External, Middle, And Inner Ear Flashcards
(47 cards)
1
Q
Auricular infections?
A
- Perichondritis
- Ramsay-Hunt syndrome
2
Q
What is Perichondritis?
A
- Infection of the auricular cartilage
- Pathogens: Pseudomonas aeruginosa, S. aureus, Streptococcus
- Risk of cauliflower ear
3
Q
What is ramsey hunt syndrome?
A
- Herpes zoster with a facial nerve palsy
- Pathophysiology: primary infection or reactivation of HSV
4
Q
What things can cause an obstruction of the external auditory ear canal?
A
• Cerumen • Foreign body • Keratosis obliterans • Polyps
5
Q
What is the image showing?
A
Cerumen blocking the ear canal
6
Q
Explain forgein bodies in the external ear canal?
A
- If you do not know what the object is, DO NOT IRRIGATE. Also, you do not always know the status of the tympanic membrane.
- Plant materials or insects will swell.
- Use an operating otoscope or a microscope to remove the foreign body in conjunction with a Hartman forceps or an alligator forceps.
7
Q
keratosis obliterans?
A
External auditory canal cholesteatoma caused by blockage of the EAC permitting accumulation of epithelial debris
8
Q
Otitis externa can happen from what?
A
• Allergic • Excematoid • Bacterial • Fungal • Viral
9
Q
History and PE of bacterial acute otitis externa?
A
- History – Pain – Tenderness – Itching – Hearing loss
- Physical examination – Swollen external auditory canal – Erythema (variable) – Watery, scant exudate – Pronounced tenderness
10
Q
Common type of bacterial acute otitis externa?
A
• Diffuse (“swimmer’s ear”)
–Most common form of bacterial AOE
–Optimally managed with ototopical agents
11
Q
Principles of treating bacterial acute otitis externa?
A
- Clean the canal
- Topical therapy
- Suitable pain management
12
Q
What is an issue using aminoglycosides (neomycin)?
A
Neomycin Sensitization
- Incidence increasing due to widespread, long-standing use
- Cross-reactivity with other aminoglycosides
- Routine use not recommended because of high risk for sensitization
13
Q
What is otitis media?
A
- Otitis media (OM): A term for any inflammatory middle ear condition.
- Acute suppurative otitis media: – Early TM appearance: still transparent, bulging – Middle phase: suppurative (purulent fluid behind TM) – Late phase: weeping and possible rupture
- Otitis media with effusion(OME): After the acute phase passes, sterile fluid remains which will either clear in about 90 days of may become re-infected.
14
Q
Adults with middle ear effusion?
A
Concern for malignancy.
Thorough exam of head and neck to include the larynx and nasopharynx.
15
Q
Acute otitis media can manifest with what?
A
• Acute otitis media (AOM)
– Without perforation
– With perforation
– With tympanostomy tubes (AOMT)
16
Q
Overview of chronic otitis media?
A
- Chronic middle ear effusion
- Chronic nonsuppurative otitis media – Cholesteatoma – Dry perforation
- Chronic suppurative otitis media – Without cholesteatoma – With cholesteatoma
17
Q
treating acute otitis media ?
A
• Systemic antibiotics are the mainstay of therapy for AOM in ears with intact tympanic membranes
18
Q
Explain tympanostomy tubes?
A
- Myringotomy with insertion of tympanostomy tubes is the most common type of surgery that children in North America and Europe undergo
- Estimated 1 million operations are performed in Canada and the U.S.annually Usually as an ambulatory procedure
- Primary indications for tympanostomy tube insertion are recurrent episodes of acute otitis media and otitis media with persistent effusion.
Risks of leaving middle ear disorders untreated: hearing loss, which raises concerns about possible negative consequences for speech development, language acquisition and learning.
Questions have been raised, however, about the effectiveness of this surgery, the appropriate management of children with recurrent episodes of acute otitis media and otitis media with persistent effusion, the economic cost and the numbers of procedures performed.
19
Q
Indications for Tympanostomy tubes?
