Otology (including diseases) Flashcards

1
Q

What are the pinnal conformations in cats?

A

Erect (normal)
four ears
folded ears
curled ears

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2
Q

What occurs in cats with the four-eared condition?

A

small extra pinna bilaterally
reduction of the size of their globes
slightly undershot jaw
normal body size

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3
Q

What breed of cat has folded ears?

A

Scottish Fold
- born with normal ears
- after about 4 weeks the ears fold rostrally
- all have some degree of osteochondrodysplasia of the distal limbs

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4
Q

What breed of cat has curled ears?

A

American curl
- ears fold back at pinnal apex

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5
Q

What is the musculature of the pinnae like?

A

muscles of the pinna are numerous and act to move the ear
- Rostroauricular muscles
- Caudoauricular muscles
- Ventroauricular muscle

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6
Q

What is the antitragus?

A

thin, elongated piece of cartilage caudal to the tragus and separated from it by the intertragic incisure
has medial process, lateral process

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7
Q

What is the intertragic incisure?

A

the anatomic region used to guide the otoscopic cone or otoendoscope into the ear canal for the otoscopic examination

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8
Q

What is hair like in the ear canal?

A

most breeds: hairs are fewer, simple, not present the length of the ear canal
- very few fine hairs are found distal to the tympanic membrane
- should decrease in number from distal to proximal
Cocker spaniels: excessive compound hair follicles in the horizontal ear canal

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9
Q

What are ceruminous glands?

A

modified epitrichial glands in the ear canal
- some open directly onto skin like atrichial glands
Cockers, English spaniels and Labrador retrievers have more than usual
may become hyperplastic with chronic otic disease
- may initially appear as prominent white specks along the canal
- Cockers more prone to hyperplasia
Cerumen formed from exfoliation of cells and glandular secretions
- Protective role with IgA, IgG, IgM – mostly IgG
More are present in the lower 1/3 of the canal
Located below sebaceous glands (like other epitrichial glands)

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10
Q

How does vasculature pass from the concave to convex pinna?

A

via foramina in elastic auricular cartilage

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11
Q

What is the tragus?

A

quadrangular plate of cartilage that forms lateral boundary of canal (opposite of anthelix)

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12
Q

What is the anthelix?

A

low ridge on medial wall of canal

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13
Q

What is the cavum conchae?

A

circular cavity created by the anthelix, tragus and antitragus
Basal conchae twists as it forms tube (vertical ear canal)
Proximal auricular cartilage creates funnel shape

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14
Q

What is the anular cartilage?

A

Separate cartilaginous band, overlaps with osseous external acoustic meatus
- Gives ear canal flexibility, articulates with meatus via ligaments

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15
Q

What organisms are present in canine and feline ear canals?

A

Normal: Staph, Strep, bacillus, E. coli, Corynebacterium, micrococcus, yeast
Otitis: Staph, Strep, Pseudomonas, Proteus, Corynebacterium, Enterococcus, E. coli, yeast

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16
Q

What is cerumen?

A

Emulsion that coats the ear canal
Contains desquamated keratin, sebaceous and ceruminous excretions
In otitis it has lower lipid content and is more acidic
The clearing mechanism is altered in otitis

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17
Q

What is the pH of dogs ears?

A

Normal= 4.6-7.2
Otitis:
- Acute= 5.2-7.2
- Chronic= 6.0-7.4 (organisms change?)

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18
Q

How is the tympanic membrane typically oriented relative to the central axis of the horizontal external acoustic meatus in dogs?

A

45-degree angle
* can be used to advantage when removing saline from ear after flush

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19
Q

How many layers is the tympanic membrane?

A

3
Inner layer - epithelium from pharyngeal pouch origin
Central layer - fibrous connective tissue from pharyngeal wall
Outer layer - stratified squamous epithelium from pharyngeal groove and part of external ear canal

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20
Q

What is the pars flaccida?

A

Dorsal part of the tympanic membrane
Has small blood vessels
Can bulge with otitis media due to pressure (rarely found in normal dogs)
Histopathology: collagen, rare mast cells, and keratinized epithelium
- no histopathology difference between bulging and not

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21
Q

What is the pars tensa?

A

Ventral part of tympanic membrane
Very thin but extremely tough and robust
Has radiating ridges
The stria mallearis is visible
- has a concave shape due to internal surface tension from this attachment
Histopathology: more collagen, no inflammatory cells, keratinized epithelium

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22
Q

What is the stria mallearis and how is it different between dogs and cats?

A

outline of the manubrium of the malleus visualized through the pars tensa
- tension from this makes the tympanic membrane have a concave shape
Dog: hook- or C-shaped
- concave aspect of the “C” facing rostrally
Cat: straight
Umbo is the point of the greatest depression

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23
Q

How long should a normal tympanic membrane take to heal following a myringotomy?

A

regenerate by day 14
Complete healing between 21 and 35 days
Will be thicker than normal (scarring)

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24
Q

What maintains the thinness of the tympanic membrane and self-cleaning function of the external ear?

A

epithelial migration
- tympanum follows centrifugal/outwards pattern of epithelial migration
- never migrates from pars flaccida to pars tensa or vice versa
if it fails you will get cerumen accumulation

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25
Q

What is impedance mismatch?

A

because fluid has higher impedance than air, a direct transfer of a pressure wave from air to water is insufficient to move through the internal ear fluid compartment

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26
Q

How does the middle ear function to overcome impedance mismatch?

A

1) the surface area of the tympanic membrane is much larger than the surface area of the foot plate of the stapes on the oval window
2) incus and malleus act as a lever system
*together they amplify the pressure wave

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27
Q

What are the functions of the external ear canal?

A

Collect sound waves
Conduct sound waves to the tympanic membrane
Determine the origin of the sound waves

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28
Q

What glands do external ear canals have?

A

Sebaceous glands
Ceruminous glands

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29
Q

What are the parts of the middle ear?

A

Tympanic membrane
Auditory ossicles
Tympanic cavity

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30
Q

What is the histologic appearance of the tympanic membrane?

A

Outer and inner epithelium
Core of collagen
Hairless, glandless

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31
Q

What are the two elastic cartilages of the ear canal?

A

Auricular
Annular

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32
Q

What is the mean middle ear cavity volume of mesaticephalic dogs?

A

1.5 mL

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33
Q

What three parts can the tympanic cavity be divided into?

A

Epitympanic recess - smallest, occupied by the head of the malleus and incus
Tympanic cavity proper - adjacent to the TM
Ventral cavity - largest part; contains the septum bulla
- cannot see much of it with a rigid otoscope

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34
Q

What houses the cochlea?

A

promontory of the petrous portion of the temporal bone
- on the medial wall of the tympanic cavity proper
- opposite the mid-dorsal aspect of the TM

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35
Q

Where is the cochlear (round) window located and what is its function?

