Audiology Test 3

Front 1

Otoacoustic Emissions (OAEs)

Back 1

Sounds that have very low amplitudes, and are almost inaudible. Research has shown they are generated by the OHCs.

Front 2

Outer Hair Cells (OHCs)

Back 2

-Change length in response to simulation
-Push and pull on BM
-Responsible for our ability to hear very soft and very loud sounds

Front 3

Spontaneous OAEs

Back 3

Continuous tonal signals that occur without any stimulation. They are present in about 50% of normal ears.

Front 4

Evoked OAEs

Back 4

Otoacoustic Emissions that are produced in response to acoustic stimulus. Two kinds.

Front 5

Transient Evoked OAEs

Back 5

-Evoking stimulus: clicks or tone pips.
-The ear produces a broadband sound in response.

Front 6

Distortion Product OAEs

Back 6

-Evoking stimulus: two steady pure tones that are presented simultaneously and referred to as "primaries" (f1 and f2)
-f2>f1; typically f2/f1= 1.22
-Cochlea response is non-linear

Front 7

DP-gram

Back 7

-Plot of DPOAE amplitudes as a function of f2
-Each point reflects the "health" of cochlea (OHCs) at the f2 frequency
-f2 placed on x-axis, and amplitude on the y-axis

Front 8

Normal EOAE

Back 8

Cochlea must generate the emission.

Front 9

EEG (Electroencephalography)

Back 9

Measuring electrical activity from the brain. Measured by electrodes placed on the scalp.
-Ongoing activity is random.

Front 10

Evoked Potentials (EPs)

Back 10

Changes in brain activity in response to specific stimuli.
-Responses from the EEG
-Compared to ongoing neural activity, these responses to stimuli are very small.
-Responses are measured by averaging.

Front 11

Latency

Back 11

The timing of a response relative to the stimulus.

Front 12

Electrocochleography (ECoG)

Back 12

The earliest responses that are recorded come from the cochlea.

Front 13

Event-related Potentials (ERPs)

Back 13

The latest responses that are recorded come from the auditory cortex.

Front 14

Auditory Brainstem Response (ABRs)

Back 14

The response that has the widest clinical application.
-Occurs in the first 10-15ms after the stimulus.
-Generated by the auditory nerve and auditory brainstem.
-Normal response implies normal cochlea, auditory nerve, and brainstem.
-Evoked by tone pips or clicks.
-Response is 5-7 small waves.

Front 15

APGAR scores

Back 15

-Taken at 1, 5, and 10 minutes after birth.
-Assess respiratory effect, muscle tone, heart rate, color, reflex, irritability.
-Score of 1-10 is given.

Front 16

Startle Reflexes

Back 16

-Contraction of muscles around eyes in response to loud sounds.
-Problems: agreement among technicians, can miss mild to moderate losses.

Front 17

Goal of Healthy People 2010

Back 17

Increase the numbers of infants screened, receiving diagnostic evaluations, and receiving early intervention services.

Front 18

Hearing Loss Prevalence in Newborns

Back 18

-Approximately 12,000 children each year
-Up to 3 per 1000 births each year

Front 19

Prior to UNHS

Back 19

-Average age: 30 months of age
-Severe-to-profound HL may be identified somewhat earlier
-Mild-to-moderate HL not until school age in many cases

Front 20

Joint Committee on Infant Hearing (JCIH)

Back 20

-All infants should be screened using objective, physiologic measures at birth
-Monitor infants who pass newborn screening but have risk factors for late-onset/progressive hearing loss

Front 21

Early Hearing Detection and Intervention (EHDI)

Back 21

1) Screening by 1 month (typically in hospital)
2) Identification by 3 months
--Diagnostic and Intervention by 6 months

Front 22

Microtia

Back 22

Very small size pinna

Front 23

Anotia

Back 23

Absent pinna

Front 24

Stenosis

Back 24

Narrowing of the ear canal--smaller the deeper you get.

Front 25

Atresia

Back 25

Cartilaginous or bony portion or the entire ear canal has not formed at all.

Front 26

CHARGE syndrome

Back 26

Associated with anomalies of the pinna and external auditory canal.

Front 27

External Otitis

Back 27

Infection that occurs in the skin of the external auditory canal.
Ex.) Swimmer's ear

Front 28

Osteomas

Back 28

-Bony tumors found in the EAC
-Not a problem unless they cause a hearing loss/lead to external otitis (conductive HL)

Front 29

Exostoses

Back 29

Bony protrusions in the bony wall of the EAC.

