Otology and Ophthalmology Flashcards
Tonotropy
different frequencies lead to vibration at specific location on basilar membrane
low frequency sounds are heard at ?
apex near helicotrema (Wide and flexible)
high freq sounds are heard at ?
base of cochlea which is thin and rigid
Weber test: localized to affected ear
Rinne test: abnormal because bone conduction >air
conductive hearing loss
Weber test: localized to unaffected ear
Rinne test: normal, air >bone
sensorineural hearing loss
Noise induced hearing loss: damage to? loss of what freq first?
damage to the sterociliated cells in organ of corti
loss of high frequency first
Age related progressive hearing loss
presbycusis
destruction of hair cells at cochlear base (loss of high freq)
OVergrowth of desquamated keratin debris within the middle ear space
cholesteatoma
may erode ossicles, mastoid air cells resulting in conductive hearing loss
painless otorrhea
Meniere disease triad
sensorineural hearing loss vertigo
tinnitus
type of peripheral vertigo that involves inner ear etiology vs central that is a brainstem or cerebellar lesion
Layers of eye (inside to out)
Retina (inner)
Choroid (middle)
Sclera (outer)
Most common cause of conjunctivitis (inflammation of the conjunctiva –> red eye)
viral due to adenovirus
sparse mucous discharge, swollen preauricular node, self resolving
Hyperopia
farsighted
eye too short for refractive power of cornea and lens –> light focused behing retina
convex lens needed
Myopia
nearsighted
eye too long for refractive power of cornea and lens –> light focused in front of retina
concave (diverging) lens
Presbyopia
aging related impaired accomodation (focusing on near objects)
aqueous humor pathway
90% via the trabecular outflow
10% via the uveoscleral outfloq
trabecular outflow
drainage through trabecular meshwork –> canal of schlemm –> episcleral vasculature
increases with M3 agonist
Uveoscleral outflow
drainage into uvea and sclera
increases with prostaglandin agonist
Aq humour
produced by nonpigmented epithelium on ciliary body
decrease by beta blockers, alpha 2 agonists, and carbonic anhydrase inhibitors
Iris dilator muscle
alpha1
Iris sphincter muscle
M3
Patient presents with increased intraocular pressure and progressive peripheral visual field loss
Glaucoma
optic disc atrophy with characteristic cupping(thinning of outer rim of optic nerve head)
Open angle glaucoma
the angle in your eye where the iris meets the cornea is as wide and open as it should be, but the eye’s drainage canals/trabecular meshwork become clogged over time with WBC,RBC, retinal elements, causing an increase in internal eye pressure and subsequent damage to the optic nerve.
associated with increased age
Closed angle/narrow glaucoma
primary cause - enlargement or anterior movement of lens against central iris (pupil margin) causing obstruction of aq flow through pupil. Fluid builds up behind iris and pushes peripheral iris against cornea and impedes flow through trabecular meshwork
secondary cause-hypoxia from retinal disease induces vasoproliferation in iris that contracts angle
Chronic vs acute closed angle glaucoma
chronic -damage to optic nerve and peripheral vision
acute- true emergency. increased IOP pushes iris forward and closes the angle abruptly.
sudden vision loss, halos around lights, frontal headache, fixed and mid dilated pupil
mydriatic agents contraindicated
anterior uveitis? posterior uveitis?
anterior is iritis
posterior is choroiditis and or retinitis
may have hypopyon (accumulation of pus in anterior chamber) or conjunctival redness
associated with systemic inflammatory disorders like RA or HLA-B27 associated conditions
Age related macular degeneration
degeneration of macula (central area of retina) causes distortion (metamorphopsia) and eventual loss of central vision (Scotomas)
dry-nonexudative
wet-exudative
Deposition of yellowish extracellular material in between Bruch membrane and retinal pigment epithelium with gradual decrease in vision
dry age related macular degeneration
Rapid loss of vision due to bleeding secondar to choroidal neovascularization
wet age related macular degeneration
treat with anti-VEGF (vascular endothelial growth factor) injections
Type of diabetic retinopathy
nonproliferative- damaged capillaries leak blood and lipids and fluid seep into retina causing hemorrhages and macular edema
proliferative - chronic hypoxia results in new blood vessel formation with resultant traction on retina
Flame shaped retinal hemorrhages, AV nicking, microaneurysms, macular star, cotton wool spots
hypertensive retinopathy
increased risk of stroke, CAD, kidney dz
presence of papilledema requires immediate lowering of BP
Papilledema
is a condition in which increased pressure in or around the brain causes the part of the optic nerve inside the eye to swell
optic disc swelling that b/l due to increased ICP
enlarged blind spot and elevated optic disc with blurred margins
Retinal vein occlusion
blockage of central of branch retinal vein due to compression from nearby arterial atherosclerosis
retinal hemorrhage and venous engorgement
“blood thunder appearance”
Retinal detachment
separation of neurosensory layer of retina (photoreceptor layer with rods and cones) from outermost pigmented epithelium (important for protecting the retina from light) –> degeneration of photoreceptors –>vision loss
could be secondary to diabetic traction etc
crinkling of retinal tissue and changes in vessel direction
Patient complains of flashes and floaters and then loss of vision in one eye as if a curtain was drawn down
SURGICAL EMERGENCY!
