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
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
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
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
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
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
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
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
9
Q
HTN
A
-increase risk of oocular vascular abnormalities like HTN retinopathy and storkes
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
11
Q
HTN retinopathy managment
A
- control blood pressure
- tx of edema and hemes: laser photocoagulation, anti- VEGF injections or corticosteroid injections
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)
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
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)
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
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