A

caudolateral portion of the promontory
covered by a thin membrane
- oscillates to dissipate vibration energy from perilymph

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36
Q

Where is the vestibular (oval) window located and what is its function?

A

dorsolateral surface of the promontory
- medial to the pars flaccida
covered by a thin membrane (18-20x smaller than TM)
- stapes should insert into it to transmit sound waves

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37
Q

What is different between the middle ears of cats and dogs?

A

Dog: bulla septum is a small, incomplete ridge
- only contacts the petrous portion of the temporal bone rostrally
Cat: bulla septum bulla is nearly complete
- separates the tympanic cavity into two compartments
*Dorsolateral (pars tympanica) - smaller, accessed with myringotomy
–> Auditory ossicles, ostium of auditory tube, TM
*Ventromedial (pars endotympanica) - larger, air-filled chamber
- connected through a foramen between septum and petrous bone
- have T-ossicle, conical cartilage in dorsolateral compartment

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38
Q

What is the auditory tube?

A

Canal from nasopharynx to rostral tympanic cavity proper
- Pressure equalizer
- 3 parts: cartilaginous (medial), junctional, osseous (distal, middle ear)
- Opened by tensor veli palatine
–> Innervated by mandibular branch of trigeminal n (same as tympani)
- may be impaired in brachycephalics

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39
Q

What are the auditory ossicles?

A

1) Malleus - largest
- manubrium part attaches to the TM
- muscular process attaches to the the tensor tympani muscle
- attaches to the incus
2) Incus - between the malleus and the stapes
3) Stapes - smallest
- anchored in the oval or vestibular window by its annular ligament
- functions as a piston
- stapedius muscle inserts onto it

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40
Q

What is the tensor veli palatini?

A

This muscle tenses the soft palate to helps equalize air pressure in the tympanic cavity
Associated with the auditory tube

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41
Q

What is the tensor tympani?

A

This muscle tenses the tympanic membrane, which reduces noise during chewing
Associated with the malleus

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42
Q

What is the stapedius muscle?

A

a small muscle in the middle ear that stabilizes the stapes bone and reduces sound transmission when exposed to loud noises
*acoustic reflex

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43
Q

What are the common organisms of the middle ear in dogs and cats?

A

Normal: Staph, Strep, E. coli, Enterococcus, bacillus, Bordatella, Branhamella, Clostridium, yeast
Otitis: Staph, Strep, Pseudomonas, Proteus, Corynebacterium, Enterococcus, yeast

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44
Q

Where are the sympathetic nerves located in the tympanic cavity?

A

A portion passes through the dorsomedial aspect of tympanic cavity proper near the cochlear window
- In dogs it mostly runs through a channel in the petrous bone
- In cats it more exposed so cats may be more prone to Horner’s

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45
Q

Where is the facial nerve located in the tympanic cavity?

A

Goes through the facial canal in the petrous portion of the temporal bone
- this is is incomplete within the region of the stapedius muscle
–>around the round window/lateral to the vestibular window

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46
Q

What is the chorda tympani?

A

Branch of the facial nerve that passes near the pars flaccida before exiting the middle ear to innervate the tongue (taste)

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47
Q

What is the most dense bone in the body?

A

petrous portion of the temporal bone
forms the medial margin of the middle ear

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48
Q

What is the pathway that nerve impulses travel from the ear to the brain?

A

Cochlea –>
up the auditory nerve –>
*Cochlear nucleus –>
*Superior olivary complex –>
*Lateral lemniscus –>
*Inferior colliculus –>
*Medial genticulate –>
*Auditory cortex

*part of the central auditory nervous system

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49
Q

How is the cat externa ear canal different than that of a dog?

A

It is relatively short and straight ear canal
*humans are even more so
Points more anterior not ventral

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50
Q

In which bone of the skull is the inner ear housed?

A

bony labyrinth within petrous temporal bone

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51
Q

What are the parts of the inner ear?

A

Bony labyrinth outside, membranous inside
Auditory
*Cochlea
Vestibular
*Vestibule (saccule and utricle)
*Semicircular canals

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52
Q

What is the role of the vestibular system?

A

Responsible for maintaining equilibrium and balance
Detects static position of head
Detects acceleration, deceleration, rotation
Coordinates head movement with:
-Movement of eyes via vestibulo-ocular projections of CNS
-Movement of trunk and limbs via vestibulo-spinal projections of CNS

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53
Q

What are the 5 organs of the vestibular system?

A

3 semicircular ducts (anterior, posterior, horizontal - oriented at right angles)
- with 3 ampullae
Utricle and Saccule (the otolith organs)
- each with a macula

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54
Q

What do the semicircular ducts do?

A

Hair cells to detect endolymph movement
Detect angular acceleration of the head (rotation)

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55
Q

What do the otolith organs do?

A

Detect linear acceleration of the head
- Utricle: degrees of tilting of the head
–> oriented in a horizontal plane
- Saccule: linear movement in the vertical plane
–> oriented in a vertical plane

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56
Q

What is the crista (ampularis)?

A

Found in the ampullae of each semicircular canal
Ridge or cone-shaped structure
covered in receptor cells called “hair cells”
- cupula is a gelatinous substance covering stereocilia of hair cells

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57
Q

What is the vestibule of the middle ear?

A

A perilymphatic chamber that contains the utricle and saccule

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58
Q

What is the structure of the macula of the utricle or saccule and how do they function?

A

Have support cells & hair cells
Hair cells of macula embedded in gelatinous substance
Over this is a gelatinous substance containing tiny calcium carbonate crystals
–> = otoconia or otoliths
Otoliths have greater density than endolymph so as the head moves, otoliths under the pull of gravity cause deflection of the apical cilia of hair cells

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59
Q

What is the scala vestibuli?

A

a fluid-filled chamber in the inner ear’s cochlea that spirals from the oval window to the cochlea’s apex

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60
Q

What are the 3 ducts of the cochlea?

A
  • Scala vestibuli - superior
    Scala media (cochlear duct) - medial
  • Scala tympani - inferior

*two main compartments

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61
Q

What is Reissner’s membrane?

A

Floor of scala vestibuli
Roof of scala media (cochlear duct)

*forms a selective barrier between endolymph and perilymph

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62
Q

Where is the basilar membrane of the cochlea?

A

Floor of the cochlear duct
Roof of the scala tympani

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63
Q

Which chambers of the cochlea contain perilymph?

A

Scala vestibuli
Scala tympani

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64
Q

Which chambers of the cochlea contain endolymph?

A

Scala media
*technically within the membranous labyrinth

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65
Q

What is the difference between endolymph and perilymph?

