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2017 EENT Clin Med Group > Hearing Disorders COPY > Flashcards

Hearing Disorders COPY Flashcards

1
Q

Sensorineural Hearing Loss: Most common population

A
  • Sensorineural hearing loss risk increases with age
  • Higher in men than women

_______________________

  • Occur in the inner ear (sensory) or auditory nerve/auditory pathway (neural)
  • Hearing levels for different frequencies are usually unequal, typically resulting in better hearing for low- than for high-frequency tones.
  • Sensory hearing loss=deterioration of the cochlea, usually due to loss of hair cells from the organ of Corti.
  • Neural hearing loss=Due to lesions which involve CN8, auditory nuclei, ascending tracts, or auditory cortex.

______________________

Assessment

  • Weber: Lateralizes to the opposite side of the affected ear. Example: If Weber lateralizes right, then SNHL is likely present in the left ear.
  • Rinne: AC>BC. But patient will indicate the sound has stopped earlier than a normal patient.
  • Otoscopic exam is often normal

Common sensorineural hearing loss causes:

  1. Presbycusis (gradually progressive, predominantly high-frequency loss with advancing age)
  2. Ototoxic drugs
  3. Meniere Disease
  4. Noise-induced
  5. Acoustic neuroma
  6. Trauma (cochlear damage)
  7. Hereditary

Treatment

  • Usually not correctable with medical or surgical therapy, but may be prevented or stabilized. Exception: sudden hearing loss may respond to corticosteroids if delivered within several weeks of onset.
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2
Q

Physiology of hearing

A
  1. Sound waves enter outer ear, travel through ear canal to tympanic membrane (eardrum)
  2. Tympanic membrane vibrates with incoming sound and sends the vibrations to 3 tiny bones in middle ear
  3. Bones in middle ear amplify sound vibrations and send them to inner ear (cochlea). These activate tiny hair cells in inner ear.
  4. Hair cells release neurochemical messengers
  5. Auditory nerve carries this electrical signal to the brain, whicht ranslates it into sound
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3
Q

Which division of the ear?

Otitis Externa

A

EXTERNAL

-

Pinna, Auditory Canal

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4
Q

Which division of the ear?

Exostosis/Osteoma

A

EXTERNAL

-

Pinna, Auditory Canal

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5
Q

Which division of the ear?

Cerumen Impaction

A

EXTERNAL

-

Pinna, Auditory Canal

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6
Q

Which division of the ear?

Otitis Media,

A

MIDDLE

-

Tympanic Membrane, Ossicles, Eustachian Tube

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7
Q

Which division of the ear?

Cholesteatoma

A

MIDDLE

-

Tympanic Membrane, Ossicles, Eustachian Tube

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8
Q

Which division of the ear?

Otosclerosis

A

MIDDLE

-

Tympanic Membrane, Ossicles, Eustachian Tube

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9
Q

Which division of the ear?

eustachian tube dysfunction (ETD)

A

MIDDLE

-

Tympanic Membrane, Ossicles, Eustachian Tube

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10
Q

Which division of the ear?

Meniere’s

A

INNER

-

Cochlea, Semicircular canals, Auditory Nerve

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11
Q

Which division of the ear?

Benign Paroxysmal Positional Vertigo (BPPV)

A

INNER

-

Cochlea, Semicircular canals, Auditory Nerve

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12
Q

Which division of the ear?

Acoustic Neuroma

A

INNER

-

Cochlea, Semicircular canals, Auditory Nerve

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13
Q

Which division of the ear?

Sensorineural HL

A

INNER

-

Cochlea, Semicircular canals, Auditory Nerve

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14
Q
  • The inner ear consists of a system of fluid-filled tubes and sacs called the ________.
  • It serves two functions:
    1. ________
    2. ________
A
  • Labyrinth
  1. hearing
  2. balance
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15
Q

• The _______ is a snail-shaped tube filled with endolymph fluid and sensitive nerve endings that transmit sound signals to the brain in order to produce normal hearing.

