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Pathologies > Outer Ear Disorders > Flashcards

Outer Ear Disorders Flashcards

1
Q

Aural Atresia Symptoms

A

can involve 1 or both ears and is the absence of EAC or presence of blind pouch in the canal.

Will give a conductive loss and if bilateral and untreated it can significantly delay speech.

Stenosis of the ear can also lead to collection of skin epithelial cells in external auditory canal (External canal cholesteatoma) –> inflammation, pain and/or discharge

If it involves the ME, then TM is absent and ossicles can be malformed or absent

If involving inner ear, less common due to distinct embryologic tissues

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2
Q

Aural Atresia Incidence/Prevalence

A

males affected more frequently, unilateral is 3x more common than bilateral, right ear tends to occur more than left, atretic portion of canal is usually bony not membranous, occurs 1/10,000-20,000 births

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3
Q

Aural Atresia Etiology

A

congential can occur in conjunction with syndromes (CHARGE, Pierre Robin, VATER, Goldenhar, Treacher Collins)

-Ossicles form from 4th gestational week-16th, at week 8 first brachial groove forms plug of cells migrates medially to oppose development of middle ear cleft --> cells hollows out to form epithelial lined EAC during 6th month of gestation ---any interruption results in ossicular malformation or atresia of canal
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4
Q

Aural Atresia Type A

A

a. Type A: meatal atresia, lateral cartilaginous portion of canal (narrowed preventing cerumen and skin cells to exit external canal)

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5
Q

Aural Atresia Type B

A

b. Type B: partial atresia, narrowing of cartilaginous and bony portion of canal (narrowed ear canal allows visualization of TM but malformations of ossicles are common)

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6
Q

Aural Atresia Type C

A

c. Type C: total atresia, complete atresia of cartilaginous and bony portions of canal, but ME and mastoid are aerated, TM typically absent and ossicles fused and adherent to atretic plate (bone adjacent to ME)

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7
Q

Aural Atresia Type D

A

d. Type D: hypopneumatic atresia similar to type c but mastoid is poorly pneumatized and facial nerve has aberrant course within temporal bone

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8
Q

Audiology of Atresia

A
  1. Audiology: Evaluate infant with ABR (typically present significant conductive loss), after perform BC on atresia side and place masking on the other side, bilateral atresia need to use BC ABR but cannot know for certain which ear has better hearing
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9
Q

Medical Assessment of Atresia

A

Need to examine if there are any craniofacial anomalies, facial nerve, any degree of microtia, CT scanning to determine location and severity of compromise

Possible surgical intervention depending on SN function and inner ear malformations: a score of 5 or less (grading scale based on point for normal radiographic appearance) disqualifies someone from surgery –> aural atresia typically repaired at age 1-2 years of age and microtia repaired 6-7 years of age —> Drill new EAC within temporal bone and carefully avoiding mastoid air cells, middle cranial fossa dura mater and facial nerve, TM graft made

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10
Q

Aural Atresia

A

ear canal fails to develop resulting in abnormally closed/absent canal

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11
Q

Eustachian Tube Dysfunction

A

Eustachian tube with ME opening in anterior medial aspect of ME, proximal 1/3 of tube passes through petrous portion of temporal bone, distal 2/3 is primarily cartilaginous, terminates in superior lateral aspect of nasopharynx, tensor veli palatini and levator veli palatini responsible for opening/closing of Eustachian tube. AT REST=CLOSED, negative pressure retracts TM (otitis media)

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12
Q

Eustachian Tube functions

A

Functions: 1. ventilation of ME 2. protection from nasopharynx 3. clearance of secretions of ME

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13
Q

Eustachian Tube Dysfunction Symptoms

A

negative ME pressure (pain, pressure in ear), serous fluid collection (otitis media with effusion), autophony (perception of one’s breath and speech excessively loud)–constantly open tube

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14
Q

Eustachian Tube Dysfunction Incidence

A

affects 70-90% of kids by age 2 years, more common in kids under 5, males and Native americans, low SES

