Exam 2 Study Guide Flashcards

1
Q

Will people with ANSD have robust OAEs?

A

Yes
But some lose them over time due to a compromised blood flow

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2
Q

Are OAEs a useful prediction of cochlear function?

A

Yes

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3
Q

Are OAEs useful for determining site of lesion?

A

Yes
Especially between sensory and neural

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4
Q

Are OAEs a test of hearing?

A

No
Peripheral hearing sensitivity is inferred from OAEs
Only tells us function of cochlear OHCs

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5
Q

Why are OAEs an almost direction measure of OHC function?

A

The middle ear function is also a factor

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6
Q

Are OAEs used in isolation for NBHS?

A

Yes
With the goal of distinguishing infants with normal or near-normal hearing from those who need further evaluation

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7
Q

In diagnostic cases, are OAEs used as a cross check?

A

Yes

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8
Q

What hearing loss can we miss with an OAE screening?

A

ANSD
Mild losses (remember OAE criteria)
Atypical configuration (for example low frequency losses or only HF losses)
Delayed onset or progressive losses
Neural and/or genetic IHC loss only (normal OHC) which are rare

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9
Q

What does dysfunction of some OHCs present as in an OAE?

A

Reduced OAE amplitude without affecting hearing sensitivity for pure tone signals at audiometric freq (can be different from OAE)

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10
Q

What patients will have abnormal OAEs but normal audiograms?

A

tinnitus
hazardous noise/music exposure
ototoxicity
vestibular pathology

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11
Q

What patients will have normal OAEs but abnormal audiograms?

A

Functional, non-organic, psychogenic hearing loss
central auditory nervous system dysfunction
VIIIth Nerve (neural) auditory dysfunction
Those with exclusively inner hair cell damage (e.g., carboplatin toxicity or genetic abnormality)

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12
Q

What amount of hearing loss are typically OAEs no longer seen?

A

Exceeding 25 to 35 dB

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13
Q

What are the 3 outcomes of OAEs?

A

Amplitude is normal (relative to an appropriate normative region),
Amplitude is abnormal (OAE is present but below normal limits), or
There is no evidence of reliable OAE activity above an acceptably low noise floor (Absent).

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14
Q

What is a pass for TEOAE?

A

Absolute emission greater than or equal to -10 dB SPL
SNR (relative value) greater than or equal to 3-5 dB (varies)
Reproducibility of 70% or greater

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15
Q

What is a pass for DPOAE?

A

Absolute emission greater than or equal to -10 dB SPL
SNR (relative value) greater than or equal to 6 dB (3-5 dB some)
Replicates

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16
Q

What is the role of the MOC and the efferent system?

A

Protection from acoustic trauma
Hearing in noise
Role in Attention
Role in Auditory Training

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17
Q

Does the OCB contain both crossed and uncrossed bundles?

A

Yes

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18
Q

Where do MOC fibers terminate?

A

At the based of the OHC

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19
Q

Where for the LOC fibers terminate?

A

On the dendrites of the auditory nerve fiber

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20
Q

What is responsible for suppressing OHC motility?

A

MOC

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21
Q

Does the presentation of a sound ipsi or contra to the ear that is having an OAE result in reduced OAE amplitudes?

A

Yes

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22
Q

Is sound-induced suppression normal?

A

Yes
Lack of suppression implies dysfunction of the efferent auditory system

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23
Q

When is suppression the greatest?

A

In the 8 to 18 ms range

24
Q

What stimuli is suppression greatest for?

A

Low intensity

25
Q

Is suppression greatest from binaural noise?

A

Yes

26
Q

What is the most powerful suppression stimulus for TEOAEs?

A

White noise

27
Q

Does the MOC appear to be more efficient in the right ear than the left?

A

Yes

28
Q

Do ANSD patients have suppression?

A

No

29
Q

Do some hyperacusis patients how abnormally large suppression effects?

A

Yes

30
Q

Can tinnitus patients show impaired efferent activity?

