Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

AUDE 6120 > final exam comprehensive > Flashcards

final exam comprehensive Flashcards

1
Q

pharmacokinetics

A

how the body interacts with the administered substance
-remember ADME (absorption, distribution, metabolism, excretion/elimination)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are some common route of administration

A

enteral, topical and parenteral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what route of administration bypasses all of the body’s barriers and has a greater risk for adverse effects

A

parenteral
-intrathecal !!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

first pass metabolism and the drugs impacted by it

A

these drugs enter the liver prior to entering circulation which allows for any unnecessary toxins to be removed
-occurs to enteral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

common barrier that need to be overcome by drugs

A

cell membrane, blood brain barrier (BBB), blood labyrinth barrier (BLB) and blood placental barrier

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bioavailability

A

amount of the drug available within the circulation
-can be impacted by the route of administration, chemical form or patient factors including GI enzymes/pH metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

2 phases of metabolism

A

phase 1 : oxidation/reduction in which the chemical structure is being modified
phase 2 : conjunction/hydrolysis which inactivates the drug or enhances the drug solubility (forms a compound/breaks the bond)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

cytochrome P450 (CYP) enzyme

A

in control of mediating oxidative reactions
-this determines the rate and extent to which an individual can metabolize various drugs
-if induced, it increases the rate of metabolism
-in inhibited, it decreases the rate of metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what the equation for half life

A

t 1/2 = 0.693 (Vd)/elimination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the difference between zero order elimination and first order elimination

A

with zero order it is a constant amount that is eliminated whereas first order the more drug there is, the more drug that is eliminated
-zero is constant, first is adaptive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pharmacodynamics

A

the effects of a drug on the body
-the biochemical and physiologic actions of drugs and mechanisms of a drug action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

agonist

A

ligand that activates the receptor
-active conformation after the drug binds to its receptor
-all NTs are agonists at their sites

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

antagonists (inhibitors)

A

prevents the action of the agonists at the receptor site but there is not effect without agonists
-can be receptor, noncompetitive or competitive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

EC50 (potency) is related to the ______ of a drug ; EC50 (efficacy) is related to the __________________ by drug molecules

A

affinity ; receptor occupancy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pharmacogenomics

A

study of the role of the genome in drug response, a combination of pharmacology and genetics
-genetic polymorphisms are common in major enzymes that metabolize phase 1 and phase 2 reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

examples of polymorphisms

A

inherited variation of enzymatic hydrolysis of short acting muscle relaxant (succinylcholine) by the enzymes cholinesterase AND the CYP liver enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how can age impact drug metabolism

A

-children will have slower reactions (including slow metabolism and slow excretion)
-older adults generally have a decrease in metabolic capacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

polypharmacy

A

taking 5 or more medications at the same time, meaning within a 24 hour time period
-more common within older adults and younger people with chronic medical conditions such as diabetes, arthritis and autoimmune disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

there is an ________ risk of drug-drug or drug-disease interactions with polypharmacy

A

increased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ototoxicity/vestibulotoxicity

A

drugs or other chemical substances that cause temporary or permanent damage to the cochlear or vestibular system
-exposure can result in functional impairment and cellular degeneration of the sensory organs, neurons of the cochlea and vestibular division of the 8th nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ototoxicity typically has SNHL, in many cases it begins as high frequency SNHL. why is this the case?

A

the drugs go into the inner ear damaging the basal end of the cochlea, which is the area associated with high frequencies
-will present as a HF sloping HL as the first presentation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

after degeneration of the OHC’s how does damage continue to occur and how does that present clinically

A

damage can then spread to IHCs resulting in a mid and low frequency SNHL, degeneration of afferent nerve endings will then occur after both the OHCs and IHCs have been impacted
-as the nerve is impacted, then speech will be impacted both in quiet and in noise
-reflexes will also be impacted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

audiological signs and symptoms of toxicity

A

SNHL that can be progressive, onset typically will occur within a few days or weeks, tinnitus, aural fullness, recruitment, abnormal/absent OAEs, abnormal/absent reflexes and poor speech perception

