Quiz 2 (Inner Ear) Flashcards

1
Q

bring about transduction mechanism and allows nerves to integrate the signal

A

ihc

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2
Q

which ion channels are disrupted in connexins

A

potassium

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3
Q

what is inner ear homeostasis

A

chemical equilibrium of the IE fluids for proper functions

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4
Q

inner ear functions include

A

hair cell fxn
regulation of extracellular endo and perilymph
conduction of nerve impulses

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5
Q

major ions

A

sodium
potassium
chloride
calcium

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6
Q

Ion movement is controlled by genes, channels, and water

A

true

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7
Q

help maximize sensitivity of hair cells
metabolic support behind hearing

A

endo and perilymph

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8
Q

describe the inner ear endocochlear potential

A

intracellular potential is -80mv and high potassium in the endolymph creates + 80mV EP so this creates a 160mV differential potential

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9
Q

what is the differential potential needed for

A

to cause hair cell shearing and electrical signaling

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10
Q

EP in the vestib system is only

A

5-10mV

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11
Q

EP is higher where

A

in cochlea than vestibular system
at basilar end than apical

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12
Q

what happens after shearing of stereocilia

A

stereocilia are displaced by motion of IHC or shearing of OHC
both rush potassium into the cell

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13
Q

what happens when peri and endo fluids are the same

A

causes reduced transduction resulting in Meniere’s disease (mixing of both)

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14
Q

Stria vascularis generates

A

potassium and has connexin gap junctions that facilitate potassium transport

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15
Q

The junctions are tight and contribute to the endocochlear potential because

A

they limit intracellular leakage of ions

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16
Q

gap junction

A

for potassium

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17
Q

tight juction

A

for blood/vascular cells

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18
Q

why is stria susceptible to many genetic disorders

A

becuase it is controlled by connexin gap junctions that faciliate K+ transport

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19
Q

cochlear disorders that disrupt stria, channels, transporters, gap or tigh junctions reduce

A

EP and result in HL

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20
Q

A gap junction or nexus is a specialized intercellular connection that

A

directly connects two cells allowing molecules and ions to pass freely between the two

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21
Q

what are aquaporins

A

proteins that regulate the flow of water
play a role in water homeostasis
blood-brain barriers and blood-labyrinthine barrier
an cause viral infections if damaged

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22
Q

Increased K+ transport in the endolymph or increased endolymph production

A

endolymphatic hydrops (too much endolymph - Meneire’s - progressive fluctuating snhl)

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23
Q

Decreased K+ transport in the endolymph or decreased endolymph production

A

endolymphatic xerosis (connexin, JLNS - permanent snhl)

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24
Q

causes the most genetic HL in humans

A

endolymphatic xerosis

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25
Q

abnormal connexin gap junctions, over 50% nonsyndromic HL

A

connexin 26

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26
Q

protein that makes K+ channels, responsible for reduced endolymph in HL with JLNS syndrome

A

KCNE1 & KCNQ1

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27
Q

which condition are KCNE1 KCNQ1?

A

jlns

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28
Q

DFNA

A

Deafness, Nonsyndromic, Autosomal Dominant

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29
Q

DFNB

A

Deafness, Nonsyndromic,Neurosensory, Autosomal Recessive

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30
Q

DFNX

A

Nonsyndromic deafness, X-linked

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31
Q

temporary disorders of ion homeostasis

A

sudden hl onset
diuretic ototoxicity
autoimmune labyrinthitis
Meniere’s disease

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32
Q

what indicates HL as homeostatic issue and not hair cells

A

these disorders manifest temporary hearing loss and recovery indicates that the damage is not to the hair cells but to the ion homeostatic process

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33
Q

symptoms of cochlear disorders

A

constant or fluctuating HL
almost always SNHL (can have mixed)
speech perception issues
loudness recruitment
aural fullness
tinnitus
conditions paired with psychological issues

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34
Q

hyperacusis

A

hurts when sound is too loud

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35
Q

misophonia

A

intense emotional feeling towards specific sounds

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36
Q

noise sensitivity

A

reaction to discomforting sounds
doesn’t have to be loud

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37
Q

phonophobia

A

fear of sound
makes tinnitus worse

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38
Q

common causes of SNHL

A

presbycusis
exposure to toxic levels of noise (noise induced HL

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39
Q

what causes inner ear infections

A

mostly viruses
some bacterial (meningitis)

