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AUDE 5410 > quiz 2 > Flashcards

quiz 2 Flashcards

1
Q

otitis media (OM)

A

an infection inflammation of the ME that can result in fluid within the ME cavity
-redness of TM without effusion is referred to as acute myringtiits

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2
Q

otitis media with effusion (OME)

A

accumulation of fluid with an OM infection

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3
Q

prevalence of OME

A

-younger the child, the higher the risk
-recurrent OME during the first 3 years of life occur in around 5-10%
-may also occur in adults and if they are recurrent, look for other causes

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4
Q

there is a greater incidence in children with a history of ___________________

A

upper respiratory illness such as colds, asthma and allergies
-inflammation of URT will affect the ET by blocking it which can become more difficult to drain out and causing OME

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5
Q

why do children outgrow susceptibility to OME around 6-8 years of age

A

their eustachian tube takes adult proportions
-this changes from being short and horizontal with flaccid cartilage to longer and more vertical

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6
Q

describe the various types of etiology for OM

A

bacterial, viral, cleft palate, craniofacial disorders, ciliary disfunction, allergies, immune dysfunction, ETD and obstruction

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7
Q

acute otitis media (AOM)

A

short time onset, ME inflammation and ME fluid (effusion) are the 3 diagnostic criteria’s
-less than 3 weeks
-characterized by otalgia and redness of TM with effusion

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8
Q

why is AOM often over diagnosed

A

it is an easy diagnosis to make

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9
Q

sub acute OM

A

condition persisting 3 weeks to 3 months

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10
Q

recurrent OM

A

multiple self limiting episodes with symptom free periods between flare ups
-3 or more episodes within aa 6 month period of 4 or more episodes within a year

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11
Q

chronic OM

A

condition persisting over 3 months
-generally with effusion but without other signs of inflammation

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12
Q

middle ear effusion (MEE)

A

almost always follows AOM and can take 2-3 weeks to clear post treatment/recovery
-however can be persistent and last over 40 days with a high incidence in children

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13
Q

what are the two classifications of OM that can occur

A

by length of infection of based on fluid composition

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14
Q

serous OM (SOM)

A

clear, watery fluid
-seen with barotrauma
-retracted TM

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15
Q

mucoid OM (MOM)

A

thick and colored, gunky, pus
-appears swollen
-can rupture

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16
Q

why is it better if a doctor can rupture the TM instead of it occurring naturally

A

with a doctor, there are clean edges and can heal with less scar tissue. if it ruptures on its own, there will be rigid edges and more scar tissue

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17
Q

purulent OM (POM)

A

odorous and thick, smelly

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18
Q

glue ear

A

used to describe chronic mucoid OM
-self limiting in most cases
-can fill with gelatinous inflammatory exudate/cellular debris

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19
Q

explain some risk factors with OME

A

age (higher change with younger age), ET dysfunction, craniofacial anomalies, decreased risk for breast fed infants, day care attendance, susceptibility to URT infections, smoking in the home, family Hx of OME, male, low birth weigh or SES

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20
Q

symptoms of OME

A

otalgia, fever, redness of TM, effusion in the ME, irritability, inconsistent responses to sound, delayed speech and language development and reduced attention span

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21
Q

otoscopic findings in OME

A

-discolored/red TM
-partial/complete bulging of the TM or can be retracted
-perforation (may not be visible)
-fluid line or bubbles

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22
Q

tympanometry findings in OME

A

-type B with fluid
-type C (negative pressure)
-type B high volume seen with perforation

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23
Q

reflex findings with OME

A

when measuring or playing anything within the affected ear, it will be abnormal or ABS

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24
Q

pure tone finding with OME

A

-may be WNL, but may have worse air than bone causing a conductive components
-fluctuating HL
-possible rising or reverse slop configuration of HL

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25
Q

speech findings with OME

A

-supra threshold speech is normal
-SRT PTA in good agreement

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26
Q

what can happen if OME is left untreated

A

permanent/temporary CHL, damage to ME structures, cholesteatoma, permanent high frequency SNHL, auditory deprivation, deficits in binaural auditory processing, speech/language delays and can result in altered ABR recordings shortly after resolution

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27
Q

what is the concerning aspect for deficits in binaural processing

A

impacts hearing in noise ability

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28
Q

what is the main societal consequence of OME

A

development of multidrug resistant bacteria (i.e. MRSA) which is a concern because of the over prescription of antibiotics and not taking the entire recommended dose of antibiotics

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29
Q

what is the gold standard for diagnosing OME?