Front 30

Otitis Media (OM)

Back 30

Inflammation of the middle ear.
-2 types

Front 31

Effusion

Back 31

Fluid that accumulates in the middle ear space.
-Produced by cells lining in the ME
-Ranges from thin (serous) to glue-like
-Fluid won't go away
-About 90% of children have this before school age (btwn 4 months-4 years)
-Results from: URI, ET dysfunction, multiplying bacteria

Front 32

Acute Otitis Media (AOM)

Back 32

An infection in the middle ear-- usually secondary to URIs
-Very young children (<6 mos) go straight to antibiotics

Front 33

Otitis Media with Effusion (OME)

Back 33

-Persists beyond 8 weeks
-Chronic, but no active infection
-Chronic negative ME pressure creates a vacuum; fluid drawn out of cells lining ME
-Fluid present during AOM never clears due to ETD
-Type B (flat) Typmanogram
-Conductive Loss with 50-60 dB maximum HL

Front 34

Cholesteatoma

Back 34

A pseudotumor in the middle ear.
-Composed of accumulation of skin, keratin, fats
-Starts when skin cells enter ME
-Very destructive: may erode ossicles or can erode bone and spread into pharynx or brain
-Can cause conductive HL
-Treatment is surgery

Front 35

Otosclerosis

Back 35

Abnormal growth of spongy bone tissue over the tapes footplate-- interferes with the movement of the stapes.
-Hereditary in many cases (50-70%) and more prevalent in women.
-Progressive CHL
-Unique feature: Carhart's notch
-Physical feature: bony growth
-Treatment is Stapedectomy Surgery or Hearing Aids
-CHL

Front 36

Rubella (German Measles)

Back 36

A concern if caught during first trimester. Babies tend to be born smaller and develop more slowly. May have brain damage, blindness, heart defects, and SNHL.

Front 37

Cytomegalovirus (CMV)

Back 37

Can be contracted before birth through placenta, during birth via cervix, and after birth bia mother's milk

Front 38

Meniere's Disease

Back 38

-SNHL, typically unilateral
-Roaring tinnitus or vertigo
-Poor speech recognition
-Caused by endolymphatic hydrops

Front 39

Endolymphatic Hydrops

Back 39

Over production of endolymph or under absorption or endolymph

Front 40

Noise-Induced HL (NIHL)

Back 40

-Excessive noise exposure that causes SNHL
-Poorest THs at 3000-6000Hz, recovery at 8000
-"Noise Notch"

Front 41

Noise

Back 41

An acoustic signal which can negatively affect the physiological or psychological well being of an individual.
-Can be any sound!

Front 42

Histopathology

Back 42

Sterocillia become floppy and lose contact with tectorial membrane
-Loss of OHCs and IHCs

Front 43

Ototoxicity

Back 43

Certain medications can damage the cochlea and/or the vestibular system.

Front 44

Presbycusis

Back 44

Hearing loss due to aging.
-Sloping high-frequency HL

Front 45

Acoustic Neuroma

Back 45

A retrocochlear tumor on the 8th cranial nerve.
-Typically arises from Schwan's cells on vestibular branch.
-Usually benign and slow growing--very treatable.
-R ipsi: present
-L ipsi: absent
-R conchra: present
-L conchra: absent
-Type A Tympanogram, SNHL

Front 46

Down Syndrome

Back 46

Chromosomal disorder (extra copy of Chromosome 21)
-CHL, varying from mild to moderate
-Impacted cerumen
-Retracted tympanic membrane and ME effusion

Front 47

Treacher Collins Syndrome

Back 47

A genetic disorder-- either inherited or the result of spontaneous genetic mutation.
-Protein Treacle is thought to play critical role in the development of bones and other tissues in the face.
-Autosomal (not on the gender gene)
-Atresia, stenosis, cleft of lower eyelid, small cheekbones, small bones, cleft or incomplete soft palate
-Congenital bilateral CHL is most common, degree ranges from mild to moderate

Front 48

Usher Syndrome

Back 48

-Hereditary Syndrome (recessive disorder)
-Retinitis Pigmentosa: degeneration of retina; progressive
-Congenital HL: ranges from moderate to profound; not progressive; SNHL
-Incomplete development of atrophy of basal end of Organ of Corti in the coclea (basal end is where high frequencies are located)