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AUDE 5410 Aud-Vestib Disorders > Quiz 2 (ME) > Flashcards

Quiz 2 (ME) Flashcards

1
Q

infectious inflammation of ME resulting in fluid buildup

A

OME

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2
Q

follow AOM
-serous fluid in ME without OM (barotrauma or season allergies)

A

MEE

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3
Q

what is treatment for MEE or OME

A

watch and see usually spontaneously resolves

Persistent = myringotomy w/ PE tube

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4
Q

GOLD STANDARD FOR OM

A

pneumatic otoscopy

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5
Q

Acute onset, ME inflammation & effusion; fever otalgia malaise nausea lack of appetite

A

AOMA

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6
Q

What is treatment of AOM

A

observe in older kids & adults

antihistime/decongestants & antibiotics for 7-10 days

f/u tymps in 2-3 wks after antibiotics to allow ME fluid to absorb

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7
Q

Condition resolves on its own 7-14 days for _____% of untreated cases and ____% of treated cases; effusion can last for >2-3 wks after antibiotics & resolution of actual infection

A

81
94

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8
Q

-™ redness without effusion
-misdiagnosed as OME
form of AOM

A

Acute Myringitis

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9
Q

what are diagnostic criteria for chronic OME

A

can be asymptomatic, may have HL, may report “plugged” or “popping” feeling of ears

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10
Q

fluid in ME for prolonged periods
-Returns over again with no infection

A

chronic OME

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11
Q

OME persisting >/= 3 mos from date of onset or date of diagnosis; has effusion but no fever or otalgia

A

chronic OME

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12
Q

can lead to glue ear (ME cavity fills w/ gelatinous debris)

A

chronic ome

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13
Q

treatment for chronic OME

A

Watch & wait for 3 mos

Myringotomy if persists followed by PE tube

Tonsil & adenoid removal

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14
Q

why should antibiotics not be used in chronic OME

A

due to increase in antibiotic resistance

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15
Q

as age increases, prevalence _______ with OME

A

decreases

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16
Q

kids outgrow by age 6-8 because

A

ET becomes more slanted

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17
Q

what is bacterial reflux

A

caused by colonization of nasopharynx, incompetence of ET and - ME pressure

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18
Q

most common pathogen causing OM also found in upper respiratory tract infections

A

bacterial

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19
Q

strep throat

A

bacterial

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20
Q

most common viral infection of OM

A

respiratory syncytial virus (RSV)

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21
Q

what are other causes of OM

A

clef palate
craniofacial disorders like treacher’s & down’s
ciliary dysfunction (cystic fibrosis & karagners
environmental allergies
immune dysfunction (aids, chemotherapy)
ET abnormalities (impaired muscle, shorter tube)
obstruction (feeding tube, tumors)

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22
Q

how are ME disorder classified

A

based on duration of disease

based on fluid composition

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23
Q

3 criteria by AAP & AAFP for AOM diagnosis:

A

acute onset
ME inflammation
ME effusion

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24
Q

short term, self-limiting condition with otalgia & redness of ™ with effusion

A

AOM

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25
Q

what is severe AOM

A

moderate to severe otalgia & temp > 102 deg F

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26
Q

what is non severe AOM

A

mild otalgia & temp < 102 deg F

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27
Q

hyperemic stage AOM

A

red & angry

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28
Q

AOM with effusion

A

may or may not see fluid
loss of clear landmarks

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29
Q

AOM suppuratibe stage

A

fluid & bubbles

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30
Q

sub acute OM

A

3 wks to 3mos

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31
Q

recurrent OM

A

multiple self-limiting w/ symptom-free periods bw flare-ups
3 or more episodes w/in 6 mo period OR 4 or more episodes

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32
Q

chronic om

A

continues >3 mos
usually / fluid but no fever or otalgia
feeling “plugged or popping” of ears

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33
Q

management of chronic om

A

watch & wait for 3 mos, myringotomy followed by PE tube, tonsil removement

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34
Q

serous oM

A

clear

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35
Q

mucoid OM

A

thick & colored (pussy)

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36
Q

purulent OM

A

odorous & thick

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37
Q

glue ear

A

chronic mucoid OM

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38
Q

what is glue ear

A

chronic mucoid OM

me fills with gelatinous debris “glue” that can lead to TM retraction & bone erosion that can lead to cholesteatoma

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39
Q

watch & wait for 3 mos, myringotomy followed by PE tube, tonsil removement

A

MEE

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40
Q

can persist for around 40 days

A

ME effusion

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41
Q

high icidence in white kids

A

MEE

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42
Q

What age group do you see more OME?

