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Otoacoustic Emissions (OAEs) > Exam #2 (Final) > Flashcards

Exam #2 (Final) Flashcards

1
Q

4 Steps CRITICAL to ensure adequacy of OAE measurements

A

1) Otoscopy- r/o EE debris, vernix, or cerumen
2) Tympanometry & ARTs to r/o ME dysf
3) Stimulus calibration in a hard walled cavity to ensure target levels within +/- 2dB of 65/55 for DPOAEs & 80 SPL for TEOAEs
4) Monitor noise in levels in EE- reduce ambient, acoustical, & physiological noise so NF is

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2
Q

What do DPOAEs and TEOAEs represent?

A

Different sources & mechanisms of generation

ALSO: Mix of both reflection and distortion emissions

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3
Q

What do SOAEs and SFOAEs represent?

A

Reflection emissions

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4
Q

General diagnostic DPOAE protocol

A

In addition to standard protocol, it’s important to include 5-8 frequencies to enable assessment of cochlear processing at many frequencies.
-Restrictin freq to 1-2 frequency/octave would preclude visualization of a dip in OAEs that reflect cochlear abnormality (especially in patients with NIHL/tinnitus)

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5
Q

Normal OAEs with Normal audio

A

Normal ME

Normal cochlea

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6
Q

Abnormal OAEs w/ normal audiogram:

A 
Abnormal ME (r/o)
Abnormal cochlear OHC function
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7
Q

Abnormal Audio w/ Normal OAEs:

A 
Possible:
IHC dysfunction
Neural dysfunction
False hearing loss 
Problems w/ PTAudiometry
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8
Q

Abnormal Audiogram w/ Abnormal or Absent OAEs

A

MUST r/o ME dysfunction
OHC dysfunction if ME is normal
Possible IHC dysfunction if pure tone thresholds are >50 dB HL
Possible VIII CN tumor w/ compromised blood supple to cochlea (least likely)

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9
Q

What supplies the cochlea?

A

(Ascending)

Anterior/inferior cerebral artery (Goes though IAC & looks like bottleneck)

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10
Q

No blood supply to HCs, so where does nutrition come from?

A

Stria vascularis, which is:
Highly vascularized tissue
Highly metabolic
In the scala media

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11
Q

Stria Vascularis responsible for:

A

Providing nutrition to cochlea
Maintaining ionic composition of endolymph and endolymphatic potentials
BUT it is NOT the life support of thee organ of corti.

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12
Q

Where does the organ of corti get its blood supply from?

A

IT DOESNT! There is no blood supply, but it must get oxygen and nutrients from surrounding fluids: Perilymph and endolymph

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13
Q

What is the CMV and what is it responsible for?

A

Common modiolar vein & it’s responsible for venous drainage.

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14
Q

Considerations for clinical applications of OAEs (ototoxicity monitoring)

A

1) sensitivity to otoxicity increases when cochlear function is developing
2) Adverse effects of ototoxic drugs may be delayed after administration and may persist for days/weeks after d/c of drugs.
3) DPOAE abnormalities may be detected prior to changes in audiogram & AEPs

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15
Q

Objectives of Monitoring

A
  1. Detect early evidence of cochlear dysfunction prior to audiometric loss.
  2. If drug treatment cannot be altered, early changes in hearing help with parent/patient counseling & management with hearing aids, ALDs, etc.
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16
Q

Aminoglycosides pathophysiology:

A

Free radicals are produced during normal biochemical activities; e.g. respiration; however, they also interact w/ proteins & DNA through their oxidative activities, thus damaging the tissue.

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17
Q

(Aminoglycosides) Free Radicals

A

Are associated w/ inflammation, neurodegeneration, neurotoxicity, ototoxicity.

