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135 Cards in this Set

  • Front
  • Back

How many rods are there in each eye? Cones? Why is this unexpected?

100 million rods
5 million cones
(20:1 ratio of rods:cones - surprising because 99% of vision depends on cones)
What cells are "scotopic"?
Rods

What cells are "photopic"?

Cones
Which photoreceptors are more sensitive? less sensitive?
- More sensitive - rods
- Less sensitive - cones
Which photoreceptors are fast/slow? (what is the integration time for each)?
- Slow - rods - 100 msec
- Fast - cones - 25 msec
Which photoreceptors have high/poor spatial resolution?
- Poor spatial resolution - rods
- High spatial resolution - cones
Which photoreceptors have more/less pigment (rhodopsin)?
- More pigment - rods
- Less pigment - cones
Which photoreceptors are directionally selective?
- Cones are directionally selective
- Rods are not
What does saturation mean?
As amount of light that reaches the retina is increased, the rods response increases but when very moderate light levels are reached the rod reaches its maximum response
Which photoreceptors saturate?
Rods; cones do not saturate
What is the saturation status of rods in low and at normal room light?
Rods are saturated
What are the implications of the fact that your rods are saturated by low levels of light?
Most of the time, your vision is based on 5% of your photoreceptors (cones)
What happens to the polarity of photoreceptors in response to light?
Hyperpolarize
What is inside of photoreceptors?
Photopigments
What is inside of photopigments?
2 protein components:
- Opsin
- Chromophore:  11-cis-retinal
2 protein components:
- Opsin
- Chromophore: 11-cis-retinal
What is the chromophore inside of photopigments? Derived from what?
11-cis-retinal - derived from Vitamin A
Rods absorb most strongly in what region?
Blue-green wavelengths (~500 nm)
Blue-green wavelengths (~500 nm)
What are the different cone types? What wavelengths do they peak absorb?
- S ("blue") ~450 nm
- M ("green") ~530 nm
- L ("red") ~560 nm
- S ("blue") ~450 nm
- M ("green") ~530 nm
- L ("red") ~560 nm
Which type of cones are the least common?
S (Blue) - variable distribution - usually ~5%
S (Blue) - variable distribution - usually ~5%
Is there a certain ratio of L (red) to M (green) cones?
No - it varies from person to person (but usually always about ~5% S/blue cones)
No - it varies from person to person (but usually always about ~5% S/blue cones)
What is the principle of univariance?
- Photoreceptors cannot register the wavelength of the photons they catch
- The output depends on quantum catch, but not upon what quanta are caught
- The photoreceptor does not only respond to "blue", "green", or "red", rather it can respond to any of
- Photoreceptors cannot register the wavelength of the photons they catch
- The output depends on quantum catch, but not upon what quanta are caught
- The photoreceptor does not only respond to "blue", "green", or "red", rather it can respond to any of these, it just has a higher likelihood of responding to light that corresponds to its peak λ; also, it will absorb more photons of light from its peak λ1 than from a different λ2
Why can a photoreceptor not register the wavelength of the photon it catches?
- The number of photons absorbed from a lower intensity light at your peak wavelength
- could equal the number of photons absorbed from a higher intensity light
- Therefore impossible to distinguish wavelength / color
- The number of photons absorbed from a lower intensity light at your peak wavelength
- could equal the number of photons absorbed from a higher intensity light
- Therefore impossible to distinguish wavelength / color
Why would you be colorblind if you only had one type of photoreceptor?
- λ1 and λ2 have the same number of incident photons, pigment abosrption, and total photons absorbed
- But from way different wavelengths, so brain can't tell if these are the same color or not!
- λ1 and λ2 have the same number of incident photons, pigment abosrption, and total photons absorbed
- But from way different wavelengths, so brain can't tell if these are the same color or not!
What kind of proteins are visual pigments?
G-protein coupled receptors
G-protein coupled receptors
How are the visual pigment G-protein coupled receptors different from others (like adrenergic receptors)?