A

pneumatic otoscopy
-can deliver air and see movement of the TM

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30
Q

how can OME be diagnosed

A

-through pneumatic otoscopy
-standard otosocpy may be useful with visualize TM color, position, mobility
-head/neck examination
-audiogram
-tympanogram

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31
Q

management of OME

A

-if no symptoms, treat through observation
-medication, such as antihistmine/decongestant or antibiotics for 7-10 days is common
-myringotomy (incision)
-watchful waiting for up to 3 months for children without HL
-PE tubes can follow myringotomy
-adenoidectomy/tonsillectomy if needed

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32
Q

what section of the TM does myringotomy occur in

A

anterior inferior section

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33
Q

why are prophylactic antibiotics contraindicated

A

due to an increase of antibiotic resistance strands

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34
Q

explain some complications of OME

A

-acute mastoiditis
-ossicular erosion leading to CHL
-SNHL, generally high frequency
-facial nerve paralysis/weakness
-labyrinthe fistula
-meningitis (most common intracranial complication)
-brain abscess

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35
Q

cholesteatoma

A

pseudo-tumors that can occupy the EAC, ME cavity or extend through the mastoids bone into the brain cavity
-highly aggressive, progressively enlarging tumor like characteristics
-can cause destruction of bone

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36
Q

what has been found within cholesteatomas that could explain the aggressive behavior

A

highly invasive fibroblasts were found that are not seen within normal skin

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37
Q

what are the 3 types of cholesteatomas that can be present

A

congenital, acquired or iatrogenic

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38
Q

congenital cholesteatoma

A

present within children with the median age around 5 years
-3:1 male to female ratio
-TM can be normal without a history of perforation, otorrhea or myringotomy
-most common location is the anterior-superior quadrant

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39
Q

acquired cholesteatoma

A

more common and is often due to chronic or untreated OME or trauma leading to a TM perforation
-can also occur as a result of TM retraction in the pars flaccida or posterior superior quandrant
-a potential growth site may be area of previous ear surgery/old TM perforation
-slow growing condition initially with no symptoms

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40
Q

iatrogenic cholesteatoma

A

may result due to a blunt knife used during myringotomy
-may lead to implantation of squamous epithelium in ME cavity

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41
Q

otoscopic findings with a cholesteatoma

A

can be normal or show perforations or otorrhea
-this will depend on the stage, where it is routed, how large or small it is, etc.

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42
Q

tympanogram findings with a cholesteatoma

A

-normal if there is no damage
-type As if it is within the ME cavity
-type Ad if disarticulation has occurred
-type B, low volume if TM perforation has occurred and if filling up the ME cavity
-type B, high volume if it is big enough to fill up the ME cavity and if TM perforation is present

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43
Q

auditory sensitivity findings with cholesteatoma

A

normal : ossicular chain is intact and the cholesteatoma only caused TM perforation is present
conductive HL : if ossicular disarticulation occurred
mixed HL : also reported

44
Q

diagnosis of cholesteaatoma

A

usually can be visualized or can do a definitive diagnosis of CT scan

45
Q

how can cholesteatoma’s be managed

A

surgical removal is primary treatment
-prior to surgery antibiotic steroid drops may be prescribed to decrease inflammation and granulation tissue which can help decrease bleeding during surgery

46
Q

what are the potential complications of cholesteatoma surgery

A

-permanent CHL/mixed/SNHL
-facial paralysis
-dizziness
-tinnitus
-intracranial complications

47
Q

otosclerosis

A

focal disease that is unique to the temporal bone
-insidious and progressive condition

48
Q

ossicular ossification is specifically used for …..

A

fixation of the stapes footplate into the oval window

49
Q

what is the main site of fixation with otosclerosis

A

fissula ante fenestram
-the slit passage within the otic labyrinth wall that is anterior to the oval window
-in close proximity to the anterior portion of the stapes footplate

50
Q

what are some causes of otosclerosis

A

can be related to a viral infection or genetics

51
Q

what population is most affected by otosclerosis

A

females are more affected then males and can often be accelerated in expression during pregnancy
-single most common cause of HL in young adulthood

52
Q

otoscopic findings with otosclerosis

A

almost always normal however can be schwartze sign
-increased vascularity of the actively growing bone near oval window that is reflected through the TM as a reddish bluish discoloration or glow

53
Q

immittance findings with otosclerosis

A

generally normal or As tymps
-abnormal reflexes in most case

54
Q

pure tone findings with otosclerosis

A

early state : normal or mild CHL with rising
middle state : CHL/MHL with rising or flat configuration
late stage : flattening of the previously rising CHL or MHL
-will show carhart’s notch (dip in BC at 2000 Hz)

55
Q

speech findings with otosclerosis

A

SRT and PTA in good agreement, WRS is good as test is performed at suprathreshold levels

56
Q

how to manage otosclerosis

A

surgery or amplification
-surgery can be from a stepedotmy to a total stapedectomy
-if bilateral, the worse ear will be operated on first

57
Q

common complications of surgery with otosclerosis

A

-WRS can worsen
-oval window otosclerosis or round window otosclerosis
-hyperacusis
-facial apralaysis/weakness
-chorda tympani nerve may need to be sacrificed
-perilymphatic fistula

