Vascular/Retinal Disorders Flashcards

1
Q

What is important to remember when transporting a retinal detachment to referral?

A

patient head positioned so retinal tear is placed at lowest point of eye to minimize extension
inferior – keep head upright
temporal – keep temporal side of head down
minimize motion of eyes

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2
Q

What is the prognosis of retinal detachments?

A

90% can be cured. The worst are if the macula detaches or long time of detachment.

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3
Q

What are potential complications of retinal detachment?

A

vision loss or decreased visual acuity, recurrence, cataract formation, glaucoma

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4
Q

What is the development of the nonproliferative diabetic retinopathy?

A

asymptomatic –> symptomatic
retinopathy –> maculopathy

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5
Q

What types of macular degeneration are there and which is the most common?

A

wet and dry (much more common)

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6
Q

What is the clinical presentation of dry macular generation?

A

central vision loss, gradual, bilateral, distortion of images, scotomas, declining visual acuity

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7
Q

What are risk factors for macular generation (both!)?

A

age related, female, white, tobacco, alcohol, excessive sunlight, CAD, HTN, HLD, family Hx, hyperopia, light iris

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8
Q

What is the causation of dry macular degeneration?

A

cellular debris Densen accumulates between retina and choroid leading to scarring and atrophy

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9
Q

What helps in diagnosis for dry macular degeneration?

A

Snellen (visual acuity), Amsler grid (curvy if +), need DILATED eye exam, focused exudates called DRUSEN upon exam

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10
Q

What is the treatment of dry macular degeneration?

A

vitamins help! STOP SMOKING!!!

Pegcetacoplan & avacincaptad pegol injection

note risk of wet ARMD

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11
Q

What is the clinical presentation of wet macular degeneration?

A

RAPID onset and severe, hemorrhaging and fibrosis within the eye, bilateral CENTRAL vision loss, distortion, scotomas

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12
Q

What is the causation of wet macular degeneration?

A

new blood vessels popping up that leak blood and hemorrhage and fibrosis

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13
Q

What is the key on fundoscopy for wet ARMD?

A

fluorescein angiography can help, but really a lot of blood in eye

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14
Q

What does chronic steroid use cause?

A

glaucoma

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15
Q

How do you treat wet ARMD?

A

inhibitors of vascular endothelial growth factors (VEGF)
-mab
ranibizumab, bevacizumab, aflibercept, farcimab
brolucizumab risk of vision loss

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16
Q

What is the clinical presentation of retinal detachment?

A

curtain of vision loss, LONG LASTING, med emergency, acute onset, tunnel vision
photopsias followed by floaters

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17
Q

What are the risk factors for retinal detachment?

A

age, myopia, cataract extraction, ocular trauma, smoking, DM retinopathy

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18
Q

What are the two kinds of retinal detachment?

A

rhegmatogenous detachment “natural” MCC – fluid goes into subretinal space, detaches

tractional - scars pull on retina, exudative- fluid trapped (wet ARMD), causes detachment

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19
Q

What does the fundoscopy look like for retinal detachment?

A

retina elevated and gray/cloudy, superior temporal quadrant; wave on a beach
Positive Shafer’s sign of clumping brown pigment

20
Q

What is the treatment for retinal detachment?

A

closing retinal holes and tears through laser photocoagulation, crypexy, pneumatic retinopexy, vitrectomy

if exudative/secondary, treat underlying cause

21
Q

What is the clinical presentation of diabetic retinopathy?

A

blurry vision, decreased acuity, visual distortion, scotomas not always noticed

proliferative has more severe symptoms

22
Q

What are risk factors for diabetic retinopathy?

A

Diabetes. 99% type I get it. 60% type II. 20% already have it with uncontrolled diabetes

23
Q

What is the difference between nonproliferative or proliferative diabetic retinopathy?

A

Nonpro- circinate ring yellow exudates, cotton wool spots
pro- growth of new vessels and fibrous tissue

24
Q

What is important to always do on diabetic patients?

