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179 Cards in this Set
- Front
- Back
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What are the categories of acquired disorders of the middle ear that we discussed in class?
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Eustachian tube dysfunction
Otitis media with effusion Disorders resulting from otitis media |
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What are the types of otitis media with effusion?
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Serous
Perulent/Suppurative Mucoid |
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What are the possible sequela of otitis media with effusion?
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Mastoiditis
TM Perforation TM retraction pocket Tympanosclerosis Cholesteatoma |
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Normally, the eustachian tube is ________ and is _________ by the _________ and the ________ during acts of _________ or _________.
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closed
opened Levator Palitini Tensor Veli Palitini swallowing yawning |
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The eustachian tube allows direct communication between the _________ and the _________.
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nasopharynx
middle ear |
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What does the eustachian tube allow for?
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aeration of the middle ear
pressure equalization of the middle ear optimal functioning of the middle ear mechanisms |
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Any condition that may interfere with eustachian tube functioning may result in _____________.
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otitis media
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What are the signs and symptoms of eustachian tube blockage/dysfunction?
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feeling of blockage
otalgia due to tension on the tympanic membrane possible hearing loss and tinnitus possible dizziness/balance problems |
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What causes eustachian tube dysfunction?
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Normal pediatric craniofacial configuration
Poorer function of tensor veli palitini Walls more compliant in children - more susceptible to collapse/functional obstruction Structural Deformities Inflammation and swelling of the mucosal lining of the ET Neoplasms Functional Barotrauma |
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How does the pediatric craniofacial eustachian tube differ (than adults)
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More horizontal (10 degrees rather than 45 degrees)
Shorter than adult's |
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What are some structural deformities that may influence eustachian tube functioning?
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Craniofacial anomalies (Down's syndrome, cleft palate)
Adenoid hypertrophy (increased size/bulk) enlarged tonsils |
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What are some physician recommended procedures to force open a blocked ET?
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Valsalva - Close mouth, hold nose, blow
Toynbee - Close mouth & jaw, hold nose, swallow |
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What is otitis media?
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An inflammatory process of the middle ear cavity, often including the mastoid
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What is second only to the common cold as the most common inflammatory disease of childhood?
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Otitis Media
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What percentage of children experience at least one episode of OM prior to age 3?
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80%
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Is OM more common in certain populations?
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Yes (e.g. Native Americans)
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Can complications of OM be life threatening?
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Yes, but it is uncommon
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Otitis Media is most commonly due to __________.
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Eustachian tube dysfunction
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Is the tympanic membrane normally concave or convex?
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concave
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What is the progression of OM?
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Normal functioning
Negative pressure in middle ear Vacuum created, TM is retracted inward Bacteria are drawn up into ET and middle ear Fluid secretions trapped in ME Bacteria proliferate TM is pushed outward (bulging) Antibacterial treatment Thin fluid remains (glue ear) or return to normal |
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What are the signs and symptoms of OM?
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Otalgia
Otorrhea Fevers Restless sleep, irritability, temperament disorders Possible balance and hearing disorders |
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Classification of OM is based on ________ and _________.
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duration
type of effusion |
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Acute OM
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Sudden onset and short duration (1-21 days)
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Subacute OM
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22 days - 3 months
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Chronic OM
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Long duration (longer than 3 months)
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Serous
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sterile fluid
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Suppurative/Purulent
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bacteria
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Mucoid
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thick, glue-like, some bacteria
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Acute Suppurative OM
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Redness and swelling of TM
TM bulges outward Bulging increases and TM becomes fiery red Possible rupture of the TM and effusion into ear canal |
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Acute Serous OM
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Uninfected fluid in the ME that is yellow or straw-colored
TM may be retracted Fluid line or bubbles may be seen behind the TM |
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Chronic Suppurative OM
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Odoriferous otorrhea
TM perforation may be unresolved |
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Chronic serous OM
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Thick mucous-like fluid with glue-like consistency
Fluid is rich in proteins that can eventually erode the ossicles, bony labyrinth, etc. |
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Diagnosis of OM
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Patient signs and symptoms/case history
Visual and otoscopic exam Audiologic exam (tympanometry, pure tone, speech audiometry) |
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Management of OM
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Medication (analgesia, antibiotics, decongestants, antihistamines, steroids)
Autoinflation Myringotomy ME air injection Tympanostomy (PE tubes) Adenoidectomy or tonsillectomy |
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Mastoiditis
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Infection/Inflammation of the mastoid portion of the temporal bone
May involve the membrane lining AND bony structures |
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Mastoiditis can be classified as ________ or ________ and is often associated with episodes of __________.