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

vestibular signs and symptoms of toxicity

A

light headedness/dizziness, unsteadiness/gait abnormalities, abnormal ocular tracking and nystagmus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

nephrotoxicity

A

damage to the kidneys as a result of a drug/chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

hepatotoxicity

A

damage to the liver as a result of a drug/chemical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

neurotoxicity

A

alteration of hearing or balance by drugs/chemicals acting at the level of the brainstem or central connections of cochlear/vestibular nuclei

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

risk factors for ototoxicity

A

dosage (higher the dose, the more of a risk there is), hepatic function (liver diseases impact metabolism, increasing risk), renal function (increase risk with any renal impairment), polypharmacy, age (very young and very old are at higher risk), pre-exisiting SNHL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

drugs that are primarily ototoxic

A

amikacin and neomycin
-both aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

drugs that are primarily vestibulotoxic

A

streptomycin and gentamicin
-both aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is antibiotic therapy used for

A

targets bacteria
-affects both gram positive and gram negative bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

antibiotic antagonism

A

when one antibiotic can cancel out desired effects of the other
-for example when tetracycline and penicillin are given together the penicillin will not be effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

antibiotic synergism

A

using more than one antibiotic increases the spectrum of kill and produces a desired effect of greater magnitude
-for example if penicillin is used alone to treat enterococci bacteria it will not completely remove it however, it used in conjunction with streptomycin the penicillin will completely kill the bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

antibiotics discussed

A

aminoglycosides, penicillin and macrolides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

aminoglycosides

A

a type of antibiotic that is used to treat infections caused by gram negative bacteria that can cause life threatening infections such as endocarditis, septicemia and kidney infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

why are aminoglycosides most often administered through IM or IV

A

they have poor bioavailability if taken through oral administration
-absorbed within the gut this way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what are the primary toxicity reactions associated with aminoglycosides

A

nephrotoxic (tubular cell injury), can lead to neuromuscular blockage (respiratory paralysis) as well as both ototoxicity/vestibulotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

with aminoglycosides, toxicity is generally dose dependent until there is a _______ component

A

genetic
-aminoglycoside included ototoxicity occurs with a point mutation within the mitochondrial DNA making an individual susceptible to ototoxicity
-only cochlea will be impacted resulting in a severe to profound SNHL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

how does ototoxicity occur with aminoglycosides

A

cationic changes occur within the charge of the cell membranes allowing for drugs to enter the cell
-drug increases the intracellular calcium and generates toxic levels of reactive oxygen species (ROS) resulting in apoptosis and necrosis
-with gentamicin, this shows concentration within the stria vascularis and diffusing into the endolymph disrupting ion channels and disturbing the homestatic balance of the inner ear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

explain the progress of damage with ototoxicity and aminoglycosides

A

the OHCs are damaged first, progresses to the IHC and the rest of the organ of corti
-nerve fiber will be impacted secondary to the hair cells
-once the IHCs and nerve are impacted ability to understand speech is impacted

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

_________ is the most limiting use factor of aminoglycosides

A

ototoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

why is HFA important within ototoxicity monitoring and aminoglycosides

A

HL begins in these higher frequencies, typically beginning over 16000 so by including HFA we can catch the damage prior to it reaching 8000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

vestibulotoxicity with aminoglycosides

A

more likely to occur in people that have a history of balance problems and kidney dysfunction
-can be permanent or temporary
-can include vertigo, disequilibrium, oscillopsia or risk of falling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

explain how vestibular issues can be compensated

A

this is a central process so if vestibular signs and symptoms are unilateral, compensatory actions can occur over time
-HOWEVER if the issue is bilateral, no compensation will occur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

when aminoglycoside is given in conjunction with loop diuretics, what happens

A

causes toxicity at a higher rate as there is an enhanced entry of aminoglycosides into the cochlear fluid and tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

when aminoglycosides are given in conjunction with neuromuscular blocking agents, what happens

A

can lead to skeletal muscle weakness and respiratory depression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

when aminoglycosides are given in conjunction with vancomycin, what happens

A

there is a synergistic effect meaning and increase in toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

penicillin

A

produced by a fungus that has a bactericidal action, meaning it blocks bacterial cell wall synthesis
-examples include amoxicillin and augmentin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

usage of amoxicillin

A

otitis media
-one of the most prescribed drugs in the US for OM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

usage of augmentin

A

used for otitis media if the patient develops a resistance or no benefit from amoxicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

is penicillin ototoxic or vestibulotoxic?