A

perilymph: high in sodium and low in potassium
- like cerebrospinal fluid and plasma
endolymph: high in potassium and low in sodium
- probably formed from perilymph by selective ion transport

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66
Q

What is the stria vascularis?

A

secretory tissue
- plays a role in maintaining the high ratio of K to Na in endolymph
located in the lateral wall of the cochlear duct
has many blood vessels
contains perivascular macrophages that regulate blood vessel permeability

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67
Q

What is the spiral ligament?

A

A fibrous thickening of the cochlea wall
- Secures the cochlear duct to the bony spiral canal
- Provides mechanical support to the stria vascularis
- Anchors the basilar membrane

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68
Q

What is the path that sound waves take to to transmitted to neurologic signals?

A

Pinna & external ears collect sound waves ->
deflection of tympanic membrane ->
amplified by ossicles ->
through the vestibular (oval) window/displacement of the round window ->
to perilymph of scala vestibule ->
through to the scala tympani at the apex of cochlea ->
bend hair cell stereocilia (organ of corti) ->
hair cells interact with tectorial membrane ->
depolarize and send signals to cochlear n

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69
Q

What is the helicotrema?

A

at the apex of the cochlear labyrinth
where the scala tympani and the scala vestibuli meet

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70
Q

How many times do the scalae spiral around the modiolus?

A

modiolus = central axis, cochlear nerve goes through it
2.5 times

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71
Q

What is the organ of Corti?

A

Organ that results in hearing
Located in the scala media of the cochlea
Composed of mechanosensory cells, known as hair cells
- sits on the basilar membrane
- 3 rows of outer hair cells
- 1 row of inner hair cells
Surrounded by supporting cells
Covered by gelatinous, collagen containing tectorial membrane
- hair cells are apically embedded in this

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72
Q

What happens to sound waves at the base of the cochlea? Apex?

A

base (closest to the outer ear)
- basilar membrane is the most stiff and narrow
- high-frequency sounds are transduced (higher number Hz)
apex
- basilar membrane is wider and much more flexible and loose
- low-frequency sounds are transduced (lower number Hz)

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73
Q

What do the outer hair cells of the organ of Corti do?

A
  • Important role in adjusting the tuning and sensitivity of the IHC
  • Not actual receptors for hearing
  • more susceptible to damage than IHC
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74
Q

How do the hair cells function?

A

Hair cells are not neurons but are cellular mechanoreceptors
Have highly specialized projections:
- sterocilla (microvilli): many of them, main transducers
- kinocilia (true cillium): one of them, apical, largest
toward kinocilium = depolarizes the cell, release neurotransmitter
away from kinocilium = hyperpolarizes cell, inhibits neurotransmitter release

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75
Q

What do the inner hair cells of the organ of Corti do?

A

Change sound/fluid waves to neurologic impulses
Fluid waves in the scala vestibuli –> deflection of the basilar membrane
–> causes movement of the organ of Corti and the tectorial membrane
–> apical cilia of hair cells bend
- initially towards kinocilium = release transmitter
- then away = stop neurotransmission

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76
Q

What is the endocochlear potential in the scala media and hair cells?

A

Endocochlear potential in scala media is +80 mV, plus high K+
Inside of IHC rests around -40 mV
Inside of an OHC is around -60 mV

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77
Q

How do hair cells generate action potential?

A

There are K channels at the tips of stereocili
Deflecting hair bundle toward kinocilium stretches tips
–> so K+ flows from + charged endolymph into negative interior of hair cells
–> Depolarizes hair cells and opens Ca2+ channels
–> Increases release of neurotransmitter (probably glutamate)
–> neurotransmitters pass to afferent end of auditory nerve
–> nerve fires

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78
Q

How is the intensity of noise determined?

A

rate of action potentials firing

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79
Q

How is the frequency of noise determined?

A

part of Organ of Corti that is stimulated

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80
Q

How is the location of noise determined?

A

Determined by higher CANS centers comparing sounds from both ears

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81
Q

Where are the cell bodies of auditory nerves?

A

spiral ganglion in cochlea

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82
Q

What is the auditory nerve?

A

*Connects cochlea with brainstem
*Relay information about intensity, frequency, and timing of a sound
*Cochlear component of CNVIII
*Courses from the cochlea through a small canal in petrous temporal bone
- internal auditory meatus (IAM)

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83
Q

What are some predisposing factors of otitis externa?

A

Conformation
- stenotic canals
- hair in canals
- long, pendulous pinnae
- breed
Excessive moisture
- swimmer’s ear
- high-humidity climate
Treatment effects
- trauma from cotton swabs
- plucking hair
- irritant antiseptic solutions
- improper abx usage
Otitis media (if primary from URI)

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84
Q

What are some primary causes of otitis externa?

A

Allergy
Autoimmune/immune-mediated disease
Endocrinopathy
Epithelialization/cornification disorder
Foreign bodies (hair could be in this category)
Glandular disorders
Parasitic
- Otodectes
- Demodex
- Otobius
- Chiggers
Micro-organisms (esp Aspergillus but rare)
Viral (canine distemper)
Neoplasia/polyps
Contact reaction
- rare, occurs on non-haired portion of skin

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85
Q

What are some secondary causes of otitis externa?

A

Bacteria
Fungi/yeast
Medication reaction (if topical rxn that occurs on inflamed skin only)
Otitis media (if from otitis externa)
Overcleaning
Progressive pathologic changes

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86
Q

What do predisposing factors of otitis externa do?

A

Facilitate inflammation by permitting alteration of microenvironment
Allow for establishment of secondary infections

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87
Q

What do primary factors of otitis externa do?

A

Conditions or disorders that initiate the inflammatory process
- Epithelium of the ear canal is just an extension of the rest of the body
- Most cases of otitis are associated with an underlying derm condition

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88
Q

What is the most common primary cause of otitis externa in dogs?

A

Allergic disease (may be only clinical sign)

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89
Q

What are the most common primary causes of otitis externa in cats?

A

Parasites, polyps, allergic disease

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90
Q

What should be your top differentials in unilateral otitis externa?

A

-Foreign body
-Tumor/polyp
-CAFR, AD
+/- otitis media

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91
Q

What do perpetuating factors of otitis externa do?

A

Sustain and aggravate the inflammatory process
Prevent resolution of the otitis externa
Worsen the otitis externa

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92
Q

What are some clinical signs associated with otitis media (other than ear pain and otitis externa)?

A

Facial nerve paralysis
- Drooping of ear/lip
- Drooling saliva
- Absent palpebral reflex
- Parasympathetic nose (xeromycteria/dry nose)
- Neurogenic keratoconjunctivitis sicca (KCS)
Sympathetic nerve injury *more common in cats
- Horner’s syndrome
Conductive hearing loss

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93
Q

What is planktonic bacteria?