A

cochlea

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16
Q
  • Balance is regulated by the ________.
  • The _________ contain fluid and hair cells in a three loop structure.
  • The sac-shaped _____ and ______ provide the brain with information about head movement and motion.
A
  • vestibular organs
  • semicircular canals
  • utricle and saccule
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17
Q
  • Signals travel from the labyrinth to the brain via the cranial nerve __________, which has two branches.
  • One branch (_______) transmits messages from the cochlea,
  • while the other (________) transmits messages from the balance organs.
A
  • vestibulo-cochlear nerve (CN VIII)
  • the cochlear nerve=cochlea
  • the vestibular nerve=balance
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18
Q

What is a basic pathophysiogy of dizziness or vertigo?

A
  • • The brain integrates balance signals sent through the vestibular nerve from the right ear and the left ear.
  • When one side is affected (viral illness, otoconia or increased fluid pressure) it sends faulty signals.
  • Thus the brain receives mismatched information, resulting in dizziness or vertigo.
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19
Q

Weber lateralizes to RIGHT side: explain potential hearing deficits for right/left ears

A
  • Right ear: potential CHL
  • Left ear: potential SNHL
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20
Q

Rinne test is AC>BC. What could this result mean?

A

Normal or SNHL

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21
Q

Rinne test is BC>AC. What could this result mean?

A

Affected ear: CHL

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22
Q

Identify:

  • the perception of sound in the ear when there is no actual sound
A

Tinnitus

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

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23
Q

Identify: Tinnitus

  • Risk factors
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

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24
Q

Identify: Tinnitus

  • Presentation/Presentation types
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease
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25
Q

Identify: Tinnitus

  • Etiology
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse
How well did you know this?
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26
Q

Identify: Tinnitus

  • diagnosis
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media
How well did you know this?
1
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27
Q

Identify: Tinnitus

  • Treatment
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed
How well did you know this?
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28
Q

Identify: Tinnitus

  • Prevention
A

Tinnitus: the perception of sound in the ear when there is no actual sound

Prevention

Minimize noise exposure (85 dB or higher is associated with damage)

Risk factors

  • noise exposure
  • male gender
  • increased age
  • smoking
  • cardiovascular disease

Presentation

  • ringing, whooshing, buzzing, roaring, clicking, machinery like noise or pusling sounds
  • Occurs in one or both ears

Presentation Types

  1. Intermittent: typically benign and requires no work-up unless other symptoms present
  2. Persistent: requires evaluation, consider referral
  3. Pulsatile tinnitus: rhythmic with pulse

Etiology

  1. Idiopathic (most common)
  2. Acoustic trauma (acute-loud concert/chronic-loud machinery at work)
  3. Presbycusis (age related hearing loss)
  4. Neurological damage (MS, acoustic neuroma)
  5. Circulatory disorders (arteriovenous malformation, turbulent bloodflow)
  6. Side effect of medications (ASA, erythromycin, quinine, etc)
  7. Obstruction of ear canal
  8. Serous or purulent otitis media

Diagnosis

  • Refer to ENT
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
  • If pulsatile: MRA or carotid doppler to rule out vessel defect
  • Imaging, neuro-otologic studies as needed

Treatment

  • Acute: oral steroid taper
  • Chronic:
    • lipoflavinoids,
    • niacin/B complex vitamins,
    • tinnitus masking
    • hearing amplification if associated with hearing loss
    • white noise machine
  • Treat underlying condition
  • Reduce noise exposure, cafffeine, smoking, alcohol, stress
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29
Q

Fill in the blank: Tinnitus

  • Minimize noise exposure (_____ dB or higher is associated with damage)
A

Minimize noise exposure (85 dB or higher is associated with damage)

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30
Q

Identify: Tinnitus

  • diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
A
  • Subjective: diagnosis is based on patient’s complaint and may be supported by hearing loss on audiogram
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31
Q

Identify: Tinnitus

  • clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
A
  • Objective: clinician can hear the sound as well (stapedial myoclonus and some vascular disorders)
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32
Q

Identify:

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency
A

Presbycusis

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection
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33
Q