A

generally it does not cause toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

macrolides

A

a type of bacteriostatic meaning it does not kill the bacteria but it kills the material membrane so it cannot replicate
-example is a z-pack

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

usage of macrolides

A

otitis media, respiratory tract infections, sexually transmitted diseases and can be used when patients are allergic to penicillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

ototoxicity associated with macrolides

A

reversible SNHL that occurs at high doses through IV administration
-may also impact central auditory pathways

55
Q

risk factors for macrolide ototoxicity

A

renal failure, liver impairment, receiving an organ transplant, age, female gender, concurrent use with other ototoxic drugs and a prolonged/high dose macrolide treatment

56
Q

which antibiotic is most commonly used to treat otitis media

A

penicillin
-such as augemntin or amoxicillin

57
Q

which antibiotic is most often associated with ototoxicity

A

aminoglycosides

58
Q

classification of chemotherapeutic agents

A

platinum derived compounds (cisplatin and carboplatin), folate analog inhibitors and vinca alkaloids

59
Q

limitation with chemotherapeutic agents

A

normal cells are also subjected to the effects of chemo so needing to allow time between sessions to allow the body’s cells to not be as impacted as the cancerous cells

60
Q

what is the most ototoxic drug

A

cisplatin

61
Q

cisplatin

A

used for germ cell tumors, bladder cancer, gynecological, lung tumors, tumors of the head/neck region and from childhood tumors such as neuroblastomas

62
Q

risk factors for ototoxicity from cisplatin

A

high IV bolus, high cumulative dose, poor renal function, young or advanced age, co-administration of high dose of vinca alkaloids and poor cranial radiation therapy

63
Q

ototoxicity with cisplatin

A

can be gradual, progressive, cumulative or it can present suddenly
-cochlear loss is detected in the higher frequencies first
-some degree of reversibility but is generally is permanent
-neurotoxicity and vestibulotoxicity can also occur

64
Q

carboplatin

A

a second generation analog of cisplatin
-same uses as cisplatin
-was introduced to be less nephrotoxic however it is more vestibulotoxic

65
Q

with carboplatin, there is significant ________________ toxicity

A

bone marrow
-take out both the T and B cells which then impacts the immune system
-can lead to anemia

66
Q

mechanisms of ototoxicity with platinum derived compounds

A

caused by free radical generation and inhibition
-hair cells and spiral ganglion are most susceptible to apoptosis

67
Q

the permanent HL associated with platinum compounds is probably caused by ….

A

loss of OHCs in the basal turn, damage later then spreads to the rest of the cochlea and then degeneration of the stria vascularis also occurs

68
Q

what are critical issues to address when dealing with platinum compound ototoxicity

A

genes involved in drug transport, metabolism/DNA repair regulation, route of administration and timing relative to therapy

69
Q

folate analog inhibitors

A

folate (vitamin B) is a vital for both cancerous and normal cells so these drugs aim to deplete folate which reduces DNA synthesis of both types of cell
-inhibition of folic acid has been used as the mechanisms for elimination of rapidly dividing cells

70
Q

an example of a folate analog inhibitor is methotrexate, explain the drug

A

used to treat severe cancer of the blood, bone, lung, breast, head/neck, RA, psoriasis and cogan’s syndrome
-is highly ototoxic in children!!
-is also used with ectopic pregnancy