A

Classic method of studying bacteria
individual cellular organisms
Free floating
Each cells divides and forms a colony of the same genetic line
- though mutations do occur

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94
Q

What is biofilm?

A

Group of bacteria
- in a matrix made of polysaccharides, DNA and proteins
- together form an extracellular polymeric substance— SLIME
May be single species or a diverse group of microorganisms
- Mix of bacteria or yeast and fungus
They communicate by a variety of signals which result in changes
- Quorum sensing is one example
Promote survival in harsh environments

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95
Q

What are the clinical signs of Horner’s Syndrome?

A

Ptosis (drooping of upper lid)
Miosis (contraction of pupil) = results in anisocoria if unilateral
Enophthalmos (backward displacement of eyeball into the orbit)
Protrusion of nictitating membrane

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96
Q

When is the auditory tube open/closed and what are the muscles involved?

A

Osseous portion = always open
Cartilaginous portion = closed at rest, opens when swallow
- contraction of the levator muscle and tensor palatini muscle
- impaired in brachycephalics

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97
Q

What nerves innervate the pinnae?

A

trigeminal
facial (CN VII)
vagus
second cervical

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98
Q

What is the pathway of sympathetic innervation?

A

3-neuron pathway
- central/1st order neuron goes down the spine
- preganglionic/2nd order neuron comes back up the neck
- postganglionic/3rd order neuron goes to the brain

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99
Q

What is the pathway of the central/1st order sympathetic neuron?

A

Goes down the spine
- hypothalamus –>
- tectotegmentospinal tract (spinal cord)

100
Q

What is the pathway of the preganglionic/2nd order sympathetic neuron?

A

comes back up the neck
- horn of the 3 thoracic spinal cord segments –>
- through the cervicothoracic and cervical ganglion (does not synapse)
- fuses with the vagus nerve = vagosympathetic trunk near thoracic inlet
- synapse in the cranial cervical ganglion (ventromedial to tympanic bulla)
postganglionic/3rd order neuron goes to the brain

101
Q

What is the pathway of the postganglionic/3rd order sympathetic neuron?

A

Goes through skull to various locations
- iris dilator muscle = miosis
- smooth muscles of the periorbita/eyelids = ptosis, enophthalmos
- supply arteries of face/ears (including sweat glands) = xeromycteria

102
Q

What is different about the innervation of the third eyelid in cats?

A

Cats have sympathetic innervation of the smooth muscles within the third eyelid, a feature that is absent in dogs

103
Q

What other clinical signs are typically associated with central Horner’s syndrome?

A

altered mentation
paresis
postural reaction deficits
dysfunction of other cranial nerves
ataxia (proprioceptive)

104
Q

What can potential happen to the face of seal point cats with Horner’s?

A

Loss of pigment (tyrosinase inactivated) due to vasodilation and hyperthermia of pinnae and nose

105
Q

What is the gold standard test for confirmation of Horner’s syndrome in animals?

A

1 drop of a 5% or 10% solution of cocaine
- prevents the reuptake of norepinephrine by the postganglionic neuron
- leads to pupillary dilation in normal eyes
- eyes with Horner’s will not dilate
Does not localize the sympathetic pathway lesion

106
Q

What is typically used for localization of Horner’s syndrome

A
  • Phenylephrine 1% (some use 0.1% others use 10% to make it faster)
    • is a direct sympathomimetic
    • dilates with postganglionic lesion < 20 min
    • no effect on preganglionic or central lesion, normal eye

Sometimes hydroxyamphetamine (1%) is used
- is an indirect sympathomimetic
- Dilates with preganglionic or central lesion, normal eye < 45 min
- No effect on postganglionic lesion

107
Q

What kind of Horner’s syndrome is caused by otitis media?

A

Postganglionic aka 3rd order

108
Q

What are clinical signs associated with otitis interna?

A

Horizontal nystagmus (fast phase away from affected side)
- classified based on the direction of fast movement
–> fast phase to the right side indicates a left-sided lesion
Head tilting, falling, or rolling towards affected side
Asymmetric ataxia
Hearing loss

109
Q

What does CN VII do?

A

Facial nerve, is a mixed nerve providing somatic and visceral innervation
- motor innervation to the muscles of facial expression/digastricus muscle
- sensory innervation to the rostral two-thirds of the tongue and palate
- parasympathetic innervation of lacrimal glands, nasal mucosa glands, and salivary glands
- afferent fibers that supply the concave surface of the ear pinna

110
Q

What does CN VIII?

A

Vestibulocochlear nerve
Vestibular portion = balance
- superior division –> utricle, anterior and lateral semicircular duct
- inferior division –> saccule, posterior semicircular duct
Cochlear = hearing

111
Q

What is different about the position of the affected lip with acute versus chronic denervation of the facial nerve?

A

Acute = ipsilateral drooping
Chronic = lips are retracted farther than normal and the nostril is deviated to the affected side as a result of muscle fibrosis

112
Q

What nerve retracts the globe?

A

CN VI

113
Q

What is the incidence of facial nerve paralysis in cats following TECA-BO?

A

incidence of facial paralysis in cats following TECA-LBO is reported to be considerably higher (as many as 74% procedures) than in dogs
- usually resolves in dogs
- 20-47% can be permanent

114
Q

Both peripheral and central vestibular disease can cause a head tilt, horizontal or rotatory nystagmus, positional strabismus, and ataxia. What signs are more likely to be present with central lesions?

A

abnormal mental status (depression, stupor, coma)
ipsilateral upper motor neuron hemiparesis
general proprioceptive ataxia
conscious proprioceptive deficits
deficits of CNs V through XII (other than VII and VIII)

115
Q

What is seen with a CT versus an MRI?

A

CT scan can be used to better define bony structures
MRI allows distinction of soft tissues components, including intralabyrinthine fluid, CSF, nerves, and vessels within the internal auditory canal, as well as meninges and brain parenchyma
- allows the structures within the petrous portion to be delineated

116
Q

Other than otitis media, what are some causes of peripheral vestibular syndrome?

A

hypothyroidism
aural neoplasia
nasopharyngeal and otopharyngeal polyps
ototoxicity (esp. aminoglycosides, topical iodophors, or topical chlorhexidine
acute idiopathic peripheral vestibular

117
Q

What is canine proliferative eosinophilic otitis externa?

A

Uncommon, idiopathic inflammatory disease
Causes chronic unilateral otitis externa
Solitary or multiple polypoid masses w slender stalk obstructing canal
Histo: papillomatous, proliferative eosinophilic microabscesses; multifocal degenerate collagen and flame figures w/ or w/o palisading granuloma
Treatment is surgery

118
Q

What are some of the pathologic changes that chronic otitis externa can cause?