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18
Q

Free radical scavengers

A

Are antioxidant drugs that freely donate an electron to stabilize the molecule & thus, in this case disrupt interaction between gentamicin & iron to prevent ototoxicity

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19
Q

Vancomycin:

A
  • Non-aminoglycoside drug used to treat methicillin resistant Staph infections.
  • No clear evidence that it produces cochlear damage in itself (w/ out other ototoxic drugs administered concurrently)
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20
Q

Furosemide (Lasix)

A
  • Most commonly used loop diuretic, so named due to its action on epithelial cells in the loop oh Henle of the kidney.
  • Used to treat congestive heart failure & pulmonary edema
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21
Q

Ototoxicity monitoring implications of Cisplatin findings are

A

Long-term monitoring for delayed onset hearing loss.

-Delayed onset may be a direct consequence of retention of cisplatin long-term in the cochlea.

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22
Q

ASHA Ototoxicity Criteria:

A

(A) 20 dB of greater decrease in pure tone threshold at one test frequency.
(B) 10 dB of greater decrease at 2 adjacent test frequencies.
(C) Loss of response at 3 consecutive test frequencies where responses were previously obtained.

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23
Q

Draw a DP-gram that is representative of Auditory Neuropathy

A

Is inverted w/ amplitude on Y axis and latency (ms/div) on X axis.

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24
Q

What is a spike rate?

A

The rate of discharge when a sensory neuron is excited.

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25
Q

What happens to spike rate as the stimulus increases?

A

As stimulus ^ increases, the spike rate increases.

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26
Q

What must happen before neural impulses can generate? (Think transducers)

A

The receptor cell must receive and change the incoming physical stimulus into an electrical stimulus (thus, trans during the signal).

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27
Q

What is receptor potential?

A

When a signal is generated in the receptor cell (a cell that absorbs the stimulus and excited the sensory neuron)

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28
Q

In biological systems, electrical charge is carried by _________. This can only be one of two types of charge either enriched with ________ (also called ________) or depleted of ___________ (also called _________).

A

Electrical charge is carried by ions, enriched with electrons (also called anions -) or depleted or electrons (also called cations+).

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29
Q

Draw out temporal spectrograms of high and low pass filters with the Y axis in mPa (dB) and the X axis in milliseconds. What does this mimic?

A

A high pass filter mimics low frequency hearing losses, a low pass filter mimics a high frequency hearing loss.

(JUST DRAW DA DAMN TING)

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30
Q

In TEOAEs _________Hz energy dominates the response. The response magnitude relates to the stimulus/amplitude how?

A
  • 1500Hz
  • The response magnitude is related to the stimulus magnitude in cases where stimulus amplitude is ^increased the response magnitude ^increases.
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31
Q

In TEOAEs, at what rate does the response magnitude increase as the stimulus intensity increases?

A

An ^Increase in stimulus amplitude of 60-70 dB, the response ^increases by 20-30dB.

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32
Q

Are TEOAE responses linear or non-linear? What is the anatomical reason for this?

A

They are non-linear because of the inherent non-linear behavior of the basilar membrane.

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33
Q

How do TEOAEs relate to the perceptual thresholds?

A

They DON’T (hah!). The noise floor and ear status of the baby can change the apparent threshold, also response magnitude may show no changes even with intensity changes.

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34
Q

In TEOAE readings, high frequencies are represented at the ________ end of the time window, and low frequencies are represented at thee ________ end of the time window.

A

-High, low….really Andrew?

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35
Q

What kind of receptors are these hearing and balance organs? What does this mean and what movement is required for stimulation?

A
  • They are mechanoreceptors, meaning they sense mechanical stimuli and transducer to a receptor potential
  • This movement requires of the stereocilia (called shearing displacement).
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36
Q

What are the 4 examples of radial orientation of structures?

A

1) Base of the W pattern of a cilliary bundle points radially away from the modiolus
2) Rudimentary kinocilium seen at the top of cochlear HCs point in a radial direction
3) Horizontal cross links and vertical tip links between stereocilia are radially aligned
4) Progression of height of stereocilia are radially oriented from shortest to tallest

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37
Q

If you were to place a micro-electrode into a hair cell what would the mV range be?