58
Q

differential diagnosis for ososclerosis

A

meniere’s disease, osteogenesis imperfecta or SSCD

59
Q

trauma and the middle ear

A

blow to the head/falls, sport injuries, blast injuries, MV accidents or foreign body insertion
-can lead to ossicular disarticulation
-also can be temporal bone trauma

60
Q

ossicular disarticulation

A

separation of the middle ear bones
-occurs to trauma to head/face and can be seen with osteoporosis
-ice cream cone sign on a CT scan

61
Q

otoscopy findings with ossicular disarticulation

A

-perforation of TM
-bleeding in the ear canal with TM perforation
-rarely the TM and ear canal may appear normal

62
Q

immittance findings with ossicular disarticulation

A

-Ad due to it becoming a mass dominated system
-abnormal reflexes due to ossicles not being together

63
Q

pure tone findings with ossicular disarticulation

A

conducitve/mixed HL

64
Q

treatment for ossicular disarticulation

A

surgical repair
-amplification can occur if surgery is not successful/not an option

65
Q

temporal bone trauma

A

requires high force to sustain a fracture due to being a dense and thick bone
-can occur with or without fracture

66
Q

auditory signs of a temporal bone fracture

A

-acute or delayed CHL
-clotted blood, debris and hematoma in canal
-perforated, lacerated or disrupted TM
-ME filled with blood or CSF
-bleeding from ears
-ossicular disarticulation
-ossicular fixation due to fibrous adhesions

67
Q

vestibular signs of a temporal bone fracture

A

only occurs within ear that is involved
-benign paroxysmal positional vertigo (BPPV)
-perilymphatic fistula

68
Q

treatment for a temporal bone fracture

A

-hemotympanum
-TM usually self heals
-persistent CHL
-irreversible SNHL and tinnitus through HA and tinnitus management
-vestibular symptoms are usually self limiting for 6 months then self resolving
-antibiotics based on culture results

69
Q

paraganglioma (glomus tumor)

A

most common benign soft tissue tumor tumor of the ME, are rarely malignant, and the second most common benign tumor of the temporal bone
-progressive growth
-typically unilateral, reddish-purple, highly vascular and lobulated
-arise from paraganglia cells

70
Q

explain the heredity of glomus tumors

A

sporadic or AD with 100% penetrance
-shows no sex predisposition with both sexes being affected equally however in sporadic cases it shows females being more affected

71
Q

patients usually present after the _______ decade of life with a glomus tumor

A

5th

72
Q

glomus tumors are highly ___________ and will be shown on a MRI due to this

A

vasacularized

73
Q

glomus tympanicum

A

arises in the ME
-along the course of the jacobson nerve, primarily within the tympanic cavity
-smaller and cause early symptoms due to a narrow cavity

74
Q

signs of a glomus tympanicum

A

-pulsatile tinnitus due to vascularity of tumor
-TM may appear red due to increased vasculature
-tissue growth of TM
-tumor can inhibit ossicualr motility resulting in CHL
-tumor can cause facial nerve dysfunction and/or vertigo and SNHL if grows inward

75
Q

glomus jugulare

A

arises within the neck
-starts from internal jugular vein bulb and involves jugular foramen and the related structures
-more common and extensive then tymapnicum due to the space available to grow
-definitive diagnosis through an MRI

76
Q

signs of glomus jugulare

A

HL, otalagia, aural fullness, vertigo, difficulty swallowing (CN 9, 10 and 11), and the involvement of CN 12 indicates a more extensive disease

77
Q

why does the involvement of CN 12 indicate a more extensive glomus jugulare tumor

A

this is the nerve that is farthest away from the tumor origin and is least likely to be involved
-really is growing large is this is involved

78
Q

audiologic signs of a glomus jugulare tumor

A

-red mass can be seen if ME cavity is involved
-CHL may be present or can be mixed if neural involvement has occurred
-As if tumor is pressing on TM
-B is large tumor is pressing on TM and render’s mobility

79
Q

treatment for glomus jugulare

A

surgery or radiation
-will typically do radiation to reduce size first

80
Q

inner ear homeostasis

A

process of chemical equilibrium of the inner ear fluids and tissues
-for proper inner ear function, a tight control of ion movement across the cell membrane is necessary

81
Q

endolymphatic hydrops

A

increased potassium transport in endolymph or increased endolymph production
-i.e. meniere’s disease

82
Q

endolymphatic xesosis

A

decreased potassium transport in endolymph or decreased endolymph production
-i.e. JLNS or connexin

83
Q

what type of infections can be seen within the inner ear

A

viral and bacterial infections
-viral can be both RNA or DNA viruses
-includes AIDS and meningitis

