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
Q

What are the two pathophysiology phases of Otosclerosis?

A

Active Phase
Mature Phase

26
Q

Describe the Active phase in Otosclerosis Pathophysiology:

A

“Otospongiosis”
Osteoclasts more active
Resorption of bone
Schwartze’s sign

27
Q

Describe the Mature phase in Otosclerosis Pathophysiology:

A

Osteoblasts more active
Deposition of new bone

28
Q

What are the common sites of involvement of Otosclerosis? (4)

A

Fissula ante fenestrum (anterior part of footplate)
Round window
The anterior wall of IAC
Inner ear “cochlear otosclerosis”

29
Q

What are the common places of Otosclerosis?

A
  • 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
Q

What are the signs in the audiogram that indicates Otosclerosis?

A
  • Air-bone gap (CHL)
  • Carhart’s notch
  • Normal discrimination
  • Tympanograms (normal or As)
31
Q

What is a Cahart’s Notch?

A
  • 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
Q

How do you manage Otosclerosis? (4)

A

Depends on the degree of Hearing loss

  • Conservative (for mild cases)
  • Audiological
    • Amplification
  • Medical
    • Sodium fluoride
    • Vitamin D and calcium carbonate
  • Surgical
33
Q

Why is Otolsclerosis amplification a good option? (2)

A

For Poor surgical candidates
For Patients who don’t want surgery

34
Q

What are Otosclerosis Amplification problems? (5)

A

Canal occlusion effect
Sound quality
No amplification at night
Cost
Cosmetic

35
Q

What is the surgical device we use in Otosclerosis?

A

Bone-anchored hearing aids (BAHA)

36
Q

How does BAHA work? (3)

A
  • Titanium screw placed in the temporal bone
  • Sound processor connected to the screw causes vibrations
  • Sound energy bypasses the external and middle ears
37
Q

What is Stapedectomy?

A

A surgical management option against Otosclerosis

38
Q

What is superior semicircular canal dehiscence (SSCD)?

A

Bony defect of superior semicircular canal

39
Q

What are clinical features of SSCD?

A

Autophony (own voice echoes in your head)
Dizziness
CHL (low-freq)
Hyperacusis
Tullio phenomenon

40
Q

What is cholesteatoma? (3)

A
  • 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
Q

What are the two ways to develop cholesteatoma?

A
  • Congenital (Left)
    Gradual growth over time
    Presents early in life
  • Acquired
    Primary acquired (retraction pocket)
    Secondary acquired (TM perforation)
42
Q

What is acquired cholesteatoma associated with?

A

Associated with chronic ETD and recurrent OMs
- TM is weakened resulting in retraction pockets or perforations
Presents later in life

43
Q

Describe Primary Acquired cholesteatoma (3) :

A
  1. Chronic ETD
  2. Deep retraction pocket (pars flaccida)
  3. Collection of keratin within the retraction pocket
44
Q

Describe Secondary Acquired cholesteatoma:

A

Secondary acquired
1. Chronic ETD
2. Recurrent OMs
3. Chronic TM perforation

In-growth of keratin via the TM perforation

45
Q

What are the clinical presentations of Cholesteatoma? (3)

A
  • 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
Q

What can we see in this Otoscopic Evaluation?

A
  1. Pars flaccida (attic) crusts and CHL -> suspect cholesteatoma
  2. This isn’t just wax-suspect underlying pocket and cholesteatoma
47
Q

What are the causes of Hearing loss due to Choleosteoma? (2)

A
  1. Ossicular erosion (mostly CHL)
  2. Labyrinthine fistula (SNHL, vertigo)