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week 6 Flashcards

1
Q

what are some risk factors for CRVO?

A

OCULAR hypertension
Glaucoma
Over 50 years of age

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2
Q

what are some systemic Conditions in people under 50 associated with CRVO:

over 50?

A

o Head Injuries
o Hyperlipidemia
o Estrogen -containing preparation

over 50 associated with CRVO:
o Hypertension
o Diabetes
o COPD

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3
Q

ischemic vs nonischemic CRVO?

A

nonischemic 4X more common but the only way to tell them apart is to do FFA

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4
Q

why is there an IOP decrease in ischemic CRVO?

A

This is due to a more severe decrease in perfusion to the ciliary body which produces aqueous (decrease in aqueous production leads to a decrease in IOP)

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5
Q

what are some fundus findings in ischemic CRVO?

what is the vision like?

A 
Blood and thunder fundus= dramatic intraretinal and nerve fiber layer hemorrhages in
the posterior pole  
-CWS
-Dilated tortuous veins 
-Exuberant disc edema 
-Gross macular and retinal edema 
-Extensive capillary closure on fluorescein angiography greater than 10DD
- + APD
Vision is usually worse than 20/200
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6
Q

vision in ischemic vs nonischemic CRVO:

A

nonischemic is better than 20/200 usually unlike ischemic

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7
Q

retinoschisis:

A

separation in OPL layer

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8
Q

T/F: grid photocoagulation did reduce mac edema in crvo but not the acuity?

A

true

*also, VA outcome largely dependent on initial VA was another study finding

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9
Q

when should you refer a CRVO to a ret specialist?

A

If the CRVO looks bad and the vision is worse than 20/40 most refer to a retina specialist.
-they either inject a steroid or Anti –VEGF 
injection

ALso: Lower IOP if its high

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10
Q

What was the outcome of the SCORE study (Standard Care vs Corticosteroid for Retinal Vein Occlusion study)

A

-Testing effect of steroid injections as a treatment for macular edema associated with CRVO
Results: Intravitreal triamcinolone is superior to observation for treating vision loss associated with macular edema secondary to CRVO in patients who have characteristics similar to those in the SCORE-CRVO trial
-still have cataracts/glaucoma to think about

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11
Q

what was the Cruise study and outcome?

A

patients with macular edema after CRVO were injected with either 0.3 mg, 0.5 mg ranibizumab (Lucentis) or sham injection.

  • Patients were excluded if they had a RAPD
  • **Conclusion: Intraocular injections of 0.3 mg or 0.5 mg ranibizumab provided rapid improvement in 6- month visual acuity and macular edema following CRVO, with low rates of ocular and non-ocular safety events.
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12
Q

what is a retinal macroaneurysm?

are they uni or bilateral?

A

= isolated dilated area of a major arterial branch

  • unilateral 90% of the time
  • associated with a 5 year mortality rate
  • Also associated with: hypertension, arteriosclerosis, and retinal emboli.
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13
Q

How can you treat macroaneurysm?

A
  • Spontaneous regression is common
  • Laser photocoagulation may be performed adjacent to the macroaneurysm if not seale in 3 months and macular edema still present or progressing.
  • *Controversy exists about lasering the macroaneurysm directly as it carries the risk of rupture and vascular occlusion.

–Newer studies have found that using either Avastin or Lucentis is an effective way to treat the associated macular edema (decreasing retinal thickness and increasing VA)

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14
Q

what is valsalva retinopathy? how do you treat it?

A

Localized intraretinal hemorrhage usually in the macula region
(caused by strenuous activity i.e. weight lifting, vigorous coughing, etc.)
TX: Usually this just recovers spontaneously
break in a blood vessel in macula> rupture of small vein >recovers on its own
looks like a large pool of blood/ intraretinal heme right over the macula

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15
Q

radiation retinopathy fundus findings?

A

very similar to DM retinopathy

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16
Q

cholesterol emboli are usually from?

A

carotid

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17
Q

Fibrinoplatelet emboli (Fisher plugs) vs hollenhorst plaques

A

Fibrinoplatelet plaques are larger than Hollenhorst plaques and come from a carotid thrombus or heart thrombus.

  • dull white in color and mobile and found at bifurcations
  • Mobile- can move quickly thru arteries, may be there when you look and gone 15 minutes later
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18
Q

wher do calcific emboli usually come from?

A

These come from the aorta, carotid arteries, or heart valves and are usually single and white.