71
Q

vinca alkaloids

A

an antitumor drug that is derived from periwinkle plant
-is often given together with other drugs such as cisplatin
-used for leukemia, lymphoma, breast/testicular cancer, neuroblastoma therapy and kaposi’s sarcoma

72
Q

why is it hard to determine the exact amount of toxicity associated with vinca alkaloids

A

since it is often given in conjunction with other very ototoxic drugs, it is hard to know exactly how much toxicity this drug has

73
Q

salicylates

A

a group of drugs that includes aspirin, which is used for mild to moderate pain relief, reduction of inflammation, reduction of fever and can prevent strokes

74
Q

how can salicylates cause ototoxicity

A

they are absorbed quickly and are distributed into the cochlea through the arteries and can then accumulate within the perilymph
-shows reversible biochemical and/or metabolic changes in the cochlea with no permanent morphologic abnormality
-associated with greater than 12 regular strength aspirin tablets taken daily for several days

75
Q

ototoxicity signs with salicylates

A

high pitched tinnitus, reversible mild to moderate HL SNHL

76
Q

what is generally the first sign of ototoxicity with salicylates

A

tinnitus
-often becomes louder !

77
Q

non-steroidal anti-inflammatory analgesics (NSAIDS)

A

actions include anti-inflammatory, analgesic and antipyretic effects
-examples include ibuprofen, naproxen and indomethacin
-nephrotoxic and can impact the GI by causing ulcers

78
Q

ototoxicity associated with NSAIDS

A

reversible tinnitus and HL
-reversible dizziness is reported with indomethacin

79
Q

quinine

A

an antipyretic used for malaria
-off label usage for nocturnal night cramps
-can be found in tonic water

80
Q

toxicity associated with quinine

A

reversible bilateral HF hearing loss with a 4000 Hz notch, high pitched tonal tinnitus, dizziness/vertigo
-referred to as cinchonism which includes tinnitus, HL, dizziness, headache, nausea and vision changes

81
Q

acetaminophen

A

useful for treating mild pain and fever but there is not anti-inflammatory agents
-such as tylenol
-is hepatotoxic if taken at greater than recommended doses

82
Q

toxicity associated with acetaminophen

A

no reported temporary or permanent ototoxic or vestibulotoxic however overuse/abuse can cause rapidly progressive profound permanent SNHL
-which only occurs with multi-ingredient substances such as vicodine (acetaminophen and hydrocodone)

83
Q

diuretics

A

preventing the reabsorption of sodium into the body which excretes water decreasing the blood volume and pressure
-used for hypertension, to reduce edema in patients with congestive heart failure, liver cirrhosis or kidney disease

84
Q

what type of diuretics is believed to be ototoxic

A

loop diuretics
-including ethacrynic acid, furosemide and torsemide

85
Q

mechanism of ototoxicity with loop diuretics

A

dose related and is reversibly depending on the endocochlear potential and intra-labyrinth electrolyte changes
-reduction in magnitude of the cochlear microphonic, summating potentials and 8th nerve action potentials
-recovery y of cochlear potentials occurs gradually
-can also cause dizziness/vertigo

86
Q

HL can be reversible if ______________ is used alone

A

loop diuretics

87
Q

how can blood thinners, bleeding disorders and diabetes impact the management of an audiologic patient

A

small nicks can lead to severe bleeding
-it is important when making impressions, particularly deep canal impression, and cerumen management
-clearance from a physician or written consent from patients informing risk is prudent

88
Q

according to AAA, what is the purpose of ototoxic monitoring

A

allows for informed medical decisions
-performed for two purposes including early detection of changes to hearing status and audiologic intervention can occur when significant hearing impairment has occurred

89
Q

ototoxic monitoring can lead to audiological intervention, this can include …..

A

use of HA/assistive devices, programming HA’s to adapt to changes within hearing sensitivity (i.e. progressive HL) and educational support for children with HL

90
Q

patient populations that should be monitored

A

very old/very young patients, patients in poor general physical health, co-morbidities (in particular liver or kidney diseases), poor hydration status, genetic tendency for ototoxic susceptibility, patients that have received large or multiple doses and patients with a history of noise exposure

91
Q

overview of the general timeline for ototoxic monitoring

A

baseline data, monitoring evaluations and post treatment evaluation

92
Q

importance of having baseline data

A

this needs to occur in order to determine if ototoxicity has occurred
-the patient is their own control!!