A

Epidermal hyperkeratosis/hyperplasia
Dermal edema and fibrosis
Ceruminous gland hyperplasia and dilatation
- more common in Cocker spaniels than fibrosis
Hidradenitis
Cartilaginous calcification
May predispose to cholesteotoma due to altered migration
- Dog w OM can have stratified epidermis in middle ear from canal

119
Q

What is the treatment of facial nerve paralysis?

A

Try to find out why it is happening and reverse it
Prevent the development of a corneal lesion
- always prophylactically do artificial tears

120
Q

Other than otitis media, what are the causes of facial nerve paralysis?

A

head trauma and/or peripheral nerve trauma
intracranial neoplasms (eg, meningioma)
hypothyroidism
use of potentiated sulfonamides (hypersensitivity)
part of a polyneuropathy
idiopathic condition

121
Q

What is the most common cause of facial nerve paralysis?

A

Idiopathic (75% of dogs and 25% of cats)

122
Q

What is the treatment of vestibular disease

A

treating the underlying cause
supportive care
- Meclizine (12.5 mg PO q12 in dogs; 6.25 mg PO q12 in cats)
- Diazepam (0.1–0.5 mg/kg PO q8 in dogs; 1–2 mg PO q12 in cats)
- Maropitant (1 mg/kg SC q24 or or 2 mg/kg PO q24)
head tilt and vestibular signs that persist longer than 2 to 3 weeks are usually permanent or improve incompletely

123
Q

What antibiotics are good choices for otogenic intracranial infection?

A

Ones that cross the blood-brain barrier
- TMS
- metronidazole
- cefuroxime
- fluroquinolones
Keep going for 1 mo beyond resolution of clinical signs
- potentially base on imaging findings

124
Q

Other than otitis media, what can cause 3rd order Horner’s syndrome?

A

middle cranial fossa pathologic abnormalities (neoplasm, vascular, infection)
retrobulbar pathologic abnormalities (contusion, abscess or neoplasm)
idiopathic HS

125
Q

What does CN V do?

A

Trigeminal
Sensory: facial sensation and some taste
Motor: Jaw movement, supplies the tensor tympani and tensor palati muscles, corneal reflex
Innervation vessels of cavernous sinus and brainstem

126
Q

What did a study evaluating inflammatory cells, epithelial cells,
bacteria, and yeast in normal versus inflamed ears find?

A

Inflammatory cells
–None in normal ears
–Affected ears:
* Present in purulent exudate
* Absent in 36% of ears with ceruminous exudate
Keratinized Squamous Epithelial Cells
–No significant difference between normal and affected
Yeast organisms
–Mean number significantly higher in affected vs normal
Bacterial organisms
–Only coccoid bacteria identified in normal
–Mean counts of bacteria were significantly higher in affected vs normal

127
Q

How many bacterial organisms (mean count/10 fields) in a dog and cat is is considered normal and abnormal?

A

*All rods should be considered abnormal
Cocci:
–Cat
* 400x: < 4=n, > 15=abnormal
* 1000x: < 2=n, > 6=abnormal
–Dog
* 400x: < 5=n, > 25=abnormal
* 1000x: < 2=n, > 10=abnormal

128
Q

How many yeast organisms (mean count/10 fields) in a dog and cat is is considered normal and abnormal?

A

Cat
* 400x: <2=n, > 12=abnormal
* 1000x: <1=n, > 5=abnormal
Dog
* 400x: < 2=n, > 5=abnormal
* 1000x:< 1=n, > 2=abnormal

129
Q

What are things to consider for performing a bacterial culture and susceptibility from an external ear canal?

A

-Blood levels of drug vs topical (may be 1,000x higher!)
-Culture is a prediction of response to treatment, not guarantee
-Predictive value for a drug to fail is better than predictive value for success

130
Q

When should you consider advanced imaging for ear disease?

A

Recurrent or chronic otitis
Otic masses
Para-aural swelling or mass
Inability to open, or pain on opening, the mouth
Abnormal tympanic membrane
Neurological dysfunction
– Vestibular syndrome
– Facial paralysis
– Horner’s syndrome
– Hearing deficit

131
Q

What are the advantages and disadvantages of conventional radiography for middle ears?

A

Advantages
* Readily available
* Air and bone distinguishable

Disadvantages
* Need general anesthesia
* Soft tissue resolution poor
* Positioning is challenging
* Interpretation is challenging

132
Q

If you are doing conventional radiography for a middle ear, which views are needed?

A

Dorsoventral
Right and left lateral obliques
Rostroventral-caudodorsal (open mouth, pretty much straight down mouth)
Supplemental in cat: 10 degree ventrodorsal
- Allows visualization of bulla without superimposition of skull/jaw

133
Q

How is contrast used during a CT?

A

Iodinated contrast medium can be used to IV to improve tissue contrast
- typically iohexol
Administered IV bolus of 880 mg/kg
Highly vascular structures (tumors, inflamed tissues) enhance after contrast

134
Q

How do CTs work?

A

Based on X-ray densitometry
Principles same as conventional radiography
High kV X-ray beam penetrates patient tissue
- Some of original beam absorbed
- Others pass through
X-ray intensity behind patient is measured to form a projected image
- attenuating value (how much resistance) along each ray can be calculated
- bone = high electron density tissue = higher linear absorption = high attenuation
- fluid = low electron density tissue = lower linear absorption = low attenuation
- Hounsfield units (air = -1,000, water = 0, bone =>250)
Mathematical reconstruction of a cross-sectional image

135
Q
A

Incus

136
Q
A

Cochlea

137
Q
A

Malleus

138
Q

Name the bone

A

Promontory

139
Q
A

Vestibular window

140
Q

What are the benefits and drawbacks of positive contrast canalography?

A

Detected 14% of ears with a rupture that were otoscopically intact
False negative in 42%
- Trower et al., 1998
TM identified in 200; 22 too stenotic
Detected 3 ears with a rupture that were otoscopically intact
- Eom, et al., 2000

141
Q

Which imaging modalit(ies) for the middle ear use ionizing radiation?

A

Traditional radiography
CT
*not MRI

142
Q

What is MR signal intensity the function of?

A

-Hydrogen concentration (proton density)
-Tissue relaxation times
-Blood movement

143
Q

What happens to fluid, air, fat, and bone in a T1-weighted MR image?

A

fluid (i.e. cerebral spinal fluid or fluid in the middle ear) will be hypointense (black)
Air and cortical bone will be hypointense (black)
fat will be hyperintense (white)

144
Q

What happens to fluid, air, fat, and bone in a T2-weighted MR image?

A

fluid (i.e. cerebral spinal fluid or fluid in the middle ear) will be hyperintense (white)
Air and cortical bone will be hypointense (black)
fat will be hyperintense (white)

145
Q

What is used for contrast in MRIs?