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15
Q

Etiology of Eustachian Tube

A

shorter in kids, accounting for increase of prevalence in kids, reaches adult size by age 7 – more flat in kids than adults (45 degree angle), patulous eustachian tube associated with weight loss, pregnancy, stroke, degenerative neurologic disorders can lead to muscle atrophy

buildup of negative middle ear pressure–effusion

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16
Q

Site of Lesion for Eustachian tube dysfunction

A

nasal cavity, inflammation/mass effect obstruction, tube can be obstructed to inflammation within tube itself or functionally not open because of peritubal muscle function

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17
Q

Audiology of Eustachian tube dysfunction

A

take baseline tymp – creating positive/negative pressure asking patient to swallow several times – no change in peak pressure suggests dysfunction – if HL it will be conductive or mixed

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18
Q

Otitis Media

A

inflammation of ME –> purulent effusion can develop because of bacteria can resolve into serous effusion before complete resolution

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19
Q

Chronic Otitis media

A

presence of OM for 30 days or more

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20
Q

Acute Otitis Media

A

3 or more bouts within 6 months or 4 or more in 1 year

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21
Q

Chronic Suppurative OM

A

persistent inflammation and disease of ME

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22
Q

Symptoms of Otitis Media

A

fever, otalgia, pressure, irritability, conductive HL or asymptomatic

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23
Q

Incidence of OM

A

over 90% of caucasian and african american kids in first 2 years of life

up to age 3 kids usually experience one episode of acute otitis media per year,

middle ear with effusion occurs most in kids under 6

more often in pediatric pts in IC

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24
Q

Etiology of OM

A

Eustachian tube dysfunction, upper respiratory infection can occur in conjunction

diseases that impair the immune system, smoke exposure, lower SES

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25
Q

Audiology of OM

A

tymp, audio eval, negative ME pressure

early on to a flat tymp, typically mild range but can fluctuate

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26
Q

Medical Exam & Management

A

purulent OM may not be easily visualized due to thickening of TM

Management: antibiotics, PE tubes with 3 or more episodes in 6 months or 4 or more in 1 year

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27
Q

Cholesteatoma

A

collection of keratin-producing squamous epithelial cells within ME – can manifest with persistent perf of TM, erosion of ossicles

ME granulation tissue

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28
Q

Primary Acquried Cholesteatoma

A

squamous collection within retracted TM pocket

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29
Q

Secondary Acquired Cholesteatoma

A

squamous cell migration through TM perf into ME

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30
Q

Symptoms of Cholesteatoma

A

typically cause conductive HL when impinge on ossicles

secondary choelsteatoma with bacterial colinization leads to persistent foul-smelling otorrhea, pain and possible ossicle erosion — can damage VII when erodes bone and CAN LEAD TO MENINGITIS

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31
Q

Incidence of Cholesteatoma

A

3/100,000 for ACQUIRED

9.2/100,000 for all ages with male predominance

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32
Q

Etiology of Congenital Cholesteatoma

A

remnant of embryonic epithelial cells nests trapped in ME during development

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33
Q

Etiology of Secondary Cholesteatoma

A

result of long term Eustachian tube dysfunction

invagination of squamous epithelium with retracted TM, bacteria, ossicles can be eroded – perf TM

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34
Q

Site of Lesion for Cholesteatoma

A

Congenital: anterior mesotympanum/ protympanum

Primary acquire: most common is posterior epitympanic space / Prussak’s space

Secondary acquired: posterior aspect of pars tensa – can extend into petrous portion of temporal bone

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35
Q

Audiology for cholesteatoma

A

tymp, eval, complicance is typically reduced

amplification required depending on medical management

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36
Q

Medical Management of Cholesteatoma

A

Tympanoplasty

Mastoidectomy – maybe ossiculoplasty depending on outcome of surgery

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37
Q

Mastoidectomy

A

removal of Cholesteatoma and any diseased mucosa within air cells of mastoid by drilled cholesteatoma and diseased muscosal away

after 6-12 months can inspect ossicles

mastoid bowl must be examined regularly to remove debris and need to keep it completely dry