Identify: Presbycusis

  • risk factors
A

Presbycusis

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection

Key Characteristics

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency
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34
Q

Identify: Presbycusis

  • pathophysiology
A

Presbycusis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection

Key Characteristics

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis
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35
Q

Identify: Presbycusis

  • presentation
A

Presbycusis

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection

Key Characteristics

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway
How well did you know this?
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36
Q

Identify: Presbycusis

  • diagnosis
A

Presbycusis

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection

Key Characteristics

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone
37
Q

Identify: Presbycusis

  • treatment
A

Presbycusis

Treatment

  • Hearing amplification
  • Avoid excessive noise exposure, use hearing protection

Key Characteristics

  • SNHL associated with advanced age
  • Loss is typically symmetrical (same in both ears) and high-frequency

Risk factors

  • Age: adults over 75
  • Genetic predisposition
  • Noise exposure
  • Diabetes
  • atherosclerosis

Pathophysiology

  • Loss of functional sensory hair cells in cochlea
  • Degeneration of neural pathway

Presentation

  • Worsening hearing loss over time in both ears
  • Difficulty hearing conversations in social situations (due to ambient noise)
  • Difficulty localizing sounds
  • Tinnitus
  • Isolation due to inability to use the phone

Diagnosis

  • Diagnosis of exclusion; rule out other causes
  • Physical examination is normal
  • High-frequency symmetrical SNHL on audiogram
38
Q

Identify: Presbycusis

  • What do you expect with regard to audiogram results?
A
  • High-frequency symmetrical SNHL on audiogram
39
Q

Fill in the blank:

  • Loud noice causes damage to the hair cells in the cochlea (_____ dB or higher)
  • _______ frequency sounds are more damaging than _____ frequency
A
  • 85 dB
  • High-frequency=more damaging
  • Low-frequency=less damaging
40
Q

What is a classic audiometry finding for noise induced hearing loss?

A

Classical noise notch at 4k

41
Q

Is noise induced hearing loss symmetrical?

A

Not always (ex. rifle firing)

42
Q

Treatment of Loud Noise Hearing Loss

A
  • Monitor for spontaneous improvement if it was an acute event
  • Steroid use is widely used, but questionable for acute events
  • Hearing amplification
  • Avoidance of loud noises/music
  • Ear protection
43
Q

Identify:

  • Patients display unilateral hearing loss and unilateral tinnitus
  • Headaches or dizziness may be present
  • Facial numbness or weakness
  • Symptoms worsen over time
A

Acoustic Neuroma (Vestibular Schwannoma)

Pathophysiology

  • Slow-growing benign tumor that grows within the schwann cell layer of the vestibulocochlear nerve (CNVIII/8)
  • May not cause mass effect symptoms until many centimeters in diameter

Risk factors

  • neurofibromatosis type II
  • ionized radiation

Diagnosis

  • Audiogram shows unilateral sensorineural hearing loss
  • Speech discrimination can be worse than expected for the degree of loss
  • auditory brainstem response (ABR) can be normal with small tumors
  • MRI of the cerebellopontine angle (CPA) with gadolinium contrast

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

Treatment

  • monitor with regular imaging, audiometry (every 6 months)
  • Refer to ENT/neurosurgery for surgical excision or stereotactic radiation (gamma knife)
44
Q

Identify: Acoustic Neuroma (Vestibular Schwannoma)

  • pathophysiology
A

Acoustic Neuroma (Vestibular Schwannoma)

Pathophysiology

  • Slow-growing benign tumor that grows within the schwann cell layer of the vestibulocochlear nerve (CNVIII/8)
  • May not cause mass effect symptoms until many centimeters in diameter

Risk factors

  • neurofibromatosis type II
  • ionized radiation

Diagnosis

  • Audiogram shows unilateral sensorineural hearing loss
  • Speech discrimination can be worse than expected for the degree of loss
  • auditory brainstem response (ABR) can be normal with small tumors
  • MRI of the cerebellopontine angle (CPA) with gadolinium contrast

