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BMS200 > wk 12, lec 3 > Flashcards

wk 12, lec 3 Flashcards

1
Q

15% of people 20-69 have some degree of

A

high frequency hearing loss due to noise

Outer and inner hair cells are damaged by noise, but the outer are more vulnerable

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2
Q

presbycusis

A

Presbycusis (age-induced) hearing loss is likely due to a combination of neuronal loss and hair cell loss

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3
Q

what substances are ototoxic (toxic to hearing) and what do they damage

A

Antibiotics, chemotherapeutic agents, diuretics are often implicated

  • Many of these substances damage either the outer hair cells or the stria vascularis
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4
Q

conductive hearing loss vs sensorineural hearing loss

A

Conductive hearing loss is typically caused by physical blockages or abnormalities in the outer or middle ear, and is often treatable with medical or surgical interventions.

Sensorineural hearing loss is usually permanent, caused by damage to the cochlea or auditory nerve, and may require assistive devices like hearing aids or cochlear implants for management.

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5
Q

conductive hearing loss vs sensorineural hearing loss which frequencies are effected

A

conductive= all frequencies

sensorineural= higher frequencies

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6
Q

conductive hearing loss

A

impaired sound transmission in the external or middle ear, impacts all frequencies

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7
Q

conductive hearing loss causes

A

Trauma to the tympanic membrane, infection, plugging of the external auditory meatus/canal, otosclerosis, cholesteatoma

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8
Q

sensorineural hearing loss causes

A

▪ Presbycusis (age-induced), ototoxic agents, noise (most common)
▪ Problems with endolymph (Meniere’s), infections of the labyrinth or 8th CN, tumours (acoustic neuroma, brainstem tumours)

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9
Q

weber and rinne tests in sensorineural hearing loss

A

Rinne: AC > BC,
Weber: lateralizes to unaffected ear

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10
Q

weber and rinne tests in conductive hearing loss

A

Rinne: BC > AC,
Weber: lateralizes to affected ear

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11
Q

what frequency can humans hear? what is speech range?

A
  • Human ear can hear from 20 – 20000 Hz
    ▪ We’re best at hearing 1000 – 4000, human speech ranges
    from 500 – 2000 Hz
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12
Q

what does audiometry assess

A
  • Audiometry assesses hearing at particular tones and is much better at characterizing hearing loss than tuning fork tests
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13
Q

what is the main cause of otitis externa

A

90% of otitis externa is bacterial
▪ Usually staphylococcal, pseudomonas
aeruginosa, or E. coli

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14
Q

risk factors for otitis externa

A

Humidity, loss of cerumen (trauma, excessive Q-tip use), heat, increased pH (the ear should be acidic for barrier immunity), obstruction of the ear canal, exposure, water with bugs

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15
Q

clinical features of otitis externa

A

otalgia
ottorhhea
itchy
▪ Edema → occlusion of the ear canal →
conductive hearing loss
▪ Severe infection can lead to cellulitis (deeper layers, skin involvement)

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16
Q

hearing loss in otitis externa

A

conductive

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17
Q

treatment for otitis externa

A

topical antibiotics
▪ Make sure not to use ototoxic antibiotics with a perforated TM

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18
Q

4 types of otitis externa

A
  1. furunculosis
  2. chronic otitis externa
  3. malignant/necrotizing otitis externa
  4. otomycosis
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19
Q

what is the worst form of otitis externa (medical emergency )

A

malignant/necrotizing otitis externa

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20
Q

furunculosis (type of otitis externa)? cause?

A

otitis externa of the outer 1/3 of the ear canal, usually staphylococcal

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21
Q

chronic otitis externa cause

A

less painful, more itchy
▪ Usually caused by repetitive trauma, chronic drainage from a
middle ear infection

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22
Q

malignant/necrotizing otitis externa

A

▪ Progressive, slowly developing infection, severe otalgia, lots of otorrhea, granulation/necrotic tissue in the auditory canal
* Can be life-threatening if the infection colonizes temporal bone, intracranial structures
* Cranial nerve palsies and systemic infection also possible

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23
Q

who is malignant/ necrotizing Otitis externa more common in

A

More common in the elderly, diabetics, immunocompromised
– usually P. aeruginosa

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24
Q

otomycosis (type of otitis externa)? cause?