A

A negative (-) range from -35 to -90mV

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38
Q

What is Davis’ micro mechanical model of hair cell transduction processes(2)? What does this mean for cochlear microphonics? If you apply an alternating current across the partition what would be read?

A
  • Voltage gradient across surface forces leakage current through cell membrane
  • Mechanical movement shears stereocilia altering the resistance of the membrane
  • Alternating the current across the cochlear partition created by sound stimulation is transformed by HCs to AC voltage called thee cochlear microphonics
  • It would be read as a sinusoidal pattern
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39
Q

What makes the neural pathway nonlinear? (4)

A

1) It undergoes adaptation
2) Saturation
3) Refractory properties
4) Masking

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40
Q

Explain the blood supply pathway to the length of the cochlea

A
  • Vertbrobasilar artery (PICA)
  • Internal auditory artery passes through the internal acoustic canal and gives rise to the spiral modiolar artery
  • Arterioles supply the length of the cochlea.
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41
Q

What are the 3 cells type that make up the stria? What are they in contact with?

A
  • Marginal cells line the scala media and are in contact with the endolymph
  • Intermediate cells are in the middle layer
  • Basal cells are attached to the spiral ligament, in contact with intermediate cells
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42
Q

How does ipsilateral and contralateral acoustic stimulation suppress SSOAE amplitude?

A
  • Ipsi= suppressing signals close to or at SOAE produce the greatest effect
  • Contra= Signals can be suppressed if the signal intensity is above IA and does not produce an acoustic reflex threshold
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43
Q

Different OAE generation mechanisms produce differences in _________ _______________ as a function of frequency.

A

Phase behavior

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44
Q

Explain the generation of OAE fine structures. (2 parts)

A
  • Frequencies are varied, non-linear phase rotates slowly, linear phase rotates rapidly.
  • This interaction produces constructive and destructive interference causing DPOAE amplitudes to show a pattern of peaks and valleys
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45
Q

Where are DPOAEs generated from, relating to the input tones? What 2 things does the generating region depend on?

A

-Generated in the frequency region where the energy of the two primary tones overlap.
It depend on the stimulus levels of the two tones and their frequency ratios.

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46
Q

For low to moderate intensities below 70dB, when L1-L2 is greater than 10dB and L1 is greater than L2, cochlear stimulation occurs mostly at the _____ site on the basilar membrane. When L1 = L2, cochlear stimulation occurs where?

A
  • Mostly at the f2 site.

- Occurs at the geometric mean of f1 and f2.

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47
Q

For high intensities above 70 dB, when L1=L2 and f1 and f2 excitation regions are ________ so that _________vibrations approximate ___________ vibration as what site on the BM?

A

For high intensities above 70 dB, when L1=L2 and f1 and f2 excitation regions are “BROAD” so that “F1” vibrations approximate “F2” vibration as what site on the BM?

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48
Q

What does truncation of your time window do to your TEOAE measurement? What ms time window is ideal?

A
  • Truncation enables response reproducibility and decreases noise.
  • 8.2ms is ideal
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49
Q

How many dB does the response amplitude of infant TEOAEs exceed adult OAEs? What are some of the best responses within the 95th percentile?

A

-10dB or more over adult TEOAEs, some of the best responses were at 26dB SPL

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50
Q

Between 31-42 weeks post conceptual age response amplitudes increase by ____ dB over that time. The maximum infant TEOAE amplitude is at ______ weeks PCA.

A

-10dB over that time, maximum is at 47 weeks.

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51
Q

What is the success rate of screening an infant within 36 hour after their birth? How many hour is a good reference for a 95% success rate?

A

75% within first 36 hours, 108 hours old would have 95% success rate

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52
Q

TEOAE Avg. infant dB response 24 hours after birth?