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acute
chronic OM |
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Symptoms of mastoiditis
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Feelings of aural fullness
Pain Edema Tenderness behind the auricle |
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Acute mastoiditis typically shows ____________ hearing loss.
Chronic mastoiditis typically shows ___________ hearing loss. |
conductive
mixed (conductive with a sensory component) |
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Possible medical complications of mastoiditis
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meningitis, brain abscess, cerebellar abscess
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If antibiotics are ineffective for mastoiditis, _________.
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Mastoidectomy to allow for drainage of mastoid air cells
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Mastoidectomy
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Operation to expose mastoid air cells, ME space and ossicles
Useful in eradicating chronic infections and the removal of cholesteatomas (also can expose the facial nerve) |
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TM perforation
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TM can spontaneously rupture from acute and chronic OM
Can also spontaneously heal but if tear remains, can result in mild to moderate HL Marginal or central TM locations |
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Degree of loss with TM perforation
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Can vary depending on size and location of perforation
Pars flaccida (marginal) - less HL Pars tensa, malleus disconnection and larger area (central) - greater HL |
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Myringoplasty
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Tissue graft is used to close a perforation of the TM
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Tympanoplasty
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Reconstructive surgery of the ME
Classified according to the magnitude of the reconstructive process |
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Monomeric TM
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Portion of the membrane is missing the fibrous middle layer
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TM retraction pockets
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Retraction due to negative pressure
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Atelactasis
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Absence or lack of air in the ME cavity
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Tympanosclerosis
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A form of membrane thickening caused by calcification plaques on the TM and nodular deposits
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What can cause tympanosclerosis?
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Chronic OM
Insertion of ventilating tubes |
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What can result from tympanosclerosis?
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Conductive hearing loss (especially if ossicles are involved) that is greater for lower frequencies (more mass)
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What are other names for cholesteatoma?
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pseudotumor, pearl tumor, keratoma
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Cholesteatoma
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Made up of debris
Skin growth can develop from perforations of the TM = acquired cholesteatoma |
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Risk differences for cholesteatoma in perforation locations
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Central - low risk of developing keratoma
Posterior-superior pars tensa margin - marked risk Pars Flaccida/Attic - serious risk |
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What can result from a cholesteatoma?
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TM perforations and foul smelling otorrhea
Erosion of the ossicles and surrounding bones Fistulas - meningeal complications Sensorineural HL and vestibular problems Facial nerve paralysis May/may not affect hearing if detected early |
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Types of HL that can result from a cholesteatoma
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Conductive - TM perforation and/or ossicular erosion has occurred
Mixed and/or SNHL - labyrinthine fistulas None - ME or IE structures are not involved (i.e. attic) |
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Can a cholesteatoma regrow?
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Yes, if it wasn't completely removed.
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Audiological intervention for a cholesteatoma
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Audiologic monitoring
Amplification if necessary Aural rehabilitation therapy - speechreading, auditory training, compensatory strategies |
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Congenital
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Present at birth
Does not signify any particular cause |
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How often does congenital deafness/profound hearing loss occur?
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1 out of every 1000 births
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Aplasia
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Defective development or congenital absence of tissue or organ
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Dysplasia
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Abnormal tissue or organ development
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What are the bases of SNHL?
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Michel Anamoly
Mondini Dysplasia Sheibe Dysplasia |
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Michel Anamoly
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Aplasia of the inner ear and in some cases, also no VIII nerve
Occurs in 1% of profoundly deaf population |
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Mondini Dysplasia
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Congenital anomaly of osseus and membranous labyrinth
-Aplastic cochlea -Deformity of vestibule and semicircular canals -Partial or complete loss of auditory and vestibular function |
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Scheibe Dysplasia
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Cochleosaccular dysplasia
-intact bony labyrinth but cochlea and saccule affected -atrophy of O of Corti -utricle and SCC are spared |
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What is the most common inner ear anomaly?
