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9530 > w7 > Flashcards

w7 Flashcards

1
Q

Cochleotoxic

A

: results in cochlear damage and CN VIII; auditory dysfunction

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2
Q

Vestibulotoxic

A

results in damage to vestibular end organs & CNVIII; vestibular dysfunction

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3
Q

ototoxic Symptoms

A

Tinnitus (typically)- constant, high pitch
SNHL (typically)- High freq with progression to mid/low freq (most agents); mid frequency (loop diuretics); difficulties understanding speech in noise
Vestibular dysfunction: disequilibrium, imbalance, vertigo & nystagmus
- may go unnoticed by patients until a communication problem becomes apparent

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4
Q

2 main classes responsible for permanent otoxic damage:

A
  1. aminoglycoside antibiotics
  2. antineoplastic (chemotherapeutic)- may be reversable initially
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5
Q

aminoglycoside antibiotics

A

resistant bacterial infections, induced vestibulotoxcity for relief of vestibulopathy

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6
Q

antineoplastic medications

A

tumor treatment

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7
Q

Diuretics

A

management of excess body fluid

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8
Q

Drug administration

A

Systemic application (bilateral effects): affecting whole body (i.e., intramuscular, intravenous, oral
Topical (unilateral affects): skin or mucous membrane application, apply drug to specific target
Cochlea (unilateral effects) Round window: drug applied to surface of round window
Direct perfusion: invasive procedure by injecting drug directly into perilymph or endolymph

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9
Q

Salicylates

A

pain, anti-inflammatory

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10
Q

ototoxic incidence

A

Incidence varies depends on definition of ototoxity, classification of medication & drug type (loop 1-6% and antineoplastic drug cisplatinum 25-90% , dosage schedule

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11
Q
  • ototoxic drugs can induce stress signals which initiate cell death occurring via 2 mechanisms (which interact)
A

necrosis and apoptosis

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12
Q

apoptosis HC death

A

apoptosis: active, programmed cell death, controlled process by which cells self-destruct
- no inflammation of neighbouring tissue

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13
Q

necrotic HC death

A

Necrosis: passive form of cell death, unregulated release of cellular debris into the intracellular space
- neighbouring phagocytes find difficulty in locating and eliminating cell by-products (immune response)

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14
Q

oxidative stress

A

when free radicals are floating around causing stress on cell until they find electron they are looking for; free radicals start to steal electrons from other cells

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15
Q

stress signalling in auditory haircell death

A
  1. Oxidative stress: occurs early in the damage process
    - Accumulation of intracellular free radicals in the form of reactive oxygen species (ROS) and reactive nitrogen species (RNS)
    - Oxidative stress results from an imbalance between ROS and antioxidants
    - Excess ROS and RNS cause damage by reacting with DNA, proteins, cytosolic molecules, cell surface receptors, and breaking down membrane lipids
  2. Expression of extracellular pro-inflammatory cytokines & other cell death signals
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16
Q

aminoglycosides

A

Damage is progressive affecting serval different cochlear structures with OHC most sensitive (then IHC then spiral ganglion, stria vascularis & support cells), base more sensitive than apex (progress from high to low frequencies)
- May be cochleotoxic or vetsibulotoxic or both
- Permanent SNHL
- Individual susceptibility may be inherited

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17
Q

cispaltin

A

used for cancer
- Highest ototoxic potential
- Earliest symptoms: tinnitus and high freq hearing loss
- Irreversible bilateral SNHL progress from high to low freq.
- OHC and stria vascularis most susceptible to damage
- Base more sensitive than apex
- Severe degeneration: support cells, collapse of Reisner’s membrane, eventual destruction of entire organ of corti replaced by epithelium

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18
Q

side effects of cisplatin

A

ototoxicity, nephrotoxicity, neuropathies, nausea, vomiting

19
Q

carboplatin

A

similar to cisplatin but incidence of SNHL lower, mixed OHC and IHC damage

20
Q

carboplatin chinchilla model

A

IHC most susceptible with sig. loss, ohc damage occurs with later progression (ONLY Found in chinchilla)

21
Q

loop diuretics

A

treat fluid volume overload
Ototoxicity low incidence of HL compared to aminoglycosides and antineoplastics
- Tinnitus, usually reversable SNHL, risk of permanent loss with cumulative dose
- Known to exacerbate aminoglycoside and cisplatin ototoxicity
Anatomical changes: stria vascularis: edema, damage/swelling of hair cells