A

Gadolinium DTPA
-Paramagnetic substance with unpaired electrons.
-Causes adjacent hydrogen nuclei to relax more quickly
-Contrast-enhancing structures will appear hyperintense (white) on T1-weighted studies

146
Q

On CT, how does the middle ear of normal brachycephalics look different than those of mesocephalics?

A

smaller
flatter
TB thickness is different between rostro-ventral (thicker) and caudo-ventral
- not seen with mesocephalics
- comparatively may appear thicker
more likely to have incidental fluid in the middle ear
have a thicker soft palate

147
Q

How do ceruminolytics work and what are some examples?

A

Hydrate desquamated sheets of corneocytes, inducing keratolysis and disintegration of cerumen
Ex. Docusate sodium, triethanolamine polypeptide oleate, urea or carbamide peroxide, salicylic acid, squalene, mineral oil, propylene glycol, glycerin
*urea or carbamide peroxide for in-hospital only because they need to be flushed out
*1997 found 25% squalene to be non-toxic

148
Q

How do surfactants work and what are some examples?

A

-Decrease surface tension between water and lipids or organic solids to break up and help remove debris
-Sodium lauryl sulfate, cocamidopropyl betaine

149
Q

What are two commonly used components of ear medications that can frequently cause topical reactions?

A

–Neomycin
–Propylene glycol

150
Q

Why are aminoglycosides in a lot of topical ear medications?

A

They have good activity against most otic pathogens
–Gram positive
–Gram negative (some not as good against P. aeruginosa)

*ototoxicity is a concern though
*are inactivated in purulent debris

151
Q

What is in Tresaderm?

A

Thiabendazole
dexamethasone
neomycin sulfate

152
Q

What is Otomax?

A

Gentamicin sulfate
betamethasone valerate
clotrimazole

153
Q

What is Mometamax?

A

Gentamicin sulfate
mometasone furoate
clotrimazole

154
Q

What is in Panalog/Entederm?

A

Nystatin
neomycin sulfate
thiostrepton
triamcinolone acetonide

155
Q

What is in Synotic?

A

0.01% fluocinolone acetonide
DMSO

156
Q

What is in EasOtic?

A

Gentamicin sulfate
hydrocortisone aceponate
miconazole

157
Q

How well does topical polymyxin B work for ear infections?

A

Good activity against gram-positive and gram-negative organisms
* Esp useful for Pseudomonas aeruginosa
* Also E. coli, Enterobacter, Klebsiella
* Not effective against Proteus
Inactivated in purulent debris
Synergistic when combined with miconazole against gram-negatives and Malassezia

158
Q

What is in Surolan?

A

Polymyxin B
Miconazole
prednisolone

159
Q

How well does topical florfenicol work for ear infections?

A

-Good activity against Staphylococcus pseudintermedius and E.coli
-Not effective against Pseudomonas aeruginosa

160
Q

What is in Osurnia?

A

Florfenicol*
Terbinafine*
betamethasone acetate

*lower concentrations than Claro

161
Q

What is in Claro?

A

Florfenicol*
Terbinafine*
mometasone furoate

*higher concentrations than Osurnia

162
Q

How well do topical fluroquinolones work for ear infections?

A

Good against gram-positive and gram-negative aerobes
-Staphylococcus pseudintermedius
-E. coli, Proteus spp., Enterobacter spp., Klebsiella spp.
-Pseudomonas aeruginosa
Little or no efficacy:
-Streptococcus spp., Enterococcus spp.
-Anaerobes
Reserve infections resistant to other antimicrobial agents and susceptible Pseudomonas aeruginosa infections

163
Q

What is in Baytril otic?

A

Enrofloxacin
silver sulfadiazine

164
Q

What is in Posatex?

A

Orbifloxicin
Posaconazole
mometasone furoate

165
Q

How does TrisEDTA work?

A

Cell surfaces of gram- negative bacteria are damaged by exposure to EDTA
- due to release of lipopolysaccharides, proteins, and phospholipids
–> Leakage of cellular components and increased permeability of antibiotics
Tromethamine enhances the effect of EDTA

166
Q

What is primary secretory otitis media?

A

Seen primarily in KCKS (also reported in other breeds like Boxers)
Sterile (typically) accumulation of mucoid material
- may be due to increased production
- decreased drainage through auditory tube
–> ineffective tensor veli palatine
- or a combination

167
Q

What nerves are involved in innervation of the pinna?

A

Trigeminal (mandibular branch, sensory)
- auriculotemporal branch
Facial (motor and sensory)
Vagus
Second cervical n
- great auricular branch

168
Q

What nerves are involved in innervation of the middle ear?

A

External acoustic meatus n (branch of auriculotemporal from mandibular n.)
Lateral internal auricular n (branch of facial n)

169
Q

What clinical signs are commonly seen with PSOM?

A

guarded and horizontal neck carriage (64%)
neurologic signs (ataxia, facial paralysis, nystagmus, head tilt or seizures) (25%)
otic pruritus without otitis externa (15%)
- potentially “phantom”/neck scratching
otitis externa (15%)
impaired hearing (13%)
- on BAER testing there is variable conductive hearing loss from none to a lot
fatigue (7%)

170
Q

What causes sensorineural hearing loss?

A

to injury to the cochlear hair cells in the inner ear (sensory) or to the auditory nerve (neural)

171
Q

What causes conductive hearing loss?

A

abnormal propagation of sound through the external, middle, and inner ears

172
Q

According to the Orthopedic Foundation for Animals, what is the the only acceptable testing modality for diagnosing canine deafness?

A

BAER test

173
Q

Evaluation of the BAER includes which assessments?

A

Wave morphology
Waveform repeatability
Absolute wave latencies and wave amplitudes
Interwave latencies
Interaural comparisons

174
Q

Can you use chemical restraint when performing a BAER test?

A

Yes

175
Q

Can a BAER test differentiate between conductive and sensorineural deafness?

A

If it is a screening test with just air-conducted clicks and tone-pip/tone-burst stimuli then no
If it includes bone-conducted click stimuli then yes (bypasses the middle ear)

176
Q

What pattern does conductive hearing loss create on a BAER test?

A

prolonged wave I
interwave latencies I through III and I through V are normal
the LI curve parallels the normal curve though is shifted to the right

177
Q

What kind of deafness does this BAER test indicate?

A

Conductive

178
Q

What is happening to puppy 1?

A

Normal hearing

179
Q

What is happening to puppy 2?

A

Deaf in left ear

180
Q

What is happening to puppy 3?

A

Deaf in right ear

181
Q

What drugs are of highest concern for ototoxicity?

A
182
Q

What is happening to puppy 4?

A

Deaf in both ears

183
Q

What two drugs have the highest concern for ototoxicity?

