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OPHTHALMOLOGY BCSC > Retina > Flashcards

Retina Flashcards

1
Q

90% of cones are located in or outside of foveal region?

A

outside

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2
Q

what is definition of fovea? foveola?

A

fovea only has photoreceptors (highest density is at 4mm from center or 12 deg from fixation)
foveola only has cones.

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3
Q

describe attachment of cones vs rods to their respective bipolar cells?

A

cones attach 1 to 1 to their bipolar cells

many rods attach to 1 bipolar cell.

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4
Q

what is ILM

A

foot plates of muller cells–attached to posterior cortical gel of vitreous

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5
Q

what is ELM

A

zonular attachments between photoreceptors and muller cells.

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6
Q

central retinal artery divides in to how many branches?

A

4.

sometime there’s a cilioretinal artery

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7
Q

what are the 4 layers of retinal vessels?

A
  1. radial peripapillary capillary network (in RNFL)
  2. superficial vascular plexus (in ganglion layer)
    3/4 deep capillary plexus (2 capillary beds on either side of the INL.
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8
Q

starting from which layer does the choroidal circulation supply the retina?

A

from outer plexiform layer outward

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9
Q

Functions of the RPE (7)

A
  • absorbs light
  • phagocytosis rod/cone outer segments
  • participates in retinal and polyunsaturated fatty acid metabolism
  • maintains subretinal space
  • forms outer blood-ocular barrier
  • Heals and forms scar tissue
  • regenerates and recycles visual pigment
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10
Q

rods and cones shed their outer segment with daily circadian rhythm how?

A

rods shed discs in AM
cones shed them at dusk

–discs are phagocytosed by RPE cells

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11
Q

5 layers of Bruch’s membrane?

A
  • basement membrane of RPE
  • inner collagenous zone
  • middle layer of elastic fibers
  • outer collagenous zone
  • basement membrane of endothelium of choriocapillaris
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12
Q

Choroidal blood enters through posterior ciliary arteries. The choroid has two layers . what are they?

A
  1. Outer larger caliber choroidal vessels (Haller layer)

2. Inner smaller caliber vessels (Sattler layer)

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13
Q

choroidal circulation

A

posterior ciliary arteries–>choriocapillaris–>venules–>vortex veins (4 or 5 per eye)–>superior and inferior ophthalmic veins

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14
Q

What is the leading cause of blindness in the developed world in people over 50

A

AMD

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15
Q

AMD risk factors (8)

A

Female sex, Family hx, HTN, HLD, CVD, highter waist to hip ratio in men, hyperopia, light colored iris

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16
Q

Race predilection of AMD

A

european americans highest, african americans lowest

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17
Q

Genetic associations with AMD?

A

lipid transport metabolism genes (APOE)
Collagen matrix genes (COL8A1)
all trans retinaldehyde photoreceptor clearaance genes ABCA4
and angiogenesis genes (VEGFA)

Genetic association is controversial as there are many modifyable risk factors.

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18
Q

size of small drusen vs intermediate vs large?

A

small <63microns, intermediate 63-124, large >124 (associated with risk of progression)

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19
Q

what are types of drusen shapes?

A

hard, soft, confluent.

soft and confluent are at more risk of progression to CNV and atrophy

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20
Q

appearance of drusen on FA?

A

small hard drusens can appear as window defects

large/confluent/soft drusens can have late staining

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21
Q

focal atrophy vs geographic atrophy of RPE?

A

geographic atrophy of RPE is when there’s continuous atrophy diameter >175 microns

GA generally are parafoveal until late stage when it will involve central vision.

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22
Q

AREDS study

A

vitamin C 500 mg, vit E 400 IU, beta carotene 15 mg, zinc oxide 80 mg, cupric oxide 2 mg.

Those with intermediate and advanced AMD had 25% less progression and 19% reduction in rate of vision loss in 5 years (>3 lines)

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23
Q

What is the 4 point grading scale for from AREDS study?

A

1 pt for 1 or more large drusen
1 pt for any pigment abnormalities
1 pt bilateral intermediate drusens
2 pts for any NV AMD

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24
Q

AREDS2 central question? outcomes?

A

tested whether replacing beta carotene with xanthophylls (lutein/ zeaxanthin) and adding omega 3 long chain polyunsaturated fatty acids would reduce AMD progression.

  • lutein/zeaxanthin are similar to beta carotene and beta carotene had more risks of lung cancer in smokers
  • LCPUFAs did not have significant effect in reducing progression of AMD.
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25
Q

CNV classifications. Type I, Type II, Type III

A

Type I CNV new vessels originating from choriocapillaris grow through a defect in bruch membrane to sub RPE space. Can create fibrovascular PED typically with irregular contour.
Type II CNV originates between RPE and retina–appears lacy/gra green lesion.
Type III CNV vessels grow downward from retina to RPE.

Left untreated NVMs become hypertropic fibrotic scars with discform apperance and photoreceptor damage.

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26
Q

Pattern of Classic CNV on FA?

A

bright lacy well defined hyperfluorescent lesion that appears in early phase and progressively leaks by late phase.

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27
Q

Pattern of Occult CNV on FA?

A

more diffuse hyperfluorescence either has PED or late leakage from an undetermined source.

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28
Q

which type of CNV is associated with classic CNV on FA and which is associated with occult?

A

Classic–type 2 CNV

Occult–type 1 CNV

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29
Q

what are retinal angiomatous proliferations?

A

RAPs are type III CNV

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30
Q

What is polychoroidal vasculopathy

A

variant CNV type I that presents with multiple recurrent serosanguinous RPE detachments.
Eval with ICG!!
“string of perals” configuration;
more common in asian ancestry.
Can have VH
Tx: photodynamic therapy with or without ranibizumab (lucentis) is better than ranibizumab alone. (EVERST study)

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31
Q

Paracentral Acute Middle Maculopathy is acute ischemia of the macular capillary layers. What are the two types?

A

Type 1 affects the superficial capillary plexus between outer plexiform and inner nuclear layer resulting in INL thinning.
Type 2 affects capillary plelxus in outer plexiform and outer nuclear layer causing disturbance in ISOS/ellipsoid region.

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32
Q

CRAO visual outcome usually ~20/400 for most. Some people with 20/40 vision most likely has what structure

A

cilioretinal artery.

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33
Q

Differential diagnoses for CRAO

A

most are due to atherosclerosis
embolic from arrythmia/MVP
vasculitis–GCA vs infectious
Hypercoagulability–trauma, sickle cell, other coagulopathies

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34
Q

management of CRAO. rule of thumb

A

most important is stroke workup. most common cause of death is CVD
Can do ocular massage or IOP lowering drops.
Should monitor closely for NV usually occurs in 1-2 months.

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35
Q

Ophthalmic artery occlusion etiologies? 3

A

embolic, ICA dissection, orbital mucormycosis, cosmetic filler injections

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36
Q

causes of macroaneurysms?

A

systemic HTN, prior vascular occlusions.

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37
Q

treatment of macroaneurysms?

A

laser.

antiVEGF hastens resolution of bleed but does not improve visual outcome.

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38
Q

What are salmon patches in SS retinopathy

A

peripheral arteriolar occlusion

39
Q

what are refractile spots in SS retinopathy

A

resorbed hemorrhages with hemosiderin deposition within ILM

40
Q

What are sun bursts in SS retinopathy

A

RPE hypertrophy/hyperplasia

41
Q

proliferative sickle retinopathy is most common in which populations?

A

SC> SThal>SS

42
Q

pathogenetic sequence of PSR?

A

peripheral arteriolar occlusion/nonperfusion–>arteriolar anastomosis–>seafan neo–>VH–>tractional detachment.

43
Q

neovascularization 2/2 PSR –you should decide to perform PRP with caution why

A

RRD is more common s/p PRP for PSR than PDR.

44
Q

scleral buckle is relatively contraindicated in SS patients. why

A

risk of anterior ischemia.

45
Q

CME results in petaloid pattern in which layer

A

Henle’s layer

46
Q

CME ddx

A

diabetic retinopathy, CRVO/BRVO, uveitis, retinitis pigmentosa, irvine gass syndrome, prostaglandins, choroidal NV, X linked hereditary retinoschisis.

