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Ophtho > Retina > Flashcards

Retina Flashcards

1
Q

List the layers of the retina

A

ILM NFL GCL IPL INL OPL HFL (henle fiber layer) ONL XLM Photoreceptors RPE

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2
Q

What are the 3 types of cones?

A

Short wavelength. S cone (formerly blue) Medium wavelength. M cone (formerly green) Long wavelength. L cone (formerly red) - easy to remember because blue is the shortest wavelength in the visible spectrum of light, red is the longest and green is in between - note: blue-yellow (S cones) is rare in inherited disease and can be an important early marker for acquired disease

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3
Q

How do test photostress recovery time?

A

Shin a bright light from the ophthalmoscope on the patients macula for 10 seconds then record the time taken for Snellen Va to return to within 1 line of preblanch levels. Normal subject will take 1 minute. Recovery time increases with age.

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4
Q

How to test dark adaptation? What’s the machine called? what is it useful for?

A

Use a Goldmann-Weekers adaptometer Light adapted Extinguish light present serious of dim-light targets 11 degrees below fixation first plateau occurs at 5-10 mins representing the cones second plateau occurs at ~30 mins representing the robs useful to defect night blindness. malingering is easily recognized. useful in demonstrating the degree of cone adaptation in cone dysfunction syndromes

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5
Q

What are the methods for testing colour vision?

A

Anomaloscope: most accurate, not really used Ishihara and Hardy-Rand-Rittler - tests for defective colour vision. Quick but not effective in classifying the deficiency Panel tests: Farnsworth-Munsell 100 and Farnsworth Panel D-15. Sensitive but time consuming. D-15 quicker. Can discriminate between retinal diseases vs congenital and acquired defects (colour deficiencies show precise defects) whereas retinal disease shows irregular patterns

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6
Q

RF for AMD

A

AGE! Female HTN, hyperchol, CVD, FHx Smoking Hyperopia Light iris color White

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7
Q

What are 2 major susceptibility genes for AMD

A

CFH (1q31) - codes for complement factor H ARMS2 (10q26) - gene product poorly understood

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8
Q

Where are basal laminar and basal linear deposits?

A

Basal laminar - between the plasma membrane and the basement membrane of the RPE

Basal linear - within the inner collagenous zone of Bruch membrane (memo basal linear is in Bruchs)

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9
Q

What are the size categories for drusen?

What is a drusenoid PED?

A

Small (< 67 um)

Intermediate (63-124 um)

large (>125 um) – 125 um width of blood vessel

drusenoid PED: confluent large drusen that coalesce into a PED (>350 um)

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10
Q

AREDS study: Risk of progression to stage 4 AMD in patients with stage 2 and stage 3? what is defined by stage 2/3?

A

Over a 5 year period risk of progression to stage 4

Stage 2: many small drusen or few intermediate drusen. 1.3%

Stage 3: many intermediate drusen or even a single large druse (stage 3). 18%

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11
Q

4 types of drusen

how do soft and hard drusen show up on FA?

Findings on OCT?

A

hard: discrete and well demarcated. well-defined focal areas of lipidization or hyalinization of the RPE-bruch membrane complex.

  • Typically window defect on FA
  • OCT: sub RPE elevations or small RPE detachments with no IRF and SRF

soft: amorphous and poorly demarcated. diffuse thickening of hte inner aspects of the bruch membrane (basal linear deposits) - more likely to progress to atrophy or CNV than an eye with only hard drusen.

  • Typically slowly and homogenously stain late because of pooling of FA in the sub-PED compartment.
  • OCT: sub RPE elevations or small RPE detachments with no IRF and SRF

Reticular pseudodrusen: seen on FAF, smaller then soft drusen, superior macular region, associated with progressive atrophy, GA, CNV.

  • OCT - above the RPE

Drusen in pts < 50: familial or early-onste drusen. Include: large colloid drusen, malattia leventinese, and cuticular drusen.

