Clinical ENT Flashcards

24 sample cards from the ENT deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. Auditory Pathway: List the main relay stations of the central auditory pathway from cochlea to cortex.

   Spiral ganglion → cochlear nuclei → superior olivary complex → lateral lemniscus → inferior colliculus → medial geniculate body (thalamus) → primary auditory cortex (Heschl's gyrus, area 41/42 of the temporal lobe). Mnemonic: E.C.O.L.I.M.A.

2. Auditory Pathway: At what point does the auditory pathway become bilateral, and what is the clinical consequence?

   From the superior olivary complex upward, information is carried bilaterally (each ear projects to both hemispheres). Therefore a unilateral central lesion (above the cochlear nuclei) does not cause complete deafness in one ear.

3. Auditory Pathway: What is the primary role of the superior olivary complex?

   Sound localization. It compares interaural time differences (ITD, via medial superior olive, for low frequencies) and interaural intensity/level differences (ILD, via lateral superior olive, for high frequencies) between the two ears.

4. Vestibular System: What are the two types of vestibular receptor organs and what does each detect?

   The three semicircular canals (cristae ampullares) detect angular/rotational acceleration. The otolith organs — utricle and saccule (maculae) — detect linear acceleration and gravity/head tilt (utricle mainly horizontal, saccule mainly vertical).

5. Vestibular System: How do otolith organs (maculae) sense linear acceleration and gravity?

   Hair cell stereocilia are embedded in a gelatinous otolithic membrane topped by calcium carbonate crystals (otoconia). Linear acceleration/gravity shifts the dense otoconia, bending the hair cells and altering firing rate.

6. Vestibular System: What is the vestibulo-ocular reflex (VOR) and its purpose?

   A reflex that produces eye movements equal and opposite to head movement to keep gaze/image stable on the retina during head motion. It is mediated by semicircular canal input to the extraocular muscles via the vestibular nuclei.

7. Vestibular System: Describe the ampullopetal/ampullofugal (Ewald's laws) response of a semicircular canal hair cell.

   Hair cells depolarize when stereocilia bend toward the kinocilium and hyperpolarize when bent away. In the horizontal canal, endolymph flow toward the ampulla (ampullopetal) is excitatory; in vertical canals it is inhibitory.

8. Central Pathways (vestibular): Name the four vestibular nuclei and two major output tracts controlling posture.

   Superior, inferior, medial, and lateral vestibular nuclei (in the pons/medulla). Outputs include the vestibulospinal tracts (posture/balance) and the medial longitudinal fasciculus (MLF, coordinating eye movements/VOR).

9. External Ear Disorders: What organism most commonly causes malignant (necrotizing) otitis externa, and in which patients?

   Pseudomonas aeruginosa, typically in elderly diabetics or immunocompromised patients. It is an invasive infection spreading to the skull base (temporal bone osteomyelitis) and can cause cranial nerve palsies.

10. External Ear Disorders: What is otitis externa ('swimmer's ear'), and its classic examination finding?

    Diffuse inflammation/infection of the external auditory canal (often Pseudomonas or Staph aureus, or fungal). Classic finding: pain on movement of the tragus/pinna (tragal tenderness) and a swollen, discharging canal.

11. Middle Ear Disorders: Contrast acute otitis media (AOM) with otitis media with effusion (OME/'glue ear').

    AOM: acute infection with a bulging, erythematous tympanic membrane, pain, and fever (often S. pneumoniae, H. influenzae, M. catarrhalis). OME: non-infected serous/mucoid fluid behind an intact retracted TM causing conductive hearing loss, no acute signs.

12. Middle Ear Disorders: What is a cholesteatoma and why is it dangerous?

    An abnormal collection of keratinizing squamous epithelium (skin) in the middle ear/mastoid. Though benign, it erodes bone — can destroy ossicles, cause facial nerve palsy, labyrinthine fistula, or intracranial complications. Classic sign: painless, foul-smelling otorrhea.