A

Aminoglycosides (eg, gentamicin, amikacin)
cisplatin

184
Q

What is the primary cause of permanent deafness due to ototoxicity?

A

Loss of sensory cells (hair cells) in the internal ear is the primary cause of permanent deficits in hearing or balance.

185
Q

What classes of drugs/factors have high potential for ototoxicity?

A

Aminoglycoside antibiotics (Streptomycin, neomycin, gentamicin)
Antineoplastics (Cisplatin, carboplatin)
Diuretics (Ethacrynic acid, furosemide)
Metallo compounds (Arsenicals including melarsomine, mercurials)
Antimalarial (Quinine)
Analgesics, antipyretics (Salicylates) - temporary
Polypeptide antibiotics (Viomycin, vancomycin, polymyxin B)
Macrolide antibiotics (Erythromycin)
Solvents (propylene glycol, DOSS, carbamide peroxide, triethanolamine)
Environment (Noise, age)
Aqueous Tobramycin
Aqueous ticarcillin
Alcohol based solutions

186
Q

What is a well-defined high-risk factor for aminoglycoside-induced hearing loss in humans?

A

mitochondrial mutations
- mammalian mitochondrial RNA contains similar subunits to the 30S

187
Q

What pattern of ototoxicity does gentamicin cause?

A

cochleotoxicity and vestibulotoxicity
- predilection for balance

188
Q

What pattern of ototoxicity does amikacin cause?

A

preferential for cochleotoxicity

189
Q

What is the estimated incidence of ototoxicity in humans, including cochleotoxicity and vestibulotoxicity, due to aminoglycosides?

A

15% to 50%

190
Q

Is there a relationship between nephrotoxicity and ototoxicity from aminoglycosides?

A

no statistically significant relationship to ototoxicity and the incidence of co-occurrence is only 4.5%

191
Q

How do aminoglycosides affect fetuses?

A

cross the placental barrier and have the potential to cause deafness in the fetus
- esp during “critical period” when the inner ear is developing

192
Q

What is the primary target of ototoxicity caused by aminoglycosides?

A

sensory hair cells, predominantly the outer hair cells (OHC), in the cochlea
- these cells are non-regenerative
- start to die off in base then progress to apical region
sensory hair cells of the vestibule, first lost in the apex of the cristae ampullares

193
Q

What frequencies of hearing are lost first with ototoxicity due to aminoglycosides?

A

higher frequencies (produced in the basal turn) –> progress to lower

194
Q

What are the secondary targets (more common wit high doses or prolonged time) of ototoxicity caused by aminoglycosides?

A

stria vascularis
spiral ganglion cells of the nerve connection to the brain
striolar regions of the maculae in utricle and sacculus

195
Q

What type of hearing loss (permanent or temporary) typically occurs with aminoglycosides?

A

permanent

196
Q

What type of hearing loss (permanent or temporary) typically occurs with cisplatin?

A

permanent, mostly irreversible

197
Q

What type of hearing loss (permanent or temporary) typically occurs with furosemide?

A

temporary

198
Q

What frequency range of hearing loss is typically associated with aminogycosides?

A

High frequencies with progression to lower frequencies

199
Q

What frequency range of hearing loss is typically associated with cisplatin?

A

High frequencies with progression to lower frequencies

200
Q

What frequency range of hearing loss is typically associated with furosemide?

A

Middle frequencies

201
Q

What is the progression of hair cell loss typically seen with aminoglycosides?

A

Beginning in the base and progressing toward the apex

203
Q

What is the progression of hair cell loss typically seen with cisplatin?

A

Beginning in the base and progressing toward the apex

204
Q

What is the progression of hair cell loss typically seen with furosemide?

A

None

205
Q

What changes in the stria vascularis are typically seen with aminoglycosides?

A

Gross degeneration only at later stages of intoxication

206
Q

What changes in the stria vascularis are typically seen with cisplatin?

A

Generally observed; mostly in intermediate cells

207
Q

What changes in the stria vascularis are typically seen with furosemide?

A

Temporary effects on intermediate cells and strial edema

208
Q

What changes in the cochlear nerve are typically seen with aminoglycosides?

A

Nerve degeneration after hair cell loss

209
Q

What changes in the cochlear nerve are typically seen with cisplatin?

A

Damage at the basal coil, and decrease in function

210
Q

What changes in the cochlear nerve are typically seen with furosemide?

A

Temporary impairment of function

211
Q

What side effects on balance are typically seen with aminoglycosides?

A

Possibly severe with some (esp gentamicin) but not all aminoglycosides

212
Q

What side effects on balance are typically seen with furosemide?

A

none (though vertigo is reported as an infrequent side effect in humans

213
Q

What side effects on balance are typically seen with cisplatin?

A

none

214
Q

What is thought to be the molecular mechanism of ototoxicity for aminoglycosides?

A

overproduction of reactive oxygen species (ROS) aka free radicals
triggers several well-defined pathways of cell death in the affected cells
- caspase activation and caspase-independent apoptotic/necrotic pathways

215
Q

What antioxidants are effective against the renal side effects of gentamicin in dogs?

A

silymarin and vitamin E

216
Q

How can the nephrotoxicity of cisplatin be reduced?

A

adequate pretreatment and posttreatment hydration and
concomitant diuresis

217
Q

What kind of category of ototoxicity does cisplatin cause?

A

cochleotoxicity, does not affect the vestibular system

218
Q

How is the ototoxicity of cisplatin related to dose?

A

dose-dependent and may continue to progress after the administration of the drug
is completed

219
Q

What is the primary target of ototoxicity caused by cisplatin?

A

more complex than that of the aminoglycosides
affects a variety of cell types within the cochlea
- loss of OHCs is a major pathologic feature
- reduction of the endocochlear potential generated by the stria vascularis
- pathologic change to spiral ganglion cells.
- compromised function of vestibulocochlear nerve fibers

220
Q

What is thought to be the molecular mechanism of ototoxicity for cisplatin?

A

the excessive production of ROS
- via an internal ear-specific NADPH oxidase, NOX3

221
Q

What might reduce the ototoxicity seen with cisplatin?

A

antioxidants like glutathione, superoxide dismutase, vitamin C, vitamin A, vitamin E, and transferrin

222
Q

How can loop diuretics affect the incidence of ototoxicity for either aminoglycosides or cisplatin?

A

potentiate cisplatin and aminoglycoside-induced hearing loss to the extent that combination treatment may lead to complete deafness even at individually safe doses of the two agents

223
Q

What is the pathology behind the ototoxicity of loop diuretics?

A

primarily act on the nonsensory tissues of the internal ear (not easily measured)
- a decreased endocochlear potential
- reduced the amplitude of the vestibulocochlear nerve action potential
- edema in the stria vascularis with degeneration of intermediate cells
These changes are reversible

224
Q

When are animals the most susceptible to side effects of loop diuretics?

