Eyes and Ears Flashcards

1
Q

Lens and Layers

A

• Lens and its layers– responsible for focusing the light that enters through the pupil onto the retina; transparent proteins fill the center
o Capsule – secreted by subcapsular epithelium; ALIVE
o Subcapsular epithelium
o Lens fibers

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2
Q

Sclera and Vitreous Humor

A
  • Sclera – tough outer white part of the eye

* Vitreous humor – jelly-like substance that makes up majority of the eye

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3
Q

Retina Structure

A

– back of the eye; interprets the different light that passes through the cornea, pupil, and lens
o Nerve fibers from retina converge at the optic disk to form the optic nerve
o Interconnecting neurons – sense hyperpolarization of rods and cones and communicate the information to the ganglion neurons
 Send signal to primary visual cortex of the brain in the occipital lobe
o Macula – middle of retina and contains the fovea
o Fovea – indentation as a result of lack of ganglion cell axons in the area; where light from lens is primarily focused
 Where majority of rods and cones are localized

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4
Q

Rods and Cones General Mechanism

A

o Rods and cones are situated behind the optic nerve, ganglion, and interconnecting neurons
o Rod cells – interpret light and dark; black/white
 Light – Na+/Ca+ ion channels are closed  hyperpolarizes the cells (-75mV)
• Na+/K+ pump continues to work
 NO light – Na+/Ca+ ion channels open  depolarizes the cells (-45mV)
 NO action potentials
o Cone cells – 3 diff. populations (red, green, blue) – each interpret different wavelength of light
 Red gene is on X chromosome so guys more likely to be red color blind

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5
Q

Retina Mechanism in Response to Light

A

o Light hits rods  converts 11-cis-retinal to trans-retinal  activates rhodopsin
o Rhodopsin is connected to intracellular G protein  replaces GDP with GTP  T-alpha-GTP complex activates phosphodiesterase (PDE) which breaks down cGMP  decrease in cGMP closes the Na+/Ca+ channel  hyperpolarization
o Guanylyl cyclase raises intracellular cGMP concentration  reopen the Na+/Ca+ channels  depolarizing the cell  trans-retinal is converted back to 11-cis retinal
o EXTREME LIGHT: all the cells hyperpolarize and need to undergo recover/adaptation which takes a few seconds (reason why we still see light even after we look away from the sun)

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6
Q

After Rods and Cones

A

o Send signals to horizontal cell s and then bipolar cells
o Bipolar cells transfer information to ganglion cells
o Ganglion cells generate action potentials along axons to the optic nerve

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7
Q

Pigmented Epithelium

A

– found inferior to the rod and cone cells
o Important for there to be a black background in order to stimulate a specific rod/cone
o Pigment produces melanin which causes the retina to be black and absorb light
o If epithelium wasn’t pigmented the light would be reflected back after it hit and vision would not be as accurate because more cells would be excited

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8
Q

Occulocutaneous albinos

A

– suffers from unpigmented retinal epithelium
o Vision has a lot of glare due to over activation of rod and cone cells
o Eyes are pink because light bounces off the red capillaries in the retina instead of being absorbed by the black retina

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9
Q

Peripheral Movement

A

– brain uses peripheral light receptors to notice movement; we turn our eyes to the sight of the movement to focus the image on our fovea to see it better

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10
Q

Hemidecasation and Visual Pathway

A

o Optic nerve  optic chiasm  lateral geniculate body of thalamus  optic radiations  visual cortex of the occipital lobe
o Medial portion of retina crosses over to opposite side of brain at optic chiasm
o Allows nerves from right and left field of vision to merge together allowing the brain to process the information together
o Right visual field hits medial right eye and lateral left eye and is processed on left side of brain
o Left visual field hits medial left eye and lateral right eye and is processed on right side of brain
o As you focus on something, the medial and lateral portions get more out of sync

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11
Q

Bitemporal hemianopia

A

– typically caused by pituitary tumor; damage the optic chiasm

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12
Q

Muscles of the Eye

A

– controlled by cranial nerves 3,4,6
o Medial rectus – inserts medially – CN 3
o Superior rectus – inserts superior – CN 3
o Inferior rectus – inserts inferiorly – CN 3
o Lateral rectus – inserts laterally – CN 6
o Superior oblique – pulls eye down and rotates
 Runs through the trochlea (hinge/pivot)
 Cranial nerve 4
o Inferior oblique – pulls eye up and rotates – CN 3

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13
Q

Strabismus, Diplopia, Amblyopia, Nystagmus

A

• Strabismus – failure to converge; can cause diplopia
• Diplopia – cross-eyed, double vision
• Amblyopia – lazy eye
• Nystagmus – alternating smooth and jerky eye movements; can be normal or pathological
o Pathological – caused by problem with vestibular system; eye will drift away and snap back

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14
Q

Myopia and Hyeropia

A

• Myopia – near sighted (cant see far); parallel rays of light are brought to a focus in front of retina
o Child may develop if they regularly read or watch TV up close
• Hyperopia – far sighted (cant see near); parallel rays of light come to a focus behind the retina in the unaccomodative eye

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15
Q

Simple Myopia Astigmatism, Presbyopia

A

• Simple myopia astigmatism - lens is not symmetrically shaped, making it difficult for light to be focused
o Vertical bundle of rays is focused on the retina; horizontal rays are focused in front of retina
• Presbyopia – involves loss of near vision due to loss of accommodation; eyes “stuck” in distance vision
o Lens doesn’t bend as well; natural position of lens is to see distance and bends in order to focus on near vision
o Occurs in older people