13. Middle Ear Disorders: What is otosclerosis and its characteristic clinical picture?

    Abnormal bone remodeling causing fixation of the stapes footplate at the oval window, producing progressive conductive hearing loss (later possibly sensorineural). Autosomal dominant, worse in pregnancy; may show 'Schwartze sign' and Carhart's notch on audiogram.

14. Inner Ear Disorders: What is the classic triad/tetrad of Ménière's disease and its pathology?

    Episodic vertigo, fluctuating sensorineural hearing loss (low-frequency), tinnitus, and aural fullness. Pathology: endolymphatic hydrops (excess endolymph). Attacks last minutes to hours.

15. Inner Ear Disorders: What causes benign paroxysmal positional vertigo (BPPV) and what maneuver diagnoses it?

    Displaced otoconia (canaliths) in a semicircular canal (usually posterior), causing brief vertigo with head position change. Diagnosed by the Dix-Hallpike maneuver (elicits rotatory nystagmus); treated with the Epley repositioning maneuver.

16. Inner Ear Disorders / Weber & Rinne: How do Rinne and Weber tests differentiate conductive from sensorineural hearing loss?

    Rinne: normal/SNHL = air conduction > bone conduction (positive); conductive loss = bone > air (negative) in the affected ear. Weber: lateralizes TO the affected ear in conductive loss, and AWAY from the affected ear (to the better ear) in sensorineural loss.

17. Rhinitis: Contrast allergic rhinitis with vasomotor (non-allergic) rhinitis in mechanism.

    Allergic rhinitis is an IgE-mediated type I hypersensitivity to allergens (mast cell histamine release) causing sneezing, itch, clear rhinorrhea, eosinophilia. Vasomotor rhinitis is non-allergic, non-IgE autonomic dysregulation triggered by temperature/odors/irritants, with congestion but little itch.

18. Sinusitis: How are acute and chronic sinusitis defined by duration, and which sinus is most commonly affected in adults?

    Acute rhinosinusitis: symptoms <4 weeks (chronic: ≥12 weeks). The maxillary sinus is most commonly affected. Most acute cases are viral; bacterial suggested by symptoms >10 days, purulent discharge, facial pain, and 'double-worsening'.

19. Sinusitis: What is the osteomeatal complex and why is it key in sinusitis?

    The final common drainage pathway for the frontal, maxillary, and anterior ethmoid sinuses into the middle meatus. Obstruction/mucosal edema here blocks drainage and ventilation, predisposing to recurrent/chronic sinusitis.

20. Nasal Polyps: What are nasal polyps, and what important condition should be excluded in a child with polyps?

    Benign, edematous, inflammatory outgrowths of nasal/sinus mucosa (often pale, grape-like, insensate). In children, cystic fibrosis must be excluded. In adults, associations include asthma and aspirin sensitivity (Samter's triad).

21. Nasal Polyps: What is Samter's triad (aspirin-exacerbated respiratory disease)?

    The triad of nasal polyps, asthma, and aspirin (NSAID) sensitivity. Due to abnormal arachidonic acid metabolism with overproduction of leukotrienes when COX is inhibited.

22. Pharyngitis: What are the Centor criteria used for, and name them.

    They estimate the probability that pharyngitis is due to Group A Streptococcus (guiding antibiotic use). The four criteria: (1) tonsillar exudate, (2) tender anterior cervical lymphadenopathy, (3) fever >$38^{\circ}\text{C}$, (4) absence of cough. (Modified adds age.)

23. Pharyngitis: What is the most common cause of acute pharyngitis overall, and the most important bacterial cause to treat?

    Most cases are viral (e.g., rhinovirus, adenovirus, EBV). The most important bacterial cause is Group A beta-hemolytic Streptococcus (Streptococcus pyogenes), treated to prevent rheumatic fever and suppurative complications.

24. Pharyngitis: What is a peritonsillar abscess (quinsy) and its classic features?

    A collection of pus between the tonsillar capsule and the pharyngeal constrictor muscle, usually a complication of tonsillitis. Features: severe unilateral sore throat, trismus, 'hot potato' muffled voice, uvular deviation to the opposite side, and drooling.

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