Visual pigments are activated by light instead of a chemical ligand
Visual pigments are activated by light instead of a chemical ligand
What protein makes up 90% of the protein composition in the outer segment?
Rhodopsin (key functional and key structural protein!)
Rhodopsin (key functional and key structural protein!)
What is the first thing that happens in phototransduction?
Isomerization of 11-cis-retinal to 11-trans-retinal
Isomerization of 11-cis-retinal to 11-trans-retinal
What happens when 11-cis-retinal isomerizes to the trans formation?
Induces a conformational change in rhodopsin/opsin
Induces a conformational change in rhodopsin/opsin
What happens when opsin becomes activated (by conformational change)?
Stimulates a G protein (called transducin)
Stimulates a G protein (called transducin)
What does transducin (the G protein) activate?
cGMP Phosphodiesterase
cGMP Phosphodiesterase
What is the action of phosphodiesterase?
Hydrolyzes cGMP to GMP
Hydrolyzes cGMP to GMP
What happens when cGMP levels go down due to PDE?
Low cGMP closes Na+ and Ca2+ channels and hyperpolarizes the cell
Low cGMP closes Na+ and Ca2+ channels and hyperpolarizes the cell
How much amplification occurs when the activated opsin stimulates tranducin (G-protein)? How long does this take?
Amplification ~ 700x within 100 msec
Amplification ~ 700x within 100 msec
How much amplification occurs when the phosphodiesterase breaks down cGMP to GMP?
1400 (i.e., a single activated rhodopsin has led to breakdown of about 1400 cGMP molecules
1400 (i.e., a single activated rhodopsin has led to breakdown of about 1400 cGMP molecules
What is the role of cGMP?
Keeps gated channels open
Keeps gated channels open
When the cell hyperpolarizes due to Na+/Ca2+ channels being closed, what happens?
- Decreased Ca2+ conc. leads to depressed PDE activity and increased Guanylate Cyclase (GC) activity
- Together these lead to increases in cGMP levels in the outer segment
What is the mechanism by which Viagra can make someone temporarily blind?
- Viagra (anod other drugs used to treat erectile dysfunction) is a cGMP phospodiesterase type 5 (PDE-5) inhibitor
- PDE-5 is present in all vascular tissue, which leads to vasodilation (erection)
- Also exerts an inhibitor action against PDE-6, isoform in photoreceptors
- Leads to increased cGMP --> opening of gated ion channels --> depolarization of cell
What are the reported visual side effects of PDE-5 inhibitors (e.g. Viagra)?
- Impaired blue-green color discrimination
- Decreased rod- and cone-driven ERG amplitudes
- Blue tinge to vision
- Increased brightness of lights
- Blurred vision
- Others show no effects
Red-green color blindness is characterized by what?
- Cone opsin (photopigment) has mutation - affects cones only
- Extremely common (8-10% of males)
* Affects cone opsins
Blue Cone Monochromacy is characterized by what?
- Absence of red/L and green/M cones
- Only have blue/S
* Affects cone opsins
Which vision problems have to do with mutations or elimination of cones?
- Red/Green Color Vision Defects
- Blue Cone Monochromacy
- Cone, Cone-Rod and Macular Degeneration
- Rod Monochromacy
What kinds of mutations cause retinitis pigmentosa (RP)?
** Mutations in rhodopsin (rod opsins)
- Mutations in PDE
- Mutations in Gated Ion channel
- Mutations in Arrestin
Which vision problems have to do with mutations or elimination of rods?
* Retinitis Pigmentosa
- Congenital stationary night blindness (CSNB)
What mutations can cause rod monochromacy?
- GMP gated ion channel mutations
- Cone transducin mutations
What does the term receptive field mean?
Region of space (or field of photoreceptors) in which the presence of a stimulus will alter the firing of that neuron
Which neurons have a receptive fields?
All neurons that are higher order than the photoreceptors
What happens to the release of NT when a photoreceptor becomes activated by light?
- Cell hyperpolarizes
- Releases less NT
- Cell hyperpolarizes
- Releases less NT
What is the action of light on photoreceptors?