93
Q

timing of the baseline evaluation

A

should be evaluated before or no later than 24 hours after administration of chemotherapeutic agents, before or no later than 72 hours following administration of aminoglycosides and then a recheck of thresholds should occur within 24 hours to determine reliability

94
Q

timeline of monitoring evaluations

A

should occur periodically throughout treatment and is usually prior to each dose for chemotherapy patients or 1-2 times per week for patients receiving ototoxic antibiotics
-is dependent on drug regimen and the physicians recommendations

95
Q

despite the monitoring schedule, it can be warranted anytime based on what factors

A

if the patient reports and increased hearing difficulty, tinnitus, aural fullness or dizziness

96
Q

timeline of post treatment evaluations

A

after treatment has stopped, evaluations should occur every 3 months for the first year then should occur annually

97
Q

why is post treatment evaluations so important

A

ototoxic HL can be progressive and it can occur 6 to 12 months after the drug is discontinued

98
Q

the national cancer institute at the national institutes of health published the common terminology criteria for adverse events (CTCAE), what is this and what does it state

A

a set of criteria for standardized classifications of adverse effects of the drug used in cancer therapy
-criteria is categorized based on changes in hearing, functional impact severity and the need for intervention

99
Q

with pediatric monitoring, this is more urgent. what are some scenarios where monitoring should occur

A

newborns who are premature, children who have been diagnosed with cancer and children who have a condition that makes them vulnerable to infections

100
Q

what are some important factors to consider with ototoxic monitoring

A

the status of patients, speed of test, cost of performing and interpreting the results and the availability of equipment/personnel

101
Q

criteria for clinically significant changes in hearing due to ototoxic medications

A

greater than a 20 dB pure tone shift at one frequency, greater than a 10 dB pure tone shift at two consecutive frequencies or threshold response shifting to a no response at three consecutive test frequencies

102
Q

when any changes in hearing are detected, what needs to occur

A

they need to be confirmed within 24 hours

103
Q

what are the ASHA testing recommendations when it comes to ototoxic monitoring

A

they recommend a full audiometric evaluation for patients that are alert and responsive
-abbreviated test battery is required for patients who tire easily or show limited responsiveness/awareness

104
Q

if any changes are noticed within the abbreviated test battery, what is the next step

A

a more complete evaluation will need to occur

105
Q

importance of adding physiologic measures for ototoxic monitoring

A

physiologic measures should be included if there is any risk for the patient becoming less responsive over the course of treatment

106
Q

what is within our test battery for monitoring

A

case history, otoscopy, pure tone audiometric monitoring (both conventional and extended high frequency), tympanometry, speech, OAEs and ABR

107
Q

importance of high frequency audiometry with ototoxic monitoring

A

this detects ototoxicity much earlier than conventional audiometry because the drugs impact the basal end of the cochlea resulting in a HF SNHL
-we need to establish a baseline for this though because there are no well accepted standards

108
Q

HFA will only be useful if we have _____________

A

the patients baseline

109
Q

why is test-retest of HFA poor in children

A

these signals typically sound very different to children
-the differences between testing can be up to 10 dB different

110
Q

when can OAEs and ABRs be used for ototoxic monitoring

A

younger children, patients with questionable reliability, unresponsive patients, patients with low cognitive abilities and very sick patients who cannot tolerate behavioral evaluation

111
Q

advantage of using OAEs during monitoring

A

they are a good indicator of early ototoxic damage as they measure the outer hair cell function

112
Q

when would ABRs be more appropriate for monitoring

A

in cases of ME dysfunction however there needs to be more caution in reading it as it could look like a conductive loss

