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145 Cards in this Set
- Front
- Back
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What is the purpose of the eustachian tube?
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allows direct communication between the nasopharynx and the middle ear for: aeration of the ME, pressure equalizing of the ME, optimal functioning of the ME mechanisms
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What muscles open/close the eustachian tube?
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levator palitini and the tensor veli palitini
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When is the ET normally closed/open?
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usually closed except when yawning, swallowing
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what are the signs and symptoms of eustachian tube blockage or dysfunction?
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- feeling of "blockage"
- otalgia due to tension of the tympanic membrane - possible hearing loss/tinnitus -possible dizziness/balance problems |
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Why might children be more likely to have ET dysfunction than adults?
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the normal craniofacial configuration- tube is more horizontal (10 degrees) versus adults (45 degrees), and shorter than adults. Walls are more compliant and susceptible to collapse/functional obstruction
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what are some causes of ET tube dysfunction?
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- poor function of tensor veli palitini
- structural deformities such as craniofacial abnormalities, adenoid hypertrophy, enlarged tonsils - inflammation/swelling of ET due to upper resp, tract infec., allergy, chronic adenoiditis -neoplasms - functional - barotrauma |
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barotrauma
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sudden changes in air pressure when flying or diving
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valsalva
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procedure for forcing open blocked ET tube- hold nose, close mouth and blow
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toynbee
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procedure for forcing open blocked ET tube- close mouth/jaw, hold nose, swallow
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effusion
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the escape of fluid into tissue or a cavity
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otitis media
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- inflammatory process of the ME cavity which often includes the mastoid
- secondary only to the common cold as most common childhood disease |
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what % of children experience OM prior to age 3?
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up to 80%
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what populations are more likely to experience OM?
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Native American
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What is the most common cause of OM?
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eustachian tube dysfunction
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how does OM occur?
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the ET becomes swollen, creates vacuum in ear, bugs are sucked up into cavity, fluid accumulates, bacteria proliferate in fluid, TM no longer retracted but bulges.
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What is chronic otitis media with effusion?
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of long duration, greater than 3 months.
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What is acute OM?
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sudden onset and short duration of 1-21 days
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What is subacate OM?
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22 days-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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what is shannell and crystals favorite word Dr. Darling says?
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Envaginate
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what are signs/symptoms of OM?
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- otalgia
- otorrhea - fevers -restless sleep, irritability, temperment disorders -possible balance, hearing disorders |
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acute suppurative OM
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- redness/swelling of TM
- TM begins to bulge outward as fluid collects - outward bulging increases, effusion of the ear canal may occur with spontaneous rupture of the tm |
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acute serous om
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serous OM characterized by presence of uninfected fluid in the ME
- may be yellow or straw color - tm may be retracted - sometimes fluid line or bubbles seen behind tm |
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chronic suppurative OM
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- characterized by odoriferous otorrhea (ew)
- TM performation may be unresolved |
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chronic serous om
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- thick, mucous like fluid is present
-fluid has a glue consistency - rich in proteins that eventually errode the ossicles, bony labyrinth, etc. |
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how is OM diagnosed?
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- patient signs/symtoms/case history
-visual/otoscopic exam - audiologic exam- immittance audiometry, pure tone and speech audiometry |
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otologic management
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- medication- antibiotics, anlgesia, possibly decongestants, antihistamines, steroids
- autoinflation -myringotomy - middle ear air injection - tympanostomy -possible adenoidectomy and tonsillectomy |
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tympanostomy
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a pressure equalizing or ventilating tube is placed to drain the fluid from the ME cavity
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What are other possible disorders and complications arising from OM?
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-mastioditis
-TM perforations - TM retraction pockets - tympanosclerosis -cholesteatoma |
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mastoiditis
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- infection/inflammation of the mastiod portion of the temporal bone
- membrane lining as well as bony structures may be infected -classified as acute or chronic -often associated with episodes of acute or chronic OM |
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what are the symptoms of mastoiditis
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- aural fullness
-pain - edema - tenderness behind auricle |
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is their hearing loss with mastoiditis?
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- acute typically shows a conductive HL due to inadequate drainage, chronic typically shows mixed hearing loss- fluid gets into cochlea
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mastoidectory
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-mastoid air cells removed
- allow for surgical drainage of mastoid air cells -useful in eradicating chronic infections of the ear and removal of cholesteatomas |
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TM perforation
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- spontaneous rutures/perforations can result from middle ear effusion associated with acute/chronic om
-can spontaneously heal, however if remains can cause mild/moderate HL -degree of HL depends on size and location of perforation |
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what areas of TM perforation are assocaited with more/less HL?
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pars flaccida- less HL
pars tensa, malleus disconnected, greater area (central)- more HL |
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what is one of the dangers of TM perforations?
