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Audiology Advanced Medical


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Describe Weber Test
Tuning fork test for lateralization
-Use 512 or 1024 tuning fork
-start fork vibrating by tappin on hand
-place base of tuning fork firmly on top of patients head
-ask patient where sound is heard

Describe Rinne Test
Tuning fork test to determine SN or conductive HL
-Place vibrating fork on mastoid bone behind ear
-when pt no longer hears it move fork near patient ear opening.
-usually pt will hear via air conduction longer than bone

What is the schwaback test
Tuning fork test which compares the testers own normal hearing with the pts
-set fork to vibrate
-go back and forth between pt and yourself
-see who can hear it longer
-if you hear it longer, may indicate that the pt has a hearing loss

Why is CBC useful in OE pathology?
RBCs if too many , may indicate dehydration
-if too many may be a problem with hemorrhaging or some type of anemia
WBC count
-serve as defense against micro organismns
-too many or too few indicative of possible pathology
-too few - drug intoxication
-too many in leukemia

White cell differential break down
neurtophils- increased in infection
-eosinofils - increased in allergic reactions and in response to some parasites
-basophils - increased in allergic reactions & disease
-lymphocytes - seen in some bacterial infections
-monocytes - increased when there is recovery from infection

3 components of impedance?
Mass reactance
-mass of ossicles
-predominant in High Freq
Compliant reactance
-stiffness of ligaments and muscles
-predominant in low freq(adding stiffness has greater effect on low freq)
--friction of Inner ear fluids against motion of footplate
-doesn't vary with freq

Broad catagories of lesions of the CNS
-Atherosclerosis & EVA
-blood system deficits that interrupt transport of oxygen & nutrition
Space occupying -
-tumors, meningioma
-low velocity - linear fractures
-high velocity - puncture or depression in skull

Space occupying lesions
-Astrocytomas- arise from small star shaped cells called astrocytes - grow in brain and spinal cord
-Brain stem gliomas - generally cannot be removed = high grade astrocytomas
-ependymomas-usually develop in lining of the ventricals, most common in childhood
-oligodendriogliomas - arise in cells that produce myelin. Usually arise in cerebrum, slow growing, usually non spreading, occur in middle aged adults but others too

Schwannomas begin where usually?
On the sheath of the auditory /vestibular nerve
Temporal lobe tumors, symptoms?
Depends on the location within the lobe
-partial seizures
seizures -cclouding of consciousness & automatic motor movements
-may do complex acts w/o knowing it
Posterior temp lobe
-get elemental flashes of lights
-visual hallucinations

Mid temporal lobe symptoms
Depends on hemisphere involved
if tumor in dominant hemisphere:
-lip smacking and anomia

symptoms of increased cranial pressure
-unilateral headache - worse upon awakening
-vomiting , nausea
-papilledema -choked optic disc - get a blind spot
-head enlargement in child
-changes in reflexes
-change in ability to regulate body temperature

Tumors of the Meninges

Tumors of the skull
-osteitis deforman

Intra cerebral hemorrhage caused by rupture of vessel called?

caused by?

CVA or cerebralvascular accident
-congenital or acquired aneurysms
-acute infections
-systematic disease

Central pathology
-tissue death - necrosis due lack of oxygen
What is a Bruit?
-sign that can be heard by physician
-turbulance in the carotid
-confirmed by carotid arteriography or sonogram

Neural tissue deprivation of oxygen =
TIA - transient ischemic attack
-may last 1-2 hours
-passage of embolism
-considered evolving strokes

Circulatory /vascular
atherosclerosis - artery wall thickens due to build up of placque ie cholesterol
-causes an inflammatory response of the walls of the artery
-most commonly affects -aorta, coronary arteries in lower extremities

Atherosclerosis symptoms
none until a thrombosis, embolism or aneurysm occurs
Cerebrovascular accident
-a stroke, occurs when a blood vessel (artery) that supplies blood to the brain, bursts or is blocked by a clot
-numbness, weakness or paralysis of face, arm or leg typically on one side of body
-vision problems, dimness, blurring, double vision, loss of vision
-confusion, trouble speaking or understanding
-trouble walking, dizziness, loss of balance
-severe headache

Thrombosis =

Embolism =

Thrombosis = formation of a clot
once it breaks off...
embolism = a clot that moves from its point of origin until it lodges in a narrow blood vessel & causes blockage, circulatory deprivation