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Scheibe Dysplasia - occurs in 70% of cases
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How many cases of congenital HL/deafness are due to genetic factors?
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50-60%
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What are the types of congenital genetic HL/deafness?
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Chromosomal aberrations
Mitochondrial defects/mutations Single gene defects/mutations Polygenic or multifactorial inheritance |
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How many known genetic causes of HL are there?
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Over 400
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How many cases of congenital HL/deafness are due to nongenetic factors?
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40-50%
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What are some causes of congenital nongenetic HL/deafness?
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Maternal infections
Anoxia Ototoxins Trauma Prematurity/low birth weight |
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Patterns of inheritance of genetic HL
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70% autosomal recessive
15% autosomal dominant 15% all other forms - 2% atributed to X-linked pattern |
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Syndromic vs. nonsyndromic genetic HL
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60-70% non-syndromic
30-40% syndromic |
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Syndrome
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Collection of associated abnormalities and symptoms
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Connexin 26
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Ear sensory cells are stimulated
Potassium ions enter "gap junctions" and are recycled If Connexin 26, potassium ions cannot be recycled Sensory cells don't function properly Loss of hearing |
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Mutations of the gene that codes for CX26 is estimated to be responsible for _________ of all recessive cases of non-syndromic congenital HL
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Approximately half
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Occurrences of mutations of CX26
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1 in 2500-5000
Males/Females in equal frequency |
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Do higher frequencies of the mutations of CX26 occur in some populations?
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Yes
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Clinical features of CX26 mutations
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Typically congenital
Mild to profound SNHL (more commonly severe to profound) Can be progressive or non-progressive |
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How many different mutations of CX26 have been found?
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>90
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What is the common form of autosomal recessive syndromic SNHL that we talked about in class?
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Usher
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Usher Syndrome
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Most common eye/ear disorder
Prevalence rate of 3.5/100,000 Basis for about 3-10% of all children with severe or profound SNHL |
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What are the clinical findings of Usher syndrome
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Hearing loss
-Bilateral SNHL -Moderate to profound -Typically congenital -Can be progressive Visual Deficits -Decrese/loss of the rod cells in retina -Nightblindness, tunnel vision -Onset early teens to 20s -Total blindness in adult life in about 50% of cases Some people have varying problems with balance |
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What is the common form of autosomal dominant syndromic SNHL that we talked about in class?
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Waardenburg Syndrome
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Waardenburg Syndrome
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Autosomal dominant syndrome but with variable expressivity
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What are the characteristics of Waardenburg Syndrome?
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Partial albinism
Laterally positioned medial canthi Different colored eyes or bright blue eyes Hearing loss (in 25% of cases) -Congenital SNHL -Slight to profound -Unilateral or bilateral -Varying configurations |
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Condition that can be inherited in an X-linked dominant fashion
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Alport Syndrome
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Alport Syndrome
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Involves progressive hearing and kidney problems
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If a man has the X-linked form of Alport syndrome, _________ of his daughters will have it and _________ of his sons will have it.
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all
none |
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If a woman has Alport syndrome, she will have ____________. Her children will have a ___________ chance of inheriting it but it will be more severe in her ___________.
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mild hearing and kidney problems
50-50 sons |
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Prevalence of Alport syndrome
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1 in 50,000 live births
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Most kids with ___________ are born to parents with normal hearing
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genetic HL
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How many pairs of chromosomes do we have?
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23 pairs
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Heredity
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Genetic transmission from parent to offspring
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DNA
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Chemical basis of heredity and carrier of genetic information
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Chromosome
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A structure containing DNA, which transmits genetic information
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Autosomes
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22 pairs of chromosomes containing genes that don't determine your gender/sex
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Sex Chromosomes
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One pair of chromosomes that determine your gender/sex.