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12
Q

What are the patterns of abnormalities of the RPE in AMD

A
  1. Focal hyperpigmentation. Typically blockage on FA and hyperreflective outer retinal foci on SD-OCT.
  2. nongeographic atrophy. atrophy that does not cover a contiguous area and may appear as mottling or depigmentation
  3. geographic atrophy: area of absent RPE is contiguous. Choroidal vessels more visible, outer retina thin, choriocapillaris attenuated. Window defects on FA, OCT loss of RPE and inner segments ellipsoid and photoreceptor layer. Dense hypoautoF on FAF. Often fovea involvement LATE in disease process.
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13
Q

Ddx for nonneovascular AMD

A

CSC

Pattern dystrophy

adult-onset vitelliform maculopathy

drug toxicity (ie plaquenil)

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14
Q

AREDS 2 results at 5 and 10 years. Definition of intermediate and advanced AMD?

A

Intermediate or advanced AMD

  • At 5 years
    • 25% risk reduction for progression
    • 19% risk reduction in rates of moderate vision loss
  • At 10 years
    • 44% of placebo vs 34% of supplement eyes had advanced AMD (27% RR)

Definition of intermediate and advanced:

  • Intermediate (stage 3): at least 1 large druse, 10 or more intermediate drusen or nonsubfoveal GA
  • Advanced (stage 4): nAMD, GA in only one eye
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15
Q

What is are the 4-points on the 4-point grading scale developed by AREDS for classifying the severity of AMD?

A
  • presence of 1 or more large (>125-µm diameter) drusen (1 point)
  • presence of any pigment abnormalities (1 point)
  • for patients with no large drusen, presence of bilateral intermediate (63–124 µm) drusen (1 point)
  • presence of neovascular AMD (2 points)
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16
Q

What are the AREDS2 vitamins with doses?

A

Vitamin C 500 mg

Vitamin E 400 IU

Zinc 80 mg

Cupric oxide 2 mg

Lutein 10 mg

Zeaxanthin 2 mg

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17
Q

Findings in AREDS2 study?

A

Lutein and zeaxanthin similar effect to beta carotene

LCPUFA not helpful

Lung cancer in pts who previously smoked taking beta carotene

conclusion: replace beta carotene with lutein and zeaxanthin and NOT add LCPUFAs

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18
Q

Clinical signs of CNV in AMD?

A

SRF

IRF

exudate and/or blood

pigment ring or gray-green membrane

irregular elecation of the RPE or a PED

RPE tear

sea fan pattern of subretinal vessels

intraretinal blood and CME may indicate type 3 NV (from the deep capillary plexus of the retinal circulation)

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19
Q

what are the 3 types of CNV in nAMD?

A

type 1: sub-RPE

  • vascularized serous or fibrovascular PED

type 2: sub-retinal

  • lacy or gray-green lesion

type 3

  • new vessels sprouting from the deep capillary plexus (RAP retinal angiomatous proliferation)
  • –> if these lesions progress they lead to a hypertrophic, fibrotic, disciform scar*
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20
Q

FA patterns of CNV?

A

Classic: bright, lacy, well-defined ((can be typically related to type 2))

Occult: ((can be typically related to type 1))

  1. PED
  2. Late leakage from undefined source
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21
Q

OCT patterns of CNV

  • Type 1 serous PED
  • Type 1 fibrovascular PED
  • Chronic fibrovascular PED
  • Type 2
  • Type 3
A
  • Type 1 serous PED: sharply elevated, dome-shaped lesions with hollow internal reflectivity and no assocaited SRF or IRF
  • Type 1 fibrovascular PED: lacy or polyplike hyperreflective lesion on the undersurfance of the RPE
  • Chronic fibrovascular PED: multilayed appearance
  • Type 2 neovascular membranes: hyperreflective band or plaque in the subneurosensory space (with SRF or IRF)
  • Type 3 neovascular membranes: hyperreflective focus emanating from the deep capillary plexus of the retina (with out without CME and PED)
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22
Q

Polypoidal choroidal vasculopathy

A

variant of type 1

serosanguineous RPE detachments

network of polyps (string of pearls)

typically hypertensive middle aged women (initially found in asian or african american ancestry)

often peripapillary and multifocal

OCT and ICG useful for identifying the lesions

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23
Q

MARINA findings

A
  • Objective: Lucentis/Ranibizumab (2 doses 0.3mg or 0.5mg) or sham for occult CNV
  • Result
  • 95% of lucentis eyes had Va improvement or stabilization compared with 62% of control eyes
  • Close to 40% of lucentis eyes has Va improvement > 15 letters compared with control eyes

