58. Review of Eye Physiology/Anatomy Flashcards

1
Q

What is the difference between Anterior and Posterior Chamber?

What is the difference between anterior-posterior axis and visual axis of eye?

What is the nodal point?

A

Anterior Chamber: between iris and cornea
Posterior Chamber: between lens and iris

AP: geometric middle of eye
Visual Axis: angled through fovea

N: where AP and VA axes cross (in lens)

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2
Q

What two ways does the cornea have transparency?

A
  1. Ideal Collagen Arrangement

2. Soluble VEGF receptors to mop up VEGF and prevent blood vessel growth

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3
Q

Lens

  • what is it composed of?
  • how does accommodation work?
  • what happens as the lens ages?
A

Multiple shells of lens fiber cells with HIGH protein content (crystallins)

Lens rounds for near vision: ciliary muscle constricts - relaxes zonules (lens tetherers) - rounds lens

Aging: insoluble proteins due to crystallin/membrane protein aggregation = less transparent - may progress to Cataracts

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4
Q

What are the components of the vitreous? What happens to the vitreous as you age?

A

Gel created by collagen and hyaluronic acid

Aging: collagen aggregation = liquefaction = less transparent = floaters

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5
Q

What are the two flow routs of aqueous humor?

A
  1. Conventional: Ciliary Body Epithelium - Posterior Chamber - through pupil - ant chamber - trabecular meshwork - canal of schlemm - episcleral veins
  2. Uveoscleral Route: Ant Chamber - iris root - ant surface of ciliary muscle - suprachoroidal space - sclera
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6
Q

How is aqueous formed in ciliary epithelium?

A

Two sheets of epithelium attached at basal sides

  1. Basal sides pump out Na
  2. Na entry on apical side with anions (Cl, bicarb, Ascorbate)
  3. Anions leave other apical side through channels, dragging water
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7
Q

How is IOP maintained?

How do you treat ocular htn?

A

IOP: balance of aqueous inflow and outflow
Ocular HTN: IOP>22mg; can lead to open angle glaucoma
tx: reduce inflow or increase outflow conductance
1. lower inflow: beta-blocker (timolol - blocks Cl- movement into aqueous via NKCC); CA-i (Acetazolamide - blocks bicarb movement)
2. increase uveoscleral route: PG agonists (latanoprost)
3. improve outflow conductance: muscarinics (pilocarpine) - contract ciliary muscle, relax Trabecular meshwork

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8
Q

Glaucoma: what it is, types

A

high IOP = causes damage to RGCs axons at optic nervehead (at lamina cribosa - where axons converge on eye, weakest part of eye wall)
Ways: high IOP = axon compression at lamina cribosa = reduced axonal RGC transport = RGC death = reduced vision
high IOP = reduced bloodflow to RGC = RGC death = reduced vision

types: 1. Normal Tension Glaucoma: normal IOP
2. Angle Closure/Acute Glaucoma: iris blocks TM (outflow) - tx with iridotomy

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9
Q

What are the 3 cellular and 2 synaptic layers of the retina? What 2 structures are right behind the retina?

A

(Nerve Fiber Layer)

  1. Ganglion Cell Layer (end of 2o n.)
  2. Inner Plexiform
  3. Inner Nuclear Layer (end of 1o n.)
  4. Outer Plexiform
  5. Outer Nuclear Layer (1on. cell bodies)
  6. Rods/Cones Photoreceptors - inner segments for metabolism; outer segments for light absorption

Behind retina

  1. RPE - absorb light
  2. Choroid (uvea) - rich blood supply
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10
Q

How does the structure of the fovea differ?

A

Most acute vision
thinned retina - inner layers pushed to the side
Photoreceptor fibers project sideways outside fovea
all cones

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11
Q

What artery supplies both retinal and choroidal circulation?

A

Opthalmic Artery

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12
Q

How does the retinal circulation branch? How is the flow rate of retinal circulation controlled? How much of the retina does it supply?

A

4 branches - 1 to each quadrant (artery, vein pair)
Central retinal vein returns thru optic nerve head
Fovea = no retinal circulation
Flow rate: METABOLIC CONTROL (like cerebral circ) - higher flow to more active retina or more hypoxia/hypercapnia (less flow with hyperoxia)
No autonomic control
supplies inner half of retina - 2 microcirculatory plexuses in plexiform layers
BLOOD-RETINAL BARRIER (endothelial tight junctions)

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13
Q

How does the choroidal circulation branch?

How is the flow rate controlled? what parts of the retina does it supply?

A
Short + Long Posterior Ciliary A. and Ant Ciliary A.
Supply outer retina
HIGH flow rate (100x retina)
Fenestrated, leaky capillaries
Primarily AUTONOMIC CONTROL
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14
Q

How does VEGF lead to problems in disease states? How to tx?

A

VEGF = more blood vessel formation, secreted in hypoxia

wet-AMD: more VEGF = choroidal neovascularization

Diabetic Retinopathy: more VEGF = retinal neovascularization

tx: anti-VEGF blockers = protect sight

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15
Q

What is the function of Retinal Pigment Epithelium (RPE)?

A
  1. Blood retinal barrier - tight junctions block fenestrated choroidal capillaries
  2. Light absorption - contain melanin, prevent image scattering
  3. Epithelial transport - b/w choroid and retina
  4. Visual Cycle - regenerates visual pigment (makes 11-cis retinal from all-trans retinal)
  5. Phagocytosis of photoreceptors
  6. Secretion of Growth factors to maintain choroid structure
    * site of retinal detachment* - no connections b/w RPE and photoreceptors
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