Females have two X chromosomes Males have an X and a Y chromosome |
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Monosomy
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Lack of a chromosome
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Trisomy
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Presence of 3, rather than 2 chromosomes in a particular set
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Karotype
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Photographic record of all chromosomes laid out
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Phenotype
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Trait produced by a single gene or several genes
The total of all observable features of an individual |
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Genome/genotype
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Total genetic makeup of a specific organism
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Gene
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Basic unit of heredity
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Locus
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Site of the gene on a chromosome
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Allele
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Different forms of a gene
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Homozygous
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If an allele from both parents are the same
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Heterozygous
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If an allele from both parents are different
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Dominant trait
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Gene pair is different - person is heterozygous for that trait
Only one gene needed for trait expression |
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Recessive trait
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Gene pair is the same - Person is homozygous for that trait
Both genes must be the same for trait expression |
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X-linked (sex-linked) trait
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Gene is contained within the X or Y chromosome
Can be dominant or recessive |
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Expressivity
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The degree of severity in trait manifestation
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Penetrance
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Regularity with which a trait is manifested in the person carrying the gene
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Acquired SNHL
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Not present at birth
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Impact of acquired SNHL depends on:
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Etiology
Degree of HL Configuration of HL Time course Age of onset |
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Tinnitus
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Sensation of noise or ringing in the ear
One typical characteristic of acquired SNHL |
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Recruitment
When does it typically occur? |
Abnormal sensitivity to loudness changes
Typical characteristic of acquired SNHL (especially if site of disorder is in the IE) |
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What are the causes of acquired SNHL?
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Diseases, infections, systematic disorders
Sudden onset disorders Trauma Ototoxicity Degenerative processes (aging) Noise exposure |
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Long exposure to noise can damage _________
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soft tissues of the IE
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Continuous or repeated exposure to loud sounds leads to __________.
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Destruction of sensory receptor cells in the IE
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Loss of hair cells impact _________.
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Auditory nerve fibers
Subsequent neurons in the central auditory system |
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Frequency range of greatest noise-induced SNHL
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4000-6000 Hz
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Early signs/symptoms of noise induced SNHL
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Diminished ability to hear high-pitched sounds
Difficulty understanding speech (especially of women and children) |
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Impact of noise-induced SNHL on the auditory system and hearing depends on __________, __________ and __________.
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Intensity
Frequency Duration |
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What is the three foot rule?
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If you have to shout at arm's length in order to be understood over background noise, then you are exposed to hazardous noise levels
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How many decibels is considered loud enough to cause damage?
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Over 85 decibels
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What is the goal of a hearing conservation program?
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Reduce the risk of developing a permanent noise-induced HL
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What are the elements of a hearing conservation program?
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Administrative and engineering controls
Audiometric testing Employee training and education Record keeping Program evaluation |
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What are the elements of an occupational hearing conservation program
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Administrative and engineering controls
Damage risk criterion Occupational Safety and Health Administration (OSHA) permissible exposure level OSHA exchange rate Audiometric testing Employee education |
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What are the two categories of congenital non-genetic SNHL?
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Viral infections
Protozoal and other organism infections |
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What does TORCHS stand for?
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Toxoplasmosis
Rubella Cytomegalovirus Herpes Simplex Virus Congenital Syphallis |
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Cytomegalovirus
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Largest and most complex member of the Herpes family
Able to remain dormant within the body over a long period Impairment of the body's immune system reactivates the virus |
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Initial CMV infection
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Has few symptoms but is followed by a prolonged infection
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Which cell types does CMV affect the most?
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Epithelial cells
Ependymal cells Organ of Corti Neurons of the VIII cranial nerve |
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What percentage of the population acquire CMV by age 40?
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50-85%
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How is CMV transferred?
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Person to person contact
Transplants and transfusions Mother to unborn child (congenital) Mother to newborn child |
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What is the most frequent way that CMV is transferred?
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Respiratory (airborne)
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What accounts for most cases of congenital CMV?
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Primary maternal infection during pregnancy
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Congenital CMV infection occurs in _______% of all live births.
Incidence is about _________ neonates per year. |
0.4-2.3%
40,000 |
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What percentage of babies born with CMV are asymptomatic/symptomatic at birth?
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asymptomatic - 90%
symptomatic - 10% |
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How many congenital CMV cases that are asymptomatic at birth will stay asymptomatic?
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85%
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The 10% of congenital CMV cases that are symptomatic at birth are identified as ______.
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CID - Cytomegalovirus inclusion disease
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What are the abnormalities that may be seen in newborns with CID?
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Small hemorrhagic spots
Smaller head than normal Intracranial calcifications Liver, spleen or kidney defects Retinopathy Intrauterine growth retardation |
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Do infants who are symptomatic (CMV) at birth have a high mortality rate?
