AAP Flashcards
Bacterial infections of inner ear and their symptoms?
Labrynthitis: inflammation of the membranous membrane from otitis media.
Bacterial meningitis: bilateral SNHL usually profound. Via internal auditory Meatus
Syphilis: SNHL is common. Vertigo and tinnitus can occur at later stages
Viral infections of inner ear and their loss?
CMV: in child profound loss in mother flu. Common cause on congenital hearing loss.
Rubella: bilateral SNHL. Partial collapse of reissners membrane
Measles: bilateral mixed. Mixed loss due to middle ear erosion. 40dB to 80dB flattish loss
Mumps: unilateral sudden severe to Profound, can be reversible
Herpes zoster: sudden cochlea and retro cochlea loss. Associated with pain and vesicular rash on external ear.
Antibiotics causing ototoxicity of inner ear and drugs, use and damage?
Neomycin, gentamicin, streptomycin.
Used for bacterial disorders and they damage the OHC at basal end of the cochlea.
Anti cancer drugs causing ototoxicity of inner ear and use and effect
Cisplatin and carboplatin
Used for malignant disease. Effects hair cells, stria vascularis and spiral ganglion and is permanent
Diuretics that cause ototoxicity in inner ear and use and effects?
Frusemide and ethacrynic acid. Used to turn excess water into urine. Effects OHCS’s and Stria vascularis. Is mostly reversible.
Anti malarial drugs that cause ototoxicity in inner ear and use and effects?
Quinine. Used for malaria treatment. Effects are tinnitus and damage to organ of corti.
NSAID (non steroid antiflamatory drugs) that cause ototoxicity in inner ear and use and effects?
Salicylates - aspirin. For pain relief and effects and damage are unknown. Loss reversible.
What is Menieres?
Over production of endolymph. The endolymphatic sac becomes swollen with excess fluid. Scala media fills the scala tympani and scale vestibuli. Greatest affect at the apical end of the cochlea therefore affects low frequency and low frequency tinnitus.
It is:
idiopathic (unknown cause)
Episodic (happens in episodes)
Endolymphatic (relates to endolymph)
Hydrops (excess fluid)
Describe stage 1 of Menieres
-Disabling, rotary vertigo
-nausea and vomiting
- episodes from 20 mins to several hours
-aural fullness or pressure
- sensation in affected ear
- between attacks hearing returns to normal
Describe stage 2 Menieres?
-hearing loss is more established but still fluctuates , often unilateral
- SN, low frequency loss: reverse slope
- vertigo episodes reach maximum and then subside
- pattern of attacks is extremely variable : no 2 patients the same
- tinnitus becomes more noticeable
Describe stage 3 Menieres?
- hearing loss becomes severe and permanent. Becomes primary disability
- 50% of long term sufferers develop a bilateral loss
- vertigo diminishes but unsteadiness remains
Medication for Menieres
- anti vertiginous
- diuretics
- gentamicin
- steroid injections
Passed through cochlea via TM or through grommets
Surgery treatments for Menieres
- endolymphatic sac shunt: drains the endolymphatic sac to reduce pressure. Usually will preserve the hearing.
- endolymphatic sac decompression: removal of bone over the sac to allow for its expansion
- vestibular nerve suction: severing of the vestibular nerve.
- labrynthectomy: destruction of Labrynth : no hearing
Other treatments of Menieres?
- vestibular rehabilitation ; head eye and neck movements. Hallpike manoeuvre
- diet - low sodium
- tinnitus management, hearing aids, counselling and surgical treatments if vertigo remains
Symptoms of Presbyacusis
- bilateral
- symmetrical
- sloping
- sensorineural
- slow and progressive
- both ears same degree
- mainly affects high frequencies
- cochlea + neural pathways
There is also a generic element as some will be more susceptible than others.
4 different etiologies of presbyacusis
- neural
- sensory
-metabolic - mechanical
Sensory presbyacusis
Hair cell degeneration within the organ of corti. Mainly at the basal end (doormat effect) therefore affects the high frequencies.
Neural presbyacusis
Degeneration of ganglion cells, reduction in synapses to the brain.
Loss of never cells that transmit the impulses along the auditory pathway. Not specific to high frequencies.
Metabolic presbyacusis
Atrophy of atria vascularis capillaries. No rich supply of potassium to feed into the inner hair cells - not specific to high frequencies.
Mechanical presbyacusis
Thickening of the basilar membrane. This reduces elasticity so the normal rippling affect does not happen. Base is already taut and becomes even more which has a greater affect on the higher frequencies.
Risk factors of presbyacusis
Heart disease
Noise damage
Ototoxic drugs
Diabetes
Poor diet
Stress
Problems with sensorineural hearing loss
Poor speech discrimination
Loudness recruitment
Poor frequency/ temporal resolution
Upward spread of masking
Describe Loudness recruitment
People with cochlea damage have reduced thresholds so when a sound is increased above this level the perceived rate of growth of loudness is greater than normal. This results from damage to the sensory cells of the cochlea as they recruit neighbour hair cells to hear the frequency.
Describe poor temporal resolution
Temporal resolution is the ability to detect small gaps in sound which is important for speech discrimination. With Cochlea damage this ability is lost which makes speech sound like a continuous slur