A

fungal infection of the external auditory canal, up to 10% of otitis externa

▪ Usual agent is Aspergillus (80%), next most common is Candida species
▪ More likely in:
* Diabetes, elderly, past history of HEENT surger in the
mastoid
▪ Often seen in those with poor response to antibacterial antibiotics

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25
Q

acute otitis media symptoms

A

rapid onset of signs and symptoms, including fever and otalgia

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26
Q

recurrent acute otitis media

A

3 or more episodes within a 6-month period or four or more episodes within a 12-month period - complete resolution of symptoms between episodes

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27
Q

cause of acute Otitis media

A

Usually due to auditory tube dysfunction

  • Up to age 7, eustachian tube is shorter, wider, and more horizontal than in adults – predisposes to upper airway/oral bacteria colonization
  • Blockage of the tube – swelling of adenoid lymphatic tissue, swelling due to URTI or allergic rhinitis, inadequate tensor palatini function
  • Lack of breastfeeding (breast milk has antimicrobial sustances in it)
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28
Q

pathogenesis of acute otitis media

A

▪ Obstruction of the auditory tube → air absorbed in middle ear→negative pressure→edema of mucosa with exudate and fluid accumulation→infection from nasopharyngeal secretions

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29
Q

bacteria and viruses causing acute otitis media

A

Major bacteria implicated: H. influenzae, S. pneumoniae, M. catarrhalis

▪ Major viruses implicated: RSV, influenza, parainfluenza, adenovirus

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30
Q

clinical features of acute otitis media - what is the triad

A

▪ Triad of otalgia, fever, and conductive hearing loss
* Rare to have tinnitus, vertigo, or facial nerve paralysis

▪ Otorrhea can occur if the TM is perforated

▪ Bulging, red TM (middle ear inflammation)

▪ Often the TM is opaque, bony landmarks are lost

▪ effusion can often be seen behind it, and mobility is limited (pneumatoscopy)

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31
Q

type of hearing loss in acute otitis media

A

conductive

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32
Q

otitis media with effusion (serous otitis media) cause

A

▪ Often due to untreated or unresolved AOM

  • Persistent effusion in up to 40% of children 30 days after initial AOM, continued for 3 months in 10%
  • Main concern in pediatric population is impact on hearing at early ages (prior to a year)
    ▪ Delay in language development
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33
Q

otitis media with effusion type of hearing loss

A

conductice

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34
Q

otitis media with effusion clinical feautres

A

▪ Conductive hearing loss with or without tinnitus

▪ Feeling of fullness in the ear, low-grade fever

▪ May or may not involve otalgia

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35
Q

otitis media with effusion on otoscope

A

▪ TM is translucent/gray (limited inflammation)
* Fluid behind the ear, can often see air-fluid levels or bubbles

▪ Loss of light reflex, reduced mobility on pneumatoscopy

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36
Q

treat otitis media?

A
  • Most cases resolve on their own

▪ Tympanostomy tubes can improve hearing
▪ Case-by-case treatment depending on presentation

37
Q

most common causes of tympanic membrane perforations

A

▪ Middle ear infections

▪ Trauma – can be barotrauma or physical injury to the ear

38
Q

clinical features of tympanic membrane perforation

A

▪ Sudden onset of pain, hearing loss
▪ Can include bloody otorrhea
▪ Vertigo or tinnitus
* Usually transient

39
Q

how to fix a tympanic membrane perforation

A
  • Perforations usually heal spontaneously – advisable to wear earplugs while swimming, bathing

▪ Postero-superior damage to the TM is more likely to damage the function of ossicles – more urgent referral to the HEENT

40
Q

what parts of the ear does chronic otitis media affect

A

both the middle ear and the mastoid cavity

41
Q

tympanic membrane perforation from

A

recurrent or chronic ear infections

42
Q

where is there a disfunction that causes chronic otitis media

A

Dysfunction of the Eustachian tube is a significant factor in this disease, observed in approximately 70% of patients undergoing middle ear surgery

43
Q

types of chronic otitis media

A
  1. suppurative or serous chronic otitis media
  2. benign chronic otitis media
44
Q

suppurative or serous chronic otitis media

A

describes
character of the drainage through the perforated TM

45
Q

benign chronic otitis media

A

“dry” – no active infection

46
Q

what is the most common cause of chronic otitis media

A

viral

Viruses usual cause, though bacteria are more likely to contribute in children
▪ Pathogens invade via the external canal → edema, fibrosis, perforation and persistent infection
▪ Can also be a complication of tympanostomy tubes