To turn them off!
To turn them off!
Do photoreceptors have an "all-or-none" response?
- Photoreceptors hyperpolarize and depolarize in a graded fashion
- Release NT in a graded fashion
- More depolarized --> more NT
- More hyperpolarized --> less NT
- Photoreceptors hyperpolarize and depolarize in a graded fashion
- Release NT in a graded fashion
- More depolarized --> more NT
- More hyperpolarized --> less NT
Are photoreceptors "ON" or "OFF" cells?
"OFF" - because stimulus hyperpolarizes them
"OFF" - because stimulus hyperpolarizes them
Light that is centered on the photoreceptor turns it off, so what kind of cells are they?
"OFF-CENTER" cells (all photoreceptors are "OFF-CENTER")
"OFF-CENTER" cells (all photoreceptors are "OFF-CENTER")
When a cone is depolarized, what does it release?
Glutamate
- Usually excitatory
- There is an exception in the retina
Even though cones respond the same to light, activity of a single cone gives rise to what pathways?
2 different bipolar cell types:
- On-Center
- Off-Center
2 different bipolar cell types:
- On-Center
- Off-Center
What kind of synapses are at "ON-CENTER" bipolar cells? What are the implications of this?
- Sign-reversing synapse w/ cones
- OFF-CENTER/inhibitory output from cone is reversed in sign to ON-CENTER in bipolar cell
- When light goes on in center, turns cone off, releasing inhibition, turning ON-CENTER bipolar on
- ON-CENTER bipolar cell is d
- Sign-reversing synapse w/ cones
- OFF-CENTER/inhibitory output from cone is reversed in sign to ON-CENTER in bipolar cell
- When light goes on in center, turns cone off, releasing inhibition, turning ON-CENTER bipolar on
- ON-CENTER bipolar cell is depolarized
What kind of synapses are at "OFF-CENTER" bipolar cells? What are the implications of this?
- Sign-conserving synapse w/ cones
- OFF-CENTER/inhibitory output from cone is conserved in sign as OFF-CENTER
- When light goes on, turns cone off, turning the off-center bipolar cell OFF too
- Sign-conserving synapse w/ cones
- OFF-CENTER/inhibitory output from cone is conserved in sign as OFF-CENTER
- When light goes on, turns cone off, turning the off-center bipolar cell OFF too
What kind of contact is made between on OFF-CENTER cone and an ON-CENTER bipolar cell?
Invaginating contacts on to cones - act like classical inhibitory synapses (i.e., NT release hyperpolarizes the post-synaptic on-center bipolar cells)
Invaginating contacts on to cones - act like classical inhibitory synapses (i.e., NT release hyperpolarizes the post-synaptic on-center bipolar cells)
What kind of contact is made between on OFF-CENTER cone and an OFF-CENTER bipolar cell?
Flat/Basal contacts on to cones - action of light on central photoreceptors of the off-center bipolar cells receptive field is to hyperpolarize the off-center bipolar cells
Flat/Basal contacts on to cones - action of light on central photoreceptors of the off-center bipolar cells receptive field is to hyperpolarize the off-center bipolar cells
What is released from cones when there is no light? What is the impact on the on-center bipolar cells?
- Glutamate
- Hyperpolarizing effect on the on-center bipolar cells, this is the opposite of glutamates usual excitatory action
- Glutamate
- Hyperpolarizing effect on the on-center bipolar cells, this is the opposite of glutamates usual excitatory action
What kind of receptors are on "ON-CENTER" bipolar cells?
Metabotropic
Metabotropic
What kind of receptors are on "OFF-CENTER" bipolar cells?
Ionotropic
Ionotropic
Every cone is connected to how many bipolar cells?
2 bipolar cells (on and off)
2 bipolar cells (on and off)
Under what circumstances does an on-center bipolar cell depolarize and release NT?
- Light
- Hyper-polarized cone (off-center) not releasing NT
- Light
- Hyper-polarized cone (off-center) not releasing NT
Under what circumstances does an off-center bipolar cell depolarize and release NT?