A

16

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53
Q

TEOAE Avg. infant dB response 48-72 hours after birth______

A

20-22

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54
Q

TEOAE Avg. adult response dB________

A

12 for adults

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55
Q

What is the resonant frequency of an infant? How long is their ear canal?

A
  • Resonant frequency is 5.3-7.2 kHz

- 12mm long

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56
Q

From 10 days old to 6 month how much does the resonant frequency change from infancy?

A

-It lowers for above 6kHz to 4-4.5KHz in children

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57
Q

When does an infant’s resonant frequency become adult-like and at what frequency? What is the length of the ear canal?

A
  • Becomes adult-like at around 20 months, is around 2.7kHz.

- Ear canal is 32mm by then

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58
Q

How does the presence of SOAEs affect TEOAEs?

A

Presence of SOAEs increase the overall TEOAEs amplitude

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59
Q

Draw out: TEOAEs in children are characterized by (low/high) frequency energy? How might these TEOAEs vary?

A
  • Typically Characterized by high frequency energy, mainly showing greatest energy in high frequency region of first 6ms followed by some mid and low frequency.
  • Some children TEOAEs can sustain high frequency energy across the entire window.
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60
Q

TEOAEs of normal hearing adults (threshold at 10 dB or better) have what expected dB responses? Draw this out, yo!

A

-S/n ratios of 7dB or greater at all frequency bands, across all age groups.

61
Q

If the patient has hearing thresholds at 25 dB or worse:
TEOAEs decrease with________
Presence of ___________ make TEOAEs increase^
Slight changes in hearing in older adults produces (greater/lesser) changes in TEOAEs compared to younger adults.

A
  • age
  • SOAEs
  • greater
62
Q

The most robust responses occur in the ___________ range. When would you use Tone Bursts for TEOAEs?

A
  • Occur in the mid-frequency range

- You would use tone burst OAEs during ototoxic drug therapy monitoring or post-noise exposure.

63
Q

Toneburst I/O curves saturate at ________dB ______. If a patient has OAEs as an adult, what changes in TBs as they age?

A

-Saturate at 50 dB peSPL, and there would be no changes!

64
Q

In TEOAE measurements, what would a patient with a conductive loss or abnormal temps show?

A

-An increase in noise…?

65
Q

When you are calibrating your OAE stimulus in a hard walled cavity, what range should your DPOAE dB levels be in? How many dB for TEOAEs?

A

-DPOAE target levels within 2dB of 65/55 and 80 dB stimulus for TEOAEs.

66
Q

What should your noise floor dB levels be less than?

A

10 dB SPL

67
Q

SOAEs and SFOAEs are considered to be________ emissions. DPOAEs and TEOAEs represent a mix of both_______and __________ emissions.

A
  • Reflections

- Reflection and Distortion

68
Q

Why would we need to use more than 1-2 frequencies per octave in OAE testing? How many should we be using?

A
  • We need to use more than 2 because we could miss a potential dip in OAEs that reflect cochlear abnormality, especially in patient with NIHL/tinnitus.
  • We should be using 5-8
69
Q

Frequency range for ototoxicity monitoring?

Frequency range for Meniere’s?

A
  • 2-10kHz for ototoxicity

- Low frequencies for Meniere’s testing

70
Q

How do low frequency protocols help diagnose ANSD?

A

If a patient has normal OAEs but has a low frequency hearing loss that points to a neural problem, not an OHC problem.

71
Q

What would an OAE “pass” consist of?

A

OAE minus NF is greater or equal to 6dB for most frequencies.

OAE - NF >or= 6 dB. —> PASS

72
Q

TEOAE reproducibility should be above _____%, DPOAE amplitude within _______dB for at least ______ runs. In DPOAE measures of 65/55, ______ dB should be maintained through the measure. TEOAEs are measured at _______dB for 100% of test time.

A
  • (-9%)
  • 2dB
  • 2 runs
  • Within 2 dB
  • 80 dB
73
Q

What are the 3 outcomes of a diagnostic OAE measurement? And define what each outcome is equal to.