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Yes
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What are the possible sequela of congenital CMV?
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Neurologic problems
Visual defects Physical development Motor impairment Seizure disorder Developmental differences Learning delays Hearing loss |
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Hearing loss in congenital CMV
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SNHL
May be unilateral or bilateral May be congenital or delayed onset May be mild to profound Frequently progressive Unpredictable configuration |
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Sensorineural hearing loss
Asymptomatic CMV and symptomatic CMV |
Asymptomatic CMV results in 2-7 times as many cases of SNHL than symptomatic CMV
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How soon after birth do you need to have a diagnosis to consider CMV congenital?
How is it diagnosed? |
As soon as possible
Between 3 weeks and 1 year is considered possible congenital Virus is isolated/grown from saliva, tissue or urine samples |
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How do you prevent congenital CMV?
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No way to fully prevent it but practicing good hygiene while pregnant can help.
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Is there a CMV vaccine?
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Not yet, but development is underway
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What is the problem with congenital asymptomatic CMV?
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We don't know who has it
Viral screening is not routinely performed |
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What are some possible solutions for CMV?
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Screen for CMV at birth
Test and monitor those who are CMV+ Aggressive management for those with hearing loss from CMV Educate MDs and public health officials |
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What are the two main parts of the hearing mechanism?
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The three parts of the ear and auditory nerve (peripheral system)
Pathways to the brain and the brain itself (central auditory nervous system) |
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What words are often used to describe acuity?
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Hearing
Hearing sensitivity |
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Can there be difficulties with auditory perception even though there is no hearing loss?
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Yes
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Perception
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How the auditory nervous system works (in total)
Requires normal function beyond the peripheral system |
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Acuity
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How well the ear works
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What words are often used to describe perception?
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Listening
Comprehension Understanding |
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Central Auditory Processing
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What we do with what we hear
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Auditory Attention
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Being aware and attending to auditory signals for an appropriate length of time
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Auditory Localization
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Ability to determine the location of a sound source
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Auditory Discrimination
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Distinguishing similarities and differences between sounds (phonemes, pitch, volume, environmental sounds)
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Auditory Association
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Ability to match an acoustic stimuli with its source
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Auditory Figure Ground
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Ability to discriminate a primary auditory stimulus from other background auditory stimuli (nonlinguistic and linguistic)
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Auditory Analysis/Segmentation
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Breaking a word into specific segments (sounds or syllables)
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Auditory Synthesis/Sound Blending
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Ability to blend individual sounds together to form words
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Auditory Closure
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Filling in missing or distorted acoustic information to complete a word or message
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Auditory Memory
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Retaining components of an auditory signal over a period of time
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Auditory Sequential Memory/Sequencing
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A sub-skill/subset of auditory memory
Remembering auditory information (sounds, rhythms, words, etc.) in a specific order |
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What is Central Auditory Processing Disorder?
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Difficulty in processing and interpreting auditory stimuli in the absence of a peripheral hearing loss, usually resulting in a problem in the brainstem and/or cerebral cortex.
A breakdown in function somewhere beyond the auditory nerve. |
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The term (C)APD implies that the ___________ is not working properly.
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auditory nervous system
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What function can a (C)APD have a negative affect on?
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Language
Language-dependent behaviors |
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(C)APD symptoms might...
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Range from mild to severe
Include a variety of skills Change over time |
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Prevalence of (C)APD
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2-3% children
Twice as often in males 10-20% of older adults |
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What are some etiologies of (C)APD?
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Anoxia
Infections Degenerative aging process Intra and extra axial brainstem lesions Brain tumor or abscess Cerebrovascular accidents Brain damage resulting from trauma Kernicterus (bile deposits in the CNS) Chronic otitis media Congenital defects of the brain |
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Causes of (C)APD
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In some cases, the cause is unknown
In others, it seems to be related to maturation Lesions may be specific or more diffuse |
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What do people with HL and clinicians need to be careful of in regard to further ear damage?
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If you have a HL, dangerously loud sounds will not sound as dangerously loud but will still be causing damage
Perception is not always a good indicator of destruction |
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What is a controversy about CAPD?
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Some SLPs believe that there is no such thing
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