- Dark
- Depolarized cone (off-center) releasing NT (glutamate) which depolarizes off-center bipolar cell
- Dark
- Depolarized cone (off-center) releasing NT (glutamate) which depolarizes off-center bipolar cell
Under what circumstances does an on-center bipolar cell hyperpolarize and not release NT?
- Dark
- Depolarized cone (off-center) releasing NT (glutamate) which hyperpolarizes the on-center bipolar cell
- Dark
- Depolarized cone (off-center) releasing NT (glutamate) which hyperpolarizes the on-center bipolar cell
Under what circumstances does an off-center bipolar cell hyperpolarize and not release NT?
- Light
- Hyper-polarized cone (off-center) not releasing NT
- Light
- Hyper-polarized cone (off-center) not releasing NT
When is there a situation in which glutamate's effects are inhibitory?
- In dark, cones are depolarized and releasing Glutamate
- Glutamate acts on "on-center" bipolar cells and hyperpolarizes them (inhibit)
- Usually glutamate is excitatory!
- In dark, cones are depolarized and releasing Glutamate
- Glutamate acts on "on-center" bipolar cells and hyperpolarizes them (inhibit)
- Usually glutamate is excitatory!
How can there be two different responses by bipolar cells to the same stimuli (Glutamate from cones)?
- Off-center bipolar cells have ionotropic receptors
- On-center bipolar cells have metabotropic receptors
- Off-center bipolar cells have ionotropic receptors
- On-center bipolar cells have metabotropic receptors
What is the purpose of having two parallel pathways (off and on center bipolar cells) as opposed to just one?
- Improves sensitivity
- One channel provides information concerning stimuli that are brighter than the background (On-Center)
- Other provides information regarding stimuli dimmer than the background (Off-Center)
What kind of cells do bipolar cells talk to?
- Amacrine cells (lateral connection)
- Ganglion cells
What kind of connections are bipolar to amacrine cells? What kind of responses are there?
- Lateral connection
- Many produce transient depolarizing responses
What kind of responses do ganglion cells have?
They are capable of producing action potentials
Which kind of cells in the phototransduction pathway produce the first action potentials?
Ganglion cells
What are the physiological types of ganglion cells? What kind of bipolar cell do they synapse with?
- ON-Center - connect to on-center bipolar cells
- OFF-Center - connect to off-center bipolar cells
- ON-Center - connect to on-center bipolar cells
- OFF-Center - connect to off-center bipolar cells
What kind of responses can ganglion cells have?
Sustained or transient response
What is the photosensitive type of ganglion cell that was just discovered about 8 years ago? Functions?
Melanopsin Ganglion - they are involved in Circadium rhythm and overall light sensitivity, constantly sampling environment to determine levels of illumination
What are the anatomical types of ganglion cells? Distribution?
- Parasol GC (10%)
- Midget GC (90%)
Where are the midget ganglion cells found? Why does this make sense with how prevalent they are?
Found in fovea (they make up 90% of all Ganglion Cells)
Where do parasol ganglion cells project to? Midget ganglion cells?
- Parasol GC - project to Magno layers (M)
- Midget GC - project to Parvo layers (P)
Which type of GC are bigger?
Parasol GC - large cells
Midget GC - small cells
Which type of GCs have larger receptive fields?
- Parasol - large receptive fields
- Midget - small receptive fields
Which type of GCs have more transient vs more sustained receptive fields?
- Parasol - more transient
- Midget - more sustained
What causes an increase in firing of "ON-center" ganglion cells?
- Light (hyperpolarizes cone) - less NT / glutamate
- On-Center bipolar cell is depolarized and releases more NT
- NT activates On-Center ganglion cell
- Increased firing on ganglion cell
- Light (hyperpolarizes cone) - less NT / glutamate
- On-Center bipolar cell is depolarized and releases more NT
- NT activates On-Center ganglion cell
- Increased firing on ganglion cell
What causes a decrease in firing of "ON-center" ganglion cells?