113
Q

how can cranial radiation impact the hearing structures

A

it can damage any of the auditory structures within the radiation field, extending from the external ear to the higher auditory pathways

114
Q

how can radiation cause conductive HL

A

radiation can degrade the external ear and middle ear systems through thickening the TM, stenosis of the ear canal, changes in the ET and ossicles resulting in temporary or permanent conductive HL

115
Q

how can radiation cause SNHL

A

as dose increases, it can cause degeneration of the OHCs, IHCs and the 8th nerve fibers

116
Q

timeline of radiation therapy ototoxicity

A

typically is irreversible and progressive
-is considered a late adverse effect with onset occurring several years after treatment

117
Q

tinnitus and ototoxicity

A

this is often the first thing that patients will report
-tinnitus ototoxicity monitoring interview (TOMI) was developed to detect tinnitus onset or changes in existing tinnitus perception during treatment with potentially ototoxic drugs

118
Q

vestibular toxicity monitoring

A

monitoring requires assessment of the balance system including the vestibular reflexes such as VOR by caloric and rotary chair testing

119
Q

pharmaceutical cognitive side effects

A

impaired concentration/attention, disorientation, confusion, loss of mental acuity, mental clouding, drowsiness, forgetfulness

120
Q

cognitive side effects

A

poorer WRS, poorer pure tone thresholds, poor compliance with use of HAs

121
Q

management of ototoxicity

A

counseling prior to therapy with ototoxic drugs to make patients aware of the risks, counseling patient/family after ototoxicity and the recommendations for rehabilitation, appropriate intervention with HAs or CIs, children with ototoxic HL will likely require the use of technology with remote microphone technology to improve SNR in the classroom, frequent follow up/counseling due to potential progressive loss

122
Q

despite the patient being done with treatment, monitoring should still occur. why?

A

the progressive nature of HL associated with ototoxicity puts patients at risk for up to 6-12 months after treatment has stopped. that is why the post treatment evaluation is vital

123
Q

examples of nephrotoxic drugs

A

aminoglycosides, cisplatin, MTX and NSAIDS

124
Q

how are aminoglycosides nephrotoxic? how does this relate to ototoxicity?

A

there is injury to the tubular cells from drug accumulation, which this can be reversible
-renal toxicity causes the drug to accumulate within the body and stay longer

125
Q

examples of hepatotoxic drugs

A

acetaminophen (if taken in greater then recommended doses)

126
Q

examples of neurotoxic drugs

A

cisplatin, vinca alkaloids and MTX

127
Q

what neurotoxic symptoms do vinca alkaloids cause

A

numbness, pain and dizziness

128
Q

why is ototoxic HL SNHL and not conductive

A

the ME space does not have any sensory or vestibular organs so the ototoxicity will always be SNHL
-the ME space may be impacted however the damage will be occurring within the inner ear

129
Q

examples of drugs that can cause vestibulotoxicity

A

aminoglycosides, cisplatin, carboplatin and quinine

130
Q

differential diagnosis for ototoxicity (based on the audiogram alone)

A

presbycusis, ototrauma and noise induced HL

131
Q

by looking at an audiogram alone, we cannot tell what caused the HL. how can we differentiate between ototoxicity or other diagnoses

A

through the case history and additional diagnostic testing results
-also with DD’s we will not see vestibulotoxicity symptoms

132
Q

how is the blood labyrinth barrier (BLB) involved with ototoxicity

A

remember the BLB allows only certain things to cross however certain factors can breakdown the integrity of the barrier
-ototoxins have the ability to cross this barrier through some sort of disruption in the ions of the stria vascularis
-once inside, different parts of the cochlea will be impacted

133
Q

as dosage and/or duration increases …..

A

IHCs can become destroyed damaging the apex causing SNHL in the mid to low frequencies
-degeneration of the afferent nerve endings follow causing tuning curse to become shallow!!

134
Q

reflexes and ototoxicity

A

they will be impacted, may still be present but at low levels due to recruitment
-remember we expect them up to around a 50-60 dB HL

AUDE 6120 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions