Retinopathies Flashcards

1
Q

Diabetic retinopathy

A
  • leading cause of new cases of legal blindness in all adults of all age groups
  • non-proliferative diabetic retinopathy (NPDR) - mild, moderate, severe
  • proliferative diabetic retinopathy (PDR): growing blood vessels where they should not be any
  • macular edema and/or clinicall significant macular edema (CSME): can happen at any state and most likely to cause permeate vision loss
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2
Q

Risk factors for diabetic retinopathy

A
  • longer duration of DM
  • insulin use
  • higher A1C
  • higher systolic blood pressure
  • male
  • higher incidence in Hispanic and African American
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3
Q

Pathogenesis of diabetic retinopathy

A
  • exact mechanism of action is still unclear
  • basement membrane thickening of retinal arterial capillaries gradually interfere w/ metabolic exchange and retinal nutrition
  • loss of pericytes of retinal capillaries secondary to excess glucose may weaken vascular walls leading to microaneurysm formation and fluid leakage
  • microaneurysms are the earliest clinical sign of DR
  • closure of capillaries and precapillary arteroles results in hypoxia and ischemia
  • endothelial proliferation bludding gives rise to neovascular tufts
  • hemorrhageing into perretinal space and viterous
  • fibrous and construction leads to traction retinal detachment
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4
Q

Clinical features of diabetic retinopathy

A
  • microaneurysms: capillary wall outpouching
  • dot/blot hemorrhages: ruptured microaneuryms in deeper layers of the retina
  • flame hemorrhage: rupture in more superficial layer of retina
  • retinal edema/hard exudates: loss of blood brain barrier, leakage of proteins, serum, and lipids from vessels
  • cotton wool spots: nerve fibers layer infarcts secondary to occulsion of precapillary arterioles - hypoxic
  • venous beading: increasing retinal ischemia, most significant predictor of progression to PDR
  • IRMA: intraretinal microvascular abnormalities - remodeled capillary beds w/o proliferative changes
  • macular edema: leading cause of visual impairment
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5
Q

Nonproliferative DR

A
  • mild: presence of at least 1 microaneurysm
  • moderate: presence of hemorrhages, microaneuryms, and hard exudates (need all 3)
  • severe: hemes, microaneuryms in all 4 quadrants, venous beading in at least 2 quadrants, IRMA in at least 1 quadrants
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6
Q

Proliferative DR

A
  • neovascularization
  • perretinal hemes: pockets of blood in the space between the retina and posterior face of vitreous
  • vitreal heme: diffuse haze
  • fibrovascular tissue
  • tractional detachment
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7
Q

Macular edema

A
  • can be present at ANY stage of DR
  • retinal edema within 500um of fovea
  • hard exudates withing 500 um of ofvea w/ retinal thickening
  • retinal edema greater than 1 disc size and within 1 disc area of fovea
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8
Q

DR management

A
  • # 1: glucose control
  • anti VEGF tx: for proliferative DR and macular edema: prevents new blood veseel growth
  • laser photcoagulation: for macular edema and PRD
  • vitrectomy: for PRD, vitreal hemes, and tractional detachment
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9
Q

HTN

A

-increase risk of oocular vascular abnormalities like HTN retinopathy and storkes

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10
Q

HTN retinopathy

A
  • arteriolar disease
  • increased systemic blood pressure causes anatomical changes to retinal vasculature
  • early: HTN leads to vessel wall thickening which leads to attenuation of arterioles
  • advanced: manifest by altering caliber and light reflex of arterioles
  • severe: blood flow so impaired that nutritional damages occur resulting in hemorrhaging, exudates, and edema
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11
Q

HTN retinopathy managment

A
  • control blood pressure

- tx of edema and hemes: laser photocoagulation, anti- VEGF injections or corticosteroid injections

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12
Q

Vascular occlusions

A
  • blockage of retinal vasculature, central or branch, either artery or vein
  • results in sudden painless loss of vision, partial or complete, temporary or permanent
  • Central retinal vein (CRV) vs. central retinal artery (CRA)
  • branch retinal vein (BRV) vs. branch retinal artery (BRA)
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13
Q