A

Yes

31
Q

Are there “safe” levels for ototoxic drugs?

A

No

32
Q

Can some ototoxic drugs create a reversible hearing loss?

A

Yes
Like aspirin

33
Q

Can you predict the severity of the hearing loss caused from ototoxicity?

A

No

34
Q

How can drugs damage an ear?

A

Formation of free radicals and metabolic stress
Toxicity: Platinum or other metal accumulation
Ischemia due to compromised blood flow (stop blood flow)
Mechanical damage (break of hair cells or BM)

35
Q

Will the hearing loss that results from aminoglycoside antibiotics be permanent?

A

Yes

36
Q

Will the hearing loss that results from salicylates (aspirin) be permanent?

A

No in most cases

37
Q

Will the hearing loss that results from cisplatin be permanent?

A

Yes
Hearing loss begins OHCs/stria

38
Q

Will the hearing loss that results from carboplatin be permanent?

A

Yes
Can cause OHC and IHC damage

39
Q

Will the hearing loss that results from quanine be permanent?

A

No
Typically reversible

40
Q

Will the hearing loss that results from methadone, ED meds, etc. be permanent?

A

Can be permanent or temporary

41
Q

What are some factors that can influence ototoxicity?

A

Other drugs
Other health co-morbidities
Age
Delivery (pill, IV, etc.)

42
Q

Are the very old and young the most susceptible to ototoxicity?

A

Yes

43
Q

Can genetic factors also contribute to ototoxicity?

A

Yes

44
Q

Is a baseline audiogram important for monitoring thresholds due to ototoxicity?

A

Yes
Performing standard audiometry, HF audiometry, and DPOAEs up to 10 kHz

45
Q

Why are DPOAEs preferred for ototoxic monitoring?

A

They have frequency specificity

46
Q

What is the rationale for using OAEs for ototoxic monitoring?

A

OAEs are site-specific for cochlear (sensory) auditory dysfunction
Ototoxic drugs exert their effect on outer hair cell function (not solely); OAEs are dependent on outer hair cell integrity
OAEs can detect cochlear dysfunction before it is evident by pure tone audiometry (more on this to come)

47
Q

What are best practices for ototoxic monitoring with OAEs?

A

Utilize DPOAE high frequency protocol (up to 10,000 Hz)
Utilize multiple frequencies/octave (>5 per octave)
Sensitive stimulus intensity levels (L1=65dB , L2=55dB)
Replicate DP grams to determine normal variability
Watch out for standing waves and Middle ear abnormality

48
Q

What are some OAE ototoxic monitoring testing challenges?

A

Patients may be ill, inattentive or difficult to transport
Bedside testing may be difficult due to acoustic and electrical noise
Baseline data often not available
Infectious disease and immunocompromised chemotherapy patients may be prone to otitis media
Potential for above also to have strict rules for access

49
Q

Different ototoxic scales

A
50
Q

What is oto-protection?

A

Medications or supplements given concurrently or prior to exposure to potentially ototoxic drugs to reduce likelihood or severity of hearing loss
Pedmark

51
Q

How are non-pressurized OAEs affected by ME pressure?

A

Reduced amplitudes to absent responses

52
Q

Where are OAEs most affected by ME pressure?

A

Low frequencies

53
Q

What are stimulus frequency OAEs?

A

Not yet widespread use
May be more predictive of behavioral thresholds than TEOAE and DPOAE
Uses a pure-tone stimulus and vector analysis techniques
Equipment is expensive and complex

54
Q

Does the emission for the stimulus frequency OAE originate in the same region of the cochlea as the evoking stimulus?

A

Yes

55
Q

What are some important things to remember about report writing?

A

Who is it going to? (what do they know about hearing and audiology and the effects of loss?)
Why are you sending it?
What do you want them to do about it?
Stay away from jargon!

56
Q

What does HEAR stand for?

A

History, relevant background
Evaluation–what you did
Audiological Findings–what you found
Recommendations–what you want the recipient to do about what you found