Lecture 6 and 7 Flashcards

1
Q

Extraocular muscle disfunctions

A

1) Strabismus

2) Amblyopia

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2
Q

Strabismus

A
  • Cross-eyed
  • Weakening or misalignment of the eye’s muscles
  • can lead to amblyopia
  • double vision, loss of depth perception
    -motor over sensory
    -Causes: Genetic (children), Stroke, Brain tumor
    -Treatments: Surgery, Corrective Lenses, Eye Exercises, Botox
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3
Q

Amblyopia

A
  • Lazy eye
  • The weakening of one eye’s input into the brain
    -Without as much sensory input the position of the weaker eye will wander. This will lead to misalignment

-Blurred vision
-Weak eye losses brain connectivity
-Sensory > Motor
-Causes (in 1 eye): high refractive error, deprivation (opacity of corneal or lens)
- Treatments: Corrective lenses, cataract surgery, deprivation of “strong” eye.

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4
Q

Corneal diseases

A

1) corneal abrasions / injury
2) Keratitis (infections)
3) Keratoconus (thinning)

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5
Q

Corneal abrasions / injury

A

Like the skin, any physical or chemical injury will leave the cornea damaged, scaring can lead to permeant injury and loss of vision

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6
Q

Keratitis (infections)

A

Both bacteria and other microbes can infect the cornea and conjunctiva surrounding the sclera.

Example: Acanthamoeba can infect the cornea (rare; associated with contact lens use).

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7
Q

Keratoconus (thinning)

A

Corneal thinning is rare but can cause
changes in how light is refracted into the eye leading to blurry vision.

Thinning of the cornea can lead to bulging (see image).

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8
Q

Types of cornea transplants

A

Keratoplasty –
transplant from donor tissue

Keratoprosthesis -Transplant with prosthetic cornea

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9
Q

Coloboma

A
  • Misshapen iris caused by development errors
    -Colobomas can affect other eye structures
    ▪ Eyelid coloboma
    ▪ Lens coloboma
    ▪ Retinal/macula coloboma
    ▪ Optic nerve coloboma
    ▪ Uveal/Iris coloboma
  • Causes of coloboma
    ▪ Genetic, inheritance
    ▪ Alcohol exposure during pregnancy

-Treatments (not many options)
▪ Contact lenses, cosmetic
▪ Amblyopia correction; eye patch.

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10
Q

Stages of early development:

A

1) bud off the forebrain
2) Begin fold into a cup shape
3) steal the cup shape

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11
Q

Key points of the lens and why it is clear / transparent:

A

1) The cells in the central lens do not have a nuclei and organelles

2) The cells in the central lens consist of a structural protein called crystalline

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12
Q

Cataracts

A

Cataracts – a clouding of the lens, reducing transparent, and reducing vision.

Symptoms:
* Blurry vision
* Difficult with vision in dim light
* Halos around lights
* Can not be corrected by eyeglasses

Age is a major contributor (50% of adults over the age of 75 have cataracts)
Other Risk Factors:
* UV exposure
* Smoking
* Diabetes
* Previous eye disease or trauma.
* Radiation or chemotherapy.
* Genetics

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13
Q

Mechanisms for cataracts formation:

A

-Aggregation of crystalline (crystallin is normally soluble but aggregates together during cataracts formation)

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14
Q

Treatment for cataracts removal

A

There are no drug treatments for cataracts other than surgery to remove and replacing the cataract with an artificial lens.

Goals of Cataract surgery:
1) Remove the old lens in small pieces.
2) Replace the old lens with a new artificial intraocular lens (IOL).

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15
Q

Types of refractive errors of the eye

A

1) Myopia (Nearsightedness)
2) Hyperopia (farsightedness)
3) Astigmatism
4) Presbyopia

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16
Q

Myopia

A

Nearsightedness
- Far away objects look blurry
- the focal point of light lands short of the retina.

Causes:
-Elongation of the eye.
* Incorrect cornea curvature.
* Defects in lens optics

17
Q

Hyperopia

A

Farsightness
-Images close-up will be blurry
-the focal point of light lands beyond of the retina.

Causes:
* Shortening of the eye.
* Incorrect cornea curvature.
* Defects in lens optics

18
Q

Astigmatism

A

Causes blurry vision for images close-up and far-away. It can also
cause double vision
(can cause blurriness in horizontal or vertical direction)

Causes:
* Irregular cornea shape.
* Lens aberrations

19
Q

Presbyopia

A

-Difficulties seeing close-up associated with middle-age (>45 years old)

  • Similar to hyperopia (farsightedness).
  • Cause the lens becomes less flexible with age and cannot be easily rounded to focus on objects close-up.
20
Q

Retinal Tears and Detachment

A

-occur when the retina is separated from choroid.

-Without surgical repair, these retinal injuries can lead to permeant vision loss.

-Vision symptoms include perception of a dark curtain and floaters
- Vitreous humor can pull on the retina leading to tears and detachment

21
Q

Causes of Retinal Tears and Detachment

A

Causes:
* Trauma/injury.
* Age – vitreous humor volume shrinks and pulls on retina.
* Diabetes – Scar tissue can form stiffening the retina and increasing the chance of a tear.
* Macular degeneration – vitreous humor can build up behind the retina.

