Final Exam Flashcards
Cholesteatoma
Abnormal skin growth behind TM. A cyst that arises from the pars flaccida. can expand into and beyond ME space
How does a cholesteatoma form?
in response to repeated infection or trauma, sometimes present at birth. Neg ME pressure causes a perforation or weak spot and skin grows in response which causes a pocket
Tx for cholesteatoma
course of antibiotics to reduce any current infection, surgery to remove is final Tx
Tuning Fork Difference Test
- comparison of AC BTW ears
- tells which ear is most sensitive to that Hz
- TF held alternatively BTW ears
- helpful to determine better ear
Weber Test
TF placed on center of forehead, midline of skull, nose, chin or upper teeth
- ask Pt where they hear the sound
Rinne Test
comparison of TF loudness on mastoid or next to ear
- ask which is louder?
Positive Rinne
AC > BC (NH or SNHL)
Negative Rinne
AC < BC (CHL)
Equivocal Rinne
AC = BC
Rinne Test Interpretation
negative rinne = 25 dB CHL
Problems with tuning fork tests
experience: - poor tech - improper interpretation limitation of fork: - test at freq used only - incorrect interpretation w/ limited results
Sites of possible ossicular discontinuity
- incudo-stapedial joint- most common
- separation of the incudo-malleal joint
- dislocation of the incus
- dislocation of the stapes from the oval window
- fracture of the stapes
- fracture of the malleus or incus- common
Etiology of ossicular discontinuity
- blunt head trauma
- longitudinal temporal bone fracture
- barotrauma
- penetrating trauma
- chronic otitis media
- chronic OM with cholesteatoma
- congenital malformation
Effects of ossicular discontinuity on hearing
- mild- mod severe CHL
- depends on severity of disartic
- if CHL > 40 dB, suspect disartic
- large ABG @ high Hz, suspect disartic
Tx for ossicular discontinuity
- partial or total ossicular replacement prostheses (PORP/TORP)
Causes of ossicular discontinuity surgery failure
- on going ME abnormalities
- recurrent cholesteatoma
- recurrent OM
- formation of granulation tissue or adhesions
- extrusion or absorption of the presthesis and bony anklyosis of prosthesis
- iatrogenic
Myringoplasty
reconstruction of a perforation of TM
- patching of perf that does not reach margin
tympanoplasty
reconstruction of the TM, also includes addressing ME pathology
Indications for tympanoplasty
- CHL due to TM perf or ossicular dysfx
- chronic or recurrent OM secondary to contamination
- progressive HL due to chronic ME pathology
- perf or HL persistent > 3 mos. due to trauma, infection, surgery
- inability to bathe or participate in water sports safely
Goals of tympanoplasty
- establish an intact TM
- eradicate ME disease and create an air-containing ME space
- restore hearing by building a secure connection BTW the eardrum and the cochlea
Tympanoplasty techniques
- overlay technique- lateral grafting, post-aurical approach
- underlay technique- medial grafting, canal approach
Type I tympanoplasty
TM is grafted to an intact ossicular chain
Type II tympanoplasty
- malleus is partially eroded
- TM +/- malleus remnant is grafted to incus
Type III tympanoplasty
- malleus and incus are eroded
- TM is grafted to the stapes superstructure
Type IV tympanoplasty
- stapes superstructure is eroded but food plate is mobile
- TM is grafted to a mobile foot plate
Type V tympanoplasty
TM is grafted to a fenestration in the horizontal SCC
tympanoplasty prognostic indicators
- status of ME
- presence of handle of malleus
- perf > 50%
Otosclerosis
- bony changes that occur are usually a combination of resorption and remodeling of the otic capsule bone
- abnormal new bone tissue is formed, starting soft and possibly becoming hardened or sclerotic
- first stage of otosclerosis is also known as otospongiosis
- later stage- bone growth hardens
- can occur anywhere in the otic capsule but most commonly the stapes footplate
symptoms of otosclerosis
- gradually progressive HL
- tinnitus in 50-60% of patients
- often bilateral
- sometimes vestibular involvement
- schwartz sign- red blush hue behind the TM due to vascularity of otospongiosis
