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Disease 2B > Diabetic Retinopathy > Flashcards

Diabetic Retinopathy Flashcards

1
Q

what “regulates capillary blood flow and line the capillary endothelium”?

A

pericytes

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2
Q

what is glucose attached to amino group of proteins

A

glycation end products (AGEs)

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3
Q

what is sugar alcohol that is slowly metabolized by the body

A

Sorbitol

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4
Q

Aldose Reductase converts

A

glucose to sorbitol

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5
Q

glucotoxicity can lead to damage in every system of the body but the main ones are

A

nerves, retina, and kidneys

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6
Q

2 main things that happen in the retina secondary to diabetes:

A

hypoxia and edema

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7
Q

how to AGEs play a role in diabetic retinopathy?

A
  • lead to disruption of the signals between proteins which leads to apoptosis of endothelial cells
  • increase the amount of VegF
  • cause damage to pericytes
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8
Q

what role does sorbitol play in diabetic retinopathy?

A

increase in sorbitol leads to basement membrane thickening and pericyte loss
-also plays role in cataract formation in diabetics

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9
Q

what has protein C been found to cause?

A
  • pericyte apoptosis
  • increase in VegF
  • change blood flow
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10
Q

protein kinase C is activated by

A

blood sugar

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11
Q

what changes to platelet adherence and RBC change occur in diabetic ret and what does that cause?

A

increase in platelet adherence and RBC change shape leads to increase in thickness of blood flow as well as thickening of blood vessels and decrease in the ability of red blood cells to release/ carry oxygen

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12
Q

how does oxidative stress contribute to diabetic ret?

A

overproduction of free radicals leads to blood vessel damage and pericyte loss

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13
Q

retinal capillary cell death and dropout leads to what “end result”:

A

hypoxia and breakdown of blood-retina barrier

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14
Q

what does loss of pericytes (along the endothelium of the capillaries) lead to?

A

weakening of capillary walls and loss of capillary endothelial cells

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15
Q

thickening of the basement membrane occurs due to:

A

proliferation of endothelial cells into the lumen of the vessels which further lead to hypoxia

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16
Q

what type of perfusion starts the process of diabetic ret and what leads to further damage?

A
  • hypoperfusion (hypoxia) starts the process of diabetic ret

- hyperperfusion leads to further vessel damage/progression

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17
Q

if diagnosed with diabetes before the age of 30, ___ % will develop retinopathy after 15 years but

if diagnosed with diabetes after the age of 30, ___ % will develop retinopathy after 15 years

A

97%

78%

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18
Q

1 risk factor to get diabetic ret is:

A

duration of diabetes

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19
Q

type 1 diabetes: __ % of patients will develop proliferative diabetic ret after 20 years

type 2 diabetes: __ % of patients will develop proliferative diabetic ret after 20 years

A

50%

10%

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20
Q

list of risk factors for diabetic retinopathy

A

puberty, kidney problems (check BUN, proteinuria, serum creatinine, GFR), hypertension, high cholesterol, pregnancy, genetics, ocular inflammation, sleep apnea, smoking

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21
Q

protective factors for diabetic ret

A

improving overall health issues, diet/exercise, glaucoma, myopia > -5D, carotid artery stenosis (if mild), optic atrophy, chorio-retinal scars

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22
Q

why can glaucoma be a protective factor for diabetic ret?

A

loss of ganglion cells and nerve fiber layer leads to a decrease in metabolic activity. decrease in perfusion secondary to increase in IOP

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23
Q

why is myopia a protective factor for diabetic ret?

A

longer axial length leads to retinal thinning. there is also a loss of retinal and choroidal blood flow, vessel thinning, and attenuation. PVDs are also more common and occur more quickly in myopes

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24
Q

which type of carotid artery stenosis is actually worst for diabetic ret?

A

severe: actually leads to an increase in ischemia especially if the patient already has later stages of diabetic ret

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25
Q

recent study: reducing blood sugar/Hba1c in Type 1 diabetics over a long period of time leads what reductions in getting diabetic ret and progression?