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

Treatment

  • monitor with regular imaging, audiometry (every 6 months)
  • Refer to ENT/neurosurgery for surgical excision or stereotactic radiation (gamma knife)

Presentation

  • Patients display unilateral hearing loss and unilateral tinnitus
  • Headaches or dizziness may be present
  • Facial numbness or weakness
  • Symptoms worsen over time
45
Q

Identify: Acoustic Neuroma (Vestibular Schwannoma)

  • risk factors
A

Acoustic Neuroma (Vestibular Schwannoma)

Risk factors

  • neurofibromatosis type II
  • ionized radiation

Diagnosis

  • Audiogram shows unilateral sensorineural hearing loss
  • Speech discrimination can be worse than expected for the degree of loss
  • auditory brainstem response (ABR) can be normal with small tumors
  • MRI of the cerebellopontine angle (CPA) with gadolinium contrast

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

Treatment

  • monitor with regular imaging, audiometry (every 6 months)
  • Refer to ENT/neurosurgery for surgical excision or stereotactic radiation (gamma knife)

Presentation

  • Patients display unilateral hearing loss and unilateral tinnitus
  • Headaches or dizziness may be present
  • Facial numbness or weakness
  • Symptoms worsen over time

Pathophysiology

  • Slow-growing benign tumor that grows within the schwann cell layer of the vestibulocochlear nerve (CNVIII/8)
  • May not cause mass effect symptoms until many centimeters in diameter
46
Q

Identify: Acoustic Neuroma (Vestibular Schwannoma)

  • diagnosis
A

Acoustic Neuroma (Vestibular Schwannoma)

Diagnosis

  • Audiogram shows unilateral sensorineural hearing loss
  • Speech discrimination can be worse than expected for the degree of loss
  • auditory brainstem response (ABR) can be normal with small tumors
  • MRI of the cerebellopontine angle (CPA) with gadolinium contrast

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

Treatment

  • monitor with regular imaging, audiometry (every 6 months)
  • Refer to ENT/neurosurgery for surgical excision or stereotactic radiation (gamma knife)

Presentation

  • Patients display unilateral hearing loss and unilateral tinnitus
  • Headaches or dizziness may be present
  • Facial numbness or weakness
  • Symptoms worsen over time

Pathophysiology

  • Slow-growing benign tumor that grows within the schwann cell layer of the vestibulocochlear nerve (CNVIII/8)
  • May not cause mass effect symptoms until many centimeters in diameter

Risk factors

  • neurofibromatosis type II
  • ionized radiation
47
Q

Identify: Acoustic Neuroma (Vestibular Schwannoma)

  • treatment
A

Acoustic Neuroma (Vestibular Schwannoma)

Treatment

  • monitor with regular imaging, audiometry (every 6 months)
  • Refer to ENT/neurosurgery for surgical excision or stereotactic radiation (gamma knife)

Presentation

  • Patients display unilateral hearing loss and unilateral tinnitus
  • Headaches or dizziness may be present
  • Facial numbness or weakness
  • Symptoms worsen over time

Pathophysiology

  • Slow-growing benign tumor that grows within the schwann cell layer of the vestibulocochlear nerve (CNVIII/8)
  • May not cause mass effect symptoms until many centimeters in diameter

Risk factors

  • neurofibromatosis type II
  • ionized radiation

Diagnosis

  • Audiogram shows unilateral sensorineural hearing loss
  • Speech discrimination can be worse than expected for the degree of loss
  • auditory brainstem response (ABR) can be normal with small tumors
  • MRI of the cerebellopontine angle (CPA) with gadolinium contrast

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

48
Q

What test should you order if patient has unilateral SNHL? Why?

A

IF PATIENT HAS UNILATERAL SNHL GET AN MRI!

May be an Acoustic Neuroma (Vestibular Schwannoma)

49
Q

_______ occurs when sound is not conducted appropriately through the external ear canal to the tympanic membrane and the ossicles

A

conductive hearing loss

50
Q

SNHL or CHL?

Tinnitus

A

likely SNHL

51
Q

SNHL or CHL?

Presbycusis

A

SNHL

52
Q

SNHL or CHL?

