ear 1/2 Buzz info Flashcards
what are the sensory hearing loss causes?
-noise
-head trauma
-systemic dx
-ototoxic drug
infxn:
-Meniere syndrome
-labyrinthitis
Auditory and vestibular systems use:
both hair cells to transduce mechanical forces into action potentials.
what are neural hearing loss causes?
-acoustic neuroma
-multiple sclerosis
-auditory neuropathy
infxn:
-Meniere syndrome
-labyrinthitis
Hair cells are located in
a fluid filled sensory organ called the membranous labyrinth.
The cochlea is the =
auditory component.
-afferent neurons exit cochle→ form auditory nerve
The otoliths organs utricle/saccule and the semicircular canals is the →
vestibular components of labyrinth → CN8
-Pitch (tone):measured in
HERTZ : Higher frequency= higher pitch
-the ear usually receives higher pitches @ the beginning and the apex receives the lower pitches
Intensity (loudness) : measured in
DECIBELS → amplitude
Sound travels through
ossicles→ sound vibration→ vibration in fluid mov’t that stimulate hair cells→ action potential
Hearing loss: 2 types
Most common due to :
Sensorineural (SNHL)
Conductive (CHL)
CERUMEN IMPACTION (WAX), ETD ( CHL), age related hearing loss (SNHL)
Sensorineural Hearing Loss (SNHL):
Etiology:
-genetic make up influences all causes of hearing loss
-hair cells of cochlea
-cochlear branch of CN8 ( damage to the nerve)
-areas if the brain that process auditory information
Presbycusis:
Etiology:
sx:
most frqt cause of sensory hearing loss
–progressive, predominantly high frequency and symmetric
Etiology: noise trauma, drug exposure, genetic predisposition
SX: loss of speech descrimination
-sounds > 85 dB = cochlea injury
Ototoxicity:
Cause DEATH OF SENSORY HAIRS (auditory and vestibular)
Most common ototoxic meds:
-aminoglycosides (neomycin, gentamicin)–> avoid in ototoxic ear drops in TM
-loop diuretics
-platinum based antineoplastic agents (cisplatin)
-ASA/NSAIDS
Sudden SNHL:
Dx:
-idiopathic sudden loss of hearing in ONE EAR
->20 yrs old
Diagnosis:
-Audiogram and MRI
Congenital and Genetic Hearing loss:
Congenital- present at birth
Genetic HL- discovered later
Most acquired prenatal cause:
Specific PE findings associated with :
-intrauterine infxn ( CMV)
-pre auricular pits and tags
-lateral displacement in the inner corner of the eyes
-hetero iridis
PE abn → risk abn. Of hearing
Conducting Hearing Loss (CHL):
- external or middle ear dysfunction
Conducting Hearing Loss (CHL):
4 main mechanisms= impairment of the passage of sound vibrations to the inner ear:
-obstruction: cerumen ( wax) impaction
-mass loading: middle ear effusio, ETD ( not allowing ™ to move)
-stiffness: scarring of ™
-discontinuity-oscillar disruption
Otosclerosis:
Etiology :
Sx:
PE:
Diagnostic:
abnormal overgrowth of the footplate of the stapes→ conductive hearing loss
Etio: autosomal dominant disorder of abnormal resorption and deposition of the bone in the otic capsule.
Sx: gradual progressive conductive hearing loss 20s-40s, initially low frequency hearing loss
PE: normal otoscopic exam, Weber and rinne (CHL)
Diagnostic:
Audiometry and CT temporal bone
Gross auditory Acuity :
- pt in a quiet room would repeat aloud the words presented in a soft whisper.
512 hz tuning fork is useful in differentiating conductive from sensorineural losses.
Weber test:
CHL:
SNHL:
Normal:
tuning fork is PLACED ON TOP PT HEAD and sound is interpreted by pt
Normal= sounds the same bilaterally
CHL= sounds louder in the affected ear
SNHL= sounds louder than normal in the non affected ear
Rinne test:
normal:
CHL:
SNHL:
tuning fork is placed on the mastoid bone then at the entrance of EAC.
Normal air conduction > bone conduction : can hear the sound in both places
CHL= Bone conduction > air conduction: CANNOT hear the sound @ EAC
SNHL= air conduction > bone conduction: normal
Audiometric Testing:
Pure tone testing:
-performed in sound proof room
threshold in decibels are obtained over the range of 250-8000 Hz for both air and bone conduction. ( ear phone and bone oscillator) and speech audiometry
Conductive losses-
Sensorineural losses-
C:create gap btw air and bone thresholds
S:both air and bone thresholds are equally diminished
Tympanometry:
measures how well the ™ moves
[helps see if child has ear infxn]
-small probe inserted in each ear
Otoacoustic Emissions
evaluates cochlear fxn
Auditory brainstem evoked responses:
determines the lesion is sensory[cochlea] or neural [CN8/brain].
Otoacoustic Emissions if + and = means?
Important for ?