Conclusion

  • Ranibizumab better than sham for occult or minimally classic CNV from AMD
24
Q

ANCHOR

A

•Objective: Ranibizumab/lucentis vs PDT in classic CNV

Result

  • Prevent vision loss: 95% lucentis eyes vs 64% PDT eyes
  • Loss of <15 letters Va: 90% of lucentis eyes, 65% of PDT

Conclusion

  • Ranibizumab is superior to PDT for predominantly classic CNV from AMD
25
Q

VIEW1/2

A

Objective: Evaluate 3 dosing regimens for eylea: 0.5mg q4wks, 2mg q4wks, 2mg q8wks following initial monthly injections vs lucentis 0.5mg q4wks

Conclusion

Eylea q8wks equivalent to lucentis monthly after 3 monthly loading doses

26
Q

CATT

A

•Objective

Objective: Avastin vs lucentis with monthly and PRN dosing

Conclusion

  • VA outcomes not statistically significant monthly vs PRN dosing
  • Mean gain greater for monthly vs PRN
  • Avastin noninferior to lucentis
  • systemic adverse events greater in the avastin group
  • Arterial thrombotic event similar between drugs
27
Q

Conditions associated with CNV (Ddx)

A

Degenerative (IE AMD, myopic degen, angioid streaks)

Heredodegenerative (IE vitelliform macular dystrophy)

Inflammatory (OHS, multifocal choroditis, Serpiginous, Toxoplasmosis, Toxocariasis etc etc)

Tumor (IE chroidal nevus, choroidal hemangioma, mets, hamartoma of hte rPE)

Traumatic (IE choroidal rupture, intense photocoagulation)

Idiopathic

28
Q

OHS

A

histoplasmosis capsulatum

yeast form of the fungus endemic in missippi and ohio river valleys

  • small atrophic, punched-out choroiretinal scars in the midperiphery and posterior pole
  • linear peripheral atropic tracks
  • juxtapapillary chorioteinal scarring with ot without CNV
  • No vitreous inflammation
29
Q
A
30
Q

What is the grading for the Modified Scheie Classification of Hypertensive Retinopathy?

A

Grade 0 No changes

Grade 1 Barely detectable arterial narrowing

Grade 2 Obvious arterial narrowing with focal irregularities

Grade 3 Grade 2 plus retinal hemorrhages and/or exudates

Grade 4 Grade 3 plus disc swelling

31
Q

What are some signs of HTN choroidopathy?

A

Elschnig spots: lobular nonperfusion of the choriocapillaris – tan, lobule-sized patches that become hyperpigmented and surrounded by margins of hypopigmentation

Siegrist streaks: Linear configurations of similar-appearing hyperpigmentations- follow the meridional course of choroidal arteries

RPE detachments

Bilateral exudative RD (in severe cases)

32
Q

What are the RF for BRVO?

A

age

HTN

smoking

glaucoma

NOTE : not DM

33
Q

What did the BVOS study find?

A

Extensive retinal ischemia (at least 5 DD in size) may result in neovascularization from the retina or optic nerve in 36% of eyes

Macular laser: laser-treated eyes with intact foveal vasculature, macular edema, and visual acuity in the 20/40–20/200 range were more likely to gain 2 lines of visual acuity (65%) than were untreated eyes (37%)

Scattered photocoagulation: laser to the area of retinal capillary nonperfusion effective in causing regression of NVD/NVE/NVI and reduced the risk of VH from 60% to 30%. But ischemia alone not an indication from tx if eyes can be followed.

VH in 60%–90% of such eyes if laser photocoagulation is not performed

34
Q

BRAVO

A

Objective: Assess safety and efficacy of ranibizumab in ME from BRVO

Conclusion: Ranibizumab is safe and effective for BRVO in ME

35
Q

SCORE results

A

BVO

  • triamcinolone = macular grid laser (in efficacy)
  • more cataract and elevated IOP in triamcinolone group

CVO

  • Triamcinolone superior to observation for CVO
36
Q

Iris NV in CRVO

  • what does it develop
  • what pertentage
  • what are the main RF
A

3-5 months

60%

Visual Acuity most predictive. Also non-perfusion on FA and intraretinal blood

37
Q

RF for CRVO

A

HTN

POAG

DM

hyperlipidemia

rare: OCPs, diuretics, hypercoag conditions (hyperhomocysteinemia, protein S deficiency, protein C deficiency, and disorders associated with vasculitis such as sarcoidosis and SLE)