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40
Q

two kinds of viruses known

A

RNA virus (covid & flu)
DNA

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41
Q

what is RNA virus

A

contain rna in their genome, mutate quickly due to lack of proofreading making it difficult to treat

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42
Q

what is dna virus

A

these contain dna in their genome and are more stable
smallpox, herpes, chickenpox

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43
Q

what is an example of rna virus

A

rubella & paramyxovirus

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44
Q

what is rubella virus

A

rna virus
responsible for german measles, effects A.S. if contracted by mom in first part of 2nd trimester when it is developing

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45
Q

rubella virus leads to

A

congenital HL, cataracts, cardiovascular cataracts, maybe intellectual disability

46
Q

what is paramyxovirus

A

rna virus
responsible for mumps & causes male infertility

47
Q

paramyxovirus leads to

A

parotid gland inflammation causes acquired unilateral SNHL

48
Q

example of DNA virus

A

cytomegalovirus CMV

49
Q

what is CMV

A

herpes family, most common viral disease in humans
50-80% US people have the antibodies by their 40’s
Decreased life expectancy, large liver and spleen, a “blueberry muffin” rash, and decreased immunity to fight off other diseases
Has the MOST GENES of any virus

50
Q

most common newborn virus

A

CMV

51
Q

if mom has CMV, what should they do

A

not breastfeed for first 3 weeks to avoidpassing it on

52
Q

audio findings of cmv

A

progressive profound permanent SNHL by 3-5 yrs
kids are ci candidates

53
Q

why are cmv newborns hearing unetected

A

it can be late onset or we are not screening for it

54
Q

problems cmv causes

A

neurological deficits, blindness, ID, and cardiovascular problems

55
Q

how is cmv diagnosied

A

GOLD STANDARD IS URINE POLYMERASE CHAIN DNA

can also do histological exam of inclusion bodies in saliva and lungs

CT to show intracranial calcification

56
Q

are inclusion bodies specifc to cmv

A

NO shown in many viruses

57
Q

Viral infections are destructive and causes

A

Damage to the basal turn of the cochlea (high freq SNHL)
Hair cell damage
Stria vascularis atrophy
Tectorial membrane rolls up
Reissner’s membrane collapses

58
Q

high frequencies and pure tones cause more damage than low frequencies and WBN

A

true

59
Q

what is meningitis

A

inflammation of the meninges of the brain and spinal cordwha

60
Q

etiology of meningitis

A

virus & bacteria

61
Q

primary meningitis

A

originates in meninges

62
Q

secondary meningitis

A

originates outside of the meninges and travels to them (ex: cholesteatoma or OME → mastoiditis)

63
Q

signs and symptoms of meningitis

A

Initially: high fever, neck stiffness, malaise, nausea, vomiting
Untreated: blindness, paralysis, hearing loss/deafness (causes acquired SNHL), and vertigo/off balance

64
Q

treatment for meningitis

A

antibiotics (do a spinal tap to see which one to give), mastoidectomy (if related to the ME), amplification/CI (ensure cochlea isn’t overgrown with bone, and that there is enough space to put a CI)

65
Q

what is a perilymphatic fistula

A

ME and IE have a connection to each other when normally they are self contained at either or both oval and round windows

66
Q

etiologies of perilym fistula

A

idiopathic

feeling ear “pop” after heavy lifting

randomly found during Meniere’s surgery or stapedectomy

67
Q

symptoms of perilym fistula

A

vertigo without HL
HL without vertigo
symptoms that cannot be determined from Meniere’s (SNHL, vertigo, tinnitus, aural fullness)
not episodic vertigo but disequilibrium with miscellaneous symptoms

68
Q

how to determine perilym fistula

A

presentation of complex symptoms
case history, symptoms they present with and can have different presentations of symptoms
high index of clinical suspicion
dix hallpike to see nystagmus or vertigo

69
Q

treatment of fistula

A

no heavy lifting
me exploration
surgery to seal leak

70
Q

what can happen after repair of fistula

A

preserve hearing that is left
resolve balance issues
improve tinnitus

71
Q

what is noise induced hearing loss (NIHL)

A

Hearing loss as a result of harmful noise exposure (dose/level and duration/time dependent)

72
Q

dose

A

leveld

73
Q

duration

A

time

74
Q

has most weight for human hearing

A

.5-8kHz

75
Q

noise notch bw 3-6000 Hz (peak bw 4 & 6kHz)
due to cochlea geometry & blood supply