A

young animals in their developmental period

225
Q

What is thought to be the molecular mechanism of ototoxicity for loop diuretics?

A

closely related to their pharmacologic properties
both the kidney and the ears have ion-transporting epithelia that are targeted
- increase in the Na concentration and a reduction in K activity in the endolymph

226
Q

What might reduce the ototoxicity seen with loop diuretics?

A

inhalation of oxygen
coadministration of triamterene (a potassium-sparing diuretic
iodinated benzoic acid derivatives (diatrizoate and probenecid)
organic acids (sodium salicylate and penicillin G)

227
Q

What is the spiral ganglion?

A

The section of the cochlear nerve that directly innervates the hair cells

228
Q

What are feline nasopharyngeal/aural/inflammatory polyps?

A

relatively common benign masses
arise from the mucosal lining of the middle ear, the auditory tube, or the nasopharynx
often occur in young cats, but can be identified at any age

229
Q

What are the treatment options for nasopharyngeal/aural/inflammatory polyps in cats?

A

Trans-tympanic traction-avulsion (with VO) - if in ear
Traction-avulsion with rostral soft palate retraction - if in mouth
Ventral bulla osteotomy
Potentially normograde rigid rhinoscopy-assisted traction-avulsion

230
Q

What are the most common bacterial isolates from middle ears of cats with nasopharyngeal/aural/inflammatory polyps?

A

No growth for nearly half, but the ones that did had:
Pasteurella multocida; other isolates included Staphylococcus sp., Pseudomonas aeruginosa, Mycoplasma sp., Streptococcus sp., Corynebacterium sp. and Bordetella bronchiseptica

231
Q

What percent of cats have bilateral feline nasopharyngeal/aural/inflammatory polyps?

A

As high as 24%

232
Q

What is the recurrence rate of feline nasopharyngeal/aural/inflammatory polyps following traction polypectomy

A

14.3-59% depending on the study
Lower with prednisolone?
- one study found none of the cats treated with prednisolone had recurrence

233
Q

What is the recurrence rate of feline nasopharyngeal/aural/inflammatory polyps following VBO?

A

0–33%

234
Q

What is the etiology of feline nasopharyngeal/aural/inflammatory polyps?

A

Unclear whether polyps are congenital in origin or a response to inflammation
Potentially related to chronic viral or bacterial infections

235
Q

What is the histopathologic appearance of feline nasopharyngeal/aural/inflammatory polyps?

A

well-vascularized fibrous connective tissue covered by stratified squamous or columnar epithelium
inflammatory cells, primarily lymphocytes, plasma cells and macrophages are present within the stroma and are especially dense in the submucosal areas of the tissue

236
Q

Why can the visual confirmation of complete removal of a feline nasopharyngeal/aural/inflammatory polyp vial the ear canal be challenging?

A

The auditory tube valve opening faces rostrally
Bleeding

237
Q

What are canine aural polypoid masses?

A

A benign non-neoplastic, polypoid mass in the ears of dogs

238
Q

Where do human aural inflammatory polyps typically arise from?

A

within the tympanic bulla

239
Q

Where do canine aural polypoid masses typically arise from

A

the external ear canal
* a mass like this has been reported in horses too

240
Q

What is the etiology of canine aural polypoid masses?

A

largely unknown, yet chronic OE has to be considered a contributing factor

241
Q

What is the histopathologic appearance of canine aural polypoid masses?

A

Variable though most were consistent with the fact that they arose from the canal
- few had cuboidal to columnar epithelium indicating potential middle ear origin
Keratinizing squamous epithelium covered the aural polypoid masses (APMs) in 14 of 20 dogs, with acanthosis (12 of 14), orthokeratotic hyperkeratosis (6 of 14) and ulceration (3 of 14)
Hair follicles, sebaceous glands and/or ceruminous glands were identified in 9 of 14 APMs with squamous epithelium, while 5 of 14 samples lacked adnexa. The remaining 6 of 20 APMs had either a combination of squamous to cuboidal to ciliated columnar epithelium (5 of 6 dogs) or only ciliated columnar epithelium (1 of 6 dogs)
Inflammatory cell types varied, including lymphoplasmacytic, neutrophilic and histiocytic. The inflammation was embedded in a fibrovascular stroma in 19 of 20 masses

242
Q

What is presbycusis?

A

reduced auditory perception with advancing age (primarily sensorineural but possibly conductive)
– ABIOTROPHY of hair cell/spiral ganglion cells of cochlea
–> middle and high frequencies first

243
Q

What are typically considered non-ototoxic medications?

A

Squalene
Aqueous solution of iodine
Acetic acid 2-2.5%
Chlorhexidine <0.2% in dogs (no dilution seems safe in cats)
Aqueous fluoroquinolone and gentamicin (weird)
TrizEDTA

244
Q

What is an aural cholesteatoma aka tympanokeratoma?

A

epidermoid cyst of the middle ear described in several species, including dogs, cats, humans and Mongolian gerbils (usually middle-aged)
- lining consists of stratified, keratinizing squamous epithelium
- central accumulation of a keratin debris
- does not have cholesterol and is not a neoplasm
often unilateral but can be bilateral
causes expansile pressure necrosis of tissue of the middle/inner ear
- may also cause pain on opening mouth
can lead to secondary infections

245
Q

What is the treatment for aural cholesteatomas aka tympanokeratomas?

A

Surgery often curative (50% recurrence) but palliative flushing possible

246
Q

What are the theories behind the development of aural cholesteatomas aka tympanokeratomas?

A
  • Primary form: Dysfunction/poor ventilation of auditory tube which leads to invagination of the tympanic membrane into the bulla (invagination theory)
  • Secondary forms: arises secondary to chronic otitis, trauma to the middle ear
    1) Metaplasia theory: modified ciliated respiratory epithelium in the bulla undergoes a metaplastic transformation into stratified squamous epithelium because of chronic inflammation
    2) Migration theory: breaks of tympanic membrane can lead to migration of the stratified squamous epithelium from external ear canal into the bulla → keratin formation and accumulation
    3) Invasion theory: keratinizing epithelial cells of the tympanic membrane migrate into the subepithelial space of the bulla through a basement membrane breach
247
Q

What is the ear canal like in sauropsids (reptiles and birds) and amphibia?

A

shallow or non-existent

248
Q

What is the structure of the equine ear canal?

A

pigmented cartilaginous and nonpigmented osseous part
osseous part has an hourglass shape
- angled in a dorsolateral-to-ventromedial direction and becomes very narrow
–> endoscopic instruments are usually too large to reach TM w/awake
–> can do it with sedation and local anesthesia