A

Peak bw 6-11 mos of age

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43
Q

what are risk factors for OME

A

age, ET dysfunction, craniofacial abnormalities, formula babies, day care, respiratory infections, allergies, smoking, family hx, male, low birth weight. low SES

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44
Q

who is more sucseptible to OME

A

6-11 mos, common in asian & blacks, peaks bw october & april, higher in males

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45
Q

risk of child has upper respiratory infection why does it risk OME?

A

because ET is opened to the nasopharynx and is surrounded by soft muscles and with inflammation of upper respiratory, these muscles swell and it closes off opening of ET, hard for it to

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46
Q

signs & symptoms of OME

A

Quick onset
otalgia
fever
redness of tm
effusion in me
irritability/fussiness
may not eat
no response to sounds
delayed S/L development
reduced attention span

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47
Q

what would you see in otoscopy for OME

A

tm discolored: red, opaque, yellowish, pink
partial/complete bulging of tm or retraction
normal, hypo-mobile, retracted tm
perf, discharge, cholesteatoma, retraction pockets, fluid lines/bubbles in ME

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48
Q

what would you see on immittance for OME

A

tymps: type b (effusion) or type b with HV (perf), type c (et & abnormal gradient/width)

ARTs: abnormal or absent

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49
Q

unilateral OM would present with what ART

A

only ipsi ART is present on the unaffected side
contra is abs/elevated

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50
Q

bilateral OM would present with what art

A

ipsi & contra abnormal in both ears

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51
Q

why are ARTs abnormal i OM

A

not enough sound to move the system: even as low as 10-15 dB gap

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52
Q

what would we see for pure tones for OM

A

WNL or fluctuating: CHL, mixed, SNHL

may have abg

CHL doesn’t exceed 60-65 dB (max CHL)

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53
Q

what would speech audiometry show for OM

A

normal supra threhold tests (WRS)

srt matches pta (matches hearing threshold)

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54
Q

why is srt consistent with hl but the WRS are not?

A

srt is a threshold test
wrs is suprathreshold - go 40 above the HL so it is way above the threshold and you can compensate for the attenuation

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55
Q

when should you perform head and neck exam

A

om

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56
Q

what is a rising configuration?

A

abnormal lf and rising to normal or close to normal hf hearing

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57
Q

what is a sloping configuration?

A

normal to near normal lf and hf abnormal hearing

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58
Q

what is needed for diagnosis of AOM

A

can follow URT infection
fever
otalgia
temporary HL
otorrhea
associated systemic symptoms - nausea, general malaise (feeling unwell), lack of appetite

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59
Q

what is needed for diagnosis of chronic OM

A

can be asymptomatic
may have HL
may report “plugged” or “popping” feeling of ears

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60
Q

societal complications of OME

A

$$$, OM is most common visits to the Dr., time off from work & school (lost productivity), development of drug-resistance bacteria, tympanostomy tube placement (2nd most common surgical procedure in kids)

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61
Q

comlications of OME

A

infection of mastoid bone, ossicle erosion, HF SNHL, facial nerve paralysis (rare), meningitis, brain abscess

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62
Q

sequelae of OM

A

permanent/temporary CHL,
damage to ME structures- leads to ossicular destruction & CHL , common with “glue ear”
cholesteatoma - happens with chronic or untreated OME or chronic - ME pressure
HF SNHL - innear ear structures become affected by toxins entering through the round window into the inner ear resulting in permanent SNHL
higher order auditory fxns

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63
Q

long term sequelae of oM

A

attention deficit in adulthood - learned inattention, s/l delays, academic failure, behavior problems, CAPD

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64
Q

structural changes of OME

A

altered ABR after OME resolution, larger tymp width, shallow static admittance, elevated ARTs

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65
Q

what higher auditory functions are affected in OM

A

auditory deprivations- affects language development
learned inattention
hard to process binaural auditory
issues w/ speech sound discrimination - ta vs da
issues with stops - b vs p

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66
Q

Another name for cholesteatoma?

