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Neuro Test 2 > Retina: Biochemistry > Flashcards

Retina: Biochemistry Flashcards

1
Q

ora serrata

A

transition zone between nonsensory retinal pigment epithelium and sensory retina

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2
Q

nonsensory retinal pigment epithelium

A
  • most anterior portion of retina, does not detect light here. injections can be made here
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3
Q

what are three things contained in the sensory retina?

A
  1. Macula Lutea: found at visual axis - cones predominate here and rods are few.
  2. Fovea Centralis: found at visual axis: cones predominate and are tightly packed here.
    * Thus visual axis is where there is the highest acuity
  3. Optic Disk: photoreceptors, bipolar cells and ganglion cells are NOT present here. only unmyelinated axons leaving the retina and entering the optic nerve are located here.
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4
Q

Three types of cells found in the retina?

A
  1. neuronal cells (photoreceptor, ganglion cells, interneurons)
  2. retinal pigment epithelial cells (RPE): outermost layer separating retina from choroid
  3. neuronal support (glial) cells - “Mueller cells”
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5
Q

10 layers in order of signal transduction?

A 
Pigment epithelial cells (RPE)
Photoreceptor cells
Outer limiting membrane
Outer nuclear layer
Outer plexiform layer
Inner nuclear layer
Inner plexiform layer
Ganglion cell layer
Optic nerve fibers
Inner limiting membrane
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6
Q

what are two parts of photoreceptor cells?

A

Inner segment: rich in organelles

Outer segment: series of flat membranous disks containing photopigment (undergo continuous turnover, old are phagocytosed via pigment epithelium)

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7
Q

Rods vs. Cones

A

Rods = detect light intensity, located in periphery, contain rhodopsin photopigment

Cones= detect blue, green, red, located in fovea, contain iodopsin

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8
Q

interphotoreceptor matrix

A

connection between photoreceptor and RPE

  • this is where recycling occurs
  • contains Interstitial retinoid-binding protein (IRBP); this transports retinol to pigmented epithelium and returns retinal to photoreceptor
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9
Q

photopigment regeneration:

A

the bleached photopigment consists of opsin and all-trans retinal.
- Regeneration of the photopigment occurs in the RPE where it is converted to 11-cis retinal and is returned back to the photoreceptor

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10
Q

RPE and recycling

A
  • RPE contains melanin granules.
  • phagocytosis of disks occurs here, and they are degraded in lysosomes and released into choriocapillaris.
  • Expresses retinol Re-isomerization enzyme: which converts retinol to 11-cis retinal
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11
Q

Rods ending?

A

end in rod sperule, which connects with dendrites of bipolar cells and neurites of horizontal cells

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12
Q

Cones ending?

A
  • end in pedicles

- pedicles communicate with dendrites of bipolar cells and neurites of horizontal cells

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13
Q

Photopsins

A
  • the protein that is contained in photoreceptors

- “opsins” protein is located in both rods and cones

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14
Q

photopsin of cones??

A

opsin protein + 11-cis retinal = iodopsin

  • when red, green and blue are stimulated this is seen as white light
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15
Q

what is bleaching?

A
  • when photopigment absorbs a photon of light it changes confirmation
  • rhodopsin disassembles into opsin and all-trans-retinal.
  • photopigment now acts as a GPCR, where it induces GMP from cGMP and cGMP dependent Na+ channels close.
  • hyperpolarization causes cell to stop releasing NT.
  • The photopigment is dissassembled and becomes all trans retinol.
  • all-trans-retinal is then enzymatically converted by RPE cells back to 11-cis-retinal, where it is then returned to photoreceptor where it recombines with opsin and rhodopsin molecules are regenerated.
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16
Q

rhodopsin

A

rhodopsin = opsin + 11-cis-retinal

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17
Q

Leber congenital amaurosis type II

A
  • mutation in RPE65 which results in blindness
  • RPE65 codes for Isomerohydrolase which converts all-trans retinol into 11-cis retinal in the RPE cell.
  • autosomal recessive
  • gene therapy for RPE65 has been made, and is introduced through adenoviral delivery vector into RPE
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18
Q

Bipolar cells: three types?

A
  • collect visual information from rods and cones and synapse onto ganglion cells, which are the output of the retina.
  • 1: Diffuse Cone bipolar cells make contact with pedicles of several cones.
    1. Rod Bipolar Cell receive input from multiple photoreceptors
  • 3: Midget Cone Bipolar Cells: receive input from only one single cone pedicle and communicate with only one ganglion cell (1:1 relationship may contribute to visual acuity in cones)
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19
Q

Ganglion Cells: two types?