- Dark (depolarizes cone) - more NT / glutamate
- On-Center bipolar cell is hyperpolarized and releases less NT
- Decreased NT acting on the On-Center ganglion cell
- Decreased firing of ganglion cell
- Dark (depolarizes cone) - more NT / glutamate
- On-Center bipolar cell is hyperpolarized and releases less NT
- Decreased NT acting on the On-Center ganglion cell
- Decreased firing of ganglion cell
What causes an increase in firing of "OFF-center" ganglion cells?
- Dark (depolarizes cone) - more NT / glutamate
- Off-Center bipolar cell is depolarized and releases more NT
- Increased NT acting on the OFF-Center ganglion cell
- Increased firing of ganglion cell
- Dark (depolarizes cone) - more NT / glutamate
- Off-Center bipolar cell is depolarized and releases more NT
- Increased NT acting on the OFF-Center ganglion cell
- Increased firing of ganglion cell
What causes a decrease in firing of "OFF-center" ganglion cells?
- Light (hyperpolarizes cone) - less NT / glutamate
- Off-Center bipolar cell is hyperpolarized and releases less NT
- Decreased NT acting on the OFF-Center ganglion cell
- Decreased firing of ganglion cell
- Light (hyperpolarizes cone) - less NT / glutamate
- Off-Center bipolar cell is hyperpolarized and releases less NT
- Decreased NT acting on the OFF-Center ganglion cell
- Decreased firing of ganglion cell
What are the principle targets of the melanopsin ganglion cells (ipRGC - intrinsically photosensitive retinal ganglion cells)?
- Superchiasmatic Nucleus (SCN)
- Olivery Pretectal Nucleus (OPN)
- Lateral Geniculate Nucleus (LGN)
What do the melanopsin ganglion cells have to do with the pupillary light reflex?
- One of the targets is the olivary pretectal nucleus (OPN)
- OPN underlies the pupillary light reflex via Edinger-Westphal nucleus, ciliary ganglion, and iris muscles
How does the melanopsin ganglion cells regulate melatnonin release?
- One of the targets of these GCs is the superchiasmatic nucleus (SCN)
- SCN links to pineal gland via the paraventricular nucleus (PVN) of the hypothalamus, the intermediolateralnucleus (IML) of the spinal cord, and the superior cervical ganglion (SCG)
- Together this regulates melatonin release
What is the impact of mutations in the new melanopsin ganglion cells?
Mutations have been linked to seasonal affective disorder
Why should we care about the melanopsin ganglion cells?
- Mutations linked to seasonal affective disorder
- Manipulating the pathway (w/ lights and drugs) can accelerate adjustment to time zone travel
- Introducing melanopsin into non-photoreceptive ganglion cells renders them photosensitive
What makes a Ganglion Cell photosensitive?
Melanopsin; when you introduce melanopsin into a non-photoreceptive GC it renders it photosensitive
What interconnects photoreceptors synaptically?
Elaborate system of inhibitor interneurons called Horizontal Cells
Elaborate system of inhibitor interneurons called Horizontal Cells
What do horizontal cells connect?
Laterally interconnect:
- Cones with other cones
- Rods with other rods
Laterally interconnect:
- Cones with other cones
- Rods with other rods
What kind of relationship do cones have with their neighboring cones?
A reciprocal synaptic relationship that is inhibitory
What happens when a cone is excited (in regards to the horizontal cells and neighboring cones)?
- Cone is depolarized (by darkness) and excites a horizontal cell that it synapses with
- Excited (depolarized) horizontal cells inhibit the neighboring cones via GABA (leads to hyperpolarization of the cones they synapse with)
- Inhibitory action on ne
- Cone is depolarized (by darkness) and excites a horizontal cell that it synapses with
- Excited (depolarized) horizontal cells inhibit the neighboring cones via GABA (leads to hyperpolarization of the cones they synapse with)
- Inhibitory action on neighboring cones
What NT is used by horizontal cells on photoreceptors?
GABA - which hyperpolarizes the receptors
GABA - which hyperpolarizes the receptors
What is the point of having lateral inhibition of photoreceptors by horizontal cells?