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19
Q

what are some questions you should ask about if you see a plaque in the eye?

A
  • transient monocular blindness
  • weakness of one side of face or limbs
  • new or worsening HAs
  • paresthesias/clumsiness
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20
Q

what should you do if you see plaque and pt has no TIA?

A

order carotid and echo, blood/lipid test
(or refer to internist)
-maybe start aspirin if no contraindications

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21
Q

pts should be operated on if the carotid is what % stenosed?

A

70-99%

*if pt has no symptoms but is stenosed, controversial whether to tx bc surgery has a 2-3.5% risk of death/stroke

22
Q

what is happening in a central retinal artery occlusion?

A

embolus gets lodged in CRA as it passes through lamina

23
Q

where does emboli from the heart come from?

A
  • calcific emboli from aortic or mitral valves

- fromvalves in subacute bac endocarditis

24
Q

what is happening in CRAO to gang cell/NFL?

A

swelling

25
Q

if there is a cilioretinal artery, VA will be what or better in CRAO?

A

20/50 or better

26
Q

what are some diff dx’es of transient monocular VA loss?

A
  • int carotid artery disease
  • cardiac emboli
  • postural hypotension (usually bilateral)
  • hyperviscosity syndromes
  • ocular migraine (bilateral)
  • ant ischemic optic neuropathy (temporal arteritis)
  • impending CRA or vein occ
  • rarely sickle cell
27
Q

what age and gender do you usually see CRAO in?

A

60 yos, more men than women

28
Q

how could you attempt to tx a CRAO?

A

lie person down, apply pressure (possibly with gonio lens) on and off, maybe hyperbaric chamber, AC parenteresis with needle (trying to decrease IOP to allow greater perfusion)

29
Q

what was the EAGLE study for CRAO?

A

compared tx outcome after conservative tx vs intra-arterial fibrinolysis, and actually vision was about the same in both where there were more adverse rxns in the tx group, so just leave it
CST-massage eye, BB drop, IV acetazolomide
LIF-microcatheter in oph artery w/ heparin and tPA

30
Q

T/F: you can get iris neo with CRAO?

A

true

31
Q

what is ocular ischemia?

A

ischemia secondary to carotid problems, so usually unilateral, internal carotid usually 80% stenosed

32
Q

what are some ant findings ass with ocular ischemia?

A

unilateral engirged episcleral vessels

  • uni corneal edema, descemets folds
  • mild ant uveitis
  • iris neo
  • uni ocular or orbital pain
  • posterior similar to DM retinopathy
33
Q

how do you manage ocular ischemic syndrome?

A

same as CRAO

34
Q

what fibers come down and cross over into optic tract as knee of willabrand

A

inf nasal

35
Q

macular fibers tend to cross where?

A

back of chiasm

36
Q

pressure from below and ant to chiasm yields defects where?

A

sup bitemporal

37
Q

pressure from above and behind chiasm yields defects where?

A

inf bitemporal

38
Q

pressure from the sides of chiasm yields defects where?

A

binasal

39
Q

typically the chiasm lies where in relation to the dorsum sellae?

A

post rim of chiasm lies above dorsum sellae (80% of people)

40
Q

prefixed chiasm tumor affects where?

A

pushes from bac and inf, gives bitemp central loss and maybe sup bitemp loss??

41
Q

postfixed chiasm tumor affects where?

A

pushes ant and inf, gives sup bitemp

42
Q

what is something that could compress chiasm from above?

A

craniopharyngioma, above and behind, affects sup nasal fibers=inf bitemporal defect

43
Q

give an example of what could compress the pituitary from the antero-superior aspect:

A

meningiomas most common

-also aneurysms of ant cerebral/ant comm artery

44
Q

T/F: lesions of the optic tract can cause optic atrophy?

A

true

45
Q

most optic tract lesions present as what?

A

homonymous and incongruous

46
Q

Not many people have LGN lesions, but if they do, what do they look like? will it give optic atrophy?

A

hourglass defect; no

47
Q

what kind of lesion gives pie in the sky?

A

temporal lobe lesions: affect fibers from inf retina travelling temporally in temp pole

48
Q

you get an extinction phenomenon with what kind of lesions?

A

parietal lobe

49
Q

lesions to occipital striate cortex usually cause what defects?

A
  • complete or incomplete congruous homonymous

- sometimes macular sparing

50
Q

most common vascular lesion that will affect occipital striate cortex

A

thrombosis of post cerebral or calcarine artery

PPO (10 decks)

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