47
Q

clinical features of chronic otitis media

A

▪ Otorrhea
▪ May or may not involve conductive hearing loss, tinnitus, or aural fullness
▪ Can have occasional severe intracranial complications in children

48
Q

cholesteatomas

A

non-neoplastic, cystic lesions lined by keratinizing squamous epithelium or metaplastic mucus- secreting epithelium, and filled with debris

49
Q

where do cholestetomas occur

A

middle ear

-cysts+ keratin

  • Occur in the middle ear, mostly in the posterior-superior region (sometimes called the attic)
  • Debris contains mostly keratin, other cellular debris
  • Cyst is usually between 1 and 4 cm
50
Q

three types of cholesteatomas

A
  1. primary congenital
  2. secondary acquired
  3. primary acquired
51
Q

primary congenital cholesteatomas

A

keratined epithelium is “misplaced” into area that should only have bone or simple cuboidal mucosa

52
Q

what type of hearing loss does cholesteatomas lead to

A

conductive hearing loss

53
Q

secondary acquired cholesteatomas

A

– Traumatic “implantation” of
keratined epithelial cells from the “external-ear” side of the tympanic membrane or auditory canal
* Traumatic causes include blast damage, iatrogenic (surgical, insertion of ear tubes) – not as common as primary acquired

53
Q

series impacts of cholesteatomas

A

Can cause serious bony destruction of the temporal bone→ infected cyst gains access to the dura and intracranial structures→meningitis and death

  • Cholesteatoma should almost always be removed to avoid this
  • Can also migrate and rupture into deep neck structures →another source of potentially life-threatening infection
54
Q

primary acquired cholesteatomas

A

– Recent investigations implicate a
combination of chronic inflammation and abnormal TM cell migration

55
Q

most common cause of cholesteatomas

A

primary acquired

mostly in adults

56
Q

pathogenesis of primary acquired cholesteatoma

A

– Inner surface of the TM consists of respiratory epithelium (simple cuboidal ciliated epithelium with goblet cells) that migrates over its surface in postero- superior direction
– As it migrates more rapidly in response to chronic inflammation, it becomes “stuck” to the incus
* Next stage – mucous accumulates in the pouch→chronic inflammation (often pseudomonas implicated) if it gets infected
* This is followed by implantation/conversion of some of the cells in this cyst to keratinized epithelial cells
– Note that the “outer” surface of the TM is pulled into the cystic structure
* Outer surface formed from keratinized epithelium, not respiratory epithelium

  • The “stuck” keratinized cells keep dividing, and continued inflammation is likely linked to:
    – Growth of the cystic structure
    – Activation of osteoclasts and invasion of the temporal bone
    – Conductive hearing loss as the mobility of the ossicles is impaired (remember, the inner surface of the TM got stuck to the incus)
57
Q

type of hearing loss in primary acquired cholesteatoma

A

– Conductive hearing loss as the mobility of the ossicles is impaired (remember, the inner surface of the TM got stuck to the incus)

58
Q

where do primary acquired cholesteatomas develop in

A

Tend to see them develop in the pars flaccida (postero-superior to handle of malleus) because:
* This is the direction the inner
surface of the TM “likes” to migrate
* This part of the TM has a lot of
resident inflammatory cells
* This area is close to the incus

59
Q

clinical features of cholesteatomas

A

-painless otorrhea
- conductive hearing loss
* Rarely vertigo or dysequilibrium may arise due to the inflammatory process within the middle ear or due to invasion of the labyrinth
* Facial nerve palsy, can also result from the inflammatory process or mechanical compression of the nerve

60
Q

prognosis of choelsteatomas

A

surgery

will usually have hearing loss post-op

61
Q

2 types of dizziness

A

vertiginous (vertigo) [peripheral and central]

non-vertiginous [ organic and functional]

62
Q

vertigo

A

The environment seems to be moving

63
Q

what 2 problems could cause vertigo

A
  • Caused by inner ear or brainstem-cerebellar disorders
    – Inner ear = peripheral
    – Brainstem-cerebellar = central
64
Q

organic non-vertiginous dizziness

A

a pathology that usually involves visual compromise or low blood pressure

65
Q

functional non-vertiginous dizziness

A

common in a wide range of mood disorders

66
Q

benign paroxysmal positional vertigo

A

Acute attacks of transient rotatory vertigo lasting seconds to minutes initiated by certain head positions
– Accompanied by rotatory nystagmus

