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9530 > w10 &11 > Flashcards

w10 &11 Flashcards

1
Q

Presbycusis prevalence

A

30-35% adults 65-75 40-50% those over 75

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2
Q

what is presbycusis

A

Hearing loss associated with the degenerative effects of aging

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3
Q

components of presbycusis

A

Peripheral components (cochlear and neural)
o Central components affecting CANS function
o Word recognition (worse relative to PT audiogram and worse compared to younger patients

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4
Q

presbycusis Etiology & pathology

A
  • Presbycusis specific genes yet to be identified in humans
  • Multifactorial condition involving age, ototoxic/noise and disease related factors over lifespan
    Environmental: health status (e.g., cholesterol, BP, heart disease), history of noise & ototoxic chemical exposure, lifestyle (stress, diet, exercise, smoking)
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5
Q

presbycusis Medical assessment

A
  • Physical exam & case history
  • Exclusion of other etiology’s if indicated by history or patient (retrocochlear pathologies, other medically managed disorders)
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6
Q

presbycusis audiology assessment

A

Should include speech in noise testing
- Standard (Otoscopy, tymps, OAEs, audiometry, reflexes)
- APD assessment (particularly if sig. complaints relative to PT audiogram)
- Impact on QOL *standardized assessment tools

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7
Q

Presbycusis categories by Schuknecht et al

A

Based on underlying pathophysiology and histopathological study of human temporal bone
6 different categories
4 main: sensory, neural, strial (metabolic), cochlear conductive
2 additional: mixed, indeterminate

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8
Q

Sensory presbycusis

A

Audiological: bilateral sloping high freq SNHL, speech discrimination generally good
Histopathology: degeneration of basal cochlea, IHC and OHC, OHC loss predominant, loss of supporting cells, leads to degeneration of organ of corti

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9
Q

Neural presbycusis

A

Audiological: bilateral SNHL, flat-gradual sloping audiogram, steeply sloping also possible, poor speech discrimination
Histopathology: loss of spiral ganglion cells in all 3 cochlear turns, relative preservation of organ of corti, neuronal loss greater than expected based on status of organ of corti

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10
Q

Metabolic (strial) presbycusis

A

Audiological: slow progressive bilateral SNHL, flat to gradually sloping, good speech rec.
Histopathology: atrophy of stria vascularis, pattern of degeneration can vary (patchy & more severe in middle and apical turns, diffuse throughout cochlea), sometimes associated with cyst formation, familial component identified (likely genetic)

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11
Q

Cochlear conductive presbycusis

A

Audiological findings: bilateral SNHL, gradually sloping high freq HL, good speech descrim.
Histopathology: hair cell and neural loss minimal, proposed (not observed): altered thickness and stiffness of BM, presumed effect: altered mechanical properties of BM

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12
Q

mixed presbycusis

A
  • 2 or more of the classical types of presbycusis
  • Varied audiometric findings
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13
Q

Revised conclusions about presbycusic pathology from Schuknecht et al

A
  1. Atrophy of stria vascularis common
  2. Neuronal loss common
  3. Sensory cell loss common
    Cochlear conductive removed bc no anatomical evidence to support this pathology
    Indeterminate added.
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14
Q

Prevailing dogma 1993-2020

A

Stria/metabolic and neural presbycusis predominant lesion in aging cochlea
Pure age-related HL due to degeneration of lateral wall
- Lateral wall cells degenerate (stria vascularis, spiral ligament)
- Critical structure for supporting basic physiology of cochlea
Primary degeneration of auditory nerve as indicated by loss and shrinkage of spiral ganglion

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15
Q

Neural presbycusis

A

supported by subsequent research in human temporal bone
- Annual decline of around 100 spiral ganglion cell bodies
- Human temporal bones @50-60 years 250-4000Hz remained normal, loss of 20% spiral ganglion cells over entire cochlear partition

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16
Q

T/F Damage in stria vascularis does not cause damage

A

true
No evidence to show a metabolic component
SV does not affect hearing loss

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17
Q

Central presbycusis

A
  • Age related changes in brain include CANS
  • Deprivation induced brain plasticity peripheral damage may exacerbate central dysfunction
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18
Q

Auditory periphery:

A
  • Sensitivity loss
  • Spectral processing disrupted
  • Reduced speech in noise perception
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19
Q

CANS

A
  • Decreased temporal & frequency resolution
  • Decreased inter-hemispheric communication/binaural integration
  • Reduced speech in noise perception
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20
Q

Cognitive changes

A
  • Speed of information processing slows
  • Working memory poorer
  • Attentional difficulties (noise, distraction, executive control)
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21
Q

statistics risk of HL and dementia

A

Hearing impairment independently associated with 30-30% acceleration in cognitive decline
Over 10 year period:
Mild hearing impairment increases risk of dementia by twofold
Moderate hearing impairment increases risk of dementia by threefold
Severe hearing impairment increases risk of dementia fivefold