A

pseudotumor

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67
Q

why are cholesteatomas called pseudotumors

A

highly aggressive & erosive and have tumor like characteristics by destructing bone & tissue

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68
Q

how do cholesteatomas grow

A

form keratinized epithelial layer & fibrous subepithelial layer called a matrix
keratin creates keratoma
keratoma creates inflammation that leads to formation of cholesteatomas

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69
Q

what is the etiology of cholesteatomas

A

congenital & acquired

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70
Q

congenital cholesteatomas

A

present in kids around 5 yrs
usually male
common in anterior-superior quadrant

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71
Q

acquired cholesteatomas

A

more common
chronic/untreated OME or trama leads to this
slow growing & no initial symptoms
presents with HL first

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72
Q

what leads to iatrogenic cholesteatomas

A

blunt knife, surgery procedures

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73
Q

what does iatrogenic cholesteatoma lead to

A

implantation of squamous epithelium in mE

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74
Q

what would otoscopy show for cholesteatomax

A

normal or a perf

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75
Q

what would tymps show for cholesteatoma

A

any type depending on size, location & what is damaged
normal = no damage
type as = stiffness in cavity
type ad = ossicular disarticuation
type b lv = tm perf or filled me
type b hv = tm perf and me not filled

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76
Q

what type of tymp would you see with cholesteatomas

A

depends on size, location & how much it has damaged

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77
Q

what would pure tones show

A

normal
CHL w/ ossicular disarticulation
mixed

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78
Q

hos does perf lead to different HLs

A

depending on how much the ™ is affected, gives you different hl

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79
Q

diagnosis of a cholesteatoma (not from audio)

A

can be visualized on microscopic exam

CT is used to identify damage that is caused

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80
Q

what is the management for cholesteatomas

A

primary = surgical removal

can use antibiotic steroid drops to limit inflammation and bleeding during surgery

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81
Q

surgical results for management of cholesteatomas

A

HL due to ossicles & tm removal

prosthesis laced and tm reconstructed

mastoidectomy if mastoiditis occurred

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82
Q

complications of surgery

A

HL (permanent CHL, mixed or SNHL)

facial paralysis

dizziness

tinnitus

intracranial complications (meningitis or intracranial abscess)

recurrence of it after surgery

83
Q

what are implications as audiologists working as surgical ear

A

the second bend is widened (can cause blow by)
if you don’t have a ™, earmold impression can adhere to the ossicles
PACK THE CANAL

84
Q

normal audio to mixed hl DEPENDING on where it is and stage you pick it up
same with tymp

A

cholesteatoma

85
Q

what is the configuration of otosclerosis

A

rising, can have carhart’s notch (bone dip at 2000 Hz reducing or losing ABG)

86
Q

what can carhart’s notch also be present in

A

osteogenesis imperfecta & ossicular fixation

87
Q

what is otosclerosis

A

specific to stapes footplate to oval window, disease of remodeling of otic capsule

88
Q

Fixation of other ossicles to each other is NOT otosclerosis, instead it is called

A

ossicular ossification

89
Q

fixation occurs at the

A

fissula ante fenestram (anterior to oval window and stapes fixation)

90
Q

full footplate involvement =

A

flat CHL

91
Q

can audio testing differentiate bw otosclerosis & obliterated otosclerosis

A

NO

92
Q

laying down new bone while also absorbing old bone - to make a spongy bone

A

pathogenesis

93
Q

sites of OTSC

A

obliterated in round window

cochlear

histologic

94
Q

cochlear site of OTSC

A

causes progressive irreversible SNHL

95
Q

genetic etiology of otosclerosis

A

unclear, presents as AD
incomplete penetrance
varying degree of expressivity

96
Q

recent hypothesis of OTSC

A

may be related to persistent measles virus infection in the otic capsule

97
Q

some cases of OTSC come from expression of

A

COL1A1 gene

98
Q

COL1A1 gene is also associatef with

A

osteogenesis imperfecta type 1

99
Q

approx. 50% of PT w/ type 1 develop HL indistinguishable from OTSC

A

true

100
Q

can OTSC have blue sclera?