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cholesteatomas- skin cells can migrate into ME
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myringoplasty
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procedure in which a tissue graft, usually a fascia or vein, is used to close a perforation in the TM
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tympanoplasty
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reconstructive surgery of the ME, usually classified in types according to the magnitude of the reconstructive process
Type 1- repair of TM perf alone Type 2-5- procedure increasingly more complex, more stuctures of ME involved |
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Monomeric TM
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portion of the eardrum is missing the fibrous middle layer
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Where are TM retraction pockets most likely to occur?
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in the monomeric or pars flacida portion
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what is TM retraction due to?
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negative pressure formed in the cavity secondary to ET dysfunction
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atelectasis
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absence or lack of air in a cavity, as in the middle ear space or mastoid cavity after ET dysfunction; incomplete expansion or a collapse of the structure
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What happens with TM retraction pockets?
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weakened portions of the TM are drawn back and invaginate into the ME space.
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small areas of the TM that are retracted can lead to the formation of what?
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cholesteatoma
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tympanosclerosis- what is it?
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a form of membrane thickening produced by fomation of whitish calcification plaques on the TM and nodular deposits (dense connective tissue) in the mucosa of the ME.
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What causes tympanosclerosis?
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- chronic inflammation or trauma
-secondary to chronic OM - often in association with the insertion of ventilating tubes |
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Does tympanosclerosis result in hearing loss?
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it may, especially if ossicles are involved
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Tympanosclerosis results in hearing loss of _________ frequencies?
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lower frequencies, because there is more mass to be moved by the sound waves
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What are other names for a cholesteotoma?
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"pseudotumor", "pearl tumor", "keratoma"
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What are cholesteatomas made of?
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accumulation of cellular debris/squamous epithelium (skin)/keratin
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What is an acquired cholesteotoma?
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when skin growth in the middle ear or mastoid develops from perforations in the TM
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What is the risk of a cholesteatoma developing in the pars flaccida/attic perforations?
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serious risk
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What is the risk of a cholesteatoma developing in the posterior-superior pars tensa margin?
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marked risk
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What is the risk of a cholesteatoma developing in central perforations?
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low risk
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What are the complications of cholesteatomas?
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moisture and bacteria may access the cholesteatoma and result in:
-TM perforations and foul smelling ottorrhea -erosion of ossicles/surrounding bones - fistulas in the otic capsule/mastoid cell wall that can result in meningeal complications - labyrinthine fistulas resulting in sensory HL and vestibular problems - erosion of facial nerve 8 and resultant facial nerve problems (paralysis) |
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Do cholesteatomas affect hearing?
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They may or may not, depending on their location and its effects on structures/sound transmission mechanisms. May be conductive/mixed/sensory depending on the site of damage
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How are cholesteatomas treated?
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if detected in the early stages can be surgically removed without any complications, but must remove all traces or they will "re-grow"
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What is the audiologic intervention for cholesteatomas?
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- audiologic monitoring
- amplification in cases where hearing loss has occured due to conductive and/or sensory mechanism involvement. -aural rehab therapy |
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How frequently does congenital deafness/profound hearing loss occur?
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1 out of every 1,000 births
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aplasia
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defective development or congenital absense of tissue or organ
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dysplasia
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abnormal tissue or organ development
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michel anamoly
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- causes SNHL, congenital
- aplasia of inner ear - no inner ear and in some cases no 8th cranial nerve - occurs in 1% of profoundly deaf population |
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mondini dysplasia
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congenital anomaly of ossues and membranous labyrinth
- aplastic cochlea - deformity of vestibule/semicircular canals - partial or complete loss of auditory/vestibular function |
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scheibe dysplasia
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- most common congenital innear ear anomaly- 70% of cases
- cochleosaccular dysplasia- cochlea and saccule affected, bony labyrinth intact |
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What percent of cases of congenital hearing loss/deafness are due to genetic factors?
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50-60%
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What are the congenital causes of HL that are genetic?
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- chromosomal aberrations
- mitochondrial defects/mutations - single gene defects/mutations - polygenic or multifactorial inheritance |
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What percent of cases of congenital HL are not genetic?
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40-50%
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What are non-genetic factors that cause congenital HL?
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- maternal infection
-ototoxins - anoxia - trauma - prematurity/low birth weight |
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Genetic forms of HL can be classified by patterns of __________________
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inheritance
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approximately ___% of genetic HL is inherited in an autosomal recessive pattern
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70%
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approximately ___% of genetic HL is inherited in an autosomal dominant pattern
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15%
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approximately ___% of genetic HL is inherited by a form that is NOT autosomal dominant or recessive (other)
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15%
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In what percent of genetic cases is hearing loss non-syndromic?
