Diabetic Retinopathy Flashcards

1
Q

NPDR definition

A

intraretinal vascular changes, no development of extraretinal fibrovascular tissue. Used to be known as NPDR

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2
Q

PDR

A

presence of retinal neovascularization from diabetes induced ischemia. Characterized as early PDR or PDR with high risk characteristics (HRC)

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3
Q

DME

A

caused by abnormal vascular permeability

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4
Q

Factors that lead to diabetic damage

A
  1. endothelial damage
  2. pericyte loss
    this happens from exposure to hyperglycemia leads to:
    -increased inflammatory oxidative stress
    -advanced glycation end products, and protein kinase c pathways

BM thickening and pericyte loss lead to:
Capillary occlusion and retinal nonperfusion

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5
Q

Consequences of endothelial barrier decompensation

A

retinal edema (serum leakage)

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6
Q

Recommended Diabetes follow up

A

Type 1 DM: 5 years after dx
Type 2 DM: immediately upon diagnosis
Pregnant with either DM: soon after conception and early in first trimester. FU every 1-3 months if severe NPDR or worse

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7
Q

What did the Diabetes control and complications trial (DCCT) and UK prospective diabetes study (UKPDS) show?

A

Intensive glycemic control was associated with:

  • reduced risk of new onset retinopathy
  • reduced progression of existing retinopathy

DCCT looked at type 1, UKPDS looked at type 2

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8
Q

What is metabolic memory

A

in the DCCT, patients who had intensive glycemic control in the beginning had decreased onset, progression, and need for surgery even 20 years after the study ended and the HbA1c levels converged.

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9
Q

What A1c is recommended based on DCCT and UKPDS?

A

less than 7

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10
Q

What did the ACCORD and ACCORDION study show?

A

A1c levels less than 6 slowed DR progresison even more in T2DM, but increased mortality

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11
Q

What other factors are associated with DR

A
  • HTN
  • severe carotid artery occlusive disease (part of ocular ischemic syndrome)
  • Advanced diabetic nephropathy
  • Anemia
  • cholesterolemia
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12
Q

How does DR lead to vision loss?

A

capillary leakage (DME)

  • capillary occlusion (macular ischemia)
  • sequelae from retinal ischemia (neo, vit heme, TRD, NVG)
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13
Q

What to do in DM patients who need CE/IOL

A

If DME, give anti-vegf

If severe NPDR or PDR, consider scatter PRP before cat removal.

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14
Q

NPDR damage

A

Dmg stays within ILM:

  • MAs
  • intraretinal hemorrhage
  • CWS
  • venous beading
  • IRMA
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15
Q

Criteria for Severe NPDR

A

4-2-1 rule:

  • 4 areas of MAs
  • 2 areas of venous beading
  • 1 area of IRMA
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16
Q

Severe NPDR vs Very severe NPDR

A

severe NPDR has 1/3 of 4-2-1 rule. Severe npdr has a 15% risk of progression to PDR in 1 year and 60% in 3 years.

Very severe has 2-3/3. Has a 45% risk of progression in 1 year

17
Q

Signs of macular ischemia

A

FAZ appears irregular on FA or OCTA and enlarges as the innermost capillaries become nonperfused

18
Q

Treatment of NPDR

A

There is no clear treatment mandate for eyes with NPDR wo DME (besides control of glucose, lipids, and HTN)

Anti-vegf, lasers, and steroids have shown NPDR levels

PVDs have been hypothesized to improve outcomes in diabetic eyes bc it takes away the scaffolding for NV

19
Q

Extraretinal fibrovascular proliferation progression

A
  1. New vessels with minimal fibrous tissue cross and extend beyond ILM
  2. New vessels get larger and become more fibrous
  3. vessels regress, leaving residual fibrovascular tissue that may be tethered in posterior hyaloid
20
Q

high risk PDR

A
  1. NVE w heme
  2. NVD w heme
  3. NVD that is 1/4-1/3 in size
21
Q

Possible draw back of treatment of PDR

A

treatment with PRP or anti vegfs may lead to contraction of fibrovascular tissue, and treatment may be followed by increased VR traction, vit heme, TRD, or combined TRD RRD

22
Q

DRCR.net protocol S

A

Showed that ranibizumab and prp had EQUAL VISUAL OUTCOMES

Rani had benefits of:

  • better average vision
  • reduction in peripheral visual field loss
  • reduced rates of sx
  • less DME
23
Q

Anti vegf in PDR

A

Given before vitrectomy, can help treat NVG

24
Q

Steroids in PDR

A

reduce PDR related outcomes in DR.

Rates of vit heme, need for prp, rates of NV are reduced when steroids are used for non PDR indications like DME

25
Q

PRP treatment is based on what study?

A

DRS (looked at if PRP was effective for treating DR)

26
Q

How does PRP help?

A
  1. destroys ischemic retina which produced growth factors
  2. Increases o2 tension by:
    - destroying retina which increases diffusion of O2 from choroid through scarring
    - decreases retina, which decreases o2 consumption
27
Q

How did DRS and ETDRS define full PRP?

A

1200 shots more than 500micrometers separated by 1/2 burn width

28
Q

What are adverse effects of PRP?

A
1. choroidal detachment
2 decreased night vision
3 color vision
4 contrast sensitivity
5 peripheral vision
6 pupillary dilation
7 increased glare
8 you may hit the long ciliary nerve and vessels which control pupillary accommodation and corneal innervation
29
Q

NVI/NVG

A

small tufts of NV at the border are relatively common, tx can be withheld in these eyes

Treat when there is contiguous NV of pupil and iris collarette w/wo NVA.

Tx is PRP. IVA can be used to temporize

30
Q

Diabetic retinopathy vitrectomy study

A

T1DM w severe VH benefitted from earlier vx.

while type 2 didn’t