A
  • Normal = OAE - NF is greater than or equal to 6dB
  • Present but abnormal = OAE - NF is greater than 6dB but amplitude is below 0dB
  • Absent OAEs = OAE - NF is less than 6dB
74
Q

How do we determine if standing waves are interfering with your OAE analysis? (2)

A
  • If there are spikes and dips in the recording that can’t be explained by history
  • If the spikes and dips are eliminated by adjusting the probe then they were standing waves.
75
Q

Can you have a normal audiogram with abnormal OAEs?

A

Yeah, bro, their OHCs are totes struggling.

76
Q

What are the 4 possibilities if a patient has an abnormal audiogram but normal OAEs?

A
  • IHC dysfunction
  • Neural dysfunction
  • False hearing loss (malingering)
  • Problems with pure tone audiometry
77
Q

At what age is the Eferrent system considered “mature”? How does this affect OAEs?

A
  • Mature at 1 year old

- Before the efferent system is mature, there is no efferent suppression so OAE amplitudes are enhanced

78
Q

In the 60-97 year old age group, TEOAEs were ONLY present if the subject’s PTA was better than_______dBHL. Only____% of these patients with this PTA actually showed present OAEs.

A
  • 30dBHL

- 60%

79
Q

What are the five reasons why females tend to have larger OAE amplitudes? Why is this important in your clinical measurements?

A
  • Shorter cochlea length
  • Better Hearing sensitivity
  • Lesser subclinical cochlear deficits
  • Greater number of SOAEs
  • Warmer body temperatures
  • This is IMPORTANT because you have to consider separate norms for women compared to women.
80
Q

Which ear typically has more robust OAEs? What are 3 potential reasons?

A

1) The right ear is more robust/better, has better hearing
2) Typically a greater number of SOAEs in the RE vs LE
3) Less efferent inhibition in the RE

81
Q

What are diurnal (time of day) effects of OAEs?

A

-Potentially 1dB greater OAEs in the sleeping cycle….?

82
Q

What do hypo and hyperthermia do to OAE amplitudes? What intensity levels should you be most concerned about?

A

-They cause OAE amplitudes to decline, especially at low intensity levels

83
Q

What can body position on the patient potentially do to your OAE measurements? Generally, what is happening to cause these changes?

A
  • If the patient tilts backwards to a horizontal position, or inverts (like a bat?) then it can decrease OAEs
  • The middle ear is changing, causing the OAEs to change
84
Q

How do sleep/attention influence OAE interpretation? What can anesthetics and sedatives do to OAEs? Nitrous oxide?

A
  • attention/sleep don’t affect OAEs
  • anesthetics and sedative May increase^ TEOAEs, but NOT DPOAEs
  • Nitrous oxide affects ME function, can affect OAEs
85
Q

What structure in the auditory pathway innervates OHCs?

A

The olivocochlear bundle (Think “OHCs? Oh, I O-H see, the bundle, that’s an aud path.” because the OHCs are “I” inervated by the “O” olivo “see” cochlear bundle which is an auditory pathway)

86
Q

How does presenting sound, with OHC stimulus, affect the amplitude of your OAEs? What causes this?

A

The amplitude is suppressed by the efferent auditory pathway.

87
Q

What if a patient presents with a lack of suppression?

A

This would suggest they have a dysfunctional efferent system.

88
Q

How many afferent CN VIII nerves are found in humans? Where are the two distinct type of afferent neurons found?

A

30,000 in humans, the distinct types are found in the distal region near the cochlea.

89
Q

Type I neurons are _________ in shape. They account for ___________% of all neurons. They are (myelinated/unmyelinated) and innervate what?

A
  • Radial in shape
  • Account for 90-95% of all neurons.
  • They are myelinated and innervate IHCs at their base.
90
Q

Type II neurons are _________ in shape. They account for ___________% of all neurons. They are (myelinated/unmyelinated) and innervate what?