Etiology of otosclerosis
- not fully understood
- hereditary
- endocrine, biochemical, metabolic, vascular
- pregnancy- hormonal
clinical otosclerosis
involving fixation of stapes footplate
histological otosclerosis
- involving portion of otic capsule NOT stapes footplate- remains freely mobile
Otosclerosis Audiogram
- initially flat or rising CHL
- mass component- high freq HL
- max CHL- 60-65 dB
- Carhart’s Notch
- bilat, progressive CHL
- word rec normal
- can spread to cochlea and cause SNHL or mixed
diagnosis of otosclerosis
- audio
- impedance mismatch
- family Hx
- tinnitus
- imbalance/vertigo
- CT scan
- schwartz sign
Tx for otosclerosis
- monitoring
- amplification
- diet- reduce caffeine, alcohol, salt
- medical- sodium fluoride, vit D
- surgery- stapes mobilization, stapedectomy
osteoma
- small tumor of new bone growth that is unilateral and singular
- commonly found at the junction of the cartilaginous and bony portion of the EAC
Exostosis
- new bone growth in multiple and bilateral
- arises from periosteum
- removed by grinding
- common among cold water swimmers
Usher Syndrome
genetic disorder characterized by HL, RP, vestibular probs
Retinitis Pigmentosa
- deterioration of the sensory cells of the retina
- rods deteriorate first
- pattern: night blindness, blind spots, tunnel vision
Type I Usher Syndrome
- profound HL from birth
- RP progresses early
- vestibular areflexia
Usher Syndrome Type II
- sloping high Hz HL present at birth that does not progress
- RP onset in adolescence
- normal vestib Fx
Usher Syndrome Type III
- NH and sight at birth
- progressive HL
- mod HL by teens, severe-prof by middle age
- RP begins in teenage yrs
- progressive loss of vestib Fx
Genetics of Usher Syndrome
- autosomal recessive pattern
- genes encode protein that make up cilia
Management of Usher Syndrome
- early Dx important
- CI
- mobility/balance training
- Tx RP
- genetic testing
Acoustic Neuroma
- benign slow growing tumors
- assoc. with neurofibromatosis
Symptoms of AN
- HL- most frequent initial symptom, asymmetric, high Hz, decreased speech discrim
- vertigo
- dysequilibrium
- tinnitus
- headache
- nystagmus
Diagnosis of AN
- history and physical exam
- audio
- ABR
- OAE
- vestib testing
- MRI
AN Tx Options
- observation
- surgery
- radiotherapy
- conventional
- stereotactic
4 types of presbycusis
- sensory
- neural
- strial
- cochlear conductive
Sensory presbycusis
- affecting haircells and supporting cells
- bilat, precipitous HFSNHL w/ excellent SDQ
Neural presbycusis
- loss of afferent neurons in cochlea
- same audio as sensory but SDQ poor
Strial
- due to atrophy of lateral wall of stria vascularis
- fairly flat SNHL with good SDQ
cochlear conductive
- metabolic
- possibly due to thickening of BM
NIPTS
- NIHL
- HL caused by chronic exposure to noise over a long period of time
- characteristic high frequency loss
- c/o HL and tinnitus
Acoustic Trauma
- HL caused by a single, short latency exposure
- sudden HL- greatest in ear facing towards noise
- unique audio config
Blast trauma
- HL secondary to sudden explosive force
- from change in pressure
otologic effects of blast injuries
- ME- TM perf most common, occasional ossicular chain disruption
- inner ear- may be damaged at pressures insufficient to rupture TM, initial SNHL
auditory symptoms of blast trauma
- HL - SNHL, CHL, mixed, bilat or uni, temporary threshold shift
- tinnitus
- TM rupture
- vertigo
- otalgia
- bleeding from external canal
- FB
How are people exposed to solvents and heavy metals?
- inhalation
- getting on skin
- spills
- explosions
- water contamination
- consumption
Symptoms of organic solvent exposure
- disequilibrium
- vision problems
- HL
- abnormal olfaction
- neurologic
- headaches
- memory loss
- mood swings
- coordination difficulties
- delayed reaction time
solvent effects on inner ear
- cochlear damage
- supporting cells
- OHCs
- vestib damage
- sensory cells
- synergistic effect when mixed
solvent effects on retrocochlear/central
- VIII nerve damage
- cerebellum/brainstem damage