retinal detachment
Central retinal artery occlusion
acute painless monocular vision loss
retina cloudy with attenuated vessels and cherry red spot at fovea (center of macula)
Retinitis pigmentosa
inherited retinal degeneration
starts with night blindness (rods affected first)
bone spicule shaped deposits around macula
Retinitis
retinal edema and necrosis leading to scar
Pupillary control pathway for miosis
(constriction, parasympathetic)
first neuron: edinger-westphal nucleus to ciliary ganglion via CN III
2nd neuron: short ciliary nerves to spincter pupillae mm
“short ciliary nerves shorten the pupil diameter”
Pupillary light reflex
light in either retina sends a signal via CN II to pretectal nuclei in midbrain to activate bilateral edinger-westphal nuclei–> pupil constrict bilaterally
illumination in one eye- causes bilateral pupillary constriction
Mydriasis control pathway
(Dilation, sympathetic)
1st neuron: hypothalamus to ciliospinal center of budge (C8-T2)
2nd neuron: exit at T1 to superior cervical ganglion while traveling along cervical sympathetic chain
3rd neuron: plexus along internal carotid through cavernous sinus –> enters orbit as long ciliary nerve to pupillary dilatory muscles
long ciliary nerves make the pupil diameter longer
Marcus gunn pupil
when the light shines into a normal eye, constriction of the ipsilateral (direct reflex) and contralateral eye (consensual reflex) is observed
when swung to affected eye, both pupils dilate instead of constrict due to impaired conduction of light signal along the injured optic nerve
Horners syndrome
sympathetic denervation of face
Ptosis - slight drooping of eyelid due to superior tarsal mm
Anhidrosis - absence of sweating and flushing of affected side
Miosis- pupil constriction
Horners syndrome lesion
sympathetic chain
1st neuron: pontine hemorrhage, lateral medullary syndrome, spinal cord lesion above T1
2nd neuron (stellate ganglion): pancoast tumor
3rd neuron: carotid dissection (painful)
Lateral rectus innervation
CN 6
Superior oblique innervation
CN 4
Innervation of all eye mm except superior oblique and lateral rectus
CN 3
“LR6SO4R3 chemical formula”
strongest action of superior oblique
depression when eye is adducted
when abducted it acts to intort the eye towards the nose
ptosis and “down and out”
CN III damage on motor (Central)
Diminished or absent pupillary reflex “blown pupil” often with down and out gaze
CN III damage on parasympathetic output
Cavernous sinus thrombosis would affect what CNs
4,6,V1,V2
Eyes move upward particularly on contralateral eye. When going down stairs the patient may tilt head in opposite direction to compensate
CN 4
cant see the floor with CN 4 damage
Affected eye unable to abduct and is displaced medially in primary position of gaze
CN 6 damage
lateral rectus can function and therefore medial gaze dominates
Right anopia
optic nerve lesion
complete loss in right eye
Bitemporal hemianopia
pit lesion, chiasm
loss of left field in left eye
loss of right field in right eye
Left homonymous hemianopia
optic tract lesion
loss of Left eye field in both eyes if lesion on R optic tract
Left upper quadrantanopia
right temporal lesion, MCA @ meyer loop
Left lower quadrantanopia
right parietal lesion, MCA @ dorsal optic radiation
Left hemianopia with macular sparing
PCA infarct affecting the meyer loop and dorsal optic radiation on right side
Central scotoma in left eye
macular degeneration in left eye
Meyer loop
lower retina, loops around inferior horn of lateral ventricle
Dorsal optic radiation
superior retina
takes shortest path via internal capsule
Cavernous sinus
collection of venous sinuses on either side of pituitary
drains into internal jugular vein
CN 3,4,V1,6,V2, pupillary fibers en route to orbit all pass through cavernois sinus
cavernous portion of internal carotid
Patient presents with variable ophthalmoplegia, decreased corneal sensation, horner syndrome, occasional decreased maxillary sensation
Cavernous sinus syndrome
CN 6 most susceptible to injury
Medial longitudinal fasciculus (MLF)
pair of tracts that allows for crosstalk between CN 6 and CN 3 nuclei
coordinates both eyes to move in same horizontal direction
highly myelinated for fast communication between eyes
MLF lesion seen classically in MS
lateral
lesion in MLF
internuclear opthalmoplegia
a conjugate horizontal gaze palsy
lack of communication between two eyes - when CN 6 nucleus activates ipsilateral lateral rectus, contralateral CN 3 nucleus does not stimualte medial rectus to contract
abductng eyes gets nystagmus because CN 6 overfires to stimulate CN 3
right vs left INO refers to eye with nystagmus
internuclear opthalmoplegia (INO)
ipsilateral adduction failure
Nystagmus in opposite eye