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60-70%
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In what percent of genetic cases is hearing loss syndromic?
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30-40%
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what is connexin 26?
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- non syndromic genetic
-half of all recessive cases of non-syndromic SNHL -a gap junction defect -causes potassium ions not to be recycled properly - results in sensory cells that do not function properly |
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Is connexin 26 syndromic or non-syndromic?
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non-syndromic
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connexin 26 is responsible for what percentage of recessive cases of non-syndromic congenital hearing loss?
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about half
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Is connexin 26 more common in males or females?
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it is equally common
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true or false- certain mutationsof the connexin 26 gene occur more frequently in certain populations?
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true- include caucasians, ashkenazi jews, asians
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what are the clinical features of non-syndromic connexin 26?
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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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Usher syndrome is what kind of syndrome?
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autosomal recessive syndromic
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Usher syndrome
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-most common eye/ear disorder
- bilateral SNHL - moderate to profound - typically congenital -can be progressive - total blindness in adult life in about half of cases -tunnel vision -balance problems - onset early teens to 20's |
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What are the three common forms of autosomal recessive syndromic SNHL?
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- usher
- pendred - jervell and lange-nielson |
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what are five common forms of autosomal dominant syndromic SNHL?
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- waardenburg syndrome
- branchio-oto-renal (BOR) syndrome - Neurofibromatosis Type II (NFII) - Stickler Syndrome - Epstein Syndrome |
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waardenburg syndrome
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-autosomal dominant with variable expressivity
-partial albinism (white forlock) - laterally positioned medial canthi (???) - different colored eyes or bright blue eyes - hearing loss in one quarter of cases- congenital SNHL, slight to profound, uni or bilateral, varying configurations |
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what is an x-linked syndrome we learned about?
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alport syndrome
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alport syndrome
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- x- linked dominant
- causes progessive hearing loss and kidney problems |
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what are TORCHS syndromes?
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Congenital non-genetic SNHL:
- Toxoplasmosis - rubella - cytomegalovirus - herpes simplex virus - congenital syphillis |
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what are viral infections that cause non-genetic congenital SNHL?
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- rubella
- cytomegalovirus - herpes -HIV |
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CMV
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- cytomegalovirus
- largest and most complex member of herpes family of DNA viruses - include chicken pox, shingles, cold sores, genital ulcers, infectious mononucleosis - remain dominant in the body over a long period |
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How does CMV present itself in the body?
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initial CMV infection may have few symptoms and is always followed by a prolonged, unapparent infection during which the virus resides in the cells without causing detectable damage/clinical illness. Severe impairment of immune system reactivates virus from its dormant state
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what cell types does CMV affect?
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- epithelial
- ependymal cells lining the ventricles - organ of corti - neurons of the 8th cranial nerve |
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What percent of adults have CMV by age 40?
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50-85%
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What percentage of babies born with CMV are asymptomatic
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90%, and 85% of these will remain normal.
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congenital CMV can cause what?
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- SNHL
- expressive language delays - learning disorders - small hemmorrhagic spots - smaller head than norma - intracranial calcifications - liver, kidnes, spleen defects - Infants symptomatic at birth have a high rate of mortality! |
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hearing loss in congenital CMV
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- SNHL
- uni or bi - congenital or delayed onset - mild to profound - frequently progressive -unpredictable configuration |
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does SNHL occur more often in symptomatic or asymtomatic cases of CMV?
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asymtomatic results in 2-7 times as many cases of SNHL as does symptomatic- because asymptomatic is more common. However the percent of SNHL is higher in symptomatic population
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how do we confirm congenital CMV?
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virologic confirmation must take place within three weeks
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what is the big problem with regard to congenital asymptomatic CMV?
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we dont know who has it
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what are solutions to the problem of CMV?
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-screen for CMV virus at birth
- test and monitor those that are CMV+ - apply aggressive management for those who have hearing loss and are CMV+ - educate MDs and public health officials |
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the impact of acquired SNHL depends on....
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- etiology
- degree of HL - configuration of HL (some pitches more than others?) - time course (sudden v insidious/stable v progressive) - age of onset |
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tinnitus and recruitment are the ___________ associated with SNHL
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two most typical characteristics
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is tinnitus a condition?
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no, it is a symptom of a condition
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recruitment
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abnormal sensitivity to loudness changes, especially if the site of the disorder is in the inner ear
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what are causes of acquired SNHL?
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- diseases, infections, systemic disorders
- sudden onset disorders - trauma - ototoxicity - degenerative processes - noise exposure |
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what are the two types of threshold shifts that can occur due to noise exposure?
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TTS- temporary threshold shifts, and PTS- permanent threshold shifts
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what is the SPL level of normal conversational speech?
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50-65 dB
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What is being lost when we have noise induced hearing loss?