A
  • Spiral in shape
  • Account for 5-10% of all neurons.
  • They are myelinated and innervate OHCs via invagination ( >_< )at the base.
91
Q

Type I neurons have convergent innervation, what does this mean?

A

It means there is 1 or more fibers that converge to innervate a single inner hair cell.

92
Q

Type II neurons have a divergent innervation, what does this mean?

A

A single fiber branches out and innervates several OHCs within the same row.

93
Q

In what decade was efferent innervation of the hearing mechanism discovered? Who discovered it and what was it called?

A
  • 1940s
  • Rasmussen
  • Called Rasmussen’s Bundle (real creative)
94
Q

What is the origin of IHC efferent innervation? Is it crossed or uncrossed? Myelinated?

A
  • Origin: lateral superior olive (LSO)
  • Does NOT cross
  • Unmyelinated
95
Q

What is the origin of OHC efferent innervation? Is it crossed or uncrossed? Myelinated?

A
  • Origin: Medial superior olive (MSO)
  • It DOES cross
  • Myelinated
  • Think M.O.M DOES get cross*
96
Q

Where does LSO efferent innervation terminate in your hearing system?

A

Terminates on dendrites of afferent radial fibers

97
Q

Where does MSO efferent innervation terminate in your hearing system? This suggests that what is influenced by these neurons? (3)

A
  • Terminates on base of OHCs

- Suggests that they influence the cochlear amplifier, dynamic range, and protection of threshold shifts.

98
Q

What type of neurotransmitters are associated with IHCs(2)? OHCs?

A
  • IHCs = Cholinergic and opioid neurotransmitters

- OHCs = Acetylcholine neurotransmitters

99
Q

What is the efferent pathway of the ipsilateral LSO bundle?

A

Cell bodies run from lateral SOC to the cochlea on the SAME side.

100
Q

What is the efferent pathway of the contralateral MSO bundle?

A

Cell bodies run from the MSO of one side, cross over near the floor of the 4th ventricle, travels dismally through the IAC and synapse at the base of the OHCs on the OPPOSITE side.

101
Q

How much does contralateral suppression affect the amplitude of TEOAE/DPOAEs? Does the duration matter?

A

It can suppress TTEOAEs and DPOAE amplitudes by 1-3dB, duration of contralateral stimulation does NOT matter.

102
Q

What frequencies are typically suppressed more with contralateral suppression? Any difference between TEOAE and DPOAEs?

A

The 1-2kHz region, affects TEOAEs more.

103
Q

How do differences in stimulus intensity affect OAE suppression?

A
  • Suppression is more pronounced for lower stimulus intensities.
  • vStimulus Intensity —>^OAE Suppression*
104
Q

What type of noise/stimulus produces the most suppression?

A

Broadband noise that is centered on the frequency region of OAEs tested.

105
Q

Preterm infants show (greater/lesser) suppression than full term infants? From the age of 10-80y/o suppression effects (improve/decline)?

A
  • Preterm infants have less suppression than full term infants.
  • From 10-80 y/o, there is decline in suppression effects.
  • So it can be said that as you age, suppression effects decline and its much worse off if you begin as a premie.*
106
Q

What are the left/right hand suppression differences?

A

Right-handed people will have greater suppression in the right ear.
Left-handed people will have no difference in suppression.

107
Q

What is an ipsilateral forward masking paradigm? How is it done?

A
  • A way of assessing ipsilateral suppression.

- You present the suppressor signal before your OAE evoking stimulus.

108
Q

What is two-tone suppression? How is it done?

A
  • A way of assessing ipsilateral suppression, creating suppressor tuning curves (STCs).
  • Suppressor tone is presented simultaneously with OAE stimulus at nearby frequencies.
109
Q

The tip of the suppressor tuning curve (STC) corresponds to what frequency site?