A

76% reduction in getting it

54% reduction in it progressing

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26
Q

does doxycycline show ant benefit to diabetic ret patients

A

does not appear to improve retinal function or slow progression in patients with mild to moderate NPDR

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27
Q

what are the benefits to put diabetic pt on a “Pril” drug such as Lisinopril?

A

reduced progression of diabetic ret by 50% and reduced progression of proliferative diabetic retinopathy by 80%

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28
Q

are NSAIDs used in diabetic ret?

A

may help (?) with inflammation in posterior set which may reduced chances of getting diabetic ret or progression of diabetic ret

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29
Q

what type of refractive error shifts can occur in diabetes

A

both hyperopic and myopic shifts have been associated with diabetes
(changes in thickness of lens, curvature, cortex, or milky NSC)

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30
Q

what Hb1ac and FBS is considered stable?

A

< 7.5% or FBS 180

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31
Q

what are you looking for on EOMs with diabetics?

A

CN palsies especially CN6- (esotropia seen)

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32
Q

4 pertinent negatives to note in diabetics chart

A

(-) NVI- iris
(-) NVD- disc
(-) NVE- elsewhere
(-) CSME- clinically significant macular edema

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33
Q

what is the size of what you see in the slit lamp in a 78D and 90D lens

A

78D- 1.2x

90D- 1.33x

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34
Q

the DCCT shows that control of blood sugar decreases development and progression by:

A

development by 76%

progression by 80%

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35
Q

tight control of BP leads to what % decrease in progression of retinopathy? what is considered tight control?

A

34% decrease in progression of retinopathy and vision loss

< 130/80 or <120/75 (if pt has renal damage)

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36
Q

how can cholesterol and exudates affect diabetic ret?

A

increase in cholesterol= increase in exudates

-there is a 50% increase in progression of ret if total cholesterol > 240

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37
Q

what is the mechanism behind the use of lasers for diabetic ret treatment

A
  • increase in proliferation of RPE cells
  • reestablishment of blood-retina barrier
  • seals off leaky vessels
  • decrease in oxygen demand
  • increases proliferation of end cells in retinal capillaries
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38
Q

focal laser is defined as

A
  • focal treatment

- 50-100 microns in size

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39
Q

grid laser is defined as

A
  • diffuse treatment
  • 100-200 microns in size
  • 1DD apart
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40
Q

pan retinal photocoagulation is defined as

A
  • large diameter (500 microns in size)
  • usually 1000-2000 spots
  • placed in mid-periphery
  • nasal or inf retina usually first
  • always treat CSME first
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41
Q

pan retinal photocoagulation is specifically for

A

retinal neovascularization

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42
Q

how does PRP work?

A
  • decreasing need for oxygen which decreases hypoxia which decreases Veg-F which makes regress
  • destroys retina and prevents further release of pro-angiogenic factors
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43
Q

what should always been done before PRP?

A

focal/grid laser

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44
Q

where is PRP usually done first and why?

A

nasal or inferior retina first because it is less likely to cause macular edema

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45
Q

what is the typical follow up plan for PRP

A

f/u 4-6 weeks b/c 50% of pts will show regression at this time
if neo regressed- f/u again in 3 months
if not- continue with more laser

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46
Q

where should PRP not be done?

A

not be done within 2DD of the macula and 500 microns from the nasal aspect of the nerve

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47
Q

what vision changes may happen after PRP? does VA improve?

A
  • VA does not improve
  • loss of peripheral vision
  • decrease in night vision
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48
Q

what other side effects can come from PRP?

A
  • can make macular edema worse
  • atrophic creep (if done by macula/nerve)
  • vitreous heme
  • Neo may not regress/may need multiple treatments
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49
Q

how it VegF increased?

A

retinal hypoxia

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50
Q

what does VegF lead to?

