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Ophthalmology > Lecture XI > Flashcards

Lecture XI Flashcards

1
Q

Pupil sparing CN III defect is more concerning for what type of problem? Why?

A

Systemic disease, since the nerve carries the parasympathetic fibers in the outer ring of the nerve.

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2
Q

Bilateral disc edema, with good vision, and no RAPD = ?

A

Papilledema

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3
Q

DM is the leading cause of blindness, specifically in what age group?

A

20-74

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4
Q

What are the three major ophthalmologic changes that occur with DM?

A
  • Refractive error changes
  • Cataracts
  • Retinopathy
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5
Q

What are the small organs that are affected with small vessel dz 2/2 DM? (3)

A
  • Eyes
  • Kidneys
  • Peripheral nerves
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6
Q

What is the chemical mediator of increased capillary permeability/abnormal vasoproliferative due to increase BG?

A

VEGF

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7
Q

What are the two forms of diabetic retinopathy?

A

Proliferative retinopathy

Non-proliferative form

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8
Q

What is the non-proliferative form of DM retinopathy?

A

Retinal blood vessels are leaky, which causes leakage into the macula which reduces vision

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9
Q

What is the progression of problems that occurs with non-proliferative DM? (4)

A
  • Microaneurysm
  • Leakage of intravascular fluid (hard exudates)
  • Intraretinal hemorrhages
  • Retinal ischemia (cotton wool spots)
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10
Q

What is the treatment for nonproliferative DM retinopathy?

A

No immediate treatment

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11
Q

What determines a high risk of imminent PDR?

A
  • Cotton wool spots
  • Capillary dropout
  • Venous bleeding
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12
Q

What causes the neovascularization with proliferative form of DM retinopathy?

A

Tissue hypoxia causes proliferation

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13
Q

True or false: pts with proliferative retinopathy can also have all the s/sx of NPDR

A

True

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14
Q

What are the fundoscopic findings of PDR?

A
  • Neovascularization
  • Vitreous hemorrhages
  • Fibrous proliferation
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15
Q

What eventually happens to the new blood vessels with PDR?

A

Vitreous hemorrhage

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16
Q

What are the s/sx of vitreous hemorrhage?

A
  • Floaters/cobwebs

- Sudden loss of vision

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17
Q

What should be done with vitreous hemorrhages?

A

Refer to ophthalmologist

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18
Q

What happens with scar formation in the eye?

A

Scar will cause traction on the retina–may lead to retinal detachment

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19
Q

How do people lose vision with diabetic retinopathy?

A

Several causes-but macular edema or vitreous hemorrhage and traction RD

20
Q

What are the two basic causes of vision loss with NPDR? Which is treatable?

A
  • Ischemic maculopathy

- Macular edema (generally treatable)

21
Q

What are the goals of photocoagulation with PDR?

A
  • Involute neovascular tissue
  • Prevents further neovascularization
  • Reduces risk of vitreous hemorrhage, and reduce traction retinal detachment
22
Q

What is the general idea with photocoagulation with PDR?

A

Kill off peripheral vision (Retina) to maintain central vision (blood flow to the macula)

23
Q

When is vitrectomy indicated?

A

If vitreous hemorrhage or retinal detachment

24
Q

What is a vitrectomy?

A

Suction out the hemorrhages

25
Q

True or false: proteinuria is a risk factor for macular edema

A

True

26
Q

What is the role of diuresis and BP control with macular edema in DM?

A

Improves–ACEI/ARBs particularly

27
Q

True or false: PDR is a risk factor for MI, stroke, amputation, and death

A

True

28
Q

What happens to the risk of nephropathy with the advent of PDR?

A

Increases the risk

29
Q

What is the problem with dyslipidemia in the development of DM retinopathy?

A

Increases the chances of hard exudate formations

30
Q

What are the DM screening guidelines for DM pts?

A

-Annual ophthalmologic exams

31
Q

What are the two forms of laser photocoagulation treatment options?

A
  • Focal macular laser for macular edema

- Panretinal photocoagulation for PDR

32
Q

What are the findings of HTN retinopathy?

A
  • Arteriolar sclerotic changes

- HTN changes

33
Q

What is the major challenge with identifying HTN retinopathy?

A

Appears very similar to natural age changes

34
Q

What are the characteristics findings on fundoscopy with arteriolar sclerosis?

A
  • Less transparent vessels

- Copper/silver wiring light reflex broadens d/t the thickening and fibrosis of the vascular wall

35
Q

What causes A/V nicking?

A

At the arterioles and veins share a common adventitial sheath at crossing sites causing A/V nicking

36
Q

What is the normal artery:vein ratio (size)?

A

2:3

37
Q

What is the pathogenesis of HTN causing retinopathy?

A

moderate elevation causes constriction of arterioles

38
Q

Severe acute BP rises over what mmHg causes fibrinoid necrosis of the vessels, and exudates?

A

More than 200 / 120

39
Q

What is the ophthalmologic consequence of malignant HTN?

A

Optic nerve edema and fibrinoid necrosis

40
Q

What are the three most sensitive ophthalmoscopic indications of HTN? (in order)

A
  1. attenuation of arterioles
  2. Focal narrowing
  3. A/V changes
41
Q

True or false: it may be difficult to differentiate chronic HTN from normal involutional changes

A

True

42
Q

What are venous beading seen in?

A

Advanced NPDR

43
Q

What are copper wiring of vessels seen in? Why?

A

HTN retinopathy–increased arteriole pressure

44
Q

What are the two major consequences of the neovascularization of PDR?

A
  • vitreous hemorrhage

- Fibrous proliferation

45
Q

What is the worst prognostic sign of hypertensive retinopathy?

A

Disc edema

Ophthalmology (14 decks)

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