Elderly young old what age?
Elderly older old age
old old age
85 plus
What is phonemic regression?
-loss for speech recognition disproportional to pure tone findings
-associated with aging
Define sudden SNHL
-Hearing loss that develops over the course of a few hours to a few days
-loss of at least 30dB in 3 contiguous frequencies over a period of 3 days
-HL that developed to maximal HL with in 8 hours

Sudden SNHL considered...
an otologic emergency
-most common treatment = steroids to reduce swelling, help body fight illness
-reduce salt intake

Possible reasons for sudden SNHL
-meniere's disease
-space occupying lesions
-acoustic neuroma

Toxins affecting the CNS?
heavy metals -gold, lead, zinc
- alcoholic mom - each subsequent child has worse involvement
Pathologies of outer ear
Traumas & disease
-otitis externa
-bony exostoses
-ear canal lacerations
Failures in development
-aural atresia
-preauricular pits-may be associated with syndromes & other developmental problems

Acute mastoiditis
-swelling of the tissue of the mastoid, pushes the ear forward
-otoscopy may find acute otitis media

Narrowing of the external ear canal
-can be congenital or result of insults such as OE or trauma
-congenital is associated with ossicular fixation as in osseopetrosis

Chronic Otitis Media
-COM -middle ear effusion w/o perf reported to persist > 1-3 months
-CSOM - persistent draining ear w/perf
-the larger the TM perf the more likely pt will develop CSOM
1-3% of pts with ventilation tubes develop CSOM
39 of 100,000 in 15 years & younger
-history of persistant CSOM after appropriate medical treatment, reason to consider cholesteatoma

Risks for COM/CSOM?
-multiple episodes of AOM
-living in crowded conditions
-large family
-craniofacial anomalies

Perfs can result from?
in a healthy person a perf can heal by itself

-acquired or congenital
-cyst comprised of keratine or granulomatous tissue
-most often in response to recurrent infection
-erodes surrounding structures including TM, ossicles, ear can, mastoid process, temporal bone
-very dangerous - most frequently erodes upwards, may see attic retraction

Presenting symptoms of cholesteatoma?
-foul smell from ear
-may have HL
-may have pain
-black nose
-rare vertigo
-unilateral HL progressive

Implantation theory of secondary cholesteatoma?
Proposes that squamous epithelium becomes implanted into the middle ear as a result of surgery, insertion of foreign body (PE tube) or blast injury
Metaplasia theory of cholesteatoma?
-explains that as a result of chronic or recurrent otitis media the low cuboidal epithelium of the ME becomes transformed into a keratinized stratified squamous epithelium similar to other parts of the body (nose, sinuses, bronchi) in response to chronic irritation or infection
How is congenital cholesteatoma formed?
-arise from embryonal inclusions or rests of epithelial cells
-refers to cholesteatomas present behind an intact TM, without continuity to the external ear canal and in the absence of etiological factors such as TM perf or history of ear infections
Goals of Cholesteatoma surgery
-eradication of disease
-perservation and or improvement of hearing
-prevention of residual or recurrent disease

3 most popular surgical techniques for cholesteatoma
1. Transcanal tympanoplasty - 2nd look procedures
2. Intact canal wall tympanmastoidectomy - more rapid healing, recurrance rates higher, decreased aural care
3. canal wall down tympanomastoidectomy
-provides best exposure to epitympanum & sinus tympanum
-allows for easier monitoring for recurrance
-must clean mastoid cavity periodically & cannot use hearing aid

Indications for doing a canal wall down procedure for cholesteatoma?
-disease in an "only hearing" ear
-inability to visualize using IWT procedure
-patient prone to poor follow up
-patient who is anesthetic risk

Recurrent disease after revision surgery most likely found where?

risk factor for development of recurrence?

-in attic or mesotympanum- usually developed from a retraction pocket
-eustachian tube dysfunction

Recurrance is more dependent on?
cholesteatoma location
Cholesteatoma recurrence rates are higher for ?
-in general 7-57% have a chance of recurrence
Pressure release phenomena associated with normal cochlear anatomy
-In normal ear, air conducted sound enters the vestibule through motion of stapes
-an inward motion of the stapes in the oval window is accompanied by an equal but outward motion of the round window membrane
-the fluid flow between the windows produces a pressure difference between the scala vestibuli & scala tympani resulting in motion of the cochlear partition, activation of hair cells & perception of sound