Noise induced

A

SNHL

53
Q

SNHL or CHL?

Acoustic neuroma

A

SNHL

54
Q

SNHL or CHL?

Cerumen Impaction

A

CHL

55
Q

SNHL or CHL?

Otitis media or externa

A

CHL

56
Q

SNHL or CHL?

tympanic membrane perforation

A

CHL

57
Q

SNHL or CHL?

otosclerosis

A

CHL

58
Q

SNHL or CHL?

mastoiditis

A

CHL

59
Q

SNHL or CHL?

cholesteatoma

A

CHL

60
Q

SNHL or CHL?

foreign body

A

CHL

61
Q

SNHL or CHL?

exostoses/osteomas

A

CHL

62
Q

Identify:

  • Protects the ears by trapping particulate matter
  • Provides a moisture barrier for the skin of the canal, protecting against dryness and itchiness
A

Cerumen (ear wax)

63
Q

Identify the audiogram

A
64
Q

Identify the audiogram

A
65
Q

Identify the audiogram

A
66
Q

Identify the audiogram

A
67
Q

Cerumen impaction

Etiology

A

Etiology

  • Unknown
  • Qtips and hearing aids interfere with self cleaning

Presentation

  • Hearing loss (worsens with time and water) (common for ears to clog after shower)
  • Ear discomfort
  • Dizziness/tinnitus IF impacted against TM

Treatment

  • Hydrogen peroxide or OTC wax-dissolving drops
  • Irrigation (ONLY IF INTACT TM)
  • loop curette
  • suction
  • forceps
  • Refer to ENT if: (1) failed debridement attempt (2) remove of cerumen requires brief sedation (3) audiogram should be considered if hearing does not return to normal after debridement
68
Q

Cerumen impaction

Presentation

A

Presentation

  • Hearing loss (worsens with time and water) (common for ears to clog after shower)
  • Ear discomfort
  • Dizziness/tinnitus IF impacted against TM

Treatment

  • Hydrogen peroxide or OTC wax-dissolving drops
  • Irrigation (ONLY IF INTACT TM)
  • loop curette
  • suction
  • forceps
  • Refer to ENT if: (1) failed debridement attempt (2) remove of cerumen requires brief sedation (3) audiogram should be considered if hearing does not return to normal after debridement

Etiology

  • Unknown
  • Qtips and hearing aids interfere with self cleaning
69
Q

Cerumen impaction

Treatment

A

Treatment

  • Hydrogen peroxide or OTC wax-dissolving drops
  • Irrigation (ONLY IF INTACT TM)
  • loop curette
  • suction
  • forceps
  • Refer to ENT if: (1) failed debridement attempt (2) remove of cerumen requires brief sedation (3) audiogram should be considered if hearing does not return to normal after debridement

Etiology

  • Unknown
  • Qtips and hearing aids interfere with self cleaning

Presentation

  • Hearing loss (worsens with time and water) (common for ears to clog after shower)
  • Ear discomfort
  • Dizziness/tinnitus IF impacted against TM
70
Q

Identify:

  • Typically multiple and protrude into the external auditory canal under normal mucosa
  • Associated with swimming in cold water as a child
A

Exostoses

Treatment: monitor, if they obstruct ear canal then refer to ENT

71
Q

Identify:

  • single outgrowth of the tympanic bone into the auditory canal
A

Osteoma

Treatment: monitor, if obstructs ear canal then refer to ENT

72
Q

Otosclerosis

Risk factors

A

Risk factors

  • genetic predisposition
  • female and caucasian
  • young adults to middle age adults

Etiology/pathophysiology:

  • abnormal, spongy bone growth at the junction of the stapes to the oval window in the middle ear
  • worsens over time

Presentation

  • worsening hearing loss over time in one or both ears
  • may, may not have tinnitus

Diagnosis

  • CHL on audiogram, possibly with a carhart notch at 2000 Hz
  • Normal physical exam and normal tympanogram (may see absent reflexes)
  • Temproal bone CT/exploratory surgery is diagnostic