A

breakdown of blood-retinal barrier and neovascularization

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51
Q

list 4 antiVegF drugs used

A
  • Macugen
  • Lucentis
  • Avastin
  • Eyelea
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52
Q

Microaneurysms (MA) is caused by:

A
  • weakness of capillary walls

- focal enlargement of capillary walls/outpouching

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53
Q

what is the earliest sign of diabetic ret

A

Micro-aneurysms

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54
Q

what is the treatment for ciliochoroidal effusion (fluid in between sclera and choroid) ?

A

vitrectomy or ILM strip

55
Q

in what layer(s) are dot and blot hemes located?

A

inner nuclear layer and outer plexiform layers

56
Q

what is the difference in appearance between dot and blot hemes

A

dot: small, distinct
blot: large, fuzzy borders

57
Q

hemes resolve in about

A

3 months

-absorbed

58
Q

list of the 5 different types of hemes

A
  • sub-retinal
  • sub-RPE
  • intra-retinal
  • pre-retinal
  • intra-vitreal
59
Q

heme that is between RPE and sensory retina

A

sub-retinal

60
Q

heme that is below RPE (more in choroid)

A

sub-RPE

61
Q

heme that is within retina (above photoreceptors, below ILM)

A

intra-retinal

where dot/blot hemes are

62
Q

heme that is below post hyaloid face but above ILM

A

pre-retinal

63
Q

heme that is in vitreous cavity

A

intra-vitreal

64
Q

what hemes are from larger pre-capillary arterioles and thus are located in the retinal nerve fiber which is not compact. blood is able to spread horizontally

A

flame

65
Q

what hemes are from the venous end of the capillaries and thus are located in the more compact inner nuclear/outer plexiform layer (confinement is a result of adjacent retinal cells)

A

dot/blot

66
Q

when do flame hemes resolve vs. dot/blot hemes?

A

flame hemes- 6 weeks

dot/blot- 3 months

67
Q

what are 2 things that may help differentiate if the flame heme is from diabetes vs. hypertension?

A

any vessel changes (A/V ratio that is smaller than 2/3) or more cotton wool spots than hemes are indicative of hypertension

68
Q

what is the criterion for moderate non-proliferative diabetic ret

A
  • increase in dot/blot (mod in 4 quads or severe in 1 quad)
  • MAs
  • cotton wool spots
  • venous beading (less than 2 quads)
  • IRMA (mild)
  • vascular loops/omega loops
69
Q

what is the risk for developing proliferative diabetic ret in 1 year if you have MODERATE non-proliferative?

A

12-27%

70
Q

f/u for mild non-proliferative

A

6-12 months

71
Q

f/u for moderate non-proliferative

A

3-6

72
Q

f/u for moderate non-proliferative

A

3-6 months

73
Q

what are cotton wool spots? what can they cause clinically?

A

RNFL infarct which leads to blockage of axoplasmic flow. after resolution of CWS, there is atrophy of ganglion cell and nerve fibers which leads to a “depression” sign VF defect

74
Q

what does venous beading look like and what causes it?

A

looks like sausaging

-due to weakening of blood vessel walls and sludging of blood

75
Q

what is IRMA (intra-retinal microvascular abnormalities)? what layer is it located in?

A

new blood vessel growth from existing blood vessels vs. remodeling of pre-existing vessels which shunt blood over non perfused areas (at level of sensory retina)

76
Q

how do you differentiate IRMA and neovascularization?

A
  • IRMA is intra-retinal and it doesn’t really leak on the FA
  • Neo forms more of a reticular network than IRMA
  • Neo goes across both arteries and veins
  • Neo usually has fibrovascular proliferation associated with it
77
Q

what is the 4:2:1 rule for severe non-proliferative?

A

-4 quadrants of hemes
-2 or more quadrants of venous beading
-1 moderate-severe IRMA
(1 item severe, 2 items very severe)

78
Q

f/u for severe non-proliferative?

A

1 month

79
Q

what is the risk for developing proliferative diabetic ret in 1 year if you have SEVERE non-proliferative?

A

52%

80
Q

what is the BEST indicator for potential proliferation?