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22
Q

Potential mechanisms of presbycusis

A
  1. Common causes
  2. Cascade hypotheses
  3. Cognitive load
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23
Q

Audiological management of presbycusis

A
  • Aural rehab
  • Hearing technologies (ALD, CI, HA)
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24
Q

Endolymphatic Hydrops

A

any causes for build-up of fluid
Menier’s disease is endolymphatic hydrops but not all endolymphatic hydrops is Menier’s

25
Q

inner ear homeostasis

A

equilibrium between vestibule, cochlea and endolymphatic sac

26
Q

cochlear homeostasis

A
  • Tight control of ion movement & fluid volume across cell membranes of membranous labyrinth
  • Ion homeostasis depends on complex transport systems
  • Regulation of cochlear endolymph & perilymph electrolyte composition critical for:
    o Maintenance of endoccochlear potential
    o Hair cell and nerve function
  • Stria vascularis & spiral ligament (specialized molecules, cells and tissues)
  • Ion regulation: numerous ion channels and transporters in the plasma membranes of cells lining scala media
27
Q

Cochlear homeostasis: Ion regulation

A
  • Epithelial complex:
    o Spiral ligament: fibrocytes
    o Stria vascularis: basal and intermediate cells, stria capillary cells
  • Molecules:
    o Gap junctions: facilitate transport of K+ between cells and into the intrastrial space
    o tight junctions: limit intercellular leakage of ions
    o ion exchange: specialized ion channels and Na+ K+ ATPase system
    o numerous genes regulate their expression
28
Q

Reissner’s Membrane

A

Job to separate perilymph from endolymph
If rupture lose ion homeostasis and development of clinical hearing loss and symptoms like vestibular issues

29
Q

Endolymph Duct system (EDS)

A

cochlea and vestibular organs contain separate compartments filled with endolymph fluid
- interconnected by narrow channels forming an endolymphatic duct system
o cochlea linked to the vestibular system via the reunion duct
o saccule to the ED via the saccular duct
o utricle to the ED via the utricular duct

30
Q

Inner ear homeostasis: aquaporins

A
  • Active water transport involves aquaporin channels in cells of membranous labyrinth
  • Hearing loss resulting from aquaporin dysfunction (knockout of AQP4 leads to HL)
31
Q

Site of lesion endolymphatic hydrops

A

Site of lesion: cochlear and vestibular membranous labyrinths
- Condition involves distortion/ruptures of membranous labyrinth

32
Q

EH pathology

A
  • Regulation of endolymphatic fluid homeostasis disturbed
  • Underlying mechanisms (mostly unknown)
  • Leads to: excess endolymphatic volume & distension= hydropic state
  • altered endolymph composition
  • Underlying mechanisms, altered endolymph and/or hydropic condition>cascade of additional problems
  • Causes poorly understood, likely that various mechanisms lead to:
    o Overproduction of endolymph
    o Under absorption of endolymph
    o Both of the above
33
Q

possible mechanisms & pathophysiology EH

A

Abnormal homeostasis (local regulation)
- Disruption of aquaporin channels>inappropriate fluid balances
- Disruption of ion channels & transporters can lead to inadequate ion transport>disrupt fluid volume
- Damage to other specialized molecules/cells/tissues lining the membranous labyrinth disrupt endolymph volume and composition (genetic mutations, infection)
- Inner ear environmental factors may contribute (inflammation, circulating hormones)

34
Q

Further consequences of EH

A

Altered cell biochemistry and/or excess volume trigger a cascade of additional problems:
- Disruption of ion transport > affects endolymph
- Ruptured membranes> affects endolymph
- Cochlear nerve degeneration possibly due to constant excitation at IHC-spiral ganglion synapse
o Glutamate excitotoxicity> degeneration of spiral ganglion cells

35
Q

EH Associated with different diseases or conditions:

A
  • Meniere’s disease
  • Infection
  • Trauma
  • Vascular etc.,
36
Q

Menier’s syndrome & disease:

A

vertigo & hearing loss in series of cases, due to inner ear rather than brain (pathophysiology and management remains controversial)

37
Q

Meniere’s Disease Idiopathic Endolymphatic Hydrops symptoms

A

intermittent attacks of vertigo, tinnitus, aural fullness or pressure, SNHL

38
Q

Meniere’s Disease Idiopathic Endolymphatic Hydrops etiology

A

Etiology: unknown (idiopathic), genetic predisposition in 2.6-12%, no causative genes identified

39
Q

Familial meniers disease:

A

autosomal dominant inheritance pattern (only need 1 copy of affected allele from mother or father, if inherit 60% chance of showing)