Vascular occlusion risk factors

A

-HTN
-DM
-hyperlipidemia
-blood clots and certain blood disorders
-blocked carotids
-age over 60
atherosclerosis
-birth control pills

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14
Q

Central Retinal Artery Occlusion (CRA)

A
  • unilateral, painless loss of vision
  • vision ranges from count fingers to light perception only
  • manifests as a whitening of the retina, macular “cherry red” spot, retinal arteriolar narrowing
  • may have macular sparing if cilioretinal artery present (32% of population)
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15
Q

CRA managment

A
  • lab tests
  • poor visual prognosis
  • no proven effective tx as eye is dead
  • will do workup to find underlying cause
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16
Q

Branch retinal artery occlusion

A
  • unilateral, painless, PARTIAL loss of vision
  • smaller vessel gets blocked
  • edema or whitening along distribution of the arterial branch
  • narrowing branch retinal arteriole or appearance of emboi
  • management same as CRA
  • No TX
17
Q

Central retinal vein occlusion (CRV)

A
  • blockage in the main retinal vein causing stagnation of blood within the retina
  • blood has nowhere to go so it explodes out of the vein and goes everywhere
  • diffuse retinal hemes in all 4 quadrants, tortuous veins, cotton wool spots, edema, and neovascularization
  • Ischemic vs. non-ischemic
  • vision can range
18
Q

CRV management

A
  • treat underlying cause (like HTN)
  • Tx: PRP for ischemic areas, intraviteral corticosteroid and/or anti-VEGF injections
  • The sooner they come in to be tx the better chance they have to get vision back
  • left untreated eye will die
19
Q

Branch retinal vein occlusion (BRV)

A
  • unilateral blind spot in the field of vision
  • sectoral hemorrhaging along affected venule
  • management: tx underlying cause (HTN)
  • same work-up and tx as CRV
20
Q

Age related macular degeneration (ARMD)

A
  • leading cause of irreversible vision loss in adults over 50
  • progressive deterioration of central vision due to damage to the retinal pigment epithelium in macula
  • two forms: non-exudative (dry) and exudative (wet)
21
Q

Age related macular degeneration (ARMD) risk factors

A
  • genetics: abnormal complement factor H
  • smoking - 2nd leading cause
  • age
  • cardiovascular disease / HTN
  • obesity
22
Q

Dry/atropic ARMD

A
  • 90% of ARMD cases
  • RPE disruption due to waste products from rod and cone cells (Drusen)
  • Advanced cases have chorioretinal atrophy
  • more likely to get dry than wet
23
Q

Wet/exudative ARMD

A
  • 90% of severe vision loss
  • neovascularization of the choroid under the macula
  • results in hemorrages and edema
  • disciform scarring
  • you will see vessels at the macula where there is not meant to be any because it can’t get its supply from choroid anymore
24
Q

Dry and wet ARMD tx

A
  • dry: dietary supplements, antioxidants (no really tx, but can slow it down)
    wet: Anti-VEFG injections, focal laser
25
Q

Drug-induced / toxic retinopathy

A
  • Bull’s eye maculopathy
  • crystalline retinopathy
  • nutirional amblyopia
26
Q

Plaquenil

A
  • causes Bullseye Maculopathy
  • used for malaria, rheumatoid arthritis, and SLE
  • it damages RPE cell in the macular leading to scotoma (causes cone damage)
  • rare, but vision loss is permanent.
  • Higher the dosage the higher the risk
  • need an exam every 6 month
27
Q

Tamoxifen

A
  • causes crystalline retinopathy
  • used for breast adneocarcinoma
  • crystalline in RPE of retina, near macula, results in hemes/edema
  • may also induce cataract
28
Q

Alcohol / nutritional amblyopia

A
  • painless bilateral loss of vision
  • retina may appear normal or may have optic nerve pallor
  • vision usually improves with nutritional supplementation