A

yes

101
Q

histopathology of temporal bones is identical in both

A

osteo & OTSC

102
Q

how are osteogenesis imperfecta type 1 & OTSC similar

A

AD, same audio findings, same temporal bone histopathology, & some blue sclera

103
Q

what population is most affected by OTSC

A

white young females bw 15-45 yrs

104
Q

are most OTSC unilateral

A

no 70% bilateral

105
Q

in 50% of females, HL occurs during/immediately after pregnancy

A

OTSC

106
Q

what does otoscopy reveal in OTSC

A

almost always normal tm

schwartze sign

107
Q

what is schwartze sign we see in OTSC

A

increased vascularity of bone growing near oval window

reddish/blue glow of the TM

108
Q

pure tone results of OTSC

A

early stage = normal or mild CHL w/ rising configuration

mid stage: conductive/mixed HL w/ rising or flat configuration

late stage: flattening of previous rising HL

109
Q

if OTSC is purely conductive will it exceed 60-65 dB HL

A

NO

max CHL

110
Q

what does bone conduction show in OTSC

A

poor at 2 kHz by 15-20 dB that narrows the ABG

carhart’s notch

111
Q

only present in <40% of PT’s

A

OTSC

112
Q

OTSC is the only ME condition with NORMAL TYMPS

A

TRUE

113
Q

What does tymp show for OTSC

A

type a or as

114
Q

ART in OTSC

A

abnormal in most
negative tone decay

115
Q

speech audio results in OTSC

A

SRT in agreement with PTA
WRS excellent due to suprathreshold testing

116
Q

what are the diagnostic features of OTSC

A

audio: bilateral conductive/mixed rising hl, tiniitus
case history
high resolution CT scan

117
Q

bigger ABG = better prognosis with surgery

A

true

118
Q

what is non surgical management of OTSC

A

amplification

119
Q

why do they do well with amp

A

becuase it provides enough amp to get through the ME system for understanding

120
Q

Who would surgery not be an option for? they want it but they cannot?

A

older - 70-80’s, you do not recover as quickly and have other medical issues and may have chronic issues with age
health - dead ear on the opposite side, if you have significant autoimmune conditions, if you already have a chronic infection etc.

121
Q

what is looked at pre op for OTSC

A

bone conduction
conductive compoment at least 25 dB bw 250-1000
- Rinne test at 512

122
Q

describe the rinne test

A

fork is placed at EAC and when PT cannot her it, moved to mastoid
if tone is heard longer at bone = -, CHL or mixed because bone is better than ear
if tone is heard longer at ear = + suggesting NH or SNHL

123
Q

how does surgery work with bilateral OTSC

A

poorer ear goes first
second is done a year later if other ear is stable

124
Q

what are contraindications of surgery for OTSC

A

dead contra ear
active OE/OM or TM perf
large exostosis that affects ME access

125
Q

ABSOLUTE contraindication of surgery in OTSC

A

OTSC involves the endolymphatic duct resulting in symptoms of Meniere’s disease

126
Q

what would be careful considerations prior to surgery

A

PT w/ vestib function that is important for employment

otologic issues in contra ear threatening hearing over time

SSCD

127
Q

what is a stapedotomy

A

small hole in stapes footplate during surgery

30-45 min surgery failure rate 1-3%

128
Q

partial stapedectomy

A

half removal of stapes footplate during surgery

129
Q

total stapedectomy

A

total removal of stapes footplate during surgery

130
Q

stapedotomy vs ectomy

A

otomy = laser making hole
ectomy = footplate removal

131
Q

replacement of footplate

A

Prosthesis or implant used in stapes surgery

132
Q

are current prosthesis safe in low power Mri

A

yes, in 1.5 tesla

133
Q

what are complications of OTSC surgery

A

WRS can worsen w/ cochlear involvement

oval window OTSC

round window OTSC

hyperacusis

facial paralysis

chorda tympani nerve

perilymphatic fistula

labyrinthitis

disarticulation of incus

SNHL

immediate CHL

delayed - onset CHL

134
Q

obliterates the oval window and can’t be easily managed or removed with a laser
surgery takes longer and may be difficult to assess length of prosthesis needed