47
Q

When is peak incidence of post CE CME

A

6-10 weeks

48
Q

Coat’s disease population

A

unilateral male predominant.

Children <4 has propensity to have massive exudative detachments.

49
Q

Coats disease. What is it

A

vascular dilatation–> leakage under retina–>detachment. NV is unusual.

50
Q

treatment for Coat’s disease.

A

PRP or cryo or retachment surgery

51
Q

DDx for coats disease

A

ROP, von hipple lindau, fasciocapsulohumeral macular dystrophy, dominant exudative vitreoretinopathy

52
Q 
Macular telangiectasia (Mactel 1)
population, treatment.
A

unilateral, predominantly young males.
dilatation of temporal mac vasculature.
Treatment is Aflibercept (not any other aVEGF)

53
Q

Macular Telangiectasia. (Mactel 2)

A

bilateral progressive neurodegenerative disease.
Most common of the mac tels.
–usually onset in the elderly with grey appearance of retina with superficial crystalline deposits, dilated/ectatic vessels–> atrophy.
-leakage seen on FA. OCT shows thinned central retina.
-treat with aVEGF

54
Q

Macular telangiectasia (Mactel 3)

A

very rare vasocclusivie disease. affects parafoveal region

55
Q

Von Hippel Lindau synrome.

  • Which chromosome is involved
  • What are the systemic manifestations
A

Chr 3 is involved.
Renal cell carcinoma, pheochromocytomas, CNS hemangioblastoma/retinal hemangioblastoma (large orange/red lesion with feeder vessels),

56
Q

How do you treat retinal hemangioblastomas?

A

Cryotherapy. Need to destroy the lesions as they will enlarge/become more numerous in time.

57
Q

what is racemos hemangiomas?

A

retinal blood vessels without intervening capillary bed. Thus appear engorged. This is associated with Wyburn Mason Syndrome

58
Q

What is Wyburn Mason Syndrome.

A

Syndromic congenital ipsilateral malformations of brain, face, orbit (racemos hemangioma) mandible.
buzz word: “Hemorrhage during dental extraction”

59
Q

Retina cavernous angiomas.

  • What do they look like?
  • What do you see on FA?
  • treatment?
A

saccular grapelike lesions in inner retina.
FA: slow filling. NO leakage.
-No treatment unless causes VH.–then treat with photocoagulation or cryo.

60
Q

Radiation retinopathy.

-Common findings?

A

–resembles diabetic retinopathy–

MAs, DBH, CWS, perivascular thinning, mac edema, disc edema, optic atrophy, CRVO, CNV, VH

61
Q

Radiation retinopathy can be slow progressive.
How many grays are generally associated with radiation retinopathy?
When does the retinopathy usually appear?

A

> 30 grays

appears about 18 months.

62
Q

How do you treat radiation retinopathy.

A

aVEGF. DO not laser as it worsens atrophy/ ischemia

63
Q

Valsalva retinopathy. Where are the hemorrhages usually located?

A

superficial. under the ILM

64
Q

Purtscher’s retinopathy.

pathophysiology? etiology?

A

complement mediated leukoembolization causing retinal ischemia.
-Usually from compressive thoracic/head trauma. Can also be from pancreatitis, SLE, amniotic fluid embolism

65
Q

what is Terson Syndrome?

A

acute intraocular bleed (VH, subhyaloid, superficial intraretinal) associated with intracranial hemorrhage.
–occurs 2/2 sudden increase in intraocular venous pressure. Spontaneous resolution usually occurs

66
Q

How are the 3 zones in ROP defined?

A

Zone 1 is within 60 degrees of the optic nerve
Zone 2 is radius from ONH to nasal ora serrata
Zone 3 is the entire remaining temporal retina

67
Q

What are the 5 stages of ROP

A

Stage 0 is imature retina without pathologic changes
Stage 1 is with clear demarcation
Stage 2 is with a ridge
Stage 3 is with extraretinal firbovascular proliferation
Stage 4 is partial retinal detachement
Stage 5 is total funnel RD

68
Q

What is plus disease in ROP?