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sensory cells and nerve fibers
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what range of hertz have the highest level of hearing loss for noise induced HL?
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4,000-6,000 hz
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what are the earlier signs and symptoms of noise-induced SNHL?
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-diminished ability to hear high pitched sounds
-difficulty with understanding speech, especially of women and small children |
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what happens later on with noise induced SNHL?
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- mid pitches are effected
- lower pitched sounds, including mens voices, become hard to understand |
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the impact on the auditory system and hearing depends on what noise characteristics?
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intensity, frequency, duration
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what is a rule of thumb about exposure to loud sounds?
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the louder the sound, the shorter the exposure can be before damage occurs
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when do we know if noise is too loud?
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- if person standing near you can hear your headphones they are too loud
- 3 feet rule= if you have to shout to be understood at this distance than background noise is too loud |
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how can we prevent NIHL?
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- prevention= avoid unnecessary exposure to loud sound
- reduce intensity by wearing personal hearing protection each and every time you are exposed to hazardous noise levels |
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what are the goals of a hearing conservation program?
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to reduce the risk of developing permanent NIHL
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what are the elements of hearing conservation programs?
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- administrative and engineering controls
- audiometric testing - employee training and education - record keeping - program evaluation |
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occupational hearing conservation: administrative and engineering controls
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- noise measurement to monitor exposure levels
- reduction of intensity levels - reduction of time of exposure |
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damage risk criterion
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the purpose of a damage risk criteria is to define maximum permissible levels of noise for stated duration which, if not exceeded, would result in an acceptably small effect on hearing levels over a working lifetime
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OSHA permissible levels of exposure
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90 dB time weighted over 8 hrs
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OSHA exchange rate
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a time/intensity trading relationship that helps ID equi-hazardous environments when exposure levels are not uniform
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audiometric testing in occupational hearing conservation programs
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- baseline hearing test
- annual eval - pure tone AC theshold audiogram at test frequencies 500, 1,000, 2,000, 3,000, 4,000, and 6,000 |
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employee education in hearing conservation programs
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- ID what noise is and what noise sources in workplace
- explain impact of noise on hearing -explain audiometric test results - explain the HCP policy - ID positive workplace actions/lifestyle to prevent NIHL - explain need for hearing protectors and train workers how to use |
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heredity
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genetic transmission from parent to offspring
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DNA
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deoxyribonucleic acid. Chemical basis of heredity and the carrier of genetic info which is present in the chromosomes of the nuclei of the cells
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Chromosome
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a structure in the nucleus of a cell which contains DNA, which transmits genetic information. Each chromosome carries hundreds to thousands of genes. Humans usually have 46 chromosomes (23 pairs); 22 are autosomes, 1 pair is sex chromosomes
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autosomes
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the 22 pairs of chromosomes that contain genes that do not determine your gender/sex. These are numbered from the largest (#1) to the smallest (#22) pairs
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sex chromosomes
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the one pair of chromosomes that determine your gender/sex. In humans, females have two "X" chromosomes, while males have one X and one Y. Human males determine the sex of their children.
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monosomy
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lack of a chromosome
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trisomy
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the presence of 3, rather than 2, chromosomes in a particular set
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karotype
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pattern of all chromosomes laid out, a photographic record. cultured from cells arrested in the process of mitosis or meiosis. Organized as a labelling system 1-22, X and Y
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phenotype
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the trait produced by a single or several genes; the total of all observable features of an individuals (including his/her anatomical, physiologic, biochemical and psychological makeup)
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genome/genotype
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the total genetic make-up of a specific organism
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gene
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basic unit of heredity; a section of DNA with the coded instruction for the production of a protein that is essential for growth, development, or continued functioning of an organism. Since chromosomes come in pairs, the genes also come in pairs.
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locus
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the site of the gene on a chromosome
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allele
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different forms of a gene; one of two or more different genes containing specific, inheritable characteristics that occupy corresponding positions (loci) on paired chromosomes
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heterozygous
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if an allele inherited from both parents are different; produced by different alleles at a given locus; a dominant and reccessive pair of genes for a given hereditary characteristic
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homozygous
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if an allele inherited from both parents are the same; produced by similar alleles at a given locus; like pairs of genes (both recessive and dominant) for a given hereditary characteristic
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dominant trait
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gene pair is different, a person is heterozygous for the 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 the trait, both genes must be the same for trait expression
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x 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 extent to which a heritable trait is manifested in the individual carrying the gene, degree of severity in trait manifestation. It may be so mild that it is undetectable.
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penetrance
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the REGULARITY with which an inherited trait is manifested in the person who carries the gene. If a trait is not recognized in a person who carries the gene, it can be said to be nonpenetrant- can look like it skips generations
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