40
Q

Meniere’s Disease Idiopathic Endolymphatic Hydrops prevalence

A

4-15/ 100 000

41
Q

Meniere’s Disease Idiopathic Endolymphatic Hydrops sex distribution

A

Sex: 1.3 F to 1 M

42
Q

Meniere’s Disease Idiopathic Endolymphatic Hydrops Course of disease

A

Onset: 20-60 years,4th decade typical
Acute and quiescent phases
Unilateral diseases can progress to bilateral disease: in 33% cases (after 8 yrs) 50% (after 20 yrs)

43
Q

Symptoms amplified during acute episodes (Meniere’s Disease Idiopathic Endolymphatic Hydrops) :

A
  • Episodes often occur in “clusters”
  • Acute episode associated with vertigo
  • Increased HL and/or tinnitus
  • Aural fullness
  • Nausea & vomiting
44
Q

early stages of MD idiopathic endolymphatic hydrops

A

Rupture of membranes in endolymphatic system, hair cells generally intact

45
Q

late stages of MD idiopathic endolymphatic hydrops

A

Degeneration of hair cells and cochlear neurons (particularly in cochlear apex)
- Distortion rupture and/or atrophy of tectorial and reisseners membrane
- Herniation into scala tympani via helicotrema
- Atrophy of stria vascularis
- Abnormal tissue growth in cochlear duct and vestibule

46
Q

Biochemical disruption

A

altered biochemistry may affect transduction processes causing hearing threshold loss
- Perilymph & endolymph mix: toxicity damages cells & tissues

47
Q

medical assessment MD idiopathic endolymphatic hydrops

A

Clinical diagnosis (based on clinical features alone): can be a challenge for non-specialists, no definitive diagnostic test or procedure
Usually based on patient history & symptoms: careful documentation of symptoms is basis of diagnosis and categorization of MD

Radiographic imgaging and laboratory tests may be used to exclude other underlying causes of EH
- ABR/ MRI/ CT for differential diagnosis: rule out retrocochlear & other mass lesions etc

48
Q

audiologic assessment of MD idiopathic endolymphatic hydrops

A
  • To confirm SNHL, monitor fluctuating HL
    Glycerol test may be ordered: monitor hearing thresholds which are expected to improve with glycerol ingestion
    Physiological tests: electrocochleography SP/AP
    Vestibular assessment: ENG.VNG &VEMP
    PT audiometry: initially fluctuating, low freq SNHL, progress to flat moderate-severe to severe SNHL, progression to bilateral loss, vertiginous episodes cease (Enough damage occurring to vestibular organs that they become non-functioning- this is why they cease)
  • Speech testing: poor WRS relative to PT audiometry: If traditionally normal SNHL you would expect 90-100% WRS but for someone with Menier’s may get 70-80%
49
Q

Medical management
Goal: control symptoms, especially vertigo
what is treatment

A

varies - Acute vs dormant phase
- Severity and duration of symptoms
- Conservative approach used initially to control symptoms
- If disabling & chronic: ablation of vestibular end-organ
- No therapy can prevent progression of hearing deterioration

50
Q

Medical management: conservative

A

Goal: manage symptoms during acute phase (vertigo) using pharmacological approach: vestibular suppressants & antiemetics (nausea), steroids (reduce inflammation)

51
Q

When conservative options fail

A

Goal: manage chronic & disabling symptoms (vertigo)
Vestibular ablation: pharmacology
Vestibular treatment or ablation: surgical

52
Q

Vestibular ablation: pharmacology

A
  • Vestibulotoxic aminoglycosides
  • Oral (systemic & bilateral effect)
  • Intratympanic (higher does & ear specific)
53
Q

Vestibular treatment or ablation: surgical

A

Endolymphatic sac decompression
- Vestibular neurectomy- hearing preserved
- Transmastoid labyrinthectomy- drill away SCC

54
Q

Endolymphatic sac surgery: decompress or shunt

A

Goal is to decrease endolymphatic pressure
- Remove some of mastoid bone surrounding endolymphatic sac, drain or insert valve
- Lower risk surgery, hearing preserved, varying success rates in controlling vertigo and stabilizing hearing (up to 80% success reported)

55
Q

Vestibular neurectomy-

A

section of vestibular nerve removed, hearing preserved, prevents signals from vestibular nerve from stimulating the brain, neurosurgery has higher risk: anesthesia, CSF leak, facial nerve damage

56
Q

Labyrinthectomy

A

ablation of the vestibular end organ, destroys cochlea, hearing not preserved, appropriate for those with no useful hearing on diseased side

57
Q

Audiologic management early phase

A

fluctuating hearing sensitivity & poor speech recognition accompanied by episodic vertigo
- Amplification, ALD, aural rehab (communication strategies, tinnitus, vocational rehab)

58
Q

Audiologic management late phase

A

progressive HL and bilateral burnout of hearing sensitivity
- Severe HL with poor WRS bilaterally
- Cochlear implantation

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