38
Q

DDX for CRVO

A

hyperviscosity retinopathy (dysproteinemia such as that associated with Waldenström macroglobulinemia, multiple myeloma, or blood dyscrasias (eg, polycythemia vera))

Ocular ischemia syndrome

39
Q

complications of CRVO

A

VH

iris NV

neovascular glaucoma

40
Q

CRUISE

A

Objective: Assess safety and efficacy of ranibizumab in ME from CRVO

(cRuise for Ranibizumab)

Conclusion: Ranibizumab safe and effective for ME from CRVO

41
Q

CVOS - what is the recommendation for when to do PRP?

A

20% of participants who had received the prophylactic PRP still developed iris neovascularization. Therefore, close monitoring of patients at high risk of iris neovascularization is necessary. The CVOS investigators recommended waiting until undilated gonioscopic examination revealed at least 2 clock-hours of iris neovascularization before performing PRP.

42
Q

OIS: symptoms, signs, dx

A

sx: slowly decreasing Va, aching pain, prolonged Va recovery after exposure to light
signs: appears similar to CRVO. Narrowed arteries, dilated veins (but not v tortuous), hemorrhages, MAs, NVD/NVE. IOP can be high or low.

low artery pressure which can be seen by pushing on the eye (vs CRVO which will have normal central retinal artery pressure)

FA: delayed choroidal and retinal filling

ERG: global amplitube reduction (VS CRVO which still has blood supply to the photoreceptors and therefore an electronegative ERG)

etiology: atherosclerosis, Eisenmenger syndrome, GCA, other inflammatory conditions

5 year mortality is 40% from comlications of CVD

Tx: carotid artery stenting or endarterectomy, PRP

43
Q

Ddx for CWS

What is a CWS?

A
  • DR
  • HIV-associated retinopathy
  • anemia
  • radiation retinopathy
  • sickle cell retinopathy
  • cardiac embolic disease
  • carotid artery obstructive disease
  • vasculitis
  • collagen vascular disease
  • leukemia

acute obstruction in the distribution of the radial peripapillary capillary net leads to the formation of a RNFL infarct, thereby inhibiting axoplasmic transport

44
Q

What are the main 3 varieties of emboli that cause BRAO?

A
  1. cholesterol (hollenhorst from the carotid arteries)
  2. PLT-fibrin emboli (assocaited with large vessel athersclerosis)
  3. calcific emboli (from diseased cardiac valves)
45
Q

Ddx for peripheral NV

A

Vascular disease with ischemia: PDR, BRVO, BRAO, carotid cavernous fistula, sickle cell, other hemoglobinopathies, IRVAN, ROP, FEVR, hyperviscosity syndromes, eales disease

Inflammatory disease with possible ischemia: sarcoid, retinal vasculitis (SLE), uveitis, birdshot, toxoplasmosis, MS

Miscellaneous conditions: incontinentia pigmenti, longstanding RD, choroidal melanoma, RP, retinoschisis

46
Q

What chromosome, gene and protein are involved with Best Disease?

What are the stages for Best Disease?

A

AD chr 11 - BEST1 GENE (VMD2) – encodes bestrophin which localizes to basolateral plasma membrane of the RPE and functions as a transmembrane ion channel

  • Stage I (Previtelliform): subtle RPE changes, abnormal EOG - normal vision
  • Stage II (Vitelliform): egg-yolk lesion; 30% have extrafoveal lesions - normal VA or mild vision loss
  • Stage III (Pseudohypopyon): layering of lipofuscin - vision similar to stage II
  • Stage IV (Vitelleruptive): scrambled egg - vision may be similar or mildly decreased from stage II (20/30 to 20/60)
  • Stage V (Atrophic): central RPE atrophy - vision ranges 20/30 to 20/200
  • Stage VI (CNV): occurs in 20% - VA 20/200 or worse
47
Q

What are the two important syndromes associated with oculocutaneous albinism?

A
  • Chediak-Higashi syndrome
    • Combines albinism with neutropenia and extreme susceptibility to infections as well as bleeding from deficient platelets
  • Hermansky-Pudlak syndrome
    • Platelet defect characterized by easy bruising and bleeding
    • Interstitial lung disease
    • Most of Puerto Rican descent
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Ophtho (8 decks)

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