A

NIHL

76
Q

what hearing sensitivity change will we see with NIHL

A

max damage is ½ an octave above stimulating frequency (ex: stimulating at 1 kHz but HL at 1.5 kHz)

77
Q

temporary threshold shift

A

reversible shift that can resolve 15 mins after exposure or persists up to 14 hours

produced by initial noise exposure
dull or muffled sound quality (at end of work shift or loud concert)

even if TTS shift comes back to baseline, can result in hidden hearing loss where there is no change in hearing but there is residual issues

78
Q

permenant threshold shift (PTS)

A

persistent change in sensitivity, persists after approx. 14 hrs

noise is bad and long enough that it doesn’t go back to baseline
if at 125 dB it is permanent

79
Q

Both accompanied by tinnitus (can be a useful warning if you get it after a temporary shift)

A

true

80
Q

Initial noise exposure produces TTS, but a daily dose of noise exposure that DOESN’T cause TTS WILL NOT cause PTS

A

true

81
Q

effects on me and noise

A

rare

82
Q

™ perf after blast =

A

possible concussion

83
Q

, >/= 165 dB SPL can cause

A

™ perf,

84
Q

> /= 190 dB SPL can cause

A

ossicular chain injury

85
Q

inner ear and noise

A

can result in tinnitus and oHC damage

stereocilia first lose stiffness (TTS) and after repeated damage becomes permanent (PTS)

86
Q

more intense & prolonged loud sounds =

A

greater degree of hair cell loss

87
Q

can noise cause NIHL vestib issues

A

doubtful BUT ACOUSTIC TRAUMA CAN

88
Q

COCHLEA MORE SUSCEPTIBLE TO NOISE LOSS, ME depending on loudness level

A

TRUE

89
Q

how to diagnose NIHL

A

clinical hx & audio data showing SNHL
medical exam to rule out other causes of HL

90
Q

audio configuration

A

usually symmetrical but asymmetries >/= 15 dB HL not uncommon(usually in HF - 3 to 6 kHz, with firearm use)

profound SNHL rare, LF thresholds better than 40 dB HL, HF thresholds rarely better than 75 dB HL

presbycusis can flatten noise notch

91
Q

notch flattens when noise induced meets presbycusis

A

true

92
Q

management of NIHL

A

no effective treatment
PREVENTION IS BEST MANAGEMENT
use of appropriate amplification w/ permanent HL
use of antioxidants & other chemicals that protect against NIHL (being investigated)

93
Q

what is acoustic trauma

A

form of NIHL that is a sudden, permanent HL as a result of a single event (NO TTS)

Caused by impulse noise of 165-190 dB SPL that causes direct mechanical damage to the cochlea (can also rupture the eardrum)

94
Q

Impulse noise over 140dB SPL can also cause PTS immediately

A

true

95
Q

sound intensity bw 165 to 190 dB SPL

A

ruptures or produces ™ hemorrhage
disrupt/fracture ossicular chain

96
Q

otoscopy on acoustic trauma

A

tm perf or hemorrhage

97
Q

audio results for acoustic trauma

A

similar to NIHL
noise notch at 3 & 6 kHz
HF sloping configuration
flat configuration (more common)
mixed HL = if ossicular disarticulation has occurred

98
Q

tymps of acoustic trauma

A

type Ad if ossicular disarticulation

99
Q

which parameter is abnormal in type Ad?

A

static admittance

100
Q

perf tymp?

A

type b with high ECV

101
Q

type b but not high volume?

A

peak pressure is not measured
admittance is not measured
just volume is measured

102
Q

art in acoustic trauma

A

absent if ossicular disruption

103
Q

HL may improve over 4-6 mo period if from acoustic trauma

A

true

104
Q

surgery could be used to repair ™ and ossicles if they are damaged in acoustic trauma

A

true

105
Q

why can we not replicate hair cells?

A

they are in G0 phase that stops the cell cycle
when you take it out it messes with the cycle and causes tumors throughout the body

*have to find a way to counterbalance this before regenerating hair cells

106
Q

what are blast injuries

A

type of acoustic trauma
caused by indirect impact from pressure wave created from an explosion

107
Q

blast injuries are more dangerous why

A

when bomb goes off, pressure wave causes damage
so much heat and pressure when it goes off

108
Q

damage as result of blast injury

A

™ perf, ossicular disarticulation, tinnitus, otalgia, HL and/or vertigo

109
Q

why is otologic usually initially missed

A

this is because high priority is for life threatening injuries

110
Q
A