A
- AAOHNS Referral Guidelines and Indications for Tympanostomy Tube (Child meets at least 1 criterion below)
- Severe AOM
- Hearing loss of > 30 dB threshold concurrent with a persistent effusion > 3 months
- Poor response to antibiotic for OM. Second-line antibiotic fails. Breakthrough AOM while on antibiotic prophylaxis.
- Treatment failure due to multiple drug allergies or intolerances
- Impending or actual complication of OM, such as mastoiditis, facial nerve paralysis, lateral sinus thrombosis, meningitis, brain abscess, or labyrinthitis
- OME > 3months (Consider adenoidectomy if over age 4 or second set of tympanostomy tubes)
- 6 or more months of effusions in the previous 12 months
- Recurrent episodes of otalgia or AOM (> 3 episodes/6 months or > 4 episodes/12 months)
- Persisting or recurrent ear discharge
- Retraction of the TM or pars flaccida, negative middle ear pressure, or TM perforation > 3months
- AOM with imminent air travel or barotrauma (injury following pressure changes) following air travel
- Craniofacial anomalies that predispose to middle ear dysfunction (eg, cleft palate, Down’s syndrome)
20
Q
Acute otitis media with tubes bacteriaology?
A
• Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis), Pseudomonas aeruginosa and Staphylococcus aureus, are commonly recovered as primary and secondary pathogens in Acute OM with tubes
21
Q
Explain acute otitis media with tubes treatment?
A
- Ototopical antibiotics alone are appropriate therapy in uncomplicated cases – Fluoroquinolones
- Adjunctive systemic antibiotics may be used – When ototopical treatment fails (after 7-10 days) – In children with associated streptococcal pharyngitis – When infection has spread beyond middle ear or external ear canal – With lack of adherence to ototopical therapy
- Special populations (eg, immunocompromised patients) require additional consideration
22
Q
Tympanic membrane perforations?
A
- Infection is the most common reason to develop a perforation.
- Traumatic perforations may result from penetrating trauma or blows to the ear (eg, being struck with the flat of the hand; falling from water skis with the head hitting the water surface, ear down).
- Inexpertly performed irrigation of the ear canal for wax can lead to perforation. In some settings, when irrigation for cerumen is relegated to medical assistants, otolaryngologists may see 10-20 patients per year with this injury.
- Failure of surgically created openings to heal when the tube extrudes results in chronic TMP.
23
Q
Repair of tmypanic membrane perforations?
A
- 80-90% will heal without needing surgical intervention.
- Observe water precautions with an open TM.
- May eventually need a tympanoplasty or a tympanomastoidectomy.
24
Q
What is Otosclerosis?
A
• Otosclerosis can result in conductive and/or sensorineural hearing loss. The primary form of hearing loss in otosclerosis is conductive hearing loss (CHL) whereby sounds reach the ear drum but are incompletely transferred via the ossicular chain in the middle ear, and thus partly fail to reach the inner ear(cochlea). This usually will begin in one ear but will eventually affect both ears with a variable course.
25
Treatment of otosclerosis?
• Treatment for the hearing loss caused by otosclerosis is through hearing aid application or through laser stapedotomy with placement of a piston prosthesis.
26
Components of the bony labyrinth?
Bony Labyrinth
Embryology
Components: Vestibule Semicircular canals Cochlea
27
Other components of the inner ear?
* Cochlear Aqueduct
* Vestibular Aqueduct
28
explain the Membranous labyrinth?
– Embryology
– The membranous labyrinth is enclosed within the bony labyrinth.
– Endolymphatic duct: connects the endolymphatic compartment to the endolymphatic sac.
– Periotic duct: within the cochlear aqueduct, connects the scala tympani to the posterior cranial fossa.
29
Explain the semicircular canals?
• The three semicircular canals open into the vestibule,
– Horizontal canal
– Superior canal
– Posterior canal
30
What is the shape of the cochlea?
The shape of the cochlea resembles that of a snail shell with two and onehalf turns
31
What is the Modiolus?
Modiolus: the central conical core of the cochlea.
32
what are two inner ear diseases and related to cochlear fluid?
Meniere's disease
Perilymphatic fistula
33
Features of meniere's Disease?
• Fluctuating hearing • Tinnitus • Aural fullness • Vertigo
34
Meniere's Disease tiggers?