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38
Q

Glomus Tumors

A

benign, slow growing, very vascularized tumor, arise from collection of neuroendocrine paraganglial cells – originating from neural crest cells surrounded by dense collection of capillaries and venules

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39
Q

Paragangliomas

A

glomus jugulare tumors develop from paraganglial tissue within adventita of jugular bulb – can affect hearing

40
Q

Glomus tympanicum

A

tumors develop from paraganglion, adjacent to either Jacobson’s nerve or Arnold’s nerve

confined to ME space but can extend to mastoid or EAC

41
Q

Ascending Pharyngeal ARtery

A

provides primary blood supply to glomus tumors of temporal bone

42
Q

Glomus Tumor Symptoms

A

variable, develop gradually, conductive hearing loss, otalgia, aural fullness, PULSATIVE TINNITUS

if tumor expands can compromise facial nerve–leading to paralysis, erosion of labyrinth

can result in vertigo and SNHL – can cause hypertension, palpitations, arrhythmias, diaphoresis

43
Q

Incidence/Prevalence for Glomus Tumor

A

1 per 1.3 million people, more common in caucasians and in women usually between age 40-70

can be transmitted autosomal dominant

44
Q

Etiology and Pathology of Glomus Tumor

A

benign and slow growing tumor, travels along path of least resistance – cluster of cells surrounded by dense network of capillaries and venules

metatsis occurs in 1-4% of patients, more prevalent in families with inherited disease

Chief cells & sustentacular cells

45
Q

Chief Cells & Sustentacular Cells & Glomus Tumor

A

Chief cells: neuroendocrine cells filled with vasculative compounds that can be secreted as described above

sustentacular cells: similar to schwann cells, support chief cells

46
Q

Site of Lesion for Glomus tumor

A

ME space, originate from paraganglia traveling along Jacobson’s or Arnold’s nerve on promonotory

47
Q

Audiology for glomus tumor

A

any pattern of HL, rare cases have normal hearing

76% of HL was conductive, pulsating beat to pt’s heartbeat

monitor with audio or provide amplification

48
Q

Medical Management of Glomus tumor

A

bluish or reddish mass behind TM – can erode through TM and present as mass in EAC

if secreting tumor is suspected do urine analysis – imaging studies to manage tumors

49
Q

Otosclerosis

A

metabolic bone-remodeling disease of temporal bone, primarily affects otic capsule and ossicles

50
Q

Otosclerosis Symptoms

A

conductive HL, typically unilateral but can become bilateral, tinnitus can be present, family history

vertigo/dizziness is uncommon

51
Q

Otosclerosis Incidence and Prevalence

A

most common cause of adult conductive HL – only 1% of population

more common in caucasian pts and women more affected between 20-40s, pregnancy accelerate presentation of disease

autosomal dominant transmission with incomplete penetrance

52
Q

Otosclerosis Etiology and Pathology

A

bone becomes reabsorbed, immature bone laid done in endocondral bone of otic capsule – becomes mineralized

when it occurs around oval window stapes footplate becomes fixed and fails to conduct sound into cochlea efficiently

SNHL can occur if cochlea becomes involved

53
Q

Otosclerosis Site of Lesion

A

anterior to stapes footplate, fissual ante fenestrum

round window can also become involved – involves damage to spiral ligament leading to progressive SNHL

54
Q

Otosclerosis Audiology

A

amount of conductive HL correlates with degree of stapes fixation

carhart notch at 2kHz, may demonstrate reduced compliance

55
Q

Medical Management

A

surgical intervention if HL more than 25dB, promontory may have reddish hue (Schwartze’s sign)

stapedectomy vs stapedotomy

56
Q

stapedectomy

A

removal of portion or entire stapes footplate, grafting open oval window – placement of prosthesis from long process of incus to graft