A

oval window otsc

135
Q

can cause permanent CHL
surgical removal of this type universally results in SNHL and shouldn’t be attempted
usually fix with amplification

A

round window OTSC

136
Q

increases sensitivity to sounds; usually temporary

A

hyperacusis

137
Q

due ot VII damage during surgery - rare
surgery may be stopped with CN VII is completely filling oval window niche

A

facial paralysis

138
Q

may be sacrificed
branch of VII N to anterior ⅔ of tongue
temporarily decreased taste/sensation for 3-6 mos until compensation of opposite nerve and other nerves take over

A

chorda tympani nerve

139
Q

what is a perilymphatic fistula

A

pathological communication bw inner and me

140
Q

differential diagnosis for otsc

A

menier’s
osteogenesis imperfecta
SSCD

141
Q

Menier’s symptoms related to otsc

A

vertigo
tinnitus
lf hl - SNHL in menier’s

142
Q

osteogenesis imperfecta symptoms related to otsc

A

blue sclera, noise notch, fragile bones, collagen gene

143
Q

SSCD symptoms related to OTSC

A

3rd window
LFCHL but SSD has normal ART and not in otsc
distinguished bw two by CT scan

144
Q

if you get ARTs that are normal -

A

NOT OTOSCLEROSIS
probably SSCD

145
Q

malfunction of prosthesis
failure to see malleus fixation
round window obliteration

A

immediate CHL

146
Q

what causes labyrinthitis

A

air or blood entering vestibule
mechanical trauma to utricle because it lies close to the oval window

147
Q

what is etiology of trauma

A

blows, sports, blasts, vehicle accidents, foreign body insertion

148
Q

trauma with fracture classifications

A

longitudinal, transverse pediatric and penetrating temporal bone trauma

149
Q

otic capsule sparing fracture

A

longitudinal fracture

150
Q

otic capsule disrupting fracture

A

transverse fracture

151
Q

70-90%, parallels long axis passing through EAC, ™ & roof of ME

A

longitudinal fracture

152
Q

what is a longitudinal fracture

A

70-90%, parallels long axis passing through EAC, ™ & roof of ME

153
Q

less common
goes through IAC or otic capsule

A

transverse fraction

154
Q

what is a transverse fraction

A

less common
goes through IAC or otic capsule

155
Q

what is pediatric trauma

A

from falls from heights
automobile/pedestrian accidents

156
Q

what are penetrating temporal bone trauma

A

most common are gushot sounds (50% of time injures cn 7)

157
Q

trauma without fraction classification

A

otic barotrauma
inner ear decompression sickness (IEDCS)
thermal injuries
compressive injuries
foreign objects

158
Q

what is otic barotrauma

A

occurs during descent or short shallow dive
injury that happens from failure to equalize pressure
causes sudden & severe - ME pressure

159
Q

waht is inner ear decompression sickness (IEDCS)

A

occurs during ascent or surfacing from dive
treatment is different but resembles IE barotrauma
HL & tinnitius & dizziness

160
Q

what PT should rapidly get transported to a hyperbaric chamber for recompression

A

IEDCS

161
Q

what are thermal injuries

A

lighting bolt conduction
during welding leadimg to TM perf

162
Q

symptoms of thermal injury

A

SNHL
dizziness/vertigo
facial paralysis

163
Q

compressive injuries

A

slap or struck on head
falling on water
blast injuries

164
Q

blast inuries lead to

A

HF SNHL

165
Q

foreign objects

A

occurs when PT removes cerumen
HL & vertigo
lacerations, infections, hematomas

166
Q

what conditions can we see ossicular disarticulation

A

osteoporosis or cholesteatoma or untreated ME infection

167
Q

can trauma to head or face cause ossicular disarticulation

A

yes

168
Q

common signs of ossicular disarticulation on otoscopy

A

bleeding from ears, csf, perf

169
Q

immittance results for ossicular disarticulatiomn

A

AD tymps
abnormal reflexes because ossicles aren’t together to make sound pressure needed