A

need baseline fundoscopy after diagnosis of type II, 5 years after type I, then annual dilated exam

25
How do you manage diabetic retinopathy?
optimize control of BG, BP, kidney function, lipids (could worsen before getting better..initially check every 3-4 months until managed for 18-24 months) VEGF inhibitors -- **Ranibizumab, bevacizumab, aflibercept, faricimab, brolucizumab** may do laser photocoag, corticosteroid, virectomy
26
What is the treatment for severe diabetic retinopathy?
panretinal laser photocoagulation prophylatically
27
What is the clinical presentation and cause of acute hypertensive retinopathy?
sudden onset of severe HTN >200/110 which could be from hyperthyroidism, drugs, pregnancy
28
What would confirm hypertensive retinopathy on a fundoscopy?
cotton wool spots, *dot blot and flame hemorrhages*, papilledema
29
What makes chronic hypertensive retinopathy different on a fundoscopy (note: hard to see, so just good to know)?
**AV nicking and crossing**, hemorrhage, narrowing, copper/silver wiring (severe), macular star
30
How do you treat acute hypertensive retinopathy?
emergency! Treat underlying cause! Complications: retinal detachment, optic neuropathy
31
What are the risks for acute hypertensive retinopathy?
older patients
32
what are the risks for chronic hypertensive retinopathy?
high sodium, obesity, tobacco, alcohol, family hx
33
What is the cause of chronic hypertensive retinopathy?
chronic HTN; atherosclerosis
34
How do you treat chronic hypertensive retinopathy?
increase risk of stroke -> MI, CAD, PAD, ARMD control HTN!!!!!!!!!!!! comps=retinal vein occlusion, retinal detachment, optic nerve atrophy
35
What is the clinical presentation of retinal artery occlusion?
sudden monocular vision loss -- no pain, redness, UNILATERAL this is assumed with these symptoms
36
What are risks for retinal artery occlusion?
diabetes, hyperlipidemia, HTN, young = migraines, oral contraceptives, vascular disease
37
What is the cause of retinal artery occlusions?
occlusion of CENTRAL or BRANCH artery (eye stroke), embolism/thrombosis (thrombophilic disorders, SLE, giant cell arthiritis) from atherosclerotic plaques, atrial fibrillation, endocarditis
38
What's the difference between acute and chronic papilledema?
acute = no loss of acuity chronic/severe acute = visual field loss, profound loss of acuity
39
What should you consider with retinal artery occlusion?
ask about neck pain, neck trauma --> carotid artery dissection giant cell arteritis (check inflammatory mediators); if >50 yr old with central occlusion young people check for clotting disorders!
40
What on the fundoscopy is key for retinal artery occlusion?
central =cherry red spot, "box car" segmentation, pale optic disk branch= cotton wool spots, limited to area
41
What do you do to manage retinal artery occlusion?
work up as a stroke!!!!!!! urgent referral to ER for imaging angiography, opthalmology referral lay patient flat, ocular massage, high conc. of inhaled O2, IV acetazolamide, anterior chamber paracentesis
42
What is the clinical presentation of vein occlusion?
more common --> sudden monocular loss of vision, no pain or redness maybe RAPD?
43
What is a risk for vein occlusion?
glaucoma but everything from artery too: diabetes, hyperlipidemia, HTN, young = migraines, oral contraceptives, vascular disease
44
What causes a retinal vein occlusion?
clot formation Virchow's triad: vessel damage, stasis, hypercoagulability, atherosclerosis
45
What is key on fundoscopy of retinal vein occlusions?
central = widespread hemorrhages, cotton-wool spots, optic disk swelling "blood & thunder" branch = confined to area
46
How do you treat a retinal vein occlusion?
VEGF inhibitor injection for macular edema Panretinal laser photocoagulation for neovascularization or Triamcinolone (central), implant with dexamethasone (either), focal laser coag (branch)