22
Q

Age-related Macular Degeneration (AMD)

A

Symptoms:
* Loss of the central visual field
* Distorted vision.
* Cloudy vision.

Prevalence (>40 years old):
* ~10% with early-stage AMD
* ~0.9% with late-stage AMD

23
Q

Types of AMD

A

1) Dry AMD
* Drusen formation
* Some vision loss
* Photoreceptor atrophy

2) Wet AMD
* Presence of blood in the macula
* A potential complication in late-stage AMD.
* Significant Photoreceptor
degeneration.

24
Q

Stages of AMD

A
  1. Build-up of “cell junk”
  2. “Cell junk” aggregates into a drusen.
  3. Atrophy of RPE and Photoreceptors
  4. (Wet Only) Break-down of Choroid-Retina barrier
    leads to neovascularization.
25
Q

Common treatments for AMD

A

Early-stages “Dry” AMD
AREDS 2 Multi-Vitamin

“Wet” AMD
Anti-VEGF drugs
(inhibit blood vessel growth)

26
Q

Retinitis pigmentosa (Retina pigmentosa, RP)

A

Symptoms:
* Loss of night vision
* Gradual loss peripheral vision
* Causes “tunnel vision”.
* Problems with color vision.

Prevalence:
* Occurs in 1:3000 – 1:5000 births
* Inherited (genetic)

27
Q

Molecular genetics of Retinitis Pigmentosa (RP)

A
  • > 100 gene mutations linked to
    retinitis pigmentosa.
  • Some genes are associated with
    other disorders, such as Usher
    Syndrome (Ush2a).
  • RP genes encode for proteins
    important for rod photoreceptors
    or retina pigment epithelium.
28
Q

Disease mechanisms in retinitis pigmentosa

A
  • Cellular etiology (cause or origin) of RP depends on the gene mutation:

1) Retinal cycling/metabolism.
2) Phototransduction
3) Photoreceptor structure.
4) Nuclear transcription/splicing

29
Q

What are the differences between AMD and RP

A

Age-related Macular Degeneration
* Central retina degeneration
* Cone degeneration
* Common
* Occurs later in age.
* Major cause is age.

Retinitis pigmentosa
* Peripheral retina degeneration
* Rod and Cone degeneration
* Rare
* Occurs at birth and throughout life.
* Major cause is genetic.

30
Q

Rhodopsin

A

is the light-sensitive protein that converts photons of light into a chemical signal.

  • Rhodopsin uses the organic molecule retinal to sense photons of light.
  • The change from cis retinal to trans-retinal after light stimulation causes a conformation change in the rhodopsin protein.
31
Q

Different opsins sense light in rods and cones

A

3 Opsins (color) and 1 Rhodopsin (dim light)

32
Q

Color vision deficiency (colorblindness)

A
  • Colorblindness occurs when you are unable to see color in a normal way.
  • It does not affect the sharpness of vision.
33
Q

Types of color vision deficiency

A

Red-Green Color Deficiency
* Difficulties distinguishing between green and red.
* Subtypes: Deuteranomaly, Protanomaly, Deuteranopia, and Protanopia
* Gene mutations: OPN1MW and OPN1LW (X-linked)

Blue-Yellow Color Deficiency
* Difficulties distinguishing several different colors (blue-green; yellow-red)
* Subtypes: Tritanomaly, Tritanopia
* Gene mutations: OPN1SW

Complete Color Deficiency
* No color vision, increased sensitivity to light
* Subtypes: monochromacy or achromatopsia

34
Q

Optic neuropathies disrupt…

A

the function and integrity of the optic nerve

35
Q

Symptoms and Prevalence of Glaucoma

A

Symptoms:
* Loss of peripheral vision
* Eye redness
* Eye pain & headaches

Risk Factors:
* Age
* Family History (genetic)
* Higher incidence among Hispanic
and African Americans

36
Q

Mechanisms of Glaucoma Progression

A

Disease Stages:
1) Elevation of intraocular pressure
2) Compression of optic nerve head
3) Axon degeneration of retinal ganglion cells
4) Retinal ganglion cell death.

37
Q

Main types of Glaucoma:

A

1) Angle-closure Glaucoma – when there is a blockage between the iris and lens.

2) Open-angle Glaucoma (most common) – when there is a blockage of the
trabecular meshwork or Schlemm’s canal.

38
Q

Treatments for glaucoma:

A

1) Angle-closure Glaucoma:
* Pilocarpine – relaxes muscles that may cause blockage
* Surgery

2) Open-angle Glaucoma:
* Drugs to reduce vitreous humor creation
* Surgery

39
Q

Other types of optic neuropathies

A

1) Optic neuritis
2) Nutritional / Toxic optic neuropathy
3) Diabetic Retinopathy
4) Leber’s Hereditary Optic Neuropathy (LHON)
5) Neuromyelitis optica