57
Q

stapedotomy

A

creating hole in fixed footplate with drill or laser

placing prosthesis from incus to stapedotomy site

58
Q

Temporal Bone Trauma Symptoms

A

afflicted with other injuries especially intracranial injuries – VII nerve can be impinged by bone fragment or severed completely, blood otorrhea, CSF leak

59
Q

Temporal Bone Trauma incidence/prevalence

A

car accidents 75%, barotrauma, more common in men in 30s-40s

60
Q

Etiology and Pathology of temporal bone trauma

A

significant force to lateral aspect of skull, force of more than 1800lbs per squre inch

longitudinal fractures are more prevalent and account for 70-80% of temporal bone trauma

61
Q

Site of lesion for temporal bone trauma

A

injury of otic capsule, facial nerve near geniculate ganglion

ossicles can be affected, incudostapedial joint most common site of dislocation

62
Q

Temporal bone trauma audiology

A

can be fluid/blood in EAC, ENoG can be necessary in cases of facial nerve involvement

63
Q

Temporal bone medical management

A

may need tympanoplasty if perf lasts too long – check out status of cranial nerves, ossicular disarticulation, vertigo is common, treat CSF leak

64
Q

External Otitis

A

caused by swimming in water with lots of bacteria, fungal infections

redness and swelling of tissues (pinna and EAC), little effect on hearing

65
Q

Exostoses

A

bony growths occuring in bony portion of EAC related to cold water exposure, can make it difficult to visualize TM

66
Q

Osteoma

A

bony growth (singular) just lateral of bony portion of EAC, related to cold water exposure

67
Q

TM Perf

A

can occur in pars tensa or flaccida but if occurs in flaccida – increased concern for cholesteatoma

large TM perf can result in up to 50dB HL

68
Q

Tympanosclerosis

A

white calcified plaques of connective tissue occur at/around circumference of TM and/or head of malleus

myringosclerosis is when it is only on TM – little L if only on TM

69
Q

Ossicular chain Disarticulation

A

conductive HL, hypercompliant TM

no crossed acoustic reflex even with normal hearing

otologic surgery to repair dislocation (ossiculoplasty)

70
Q

Microtia

A

Type 1: small but normal looking ear
Type 2: moderately deformed external ear
Type 3: only a little tissue visible
Type 4: anotia: no sign of any ear

somethings associated with middle ear pathology because during development pharyngeal arches are close together with same tissue (arches 1&2)

71
Q

Microtia Etiology

A

Genetic or drug related

72
Q

Microtia Audiology

A

should be normal, sound collecting quality from pinna (short wavelength HF, subtle differences in performance that require HF info)

73
Q

Preauricular tag

A

cosmetic deformity, genetic – surgical excision

may be indicative of other things going on in ME or EAC that occurred during development

74
Q

Preauricular sinus or pit

A

malformation in soft tissue near auricle

genetic – can be benign or indicate more medial pathologies – hygiene should be part of counseling because if its larger could collect bacteria/become infected

75
Q

Dermatitis

A

inflammation of skin

reddness, crusting of skin, most likely medical referral to dermatologist especially if its painful dont wat to put inserts in

76
Q

Keratosis

A

Multiple layers of thick, flakey skin

sometimes pre-cancerous (skin cancer)

77
Q

Keloid

A

build up of scar tissue

typically secondary to trauma, higher prevalence in black individuals

78
Q

Cauliflower

A

dead cartilage, typically secondary to trauma

blood clots causes cartilage to separate from overlying skin

DISORDER OF CARTILAGE – DIES excessive trauma, blood clots cause cartilage to separate from overlying skin

79
Q

Shingles

A

Can invade EAC, cannot use a HA–not going to cause a progressive HL but will interfere with HA use

viral disease wtih painful blisters

80
Q

Impacted cerumen

A

increase prevalence with aging

degeneration of elastic fibers and collagen (helps helps with migration)

increased growth and thickness of hair follicles (hold onto the wax)

drier wax, physical obstruction due to HA

57% of older pts in nursing homes, 10% of kids, 36% patients with intellectual disability – may make tinnitus louder

