Middle Ear Pathologies, Bony Diseases and Cholesteatoma Flashcards

1
Q

What are the important parts of the ME?

A
  • Some of the ossicles will not be seen through the eardrum
  • Stapes is posterior to malleus
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2
Q

What is the orientation of the ME parts in the Anterior view?

A

The shape of the eardrum looks like a dish or bowl not flat

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3
Q

What are the 3 layers of the pars Tensa?

A

Composed of 3 layers
1. Outer-squamous: epithelium/skin same cells
2. Middle-fibrous: gives rigidity to the membrane
3. Inner-mucosa: same as skin in nose

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4
Q

How big are the ossicles?

A

Smaller than a dime

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5
Q

What is the bulk of the TM called?

A

Pars tensa

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6
Q

What is the name of the section of the TM over the lateral process of the malleus?

A

Pars Flaccida (doesn’t have fibrous layer)

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7
Q

What are the three main Physiology aspects of the ME?

A
  • Aerated space
  • Eustachian tube
  • Mastoid space
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8
Q

Why does the ME need to be aerated and why do the ossicles look this way?

A

Transfer of sound energy from low-impedance air to the high-impedance cochlear fluid

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9
Q

Which way does the ME match the impedance?

A

Lever effect 2.5 dB Longer malleus to shorter incus transfer of energy

Area effect 25 dB high area eardrum to a low area stapes footplate

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10
Q

What are the typical causes of TM perforation? (6)

A

Trauma
Infection (most common)
Cholesteatoma
Tympanostomy tubes
Tympanosclerosis
Spontaneous

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11
Q

What is the difference between both these TM perforation?

A

Marginal and central perforation (worst)

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12
Q

How do you treat small perforations of the TM?

A

With time it heals by itself

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13
Q

What problems can be caused by a perforated TM? (2)

A

Recurrent infections/otorrhea
CHL (reduced immittance/energy transfer mechanism)

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14
Q

How do you manage the TM perforations? (2)

A
  1. Monitor (most heal with time)
  2. Tympanoplasty
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15
Q

What is Tympanosclerosis?

A
  1. Scarring of the tympanic membrane Aka myringosclerosis
  2. CHL is rare
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16
Q

What can cause tympanosclerosis? (3)

A
  1. Otitis media
  2. Tympanostomy Tubes
  3. TM perforation

Heals by itself

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17
Q

What is this condition?

A

TM Granulation: causes by foreign bodies being fought off by the immune system most of the time

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18
Q

What is this condition?

A

Hemotympanum

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19
Q

What is this condition

A

Retraction Pockets

20
Q

What is this condition?

A

Middle Ear Atelectasis/Collapse

21
Q

What is Bullous Myringitis?

A
  • Inflammatory condition of TM
  • Fluid-filled vesicles
  • Sudden onset of severe otalgia
  • Often follows AOM
  • Treat with antibiotics, analgesics and drainage
22
Q

What is otosclerosis?

A

Oto = ear
Sclerosis = hardening or fibrosis of the bone

A metabolic bone disease of the otic capsule (embryological origin of some of our ear structure)

23
Q

What is the epidemiology of Otosclerosis?

A
  • Typically present in the 2nd-4th decades of life
  • Rarely in children (congenital fixation of stapes)
  • More common in females (2:1)
  • Mostly Caucasians (non-existent in First * Nations/Indigenous)
  • 10% of all temporal bones showed histological changes of otosclerosis in one study
  • Becoming less common
24
Q

What causes Otosclerosis?

A

Idiopathic: tends to just appear
* Genetic
- Family history present in 50-70%
- AD with incomplete penetrance
* Hormonal
- F > M almost 2 to 1
- Accelerated during pregnancy
* Viral
- Reduced after measles vaccination

25
What are the two pathophysiology phases of Otosclerosis?
Active Phase Mature Phase
26
Describe the Active phase in Otosclerosis Pathophysiology:
“Otospongiosis” Osteoclasts more active Resorption of bone Schwartze’s sign
27
Describe the Mature phase in Otosclerosis Pathophysiology:
Osteoblasts more active Deposition of new bone
28
What are the common sites of involvement of Otosclerosis? (4)
Fissula ante fenestrum (anterior part of footplate) Round window The anterior wall of IAC Inner ear “cochlear otosclerosis”
29
What are the common places of Otosclerosis?
* STAPES footplate fixation - CHL - Better understanding in noise (paracusis of Willis) * Inner ear involvement  SNHL * HL progresses from low to high frequencies * Low-frequency tinnitus Bilateral in 70% of patients
30
What are the signs in the audiogram that indicates Otosclerosis?
- Air-bone gap (CHL) - Carhart’s notch - Normal discrimination - Tympanograms (normal or As)
31
What is a Cahart's Notch?
* At 2000 Hz, air and bone conduction come together to appear as a SNHL * Theories - Disrupted ossicular resonance/perilymph immobility - Mechanical artifact * Reverses with stapedotomy
32
How do you manage Otosclerosis? (4)
Depends on the degree of Hearing loss * Conservative (for mild cases) * Audiological - Amplification * Medical - Sodium fluoride - Vitamin D and calcium carbonate * Surgical
33
Why is Otolsclerosis amplification a good option? (2)
For Poor surgical candidates For Patients who don’t want surgery
34
What are Otosclerosis Amplification problems? (5)
Canal occlusion effect Sound quality No amplification at night Cost Cosmetic
35
What is the surgical device we use in Otosclerosis?
Bone-anchored hearing aids (BAHA)
36
How does BAHA work? (3)
* Titanium screw placed in the temporal bone * Sound processor connected to the screw causes vibrations * Sound energy bypasses the external and middle ears
37
What is Stapedectomy?
A surgical management option against Otosclerosis
38
What is superior semicircular canal dehiscence (SSCD)?
Bony defect of superior semicircular canal
39
What are clinical features of SSCD?
Autophony (own voice echoes in your head) Dizziness CHL (low-freq) Hyperacusis Tullio phenomenon
40
What is cholesteatoma? (3)
* A collection of squamous keratin * Produced from squamous epithelial cells (not normal outside of EAC) mostly appears on top of ossicles or pars flaccida * Exhibits independent growth and locally aggressive * Should really be called keratoma
41
What are the two ways to develop cholesteatoma?
* Congenital (Left) Gradual growth over time Presents early in life * Acquired Primary acquired (retraction pocket) Secondary acquired (TM perforation)
42
What is acquired cholesteatoma associated with?
Associated with chronic ETD and recurrent OMs - TM is weakened resulting in retraction pockets or perforations Presents later in life
43
Describe Primary Acquired cholesteatoma (3) :
1. Chronic ETD 2. Deep retraction pocket (pars flaccida) 3. Collection of keratin within the retraction pocket
44
Describe Secondary Acquired cholesteatoma:
Secondary acquired 1. Chronic ETD 2. Recurrent OMs 3. Chronic TM perforation In-growth of keratin via the TM perforation
45
What are the clinical presentations of Cholesteatoma? (3)
* History Otorrhea, hearing loss, otalgia, aural fullness, dizziness, tinnitus * Past medical history OMs, TM perforations, trauma, ear surgery * Most common presentation involves unilateral chronic otorrhea and hearing loss
46
What can we see in this Otoscopic Evaluation?
1. Pars flaccida (attic) crusts and CHL -> suspect cholesteatoma 2. This isn’t just wax-suspect underlying pocket and cholesteatoma
47
What are the causes of Hearing loss due to Choleosteoma? (2)
1. Ossicular erosion (mostly CHL) 2. Labyrinthine fistula (SNHL, vertigo)