A pathologic 3rd window...
On the vestibular side (superior canal dehiscence)
-allows for a portion of this acoustic energy to be transmitted (diverted) to the cupula & distension of the membranous canal wall
enlarged vestibular aqueduct
-an ear disorder involving progressive hearing loss that starts during childhood
-caused by abnormal fluid movement within the ear structures due to the large size of structures that hold fluid.May cause
-sudden HL
-fluctuating HL
-progressive SNHL
-large vestibular aqueduct

what is a perilymph fistula?
-an abnormal opening between the air filled ME and the fluid filled inner ear. two weakest points are the oval and round windows.
-A dehiscence is similar but not as serious - an erosion of bone usually found in the Superior SSC uncovering a membrane, makes the ear more sensitive to pressure and noise...hence often have supra normal BC results
Clinical findings in SCD?
-conductive HL across the audiometric range
-CHL isolated to high freq
-CHL isolated to low freq
-CHL which as air bone gaps greatest in high >2000
but can have a/b gaps in low as well

The cochlea communicates with the vestibular system via?
The Ductus reuniens (to saccule)
-pressure can be transmitted
-agents can be transmitted

Vestibular pathologies?
-BPPV related vertigo
-vestibular hydrops (Meniere's)

What is diffuse superior canal dehiscence?
broadly based lesion as in Pagets disease which may behave as a diffuse third window
What is discrete dehiscence
-anatomically discrete lesions, may be classifed by location:
Superior, lateral or posterior canal edhiscence
-bony vestibule (EVA)
-cochlea - (x-linked stapes gusher)

With SCD, Vemp thresholds are significantly ___ in the affected ear than in the uneffected ear
What is Henneberts sign
Characterized by a few beats of horizontal nystagmus seen under Frenzel glasses - due to neg or pos pressure introduced to the external ear canal
-most patients feel dizzy
Symptoms of SCD
-tullio effect - sound induced vertigo
-pressure induced vestibular symptoms
-symptomatic conductive hyperacusis autophony
-sound evoked eye movements
-hennebert's sign

Some conditions you should rule out SCD with
- X-linked stapes gusher syndrome (DFN3)
-enlarged vestibular Aqueduct
-Pagets disease affecting the otic capsule
-conductive pathology

SCD should be differentiated from ?
-perilymph fistula
-Meniere's disease
-lyme disease
-cholesteatoma (eroding the SSC)

symptoms of SSC
- increased sensitivity to bone conducted stimulus
-autophony (own voice sounds louder)
-hearing one's own footsteps
-Better bone conduction in Rinne test
-Weber test - lateralizes to side of dehiscence
-present acoustic reflexes

Some normal inner ear 3rd windows
-cochlear aqueduct
-vestibular aqueduct
-foramina associated with the passage of blood vessels

all known collectively as normal third windows

What is oscillopsia?
-oscillating vision - the visual sensation that stationary objects are swaying back and forth

What is Tullio phenomena
Sound induced vertigo
Difference between perilymph fistula and SCD?
perilymph fistula - low likelihood of comductive component, may have dizziness though
What are Vemps?
Vestibular evoked myogenic potentials
-response to a brief loud click or tone burst
-results in a large amplitude, short latency potential in a tonically contractied sterno-cleido mastoid muscle
-increased or absent response in ME path or ossicular chain abnormality
-decreased threshold of response found in perilymph fistula or SCD

What is autophony
Unusually loud hearing of a persons own voice, breathing or other self generated sounds
An inhibitory potential in response to loud sounds, non invasive assessment of otolith function & functional integrity of the inferior vestibular nerve
-generally used to investigate vestibular disorders
-biphasic response elicited by clicks or TB recorded from tonically contracted sternocleidomastoid muscle (90 dB clicks)
-considered a vestibulo-collic reflex whose afferent limb arrises from acoustically sensitive cells in the saccule with signals conducted via the inferior vestibular nerve
-applications? Menieres, vestibular schwannoma, vestibular hypersensitivity disorders, vestibular neuritis, MS, BS lesions and SCD

- not many tests for vestibular system... ENG assesses semicircular canals and superior vestibular nerve
-VEMP assesses - saccule and /or inferior vestibular nerve
- absent in Menieres
- abnormal in vestibular schwannoma
-SCD - present w/low thresholds and abnormally large amplitudes