- Improves resolution
- Greatly increases the visual system's ability to respond to edges of a surface
- Neurons responding to the edge of a stimulus respond more strongly that do neurons responding to the middle
- Edge neurons receive inhibition only from neighbors on one side - side away from edge
- Neurons stimulated from middle of a surface get inhibition from all sides
Why do neurons responding to the edge of a stimulus respond more strongly than those responding to the middle?
- Edge neurons receive inhibition only from neighbors on one side (side away from edge)
- Middle neurons receive inhibition from all sides
What is the "term" for the photoreceptors that are surrounding your "off-center" photoreceptor?
On-Surround - because light falling in the region surrounding the photoreceptor but not directly on it, turns the photoreceptor on (via horizontal cells/GABA)
Darkness falling on the central photoreceptor turns it on/off?
On - depolarizes - releases Glutamate
Light falling on the surrounding cones turns them on/off? How doe this affect the central cone?
- Surrounding cones are off - hyperpolarize
- Releases inhibitory action on central cone (further turning the central cone on - depolarized)
What makes up a midget ganglion cells receptive field?
- 1 central photoreceptor
- 5-6 surround photoreceptors
What makes up a parasol ganglion cells receptive field?
Hundred of photoreceptors - integrates over a larger area
Refractive errors are from defects in what part of the eye?
Anterior part of eye
What cells does glaucoma affect? What kind of visual disease is it?
- Ganglion cells
- Peripheral to inward disease - makes it difficult to detect (because peripheral vision isn't that important to your day to day functioning)
What happens in age-related macular degeneration?
- Resulted in RPE (retinal pigment epithelium) disfunction
- RPE's job is to turnover photoreceptor outer segment
- Waste byproducts over the years can build up
- Don't want it to turn into wet version
What can mutations to rhodopsin cause?
- Alter rod function via a number of mechanisms
- Disrupt transport of rhodopsin to the outer segment
- Can retain rhodopsin in the ER
- Can affect stability and post-translational modification
- Can result in constitutive activation
* Can lead to RPE
What are the signs and symptoms of Retinitis Pigmentosa?
- Difficulty seeing in dim lighting
- Tendency to trip easily or bump into objects when in poor lighting
- Gradual loss of peripheral vision - variable progression
- Glare
- Loss of contrast sensitivity
- Difficulty seeing in dim lighting
- Tendency to trip easily or bump into objects when in poor lighting
- Gradual loss of peripheral vision - variable progression
- Glare
- Loss of contrast sensitivity
What disease is this?
What disease is this?
Retinitis Pigmentosa
How is Retinitis Pigmentosa inherited?
- Autosomal dominant
- Autosomal recessive
- X-linked manner (dominant or recessive)
What causes retinitis pigmentosa?
- Defects in rod photoreceptors
- Also lose cones because rods provide support
What are the symptoms of Usher's Syndrome?
Progressive vision and hearing loss, also associated with reduced odor identification, vestibular dysfunction, and reduced sperm motility
What is the most common form of deaf-blindness (conginital deafness) (1:20,000)?
Usher's Syndrome
What kind of structural defects are there in Usher's Syndrome?
- Defects in motor proteins, scaffold proteins, and cell adhesion molecules
- Defects in sensory cilia (proteins found in actin core of stereocilia and the CC and Calycal process)
How does the type and severity of color vision defect change when it's congenital? Acquired?
- Congenital - type and severity are the same through life
- Acquired - type and severity fluctuate
How is the classification of the type of a color vision defect change when it's congenital? Acquired?
- Congenital - type can be classified precisely
- Acquired - type may not be easily classified; combined defects occur
How are the eyes affected for a color vision defect when it's congenital? Acquired?
- Congenital - both eyes equally affected
- Acquired - monocular differences often occur
How is visual acuity affected by a congenital color vision defect? Acquired?
- Congenital - visual acuity is often unaffected
- Acquired - visual acuity is often reduced
What types of color vision defects are more common in congenital defects?