A

F2

110
Q

High suppressor intensities have less effect on DPOAE when presented at actual DP place or 2f1-f2. Contribution of both f2 and DP place to DPOAE occurs under certain test conditions, meaning there is a primary and secondary generator of DPOAE.

A

So there.

111
Q

Energy arising from the DP place is essentially an _______ reading +/- interactions between two generators that may be responsible for what? What would the presentation of a 3rd tone do to the DPOAE amplitude?

A
  • SFOAE reading
  • Responsible for fine structure
  • A 3rd tone (in 2f1-f2 region) may decrease OR increase DPOAE amplitude.
112
Q

What important information did STC measurements reveal? (2)

A
  • Found the site of DPOAE origin

- Found out that infants have high frequency resolution at birth (in mid to high frequency region)

113
Q

Cerumen/vernix issues occur in ______% of NICU patients and _____% of normal populations?

A
  • 25% in NICU pts

- 19% in normal pts

114
Q

Negative ME pressure abolishes OAEs if the ABG is ____dB or above. A daPa of +/-100 causes a _____dB decline in TEOAEs and up to _____dB decline in DPOAEs.

A
  • Above 15dB
  • A 2-3dB decline in TEOAEs
  • Up to 8dB decline in DPOAEs
115
Q

How does a TM perforation effect OAE measurements?

A

If there aren’t any ME pathologies, they are normal across normal range or at least normal in high frequencies.

116
Q

How do OAEs present in otosclerosis?

A

They are not detectable, regardless of degree/configuration of hearing loss

117
Q

How long does neonatal amniotic fluid persist in the ME?

A

48 hours

118
Q

How long does neonatal mesenchyme persist in the ME? How long could it potentially take to be fully absorbed?

A

Mesenchyme is absorbed soon after birth, but can last up to 1 year.

119
Q

What can different anesthetic agents or sedatives do to your OAE measurements? (2)

A
  • Nitrous oxide alters ME pressure, reducing OAE amplitudes

- Chloral hydrate increases^ ME pressure

120
Q

Valid OAEs are seldom recorded when sensory hearing losses exceed ________dB?

A

35-40dB

121
Q

TEOAE absolute amplitude must be over _____dB to pass.
TEOAE SNR above _______dB to pass.
Reproducibility needs to be above_______% to pass.

A
  • 5dB
  • 3dB
  • 70% or better
122
Q

What frequencies do you have to be wary of when using TEOAEs for a diagnosis of SNHL?

A

Low frequency, 500Hz TEOAE measurements cannot be differentiated from normal to impaired ears.

123
Q

What happens to your TEOAE reliability as you increase frequency?

A

Your false negatives decline but false positives increase^

Think negative, going down and positive increasing and that is Totally Expected for TEOAE reliability

124
Q

NF at frequency of DPOAE measurements should be below ____dBSPL.
OAE amplitude can be interpreted as what 3 results?

A
  • (-10dBSPL

- Normal, abnormal, or absent

125
Q

F2/TEOAE frequency should be aligned with what?

A

The audiometric frequency that you are trying to assess.

126
Q

From a hearing loss that has thresholds from 15-30dB, what can you expect from OAE amplitudes?

A

OAE amplitude would be below normal limits but measured 5dB or more above the noise floor.

127
Q

As cochlear function develops, what happens to ototoxicity sensitivity?

A

The cochlea is more sensitive to ototoxicity while developing.

128
Q

Why do we have to monitor ototoxic drugs well after their administration? What is a half-life? In a drug with a half-life of 2 hours, what would that mean happens after 2 hours?

A
  • Because adverse effects might be delayed, and can persist for days/weeks after discontinuation of drugs.
  • A half-life is the rate that a drug is excreted from the body.
  • It means after 2 hours, half of the drug has been excreted from the body.
129
Q

What are 2 main objectives of ototoxicity monitoring?

A

1) detect early evidence of cochlear dysfunction

2) counseling and management of future changes of hearing/possibility of amplification.