Acronym for cranial nerves?
On old olympic towering tops a fin & german viewed some hops

some say marry money but my brother says big boobs matter more

Cranial nerves
Olfactory = sensory
Optic = sensory
Occulomotor = motor
Trochlear = motor
Trigeminal = both
Abducens = motor
Facial = both
Acoustic/vest = sensory
Glossopharyngeal = both
Vagus = both
Spinal accessory = motor
hypoglossal = motor

Components of Facial nerve (VII)
-chorda tympani - taste
-lacrimal branch - tears
-branch that supplies sublingual & submandibular glands (lingual branch)

What nrve inervates the tongue muscles during development?
Primary palate development
-begins to form in beginning of the 6th week
-develops from the fusion of the medial nasal prominances between maxillary prominances
-becomes small portion of the adult palate

Secondary palate development
-becomes the hard & soft palate
-begins to form during beginning of week 6 from maxillary prominances as lateral palatine processes on each side of tongue
-week 7-8 processes get longer & move upward to a horizontal location above the tongue
-weeks 9-12 fuse with each other & with nasal septum & posterior primary palate

CNS develops from what ?
-the neural tube
- the neural crest and its cells develop into the majority of cranial, spinal & autonomic cells of the PNS and ANS
The spinal meninges develop from what?
-mesenchyme around the neural tube. compresses to create primordial meninges
- 3 layers = leptomeninges
-fluid filled apace within the lepto develop into the subarachnoid space
-cerebrospinal fluid begins to develop in the 5th week of embryonic development

Catagories of ototoxic drugs?
- streptomycin
Heavy Metals
Chemotherapeutic agents

Audiologic measures for detecting ototoxicity?
-high freq audiometry
- ENGs for early detection

4 barriers to drug absorption are?
-blood brain barrier
-blood labyrinth barrier
-blood placental barrier
-blood testes barrier

Variability between drug responses in patients can be accounted for by:
-body weight
-disease states
-genetic factors

The incidence of HL among patients treated with cisplatin?
as low as 11% & as high as 91%
-generally considered ~ 40-60% in the 4000-8000 range
-ototoxicity is dose related
-71% of cisplatin HL was 1st detected in freq of 8000 Hz or above

Catagories of anti inflammatory drugs
Non steroidal /anti inflammatory drugs (NSAIDS)
Quinine - auditory & vestibular ototoxicity "cinconchism" = deafness, vertigo, tinnitus, headache, nausea, visual loss
-treatment for malaria - high dose
-usually reversable HL
-low dose - drinking - vestibular changes

Aspirin ototoxicity stats
ototoxicity occurs 11 per 1000
-elderly at higher risk even at lower doses
salicilate ototoxicity symptoms:
- nausea, vomiting, tinnitus,
-HL (mild to mod bilateral, symmetric flat or just high freq)
-mental changes
-increased respiration

The severity of aminoglycoside ototoxicity can be reduced by?
-monitoring renal function & serum levels
-once ototoxicity occurs, it may be irreversible & can even progress after cessation of therapy
are used to treat aerobic gram neg bacteria such as e-coli, enterobacter, klebsiella
poorly absorbed orally and most toxicity comes from parenteral administration

Which 2 aminoglycocides are exquisitly toxic to the cochlea?
Neomycin and Kanamycin
[parenteral use should be limited]
Loop diuretics
-exert potential saliuretic effects effects by acting on epithelial cells in the loop of Henly of the Kidneys
-ethacrynic acid - acute & sometime permanant HL
-flurosemide (lasix) significant potential for HL

How should loop diuretics & aminoglycosides be administered at same time?
Loop diuretics first
followed by
does not affect cochlear toxicity any more than the drug singly
-If you reverse the order, Organ of Corti gets severly damaged

What are some macroglides?
-Erythromycin - for legionnaires disease, ototoxic effect even at high doses is reversible
named mycins but are NOT aminoglycocides

Chemotherapeutic agents?
-cisplatin - most common
-nitrogen mustard - cochlear ototoxicity
-vincristine & vinblastine

Methods for avoiding SNHL prior to cisplatin administration
hypertonic saline
-mannitol diureses

Occupations that may place a worker at risk for HL due to ototoxic chemicals

Anti inflammatory agents
Anagesics - for aches and pains

Cardiovascular/renal agents
-diuretics (for Blood pressure)
-Dyslipidemic Agents (statins)
-anti hypertensive agents-resperine,propanol, verapamil

Immune suppressants
-immune globulin

(CMV) of herpes virus family
-most common congenital viral infection
-herpes virus family includes: chicken pox, infectious mono, fever blisters, genital herpes
-may lie dormant & reactivate at later time
-carried by people
-not associated by food, water, animals