22
Q

criteria for sig changes

A
  • > 20dB pue tone threshold at 1 freq
  • > 10dB shift at 2 consecutive test frequencies
  • > 5 db shift at 3 adjacent test freq.
  • If pre-existing profound loss: threshold shift to “no response” at 3 consecutive test frequencies
  • Confirmed by re-test
23
Q

audiological outcomes of ototoxicity

A

bilateral decline in thresholds (usually), progress from high to low frequencies, behavioural and physiological responses (OAEs, ABR) deteriorate in pattern reflecting damage to cochlea

24
Q

Monitoring program baseline evaluation

A

no later than 24 hours after chemotherapeutic
No later 72 hours after aminoglycoside antibiotics

25
Q

Ototoxicity medical examination

A

History; other medications, chemical and/or noise exposure
Physical exam: tinnitus, hearing loss, vestibular dysfunction: nystagmus
Additional assessment: audiology, vestibular, radiology if retrocochlear damage suspected

26
Q

salicylate

A

(Asprin)- anti-inflammatory effects
Ototoxicity usually reversable, tinnitus, high frequency or flat SNHL, no clear affects on anatomy, temporary threshold shift and OAE temporarily altered
Possible pathophysiological effects: OHC motility, auditory synapse

27
Q

acute SSNHL

A
  • Very sudden onset of unilateral SNHL that may be accompanied by acute vertigo, aural fullness/pressure and tinnitus
  • Medical emergency
28
Q

criteria for ssnhl

A

unliateral hl of 30dB or more in 3 adjacent frequencies
- Rapid progression occurring within 72 hours of initial symptoms

29
Q

SSNHL incidence

A

5-27/100 000 in us ; about 1% of all SSNHL

30
Q

SSNHL age

A

40-60 year olds

31
Q

sex differences

A

none Male=Female

32
Q

etiology

A

unknown 90% idiopathic; identifiable causes are neoplastic, infectious (autoimmune, neurologic, ototoxicity)

33
Q

idiopathic SSNHL

A

rapid onset
- Not explained by other identifiable cause

34
Q

audiologic assessment for SSNHL

A

Clinical features: SNHL is usually unilateral, sudden & rapid, progressive (<3days) additional symptoms: vertigo, aural fullness, tinnitus
Comprehensive audiologic evaluation: behavioural and objective tests
- Rule out retrocochlear involvement (immittance with acoustic reflexes, OAE, ABR)

35
Q

why is SSNHL an emergency

A

better prognosis if treatment starts early, rule out stroke

36
Q

case history SSNHL

A

: critical to diagnosis which is based on exclusion of other known causes
Goal is to rule out: specific treatable infections (bacterial or viral), cardiovascular/stroke, labyrinthine membrane rupture (trauma or barotrauma), mass lesions (retrocochlear) autoimmune (systematic or inner ear specific), ototoxicity

37
Q

imaging for SSNHL

A

to rule out cerebellopontine angle tumors, MS, vascular compromise, malformations

38
Q

laboratory evaluations SSNHL

A

may be considered when specific disorder is suspected (thyroid function test, bacterial infection, autoimmune disease)

39
Q

idiopathic SSNHL medical treatments

A
  • Varies with underlying condition but majority of cases are peripheral auditory (vestibular) disorder classified as idiopathic (likely viral)
  • Systemic steroids (e.g. prednisone) to reduce ear inflammation
  • Intratympanic steroids
  • Hyperbaric oxygen therapy
40
Q

order of treatment for idopathic SSNHL

A

Initial is systemic prednisode then follow up treatment with corticosteroid into ME (intratympanic delivery)
- HBOT recommended as initial with steroids or as salvage treatment for SSNHL

41
Q

prognosis trends

A

Delay in steroids=poorer prognosis
Age: younger people more favourable recovery
Mild low frequency HL recovery better than mild high frequency
Severe to profound loss=poor prognosis

42
Q

audiologic monitoring of SSNHL

A

Monitor patients for: effect of treatment & recovery in affected ear, SNHL in contralateral ear, development of associated diseases (autoimmune)
- Aural rehab for hearing that does not improve

43
Q

Following stabilization of hearing thresholds for SSNHL what do we do and when is stabilization

A

3-6 months)
o Consider amplification if residual SNHL
o CROS if no residual hearing
o ALDs
o Cochlear implant

44
Q
A

9530 (7 decks)

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