruction; treatment is repeated surgical debridement, and HPV vaccination reduces incidence.
Understand vocal fold paralysis: left recurrent laryngeal nerve is longer and more vulnerable (thoracic disease); right is shorter. Bilateral paralysis can cause airway obstruction and stridor; unilateral paralysis causes a breathy voice. Also know spasmodic dysphonia (adductor type: strained, strangled voice; botulinum toxin treatment) and laryngopharyngeal reflux (globus, throat clearing, posterior laryngitis).
Traps: attributing hoarseness to reflux without visualizing the larynx; missing airway compromise in bilateral vocal fold immobility; and confusing muscle tension dysphonia with structural pathology.
Clinical boundary: Do not wait for a duration threshold when there are concerning airway or malignancy features.
Worked example: A 60-year-old smoker with 6 weeks of hoarseness and a neck node has a laryngeal mass on flexible laryngoscopy. Proceed to biopsy and staging imaging; do not treat empirically for reflux.
Sleep-related obstruction
Sleep medicine questions center on obstructive sleep apnea (OSA) diagnosis, consequences, and treatment selection. Understand that OSA is caused by pharyngeal collapse during sleep and is associated with hypertension, cardiovascular disease, stroke, and metabolic dysfunction. Diagnosis uses an appropriate sleep assessment and testing in eligible patients; apnea-hypopnea categories must be interpreted within the named adult framework and are not pediatric thresholds.
Know the anatomic levels of obstruction: nasal, retropalatal, retroglossal, and hypopharyngeal. Drug-induced sleep endoscopy (DISE) can localize collapse. Positive airway pressure (PAP) is an important standard option in suitable patients; alternatives include oral appliances (mandibular advancement), positional therapy, and weight loss. Surgical options include uvulopalatopharyngoplasty (UPPP), hypoglossal nerve stimulation (for PAP-intolerant patients with favorable anatomy), and maxillomandibular advancement for skeletal deficiency.
Traps: recommending surgery without documenting PAP failure or intolerance; missing central sleep apnea and obesity hypoventilation; and forgetting that pediatric OSA is often treated with adenotonsillectomy. Also know that bariatric surgery can improve OSA but does not guarantee cure.
Rule of thumb: "Match the confirmed mechanism, physiological severity, anatomy and patient circumstances to the actual treatment options."
Worked example: A 45-year-old with AHI 35, hypertension, and PAP intolerance has DISE showing retropalatal and retroglossal collapse. Consider hypoglossal nerve stimulation if criteria are met, or maxillomandibular advancement if skeletal deficiency is present.