- Protanopia - complete absence of red photoreceptors
- Deutan - absence of green photoreceptors (makes it harder to discriminate red and green)
What type of color vision defect is more common in acquired cases?
Tritanopia - absence of blue retinal receptors
How are males/females affected by congenital vs. acquired color vision defects?
- Congenital - higher incidence in males
- Acquired - equal incidence in males and females
What is rod monochromacy?
- Rare hereditary condition
- Due to absence of cone-baed vision in eye
- Glare in bright conditions that is so blinding they seek to avoid it (photophobia)
- Very poor visual acuity (at best 20/200)
- Poor fixation
- Nystagmus - rapid involuntary movements of eye
- Visual field defects (namely a central scotoma due to impaired cone function - diminished area surrounded by relatively well-preserved vision)
- Serious refractive errors (especially myopia)
What causes rod monochromacy?
- Mutations in CNG channel subunits (channels that respond to levels of cGMP to open/close)
- Or mutations in GNAT2 (cone transducin)
- Cones are unable to hyperpolarize in response to light
What does it mean to be a "dichromat"?
You are missing the function of one of the three cone types
Which of the dichromacy types is sex-linked?
- Protanopia - absence of red photoreceptors
- Deuteranopia - absence of green photoreceptors
What gene is responsible for the red and green photoreceptors?
L/M gene array on the X chromosome
What are some examples of conditions that can lead to acquired defects in retinal pathology?
- Progressive rod and cone dystrophies, RPE dystrophies
- Optic neuritis
- Diabetic retinopathy
- Glaucoma
- Autosomal dominant optic atrophy
- Vitamin A deficiency
What are some drugs that can lead to acquired defects in retinal pathology?
- Digitalis
- Ethambutol
- Chloroquine
- Thioridazine
- PDE5 inhibitors
Exposure to what things can cause acquired defects in retinal pathology?
- Heavy metal exposure
- Chemicals used in plastic, rubber, and viscose rayon manufacturing plants, rotogravure printing industries, as well as dry-cleaning facilities
Which photoreceptors are dependent on the other type?
- Cones are dependent on rods, so if rods die, so will cones
- Rods are not dependent on cones, and will survive without them (rod monochromacy)
Which of the following stimuli would give rise to the largest output from an off-center ganglion cell?
Which of the following stimuli would give rise to the largest output from an off-center ganglion cell?
#1 - want center to be dark but it benefits to have some light on the surround
#1 - want center to be dark but it benefits to have some light on the surround
A 54-year-old woman comes into the clinic complaining of a reduced ability to “see things off to the side”. You perform an evaluation of her optic nerve head through a slit lamp examination and note a cup to disc ratio of 0.8. Visual field testing revealed arcuate pattern scotomas in both eyes, and interocular pressure was elevated (30 mm). The most likely cause of her vision loss is?
Glaucoma
- High cup-to-disc ratio
- High intraocular pressure
- Peripheral vision loss
A 68-year-old woman comes into the clinic complaining of a difficulty reading and metamorphopsia. Indirect fundus examination reveals multiple drusen throughout her macula. Patient has a positive history of smoking, with past ocular history is positive for cataracts (she had interocular lenses put in 7 years ago). The most likely cause of her vision loss is?
Age-related macular degeneration
- Smoking is a big risk factor
- Multiple drusen
- Metamorphopsia (distorted vision in which a grid of straight lines appears wavy and some parts appear blank)
What is metamorphopsia?
Distorted vision in which a grid of straight lines appears wavy and some parts appear blank
A mother complains that her 4 year old boy’s eyes don’t seem right. He has poor depth perception, rapid side to side eye movements, and an intense red-eye effect in photographs. Upon slit lamp examination, you note complete iris transillumination, absence of a foveal reflex, and a generally hypopigmented fundus. Skin and hair pigmentation appear normal. Family history is reported as positive, with mom’s maternal grandfather also having similar symptoms. You suspect this child has?
Ocular Albinism
- Normal skin and hair pigmentation
- Iris transillumination
- Red-eye effect