84
Q

viral infections of the inner ear

A

destructive patterns
-organ of corti gets damaged at the basal turn (high frequency SNHL)
-individual hair cells are damaged or missing
-atrophy of stria vascularis may occur

85
Q

RNA virus

A

high mutation rates and are not as stable as DNA viruses due to lack of proofreading
-rubella virus (german measles)
-paramyxovirus (mumps)

86
Q

DNA virus

A

more stable that RNA viruses due to having proofreading abilities and are less common due to the DNA duplication process
-cytomegalovirus (CMV) which belongs to the herpes virus family and is one of the most common viral diseases of the human race

87
Q

acquired immunodeficiency syndrome (AIDS)

A

caused by the microbe human immunodeficiency virus (HIV) which is a retrovirus meaning it goes from RNA to DNA in transcription instead of the normal pattern DNA to RNA
-neurotropic meaning it attacks the nervous system

88
Q

audiologic signs seen with patients that have AIDS

A

OME, otalgia, vertigo, tinnitus, aural fullness, reduced OAEs and delayed ABR inter wave latencies
-secondary symotms may occur due to ototoxic effects or recurrent/chronic OME or other infections that attack the ear

89
Q

meningitis

A

inflammation of the meninges surrounding the brain and spinal cord (dura mater, arachnoid mater and pia mater)
-can be from viruses or bacteria
-primary originates within the meninges
-secondary begins as OME that leads to mastoiditis/labyrinths and then the meninges

90
Q

initial symptoms of meningitis

A

high fever, neck rigidity (due to inflammation of the meninges that cover the spinal cord) , malaise, nausea/vomiting and in some cases coma or death

91
Q

severe/untreated infections can lead to …..

A

blindness, paralysis due to motor centers in the brain dying, HL/deafness, vertigo and balance problems

92
Q

how to treat meningitis

A

antibiotics, mastoidectomy and amplification/CI if HL is severe/profound

93
Q

perilymphatic fistula

A

abnormal connection in either oval or round window that separates the air filled ME and the fluid filled perilymphatic space of the inner ear
-remember that a fistula is an opening that should not be there that is connecting 2 systems

94
Q

common etiologies of a perilymphatic fistula

A

idiopathic, history of straining/lifting and feeling the ear pop, can occur during early or late periods of time following stapedectomy or can can spontaneous

95
Q

audiologic findings with perilymphatic fistula

A

episodic vertigo without HL, HL without vertigo, symptoms similar to menieres disease, or other symptoms with disequilibrium but not vertigo

96
Q

treatment for perilymphatic fistula

A

middle ear exploration, surgical repair for perilymph leak/sealing of the round or oval window, and patients are cautioned against heavy lifting following surgery

97
Q

noise induced HL (NIHL)

A

caused by both dose (level) and duration (how long) to exposure of sound
-can cause temporary threshold shifts and permanent threshold shift

98
Q

temporary threshold shift (TTS)

A

is reversible
-increasing in auditory threshold following exposure to loud noise
-most will resolve after around 15 minutes but can go up to 14 hours

99
Q

permanent threshold shift (PTS)

A

does not go back to normal
-change in hearing sensitivity around 14 hours after
-permanence is assumed if change is still observed on a 30 day follow up hearing test
-can be due to tip links breaking or fractured/detached stereocilia

100
Q

what effect does NIHL have on the middle ear

A

injury from noise is rare and will only occur with extremely high levels of noise
-perforations can be used as a sign for possible concussions

101
Q

what effect doe NIHL have on the inner ear

A

can result in tinnitus and those that are most vulnerable include the cochlea and OHCs
-stereocilia will lose stiffness and ability to vibrate in response to sound which results in a reversible HL or TTS

102
Q

even though there is no effective treatment, ____________ is the best management

A

prevention

103
Q

acoustic trauma

A

sudden permanent HL from a single event or exposure without intervening TTS
-includes blast injuries

104
Q

acoustic trauma is caused by impulse noise, explain this type of noise

A

sudden, short duration very loud sounds
-bombs or IEDs
-firearms and other weapons
-industrial blasts
-intensity between 165 and 190 dB SPL

105
Q

describe the levels in dB HL that can cause acoustic trauma

A

-165 to 190 dB can rupture/produce hemorrhage of the TM
-impact noise that is grater than 140 dB SPL can result in PTS

106
Q

effects on the auditory system that occur based on acoustic trauma

A

perforation or hemorrhage, may see a noise notch, variety of configurations (flat or high freq. sloping), type Ad tympanogram with ABS ARTS
-HL can improve over a 4-6 month range
-surgery may be required to repair TM and ossicles

107
Q

blast injuries

A

caused by indirect impact from a pressure wave generated by an explosion that causes an instant rise in pressure, creating a blast wave that starts at the site of the explosion and travels outward

AUDE 5410 (4 decks)

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