130
Q

When would aminoglycosides be administered? Give and example of a few.

A
  • Administered for bacterial infections (particularly gram negative aerobic bacilli)
  • Neomycin, Kanamycin, gentamicin, netilmicin, amikacin
131
Q

What aminoglycosides are very commonly used in the NICU? And what are they used for?

A
  • Gentamicin: as a prophylactic agent (sometimes)

- Tobramycin: to treat pneumonia in CF patients.

132
Q

What are the 4 types of bacterial classifications with their drawings?

A
  • Bacillus
  • Cocus
  • Bacillococcus
  • Spirochetes
133
Q

What is affected in the cochlea because of aminoglycosides? How does the damage progress?

A
  • Calciuum and ion channel metabolism membranes within the cochlea are affected.
  • OHCs and support cells show dysfunction, then damage, beginning at the base, then spreading to the apex.
134
Q

What drugs can augment the effects of aminoglycosides(3)? What condition has to be met for them to concurrently damage the cochlea.

A
  • Loop diuretics, cisplatin, ethacrynic acid

- Both drugs need to have remnants in the perilymph

135
Q

How do aminoglycosides create form-free radicals? What are free radicals?

A
  • They interact with iron to form oxidative compounds.
  • They are atoms, molecules, or ions with an unpaired electron in its outer shell, making the surrounding molecules more unstable.
136
Q

What symptoms are free radical associated with? (3)

A

Inflammation
Neurodegeneration
Neurotoxicity

137
Q

What are free radical scavengers?

A

Antioxidant drugs that freely donate an electron, stabilizing the molecules and disrupting interaction between gentamicin and iron to prevent ototoxicity.

138
Q

What 2 conditions are treated with Vancomycin?

A

Staph infections and MRSA (also C. Diff)

139
Q

What are loop diuretics? What are they used to treat?

A
  • Drugs that expel water by acting on epithelial cells in the loop of Henle (kidney)
  • Treat congestive heart failure and pulmonary edema
140
Q

What loop diuretic causes ototoxicity? What anatomical structure is affected?

A
  • Furosemide (Lasix)

- The stria vascularis

141
Q

What does damage to this previous structure do to the hearing mechanism? What hearing processes and electroacoustic measures could be affected?

A
  • It causes a decline in the endocochlear potential
  • Could affect OHC active processes like OAEs, CMs, and APs
  • CMs, ECochG, ABR, and OAEs could all be affected
142
Q

What are the 3 things that histopathological data shows involving furosemide damage on OHCs?

A

1) Impairment of oxidative metabolism
2) Splaying of stereocilia
3) Breakage of tip links and cross links

143
Q

What is Cisplatin typically used for?

A

Chemotherapeutic drugs used for tumors typically in the genitourinary tract, lung, neck, and head.

144
Q

What does cisplatin do to the hearing system anatomically? (4)

A

-Damage to OHCs, supporting cells, and Reissner’s membrane, possible damage to stria vascularis and spiral ganglion cells.

145
Q

How long could Cisplatin possibly stay in the system after treatment?

A

18 months

146
Q

How could Cisplatin possibly be prevented? What is research developing now?

A

Otoprotective drugs, similar to aminoglycosides, research developing ways to block uptake through stria vascularis

147
Q

What is the main difference between Cisplatin and Carboplatin?

A

Carboplatin affects IHCs instead of OHCs

-May not be a good tool for monitoring ototoxicity

148
Q

What is quinine used to treat? What are the first symptoms? Are they reversible?

A
  • Malaria and muscular disorders
  • First symptom is tinnitus (much like aspirin) followed by a 45dB hearing loss.
  • Yes, symptoms are reversible.
149
Q

What does quinine do to the hearing system anatomically? (2)

A

Alters BM mechanics

Interrupts active processes of OHCs

Otoacoustic Emissions (OAEs) (2 decks)

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