How is CMV spread?
- not highly communicable
-spread by direct contact
-shed in urine, saliva, semen, breast milk
-infected mom to child
-blood transfusions
-organ transplants

symptoms of CMV?
Immunocompromised people may experience more serious illness w/fever, pheumonia
-eyes -visual impairment,blindness
-lungs - pneumonia
gastrointestinal system, diahrea, ulcerations, and bleeding
-liver - hepatitus, prolonged unexplained fever
-brain - inflammation (encephalitis) seizures, coma

CMV in infants, immediate signs:
-purple skin blotches, rash or both
-enlarged spleen, liver
-poorly functioning liver

Incubation period of CMV? after exposure
3 to 12 weeks
Most common late developing symptom in CMV?
Hearing loss
other disabilities include:
-mental disability
-lack of coordination
-small head

Best protection from getting CMV?
-hand washing
-avoid contact with tears or saliva when with young children
-avoid sharing drinking glasses
-take special care when changing diapers
-practice safe sex

Incidence of CMV in infants?
10 of 1000 babies born with it but 9 will have no symptoms

one will have significant illness involving the nervous system damage or developmental disabilities

According to NIHND what % of adults are infected with CMV by age 40?
50% to 80%
AKA epidemic parotiditis
-painful swelling of salivary glands may affect testicles
-pain when chewing
-fever,headache, orchitis
-spread by droplet transmission, sharing food, drinks,kissing can spread too

Acquired rubella transmitted via air born droplet
-from upper respiratory tract
-can be present in uring, feces, and on skin
-no carrier state
-incubation period 2-3 weeks
-in 2004 congenital & acquired cases of Rubella had been eradicated by vaccine

-sexually transmitted
spirochete treponema pallidum
-5 stages:
Primary,secondary, latent, tertiary neurosyphilis

Primary stage syphilis
-symptoms delayed ~ 10-90 days after exposure
-skin lesion at point of contact -canker
-may heal spontaneously 4-6 wks later symptoms can disappear w/o treatment
-at this stage penicillin is very effective

Secondary Stage syphilis
-occurs 4-6 months later
-rash may occur on body
-sore throat
-weight loss
-enlarged lymph nodes
-renal disease

Latent stage of syphilis
-Quiescent - may appear to be gone
-discoverable by proper blood test
-in late latent- 2 years post infected, no longer infectious
-50% of those with latent syphilis will progress to late stage syph
-25% will stay in latent
-25% will make full recovery

Tertiary syphillis
1-10 years post initial infection, can be longer
-formation of granulomas called gummas
-chronic inflammatory state characterized by joint pain
loss of sensation & fine position sense

Neurological complications in syphillis
-generalized paresis of the insane (personality changes, hyperactive reflexes)
-Argyll-Robertson pupil - diagnostic sign, small irregular pupils constriction in response to focusing the eyes byt not to light
-Tabes dorsalis -disorder of spinal cord results in "shuffling" gate

Lues =
luetic deafness
-SNHL caused by syphilis
-may be fluctuating
-sudden drops in hearing is tyical
-up to and including complete SNHL
-some recovery may be obtained following treatment

diagnostic tests for Syphilis
Old test = wasserman
-FTA-ABS - fluoresent treponemal antibody absorption
must be used after primary stage

TX for syphilis

Congenital syphilis
Asymptomatic newborns- only identified on routine pre-natal screening. If not identified & treated they develop poor feeding & rhinorrhea. Early congenital syph= 0-2, after that considered late stage
Symptomatic newborns - if not still born, are born premature, enlarged liver, spleen, skeletal abnormalities, pheumonia, bullous skin disease
Other symptoms of congenital syphilis
-abnormal X-rays
-Hutchinson's triad = deafness, hutch teeth centrally notched, wide spaced peg shaped upper incisors
Keratitis - inflammation of cornea, potentily leading to blindness
-mulberry molars
-poorly developed maxillae
rhinitis can lead to saddle nose

What are the types of isolation precautions?
-droplet and contact
-airborn & contact

Use of chemicals to remove most surface microorganisms
a procedure using intense heat, steam, or gas to remove microorganisms from medical equipment. It typically requires specialized equipment. One method is the use of ethylene oxide gas within a special chamber
Contact isolation
warning designation placed on a patient if the patient has a disease or infection that is transmitted through physical contact. Use of mask, gloves, & purell after removal of gloves

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