• Caffeine • Alcohol, Aspirin products • Tobacco • Sodium • The NO CATS approach.
35
Hair cells are held how? Stimulus?
• Hair cells • The hair cells are held in position by a system of supporting cells. • stimulus for activating the hair cell. • Each hair cell is innervated at its base
36
What are the receptors on the hair cells?
• Stereocillia • Kinocillium
37
What are stereocilla?
Actin filaments within a tubular membrane
38
Mechano-electrical transduction by hair cells?
Movement of the hair bundle in the depolarizing direction leads to increases in membrane conductance, meaning that the membrane becomes more permeable to positively charged ions
39
Mechanical events that take place in the cochlea when a sound wave enters the inner ear?
Sound waves normally enter the inner ear via the oval window and are transmitted rapidly through the cochlear fluid. Movement of the oval window by the stapes footplate is met with equal and opposite action of the round window
40
The basilar membrane is a what?
Basilar membrane is a resonant structure • The basilar membrane is deflected in response to sound waves in the inner ear.
The deformation of the basilar membrane is a traveling wave.
41
How does the basilar membrane work?
Different regions of the basilar membrane respond maximally to different sound frequencies based on the local physical properties. ie The topotonical basilar membrane
Variation in the width of the basilar membrane
42
Excitation of the auditory nerve fibers?
* Shearing motion of the stereocillia
* Shearing results in depolarization or hyperpolarization
43
Afferent and efferent innervation to the organ of corti?
44
Explain begnin positional vertigo?
Typical complaint: spells of vertigo when turning over in bed, “top shelf vertigo”
Examine the patient for nystagmus and vertigo in the Dix-Hallpike position : head-hanging R and L
Vertigo lasts shorter than 1 minute
Geotropic, torsional nystagmus with upbeat component
Brought on only by positional changes
Latency of few seconds up to 45 sec
Fatigues with repeated testing
45
What is the pathophys of BPPV?
In BPPV, the otoliths become dislodged from the hair cells and membrane to which they were attached, migrate out of the utricle, and enter the semicircular canals. The posterior semicircular canal is almost always the involved canal since it is the most dependent of the 3 canals. Now when the patient turns his head, both the otoliths and endolymph start to move. Once the patient stops turning his head, the endolymph should stop moving as well. However, the otoliths continue to move and drag the endolymph with them. Angular acceleration receptors in the semicircular canal continue to fire and tell the brain that the head is still turning. The eyes, however, tell the brain that the head has stopped moving. Receiving conflicting information, the brain resolves this dilemma by rationalizing that the room must be spinning in the opposite direction.
46
What is the dix-hallpike manuver?
The Dix–Hallpike test is performed with the patient sitting[3] upright on the examination table with the legs extended. The patient's head is then rotated to one side by approximately 45 degrees. The clinician helps the patient to lie down backwards quickly with the head held in approximately 20 degrees of extension.
47
The epley manuver is what?
* The patient begins in an upright sitting posture, with the legs fully extended and the head rotated 45 degrees towards the affected side.
* The patient is then quickly and passively forced down backwards by the clinician performing the treatment into a supine position with the head held approximately in a 30 degree neck extension (Dix-Hallpikeposition) where the affected ear faces the ground.
* The clinician observes the patient's eyes for “primary stage” nystagmus.
* The patient remains in this position for approximately 1–2 minutes.
* The patient's head is then turned 90 degrees to the opposite direction so that the unaffected ear faces the ground, all while maintaining the 30 degree neck extension.
* The patient remains in this position for approximately 1–2 minutes.
* Keeping the head and neck in a fixed position relative to the body, the individual rolls onto their shoulder, rotating the head another 90 degrees in the direction that they are facing. The patient is now looking downwards at a 45 degree angle.
* The eyes should be immediately observed by the clinician for “secondary stage” nystagmus and this secondary stage nystagmus should beat in the same direction as the primary stage nystagmus. The patient remains in this position for approximately 1–2 minutes.
* Finally, the patient is slowly brought up to an upright sitting posture, while maintaining the 45 degree rotation of the head.
* The patient holds sitting position for up to 30 seconds.