A
  • have dendrites in the inner plexiform layer which synapse with bipolar cells
    1. Diffuse ganglion cells: contact several bipolar cells
    2. Midget ganglion cells: contact with a single bipolar cell
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20
Q

Amacrine cell

A
  • an association neuron which integrates signaling. Do not have an obvious axon but have tightly branched neurites.
  • function in sampling and modifying the output of bipolar cells
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21
Q

Horizontal cells

A
  • Neurites ending on cone pedicles and rod spherules

- association neurons that integrates signals

22
Q

2 types of Glial Cells?

A
  1. Mueller Cells (span the entire retina and provide support to all cells)
  2. Microglia (present in al layers and phagocytose debris)
23
Q

Fovea

A
  • located at the visual axis of the cornea
  • depression in the retina due to flattened inner layers
  • greatest visual discretion here: most neuronal interconnections located here.
  • almost exclusively contains cones (thus poor in low light)
24
Q

fovea centralis

A
  • an area of tightly packed cones in the middle of the fovea.
  • The cones are arranged at an angle to the pigmented layer, thus the outer layers do not obstruct the light pathway.
  • the outer segments of photoreceptor cells receive light that has not passed through the other layers of the retina
25
Q

Age Related Macular Degeneration… visualization?

A
  • can be visualized with Optical Coherence Tomograph (OCT); will measure the size of fovea centralis
  • AMD results when photoreceptors and retinal pigmented epithelium at macula break down.
  • damage to macula occurs rapidly and painless vision loss occurs.
26
Q

two types of AMD?

A
  1. dry AMD: photoreceptor cells and the retinal pigmented epithelium at the macula break down (most common early sign is drusen)
  2. wet AMD: new blood vessels grow under the macula, the new blood vessels leak blood and fluid raising the macula from its close association with the choriocapillaris
27
Q

Optic Nerve

A
  • occurs at the convergence of the axons of retinal ganglion cells
  • fibers traveling in are unmyelinated affarents
  • myelination begins at the optic disc
  • there is an absence of photoreceptors here resulting in a blind spot
28
Q

optic cup

A

central depression of the optic disk. It is pale in comparison with surrounding nerve fibers.

29
Q

what happens to the disk with increased intraocular pressure? what about an increase in intracranial pressure?

A
  • the disk of the optic nerve appears concave.

- the disk becomes swollen (papilledema) and the vv. are dilated when pressure increases intracrnially.

30
Q

what supplies the outer retina

A

Choroid

- supplies the photoreceptor cells and horizontal cells

31
Q

what supplies the inner layer of the retina?

A
  • central retinal artery, which arises from the optic nerve head.
  • provides blood to ganglion, bipolar and amacrine cells
  • branches run posterior to the inner limiting membrane wihtin the nerve fiber layer.
  • capillaries can be found running through the retina, but generally no deeper than the outer plexiform or nuclear layer.
32
Q

why is retinal detachment critical? two types?

A
  • detachment of the photoreceptor cell layer from the pigment epithelial layer can result in blindness. once cells die, they cannot be regenerated. RPE is needed to maintain support of visual fn.
  • choroid is needed to nourish and maintain cells
  • could occur due to hemorrhage in between RPE
  • could also occur with a tear in retina –> vitreous leakage
33
Q

Diabetic retinopathy

A

60-80% of diabetics will develop some sort of retinopathy.

34
Q

what do you see with retinopathy?

A
  1. microaneurysms (small outpouchings from retinal capillaries)
  2. cotton-wool spots (regional failure of retinal microvascular circulation resulting in ischemia)
  3. retinal vv (dilated and tortuous)
  4. retinal aa (white and non-perfused, eventually absent of endothelial cells)
  5. selective loss of pericytes (help regulate capillary blood flow)
  6. apoptosis of capillary endothelial cells
  • these changes most likely due to oxidative stress *
35
Q

2 phases of diabetic retinopathy?

A
  1. Preproliferative (Nonproliferative): increased size and number of intraretinal hemorrhage. Vision loss occurs from macular edema- but not clinically significant
  2. Proliferative: the formation of new blood vessels (neovascularization) which can protrude into vitreous area. will see hemorrhage and clouded vision. can result in detached retina. Will eventually extend into the anterior structure of the eye and cause blindness.
36
Q

How can you visualize the retina?

A
  1. fundoscopy/opthalmoscopy (Direct: reqs dilation of retina)
  2. indirect use of lens and binocular
  3. fundus photography.
37
Q

what do you see in nonproliferative DR?