-Pts w normal hearing = (+) OAEs
-Blockage in outer ear= no sounds = no vibrations come back
IMPORTANT IN NEWBORN HEARING EXAM
Pure tone testing:
requires a quiet testing environment w low levels of background noise, sound from low to high pitch is recorded on the audiograms horizontal axis
On the graph , the right ear is O and the left is X.
Auditory Brainstem response (ABR):
recording of the activity CN7 and the brainstem/brain response to an auditory signal.
Electrodes are put on the head and record the brain wave activity in response to sounds heard through headphones.
what CONFIRMS COCHLEA AND BRAIN PATHWAYS WORK TO HEAR
Auditory Brainstem response (ABR):
Tinnitus:
Etiology:
perception of sound in the absence of an actual external sound
Etiology: associated with high frequency SNHL medications, any lesions
[assoc. W depression, anxiety, personality disorders]
Tinnitus :
Sx:
Diagnostic tests:
Sx: quiet background noise ,non pulsatile, pulsatile ( hearing your heartbeat), staccato ( middle ear spasm)
Diagnostic tests:
™ studies,
screening tests: rinne/weber, audiometry ( tinnitus )
GOAL IS TO LESSEN TINNITUS AND ITS IMPACT ON QUALITY OF LIFE
Bilateral tinnitus:
prolonged noise exposure, systemic damage the cochlear hairs
Unilateral tinnitus:
™ damage, impact cerumen, meniere’s dx, recurrent ear infxn, ossicle damage, trauma
Macula detects
→ linear acceleration/deceleration, detects head tilt
Semicircular ducts/ canals:
detects ROTATIONAL ACCELERATION DECELERATION
Vestibular labyrinth
-utricle, saccule and 3 semicircular ducts
Utricle and saccule
-(linear acceleration)
3 semicircular ducts
-(rotational acceleration)
-ampullae [base of semicircular ducts] houses the sensory area [crista ampullaris]
-innervated by CN8
Vertigo:
Etio:
false sensation of motion [HISTORY IS IMPORTANT!!!]
Etio: damage to or dysfxn of the labyrinth, vestibular nerve or central vestibular structures in the brainstem.
“Spinning sense, sense of falling backward/forward, sensation /out motion, exaggerated motion
Vertigo:
peripheral and central
Peripheral: vestibular nerve or labyrinth
-sudden onset, horizontal or torsional ( eyeball movt)
Central: brainstem or cerebellum
-gradual onset
Meniere Dx/syndrome:
Positive sx:
duration!!!
compartment of inner ear due to EXCESS FLUID
Positive sx = allergies, hormonal imbalance, trauma, infxns [ SYPHILIS]
Duration: MINUTES- HRS.
Vestibular neuronitis and labyrinthitis:
Etio:
Patho:
SX:
Etio:
Vestibular neuronitis: inflammation of the vestibular portion of CN8
Labrynthitis: inflammation of vestibular & cochlear portion of CN8
Pathophysiology:
Infectious microorganisms or inflammatory mediators invade the membranous labyrinth and damage the vestibular and auditory end organs
Sx:-
-continous vertigo
VESTIBULAR NEURITIS IF NO SX →
duration:
PE:
Diagnostic:
-HSV OR VARICELLA
Duration: SEVERAL DAYS TO WEEKS
PE:
-look for recurrent infxn, rotary horizontal nystagmus
Diagnostic studies:
-audiogram
-electronystagmography
-mri of brain
Benign Paraoxysmal positional vertigo:
abnormal sensation of motion for certain positions that trigger nystagmus and vertigo. [small movt= huge movt]
Benign Paraoxysmal positional vertigo:
SX:
Patho:
-migration of OTOLITHS from utricle/sacule to the posterior semicircular canal
- otoliths dislodges→ crystal in wrong place= excess movt when there isnt
Sx: sudden onset, episodic vertigo
Benign Paraoxysmal positional vertigo:
DURATION!!!
provoked by:
PE:
if recurrent?
Duration:
LASTS 20 SECS- 1 MIN
-Provokes by changes in head position (rolling over, bending over, standing up)
PE:
-ENT and neurological exam
-DIX HALLPIKE TEST: torsional nystagmus stimulate heas movt and see nystagmus ( eye movt)
recurrent cases need MRI
Types of Vertigo testing :
Vestibulo-ocular reflex:
Electronystagmography:
Video-nystamography:
Dix hall pike maneuver:
Vestibulo-ocular reflex:allow for eye fixation on a stationary target while head is in motion. Must have intact vestibular system to work.
Electronystagmography: electrodes to record nystagmus
Video-nystamography: video cameras to record nystagmus
Dix hall pike maneuver: evokes nystagmus due to head position
new onset vertigo=
early sign of stroke, migraine
brain stem compression
Peripheral Vestibular dx:
-SUDDEN ONSET VERTIGO
-so severe that pt is unable to walk
-fatigable nystagmus
Trigger:s: diet, stress, fatigue, bright lights