Treatment

  • Refer to ENT for middle ear exploration/stapedectomy/ossicular chain reconstruction
  • Alternatively: hearing amplification and monitoring
73
Q

Otosclerosis

etiology/pathophysiology

A

Etiology/pathophysiology:

  • abnormal, spongy bone growth at the junction of the stapes to the oval window in the middle ear
  • worsens over time

Presentation

  • worsening hearing loss over time in one or both ears
  • may, may not have tinnitus

Diagnosis

  • CHL on audiogram, possibly with a carhart notch at 2000 Hz
  • Normal physical exam and normal tympanogram (may see absent reflexes)
  • Temproal bone CT/exploratory surgery is diagnostic

Treatment

  • Refer to ENT for middle ear exploration/stapedectomy/ossicular chain reconstruction
  • Alternatively: hearing amplification and monitoring

Risk factors

  • genetic predisposition
  • female and caucasian
  • young adults to middle age adults
74
Q

Otosclerosis

presentation

A

Presentation

  • worsening hearing loss over time in one or both ears
  • may, may not have tinnitus

Diagnosis

  • CHL on audiogram, possibly with a carhart notch at 2000 Hz
  • Normal physical exam and normal tympanogram (may see absent reflexes)
  • Temproal bone CT/exploratory surgery is diagnostic

Treatment

  • Refer to ENT for middle ear exploration/stapedectomy/ossicular chain reconstruction
  • Alternatively: hearing amplification and monitoring

Risk factors

  • genetic predisposition
  • female and caucasian
  • young adults to middle age adults

Etiology/pathophysiology:

  • abnormal, spongy bone growth at the junction of the stapes to the oval window in the middle ear
  • worsens over time
75
Q

Otosclerosis

diagnosis

A

Diagnosis

  • CHL on audiogram, possibly with a carhart notch at 2000 Hz
  • Normal physical exam and normal tympanogram (may see absent reflexes)
  • Temproal bone CT/exploratory surgery is diagnostic

Treatment

  • Refer to ENT for middle ear exploration/stapedectomy/ossicular chain reconstruction
  • Alternatively: hearing amplification and monitoring

Risk factors

  • genetic predisposition
  • female and caucasian
  • young adults to middle age adults

Etiology/pathophysiology:

  • abnormal, spongy bone growth at the junction of the stapes to the oval window in the middle ear
  • worsens over time

Presentation

  • worsening hearing loss over time in one or both ears
  • may, may not have tinnitus
76
Q

Otosclerosis

treatment

A

Treatment

  • Refer to ENT for middle ear exploration/stapedectomy/ossicular chain reconstruction
  • Alternatively: hearing amplification and monitoring

Risk factors

  • genetic predisposition
  • female and caucasian
  • young adults to middle age adults

Etiology/pathophysiology:

  • abnormal, spongy bone growth at the junction of the stapes to the oval window in the middle ear
  • worsens over time

Presentation

  • worsening hearing loss over time in one or both ears
  • may, may not have tinnitus

Diagnosis

  • CHL on audiogram, possibly with a carhart notch at 2000 Hz
  • Normal physical exam and normal tympanogram (may see absent reflexes)
  • Temproal bone CT/exploratory surgery is diagnostic
77
Q

Cholesteatoma

Etiology/pathophysiology

A

Etiology/pathophysiology

  • Middle ear cyst with keratin formation
  • Expansion of cyst leads to:
    • destruction of middle ear, labyrinth, mastoid air cells, and facial nerve
    • can lead to invasion of middle cranial fossa of the brain in severe cases
  • Etiology is unknown. Associated with:
    • Eustachain tube dysfunction (chronic negative middle ear pressure leads to retraction of TM, putting skin cells in the middle ear)
    • TM perforation-introduces skin cells to middle ear
    • Congenital