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16
Q

Leading Causes of Blindness (River blindness, cataracts, glaucoma, macula degeneration, diabetic retinopathy)

A

o River blindness – parasitic worms destroy retina; NOT seen in US; leading cause worldwide
o Cataracts – clouding of the lens prevents light from penetrating through; pupil is enlarged
 Diabetics – this occurs more rapid
o Glaucoma – increased pressure in the anterior chamber; pushes back on lens and causes damage to optic nerve
 Diagnose via pressure test
o Macula degeneration – degeneration of the macula; causes central (high acuity) blindness
o Diabetic retinopathy – increased vascular permeability and angiogenesis destroys retina

17
Q

Ear Systems

A

o Auditory System – external, middle, & inner ear for hearing
o Vesibular system – relays information regarding balance and rotational acceleration

18
Q

External Ear

A

o Auricle – allows sound waves to bounce off appropriately and enter the ear canal
o External auditory meatus (ear canal)

19
Q

Middle Ear

A

o Tympanic Membrane (eardrum) – translates sound waves into mechanical forces onto the auditory ossicles – malleus (hammer), incus (anvil), & stapes (stirrup)
o Stapes – transfers vibrations onto the oval window; moves back and forth as result of interactions with other auditory ossicles and creates changes in pressure in the cochlea

20
Q

Inner Ear

A

o Oval window creates pressure changes inside the cochlea – tube curled on itself and filled with a fluid known as perilymph; curls 2.5x and then curls back 2.5x
o One end of tube is connected to oval window and other is connected to the round window
o Fluid inside the tube cannot compress and the volume cannot change, therefore the round window vibrates along with the oval window

21
Q

Hearing Mechanism

A

o Oval window creates standing waves throughout the cochlea
o Each wave/harmonic has a certain frequency that equates to a certain distance within the tube
o Cochlea is lined with hair cells (specialized nerve cells) that sense where the nodes of the harmonics exist (“frequency deposition” of the sound)
o Hair cells depolarize and send their signals to the temporal lobe via vestibulocochlear nerve
o Hearing can be characterized by frequency and loudness (detected through hair cells in cochlea)
 Frequency – measured in Hz
 Intensity (loudness) – measured on exponential scale in decibels (db)

22
Q

Vestibular System

A

o 3 semicirucular canals filled with fluid (endolymph) each responsible for one dimension
o Saccule and Utricle – relay information regarding linear acceleration

23
Q

3 Semicircular Canals and Mechanism

A
  • filled with fluid (endolymph) each responsible for one dimension
     Fluid moves in the tubes and denotes 3 dimensional orientation (pitch, roll, and yaw) and rotational acceleration
     Ampulla of Semicircular ducts – at end of each tube; collection of hair cells that have stereocilia imbedded in gelatinous substance known as cupula
    • Stereocilia bend due to motion
24
Q

Saccule and Utricle Mechanism

A

– relay information regarding linear acceleration
 2 otoliths – heavy and want to stay in place
 During acceleration, otoliths create a backwards pull on gelatinous layer and cause stereocilia of hair cells to bend and sensory signal being sent to brain ; each curved so they each cover 1.5 dimension
 Hair cells line each structure and interact with a gelatinous layer
• bent forward signal inhibition/hyperpolarization

25
Q

Hair Cells and Mechanism

A

– specialized nerve cells
o Interpret the bending of their stereociliary as either stimulatory or inhibitory signal
 More stereocilia bent = greater change in the firing rate
o Resting state – stereocilia are NOT bent; sends signals to brain at a constant rate saying they are undisturbed
o Active state – stereocilia bent towards kinocilia (largest stereocilia at the apex of the cell) results in the cell being stimulated and depolarize at a faster rate
o Active state – stereocilia bent away from kinocilia results in cell being inhibited and hyperpolarize; cells fire at slower rate

26
Q

Vertigo

A

o Peripheral – problem with vestibular system – saccule, utricle, or semicircular canals
o Central – problem with the brain’s “balance” centers
o Eyes are able to fix any slight issues it detects with the vestibular system
o Closing their eyes leads to loss of balance, head spinning, and other symptoms of vertigo
o Symptoms: dizzy; motion sickness; balance loss; vision problems (trouble focusing, nystagmus)
o Incidence: ~5% of people report a year; 7% lifetime incidence; women 3x more likely

27
Q

Audiogram

A

– used to test frequency and loudness

o Can hear from 20Hz – 40,000Hz

28
Q

Hearing Loss

A

o Conductive hearing loss – problem with conduction of sound
o Sensoneural hearing loss – problem with detection of sound or brain
o Severity: 20-40db = mild; >90 db = profound
o Causes – exposure to loud noises, diseases (esp. ear infections), drugs/chemicals, genetics
o Incidence: 1 per 1000 are deaf before 18; 4 per 1000 deaf in lifetime; >10% lifetime incidence of “hard of hearing” mostly >65 yo

29
Q

Prebyacusis

A

– sloping high-frequency hearing loss; synonymous with aging process; can hear low frequency find but can’t hear high frequency sound

30
Q

Examples of Hearing Loss

A

o < 1000Hz = low frequency loss
o 1000-2000 Hz = mid frequency loss
o >2000 Hz = high frequency loss  most common with older people
o Most speech is 300-3000Hz

31
Q

Hearing Aid Syles

A

o Larger hearing aids are required for greater gain in order to prevent feedback
o Basically a microphone at one end and speaker at the other end
 Small hearing loss can have entirely IN canal hearing aid
 Large hearing loss microphone is external and speaker is deep inside ear (FARTHER apart)