81
Q

Otomycosis

A

ear infection caused by fungus

white discharge – extremely painful

not as frequently occurring, would use anti-fungal medication

82
Q

Collapsing EAC

A

affected young kids and elderly – cartilage is starting to break down

test by pressing cartilage and looking to see if lateral wall is closing in

conductive HL with normal tymps

83
Q

CT Scan

A

Cross-sectional imaging –look at different slices of skull bones

quick time, better at identifying abnormalities in the bone – often used for looking at aspects of skull

84
Q

MRI

A

protons in water molecules align along magnetic field

T1: weighted differentiates fat (lighter) and water (darker), can be run quickly – gray/white matter contrast

T2: weighted differentiates fat (darker) and water (lighter) – better at identifying changes in water concentration (edema) – better contrast resolution, visualize soft tissue & can show blood circulation –> ACOUSTIC NEUROMA

85
Q

Valsalva

A

hold nose and blow – creating positive pressure in ME space so should see movement. Have them swallow and look for a change – if can see changes in peak of tymp then indicates normal eustachian tube

86
Q

Patulous (Patent) ET

A

occurs when ET does not close – associated with weight loss or pregnancy

changes in soft tissue mass or chatacerstics

Autophony (own voice sounds very loud to you), tymps can reveal breathing patterns

87
Q

Mastoiditis

A

mastoid air cells are covered with mucosa which is in ME space – reddness in mastoid area, fullness, pain, OM, tenderness and conductive HL

less of a problem due to antibiotics and PE tubes

mastoid bowls:

88
Q

Willis Paracusis

A

occurs with individuals with otosclerosis

hearing better in background noise – LF conductive HL – noise is cut out and can hear speech people better

conductive HL acts like a low frequency filter

89
Q

Barotrauma

A

Most prevalent problem associated with airplane travel

damages tissues when pressure is different between ear and air pressure outside body that may cause pain or sensation of aural fullness

90
Q

Outer ear Barotrauma

A

occurs when object is occluding EAC and traps air within it, causes vacuum effect

91
Q

Inner Ear Barotrauma

A

unequal pressure between inner ear and pressure outside of the body, occurs predominantly in shallow water

92
Q

Middle ear Barotrauma

A

occurs when pressure between middle ear space is unequal to surroudning pressure outside the body, complications cause hemorrhaging or ruptured TM

93
Q

Barotrauma signs & symptoms

A

TM retraction, fluid or blood behind TM, perforation of TM

aural fullness or ear blockage, pain, conductive HL

inner ear: SNHL, vertigo, dizziness, immediate tinnitus or late onset tinnitus after incidence

94
Q

Longitudinal Temporal Bone Fracture

A

most common cause: car accidents 75%, motorcycle accidents, gunshot wounds

95
Q

Longitudinal Temporal Bone Fracture Symptoms

A

facial paralysis or muscle weakness–VII nerve severed or damaged

conductive HL, ossicular separation, hemotympanum: blood in ME, TM perf

blood otorrhea, CSF leak could cause otorrhea or rhinorrhea

96
Q

Medical Management of Longitudinal Temporal Bone Fracture

A

May need ENoG–place electrodes on head and stimulate auditory system with acoustic info and measure muscle resonse

steroids, tympanoplasty if TM perf doesn’t heal

97
Q

Why does Carhart’s Notch appear with otosclerosis?

A

With otosclerosis, due to fixation of stapes in oval window both inertial and osseotympanic (still utilizing ossicular chain in third way) BC is compromised. most obvious reason is seen at 2kHz which is natural resonant frequency of ME ossicles thus carhart’s notch does not represent cochlear hc damage at 2 but actually mechanical artifact of BC testing

Pathologies (5 decks)

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