​Presentation

  • Typically presents as chronic draining ear
  • CHL
  • dizziness

Physical exam

  • TM pearl
  • external ear discharge
  • audio shows CHL

Diagnosis

  • CT temporal bone

Treatment

  • Surgical excision necessary to prevent further middle ear destruction
78
Q

Cholesteatoma

presentation/physical exam

A

Presentation

  • Typically presents as chronic draining ear
  • CHL
  • dizziness

Physical exam

  • TM pearl
  • external ear discharge
  • audio shows CHL

Diagnosis

  • CT temporal bone

Treatment

  • Surgical excision necessary to prevent further middle ear destruction

Etiology/pathophysiology

  • Middle ear cyst with keratin formation
  • Expansion of cyst leads to:
    • destruction of middle ear, labyrinth, mastoid air cells, and facial nerve
    • can lead to invasion of middle cranial fossa of the brain in severe cases
  • Etiology is unknown. Associated with:
    • Eustachain tube dysfunction (chronic negative middle ear pressure leads to retraction of TM, putting skin cells in the middle ear)
    • TM perforation-introduces skin cells to middle ear
    • Congenital
79
Q

Cholesteatoma

diagnosis/treatment

A

Diagnosis

  • CT temporal bone

Treatment

  • Surgical excision necessary to prevent further middle ear destruction

Etiology/pathophysiology

  • Middle ear cyst with keratin formation
  • Expansion of cyst leads to:
    • destruction of middle ear, labyrinth, mastoid air cells, and facial nerve
    • can lead to invasion of middle cranial fossa of the brain in severe cases
  • Etiology is unknown. Associated with:
    • Eustachain tube dysfunction (chronic negative middle ear pressure leads to retraction of TM, putting skin cells in the middle ear)
    • TM perforation-introduces skin cells to middle ear
    • Congenital

​Presentation

  • Typically presents as chronic draining ear
  • CHL
  • dizziness

Physical exam

  • TM pearl
  • external ear discharge
  • audio shows CHL
80
Q

Eustachian Tube Dysfunction

Why more common in children?

A

because of horizontal position

81
Q

______ is a thin muscular tube that is responsible for equalizing the pressure in the middle ear with the pressure outside the ear. It also drains mucous from the middle ear

A

Eustachian Tube

82
Q

Normal function of eustachian tube

A

opening and closing with soft palate movement

(dysfunction=fails to open and remains closed)

83
Q

dysfunction of eustachian tube

A

dysfunction=fails to open and remains closed

(normal=opening and closing with soft palate movement)

84
Q

Causes of Eustachian Tube Dysfunction

A
  1. Inability of tiny ahirs inside the ear to remove fluid and infection
  2. Poor contractile function within the eustachian tube
  3. Narrow eustachian tube-in infants
  4. Adenoid tissue blocking eustachian tube especially in children
  5. Swollen nasal tissue due to secretions that cause of blockage of the nose
  6. Nasopharyngeal tumors in adults

**if there is a unilateral OM must check NP**

85
Q

**if there is a unilateral OM must check _____**

A

nasopharynx for tumors; rare for adults to have UNILATERAL blockage

86
Q

Problems associated with Eustachian Tube Dysfunction

A
  1. Otitis media
  2. Barotrauma–especially with flight
  3. Possibly cholesteatoma
87
Q

Eustachian Tube Dysfunction

Presentation

A

Presentation

  • Ear pain or pressure
  • Stuffiness-doesn’t clear with valsalva
  • Hearing loss or tinnitus
  • Retracted TM on exam
  • Tympanogram is flat

Treatment

  • Nasal decongestants–sudafed, afrin for 3 days max
  • nasal steroids (flonase, nasonex): nose, toes, eyes pie
  • More significant: oral steroids or do myringotomy and place a tube
88
Q

Eustachian Tube Dysfunction

treatment

A

Treatment

  • Nasal decongestants–sudafed, afrin for 3 days max
  • nasal steroids (flonase, nasonex): nose, toes, eyes pie
  • More significant: oral steroids or do myringotomy and place a tube

Presentation

  • Ear pain or pressure
  • Stuffiness-doesn’t clear with valsalva
  • Hearing loss or tinnitus
  • Retracted TM on exam
  • Tympanogram is flat
89
Q

Size of adult TM

A

8-10mm

2017 EENT Clin Med Group (13 decks)

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