67
Q

what is the most common form of positional vertigo

A

benign paroxysmal positional vertigo

68
Q

symptoms in benign paroxysmal positional vertigo

A

– Symptoms are usually brief, caused by changing head position – Typical history = worsening when getting out of bed,
extending the neck

69
Q

cause of benign paroxysmal positional vertigo

A

Usually caused by migration of a free-floating otolith [crystals in the ear] (should not be free-floating, should be attached)

70
Q

diagnosis of benign paroxysmal positional vertigo

A

– Dix-Hallpike Positional Testing
* Patient rapidly moved from a sitting position to a supine position with the head hanging over the end of the table, turned to one side at 45° and neck extended 20° holding the position for 20 s

– Onset of vertigo and rotatory nystagmus indicate a positive test for the dependent side

71
Q

Meniere’s disease vs benign paroxysmal positional vertigo timeline vs vestibular neuronitis

A

menieres= min to hours

bppv= secs to mins

vn= days to weeks

72
Q

meniere’s disease

A

Episodic attacks of tinnitus, hearing loss, and vertigo lasting minutes to hours

73
Q

cause of meniere’s disease

A

excess endolymph

– Inadequate absorption of endolymph leads to endolymphatic over-accumulation that distorts the membranous labyrinth

– Usually begins in middle age

74
Q

triggers of meniere’s disease

A

Triggered by high salt intake, caffeine, stress, nicotine, and alcohol

75
Q
  • Diagnostic Criteria for Menière’s Disease (must have all three)
A

– Two spontaneous episodes of
* Rotational vertigo ≥20 min
* Audiometric confirmation of Sensorineural Hearing Loss
* Tinnitus and/or aural fullness

76
Q

vestibular neuronitis

A
  • Acute onset of disabling vertigo often accompanied by nausea, vomiting, and imbalance without hearing loss that resolves over days leaving a residual imbalance that lasts days to weeks
77
Q

causes of vestibular neuronitis

A

– Could be viral, often associated with URTI

78
Q

acute and convalescent phase of vestibular neuronitis

A
  • Acute phase
    – Severe vertigo with nausea, vomiting, and imbalance lasting 1-5 days
    – Nystagmus
    – Patient tends to veer towards affected side
  • Convalescent phase
    – Imbalance and motion sickness lasting days to weeks
    – Spontaneous nystagmus away from affected side
    – Gradual vestibular adaptation requires weeks to months
79
Q

what is labyrinthitis

A
  • Acute infection of the inner ear resulting in vertigo and hearing loss
80
Q

labyrinthitis causes

A
  • May be serous (viral) or purulent (bacterial)
    – Occurs as a complication of acute and chronic otitis media, bacterial meningitis
  • Bacterial: S. pneumoniae, H, influenzae, M. catarrhalis, P. aeruginosa, P. mirabilis
  • Viral: rubella, CMV, measles, mumps, varicella zoster
81
Q

symptoms of labyrinthitis

A
  • Sudden onset of vertigo, N/V, tinnitus, and unilateral hearing loss
    with no associated fever or pain
    – Meningitis is a serious complication
82
Q

acoutsic neuromas effects what cell

A

Schwann cells that myelinate vestibular and/or cochlear nerve

83
Q

acoustic neuroma

A
  • Intracranial tumours that develop from Schwann cells that myelinate the vestibular and/or cochlear nerve

– Can take up much of the space of the cerebellopontine angle (80% of tumours in this area are acoustic neuromas)
– Most are from the vestibular component of the nerve

84
Q

acoustic neuroma can impact brain and nerves?

A

alway vestibular and/or cochlear nerve

– There’s quite a bit of room in that area of the brain, so often do not elevate intracranial pressure until they are quite large
– Can also impinge on the nearby facial nerve and trigeminal nerve

85
Q

risk factors for acoustic neuromas

A

– Neurofibromatosis type II (defective merlin gene)
– Ionizing radiation to the area

86
Q

clinical features of acoustic neuroma

A
  • Hearing loss by far the most common
    – Can be sudden or gradual, constant or fluctuating
    – Assume that all unilateral neurosensory hearing loss is due to an acoustic neuroma until proven otherwise
  • Vertigo is fairly uncommon, but balance difficulties are common
  • Facial weakness or numbness due to CN VII or V impingement
  • Headache due to elevated intracranial pressure
87
Q

treatment/prognosis of acoustic neuroma

A

*Microsurgery or radiation used to treat, generally survival is quite good
* 30 – 80% maintain hearing

BMS200 (40 decks)

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