A

venous tortuous dilatation in at least 2 quadrants.

69
Q

What is aggressive posterior ROP (Rush disease)

A

vacularization ending in zone I or early zone II with plus disease. –This may progressive rapidly

70
Q

What is threshold disease?

A

5 continugous clock hours of extraretinal NV

8 or more cumulative clock hours of extraretinal NV with PLUS disease located in zone I/II

71
Q

At how many weeks of gestation does retinal vascularization start? when does it complete nasally? temporally?

A

Starts at 16 weeks. completes nasally at 36 weeks and temporally at 40 weeks.

72
Q

pathophysiology of ROP?

A

< 31 weeks–vascular development ceases due to lack of hormonal growth factors (VEGF and IGF1)
31-34 weeks excess VEGF/IGF1 due to retinal ischemia.

73
Q

what type of glaucoma is associated with kids with ROP?

A

angle closure most commonly

can also have pupillary block glaucoma

74
Q

ROP screening guidelines?

A

<30 weeks of gestation; <1500 g birth weight

Unstable clinical course, IGF-1 levels/rate of weight gain.

75
Q

ROP babies with prethreshold or threshold disease should be treated within what time period?

A

within 72 hours of exam.

76
Q

When does cryotherapy play a role in ROP? Why should you be careful with cryo in babies?

A

When there’s media opacities. 5% can experience cardio/respiratory arrest.

77
Q

What is CSCR?

A

idiopathic serous detachment of retina due to leakage at level of RPE/choriocapillaris.

78
Q

CSCR typical population? other associated conditions?

A

males 35-55 years with type A personalities.

Cushings, pregnancy, sleep apnea, HTN, psychoparmcologic meds.

79
Q

What are the presenting symptoms of CSCR?

A

sudden blurred/dim vision, micropsia, metamorphopsia, paracentral scotomas, change in color, prolonged after image.

Visual acuity is often fairly good.

80
Q

Classic Fluorescein findings for CSCR

A

dot form leakage and smoke stack form leakage

81
Q

How do you treat CSCR?

A 
First, you should treat it as it can cause scotomas and secondary CNV.
Photodynamic therapy (PDT) is treatment of choice as it's effective and is not associated with recurrence (which laser photocoagulation is)
82
Q

Choroidal infarction can be caused by what two broad categories of conditions?

A

arteritic (GCA, PCA) vs nonarteritic (thromboembolic and hypercoagulable (SLE, TTP, DIC) and low perfusion (such as HTN/eclampsia) conditions)

83
Q

what is the appearance of choroidal infarction on exam?

A

yellow placoid RPE discoloration with serous RD.

Also, smaller pigmentary hyperplasia called Elschnig

84
Q

choroidal infarction spots are called what? what about chroidal infarction streaks? what about choroidal infarction triangles?

A

Elschnig spots, Siegrist streaks, and Amalric triangles

85
Q

What are Patton Lines?

A

chorioretinal folds around ONH in elevated ICP.

86
Q

tomato ketchup fundus

A

sturge weber syndrome. choroidal hemagioma (transillumination on B scan, early filling on FA)

87
Q

Uveal effusion syndrome. pathophysiology? population?

A

scleral thickening decreasing trans scleral aqueous outflow leading to marked thickening of choroid/ciliary body.
Young hyperopes with serous RD

88
Q

Leopard-spots on FA?

A

Uveal effusion syndrome vs BDUMP

89
Q

What is BDUMP (bilateral diffuse uveal melanocytic proliferation)

A

diffuse thickning of choroid, reddish/brown choroidal discoloration. Heralds systemic cancer (uterine, ovarian, lung, colon, kidney)

90
Q

BDUMP findings on autofluores and FA?

A

hypoautofluorescent

Hyperfluorescent on FA

91
Q

definition of pathologic myopia

A

-6D or AL of 26.5

92
Q

what are lacquer lines?

A

small cracks in bruch’s membrane in pathologic myopia.

93
Q

which white dot syndrome is associated with cerebral vasculitis?

A

AMPPE

94
Q

AMPPE

A

bilateral. Men=women

OPHTHALMOLOGY BCSC (8 decks)

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