170
Q

pure tone results for ossicular disarticulation

A

conductive/mixed HL
can be acute or delayed

171
Q

signs & symptoms of disarticulation

A

acute/delayed chl
injured tm
me blood or csf
bleeding from ears
bppv, concussions, perilymphatic leak

172
Q

what should be done for diagnosis of ossicular disarticulatioin

A

ct scan

173
Q

what is normal appearance of ossicles on axial CT

A

ice cream cone sign

174
Q

ball of ice cream

A

malleus head

175
Q

cone

A

body of incus

176
Q

point of cone

A

short process ofincus

177
Q

failure of ice cream configuration on ct

A

suggests ossicular chain disruption (incudomalleolar disarticulation)

178
Q

treatment for hemotympanum

A

self healing

179
Q

persistent chl treatment

A

repair ossicles or amplification if surgery not possible

180
Q

BPPV treatment

A

self healing in 6 mos or epley maneuver

181
Q

irreversible snhl & tinnitus treatment

A

ha’s & tinnitus management

182
Q

which me tumor grows largest

A

glomus jugulare because there is more space for it to grow

183
Q

another name for glomus tumors?

A

paragangliomas becuase it comes from paraganglia

184
Q

most common benign soft tissue tumor of ME & second most common benign tumor of temporal bone

A

paragangliomas

185
Q

describe glomus tympanicum

A

arises from Jacobson nerve in tympanic cavity
neuroendocrine cells give rise to these
smaller
can surgically remove
early symptoms are pulsatile tinnitus, red tm & chl

186
Q

describe glomus jugulare

A

arises from dome of internal jugular vein & is under pinna on the neck
common & more extensive with space to grow
can be silent for a long time, damage 7 &11 and grow into me cavity

187
Q

usually unilateral, reddish-purple, highly vasculated & lobulated

A

glomus tumors

188
Q

both slow progressive growth through least resistance paths

A

true (temporal bone air cells & ET

189
Q

why are glomus tumors incorrectly named

A

because they originally thought they came from true glomus complexes

190
Q

heredity of tumors

A

sporadic or AD w/ 100% penetrance

191
Q

who is more affected with tumors with sporadic heredity

A

females

192
Q

most tumors affect

A

male and female equally and can be seen in NF1

193
Q

which may have genomic imprinting involved

A

glomus tumors

194
Q

what is genomic imprinting

A

when the phenotype varies depending on who passes the gene down

195
Q

who passes the glomus tumors down

A

father

196
Q

will female offspring have phenotypic expression

A

usually not until transmission is through a male carrier

197
Q

what is the incidence of glomus tumors

A

after 5th decade, mostly sporadic, 1/3 to 1/2 associated with NF1, 10 genes linked

198
Q

adrenal gland tumor & causes hormonal problems)

A

pheochromocytoma

199
Q

signs of glomus tympanicum

A

smaller & cause early symptoms
pulsatile tinnitus, red tm, chl
if grows medially causes SNHL FN dysfunction or vertigo

200
Q

symptoms of glomus jugulare

A

remaines silent for years and grows large
HL
otalgia
aural fullness
vertigo

201
Q

if you get a pulsating tymp what should you suspect

A

glomus tumor

202
Q

audio findings of glomus tumors

A

red tm or mass in me cavity
chl or mixed
type as or b tymps that show jagged edges w/ PT’s pulse

203
Q

treatment for glomus tympanicum

A

tumor remoal

204
Q

treatment for glomus jugulare

A

need MRI for definitive diagnosis
surgery/radiation to shrink before removal

AUDE 5410 Aud-Vestib Disorders (18 decks)

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