A
  1. hemorrhages and exudates (red spots, and white spots without blood supply)
  2. ring of exudates around macula
  3. tortuous vessels
  4. flame shaped hemorrahges.
  5. macular edema
38
Q

what do you see in proliferative DR?

A
  1. neovascularization of disc and surrounding area.
  2. fibrous vitreous bands
  3. boat shaped hemorrhages (located under internal limiting membrane)
  4. ischemia in certain areas
39
Q

how can you visualize blood flow in retina?

A

fluorescein angiography: sodium fluorescein dye injected into vein of patients arm

  • can see vv. will ultimately see hemorrhaging after time
  • helps visualize neovascularization
40
Q

how can you measure the width/depth of fovea?

A

through optical coherence tomography (OCT)

  • shows retinal thickness increases in DR and ME
  • uses infrared beams
41
Q

2 types of treatment of nonproliferative DR?

A
  1. control blood glucose through strict glycemic control (insulin therapy, diet, acvitiy)
    - highly effective prevention, but can’t reverse damage already done
  2. control of blood pressure through ACE inhibitors, ANGII blockers or beta blockers (efficacy in diabetic nephropathy, less sure for retinopathy)
    - results suggest that controlling BP aids in prevention - diastolic may be biggest predictor
42
Q

Treatment for advanced proliferative DR?

A

PRP: panretinal photocoagulation -

  • Scatter laser treatment with multiple burns across a large diameter
  • treatment results in ablation of neovascularization and causes cell death of retina as well.
  • this is possible b/c of presence of absorptive pigment epithelial cell layer
  • significant pain and vision loss associated
  • does not target optic disk
43
Q

early treatment for proliferative DR?

A

Focal Laser

Directed to specific:

  • Microaneurysms
  • Microvascular lesions
  • Macular edema
  • Hard exudates
  • Painless and highly efficacious
  • Vision stabilization but not improvement
44
Q

what is vitrectomy?

A
  • removal of vitreous humor
  • used for nonclearing vitreous hemorrhage (opacity that may inhibit photocoagulation)
  • enzymatic vitrectomy: Hyaluronidase and plasmin can clear intravitreal hemorrhage.
45
Q

intravitreal injections: what two things can be injected?

A
  • inject local anesthesia infratemporally.
  • inserts 3.5 mm posterior to limbus through pars plana.
  1. glucocorticoid injections: reduce neovascularization, rapid reduction in macular thickness
    * complications: can increase IOP and lead to glaucoma
  2. VEGF inhibitors: VEGF concentration is high in vitreous chamber of DR patients. shows increase in visual acuity, effective when combined with photocoagulation (will reverse damage). VEGF inhibitors keep damage from proliferating
46
Q

Open Angle Glaucoma? Two types?

A
  • no closure of iridocorneal angle
  • increased IOP (normal: 12-22 mmHg)

Primary:

  • unkonwn cause, genetic.
  • Myocillin mutations (unknown fn. expressed in smooth m. of ciliary body)
  • largest known cause to disease

Secondary:

  • particulate material (pigmentary or exfoliative tissues shed and accumulate in meshwork)
  • Increased Episcleral venous pressure could also cause it
47
Q

how is glaucoma detected?

A
  1. tonometry: measures pressure reqd to depress the cornea (puff of air)
  2. slit-lamp examination: low power microscope with slit to examine cornea, iris, sclera and the actual trabecular meshwork
48
Q

cup-to-disk ratio

A

optic disk is donut shaped

  • orange/pink neuroretinal rim with axons of retinal ganglion
  • white physiologic cup with central depression containing central retinal artery and central retinal v.
  • should be 1:2 ratio
49
Q

pathological changes to cup-to-disk ratio

A
  • rim whitening: indicates death of retinal ganglion cells
  • fuzzy margin changes = death of retinal ganglion cells or inflammation.
  • cup diameter changes= sign of optic cupping, loss of RGC axons
50
Q

treatment of glaucoma

A

little medications

  • laser traceuloplasty: cut holes in meshwork
  • trabeculectomy: most serious, punch a hole through meshwork and canal of schlemm all the way into the sclera.
51
Q

Angle closure glaucoma, two types?

A
  1. Primary: anatomical predisposition - congenital shallow anterior chamber results in pupillary block
    - could be foward apposition of lens
    - could be due to increased posterior chamber resulting in bowing iris
  2. Secondary: inflammation, neovascularization, contraction of tissue

Neuro Test 2 (13 decks)

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