A

venous beading

81
Q

proliferative diabetic ret means you have one of what things?

A

NVD, NVE, NVI, NVA, pre-retinal hemorrhage, vitreal hemorrhage

82
Q

what areas does neo grow towards?

A

towards the posterior hyaloid surface of the vitreous and towards areas of capillary non-perfusion

83
Q

_____ is the process of growing new blood vessels

A

angiogenesis

84
Q

what are neo vessels like and what can they lead to?

A
  • they are weak and leak
  • they carry fibrotic tissue (increases risk of fibrovascular proliferation)
  • leaky vessels along the posterior hyaloid face leads to early liquefaction of the vitreous (PVD)
85
Q

4 step process of neo

A
  1. stimulus: hypoxia, cyokines (increase with inflammation)
  2. Veg-F released (vascular endothelial cell growth)
  3. Veg-F binds to receptors on blood vessels that are nearby the initial stimulus
  4. new blood vessels develop towards the source of the signal
86
Q

what is the specifications for NVD?

A

within 1DD of the optic nerve

-usually arises from large veins

87
Q

where does NVI usually start on the iris?

A

pupillary ruff

88
Q

specifications for classification Proliferative Diabetic Ret (LOW RISK)

A
  • NVD less than 1/3 the size of the disc

- NVE less than 1/2 the size of the disc

89
Q

follow up and treatment for Proliferative Diabetic Ret (LOW RISK)

A

-consult in 1-2 weeks
-treatment anti-VegF and PRP
(vitrectomy also considered)

90
Q

specifications for classification Proliferative Diabetic Ret (HIGH RISK)

A
  • NVD more than 1/3 the size of the disc
  • NVE more than 1/2 the size of the disc
  • any amount of NVD or NVE with a vitreal hemorrhage or a pre-retinal heme
91
Q

follow up and treatment for Proliferative Diabetic Ret (HIGH RISK)

A

-consult in 24-48 hours
-treatment anti-VegF / PRP
(vitrectomy also considered)

92
Q

what are collateral vessels?

A
  • vessels develop within the retina vascular framework to join obstructed to non-obstructed vessels (pre-formed capillaries)
  • not new vessels
  • thin vessels but not as tortuous as neo
  • no leakage on FA
93
Q

what affect do collateral vessels have on neo?

A

they actually help reduce the amount of neo

94
Q

what are the 3 types of collateral vessels

A
  • A to A
  • V to V
  • A to V
95
Q

optociliary shunt vessels are connections between:

A

central retinal vein and the peri-papillary choroidal veins

96
Q

when do optociliary shunt vessels show up? what do they look like?

A
  • occurs when retinal venous circulation is compromised
  • does not leak
  • thick
97
Q

what other conditions can optociliary shunt vessels show up in?

A
  • chronic glaucoma
  • CRVO
  • optic nerve sheath menangioma
  • papilledema
  • optic nerve gliomas
  • disc drusen
98
Q

what is the most common cause of decrease in vision in patients with diabetic retinopathy?

A

clinically significant macular edema

99
Q

why does CSME occur?

A

breakdown of blood-retina barrier leads to leakage of plasma and exudates (lipoproteins) from small retinal vessels in the macula (especially the capillaries)

100
Q

what is the appearance of CSME

A

circinate ring with exudates on the outside and leakage in the middle

101
Q

3 criteria for CSME

A
  1. retinal thickening at or within 500microns (1/3DD) of the center of the macula
  2. exudates at or within 500microns (1/3DD) of the center of the macula with retinal thickening (b/c exudates can be present without any active edema)
  3. retinal thickening greater than 1DD in size within 1DD of the center of the macula
102
Q

treatment options for CSME

A
  • retina consult within 2 weeks
  • controlling blood sugar (decreases risk of edema by 46%)
  • focal/grid laser
  • anti-VegF
103
Q

does treatment for CSME improve VA?

A

stabilizes VA but doesn’t really improve it

104
Q

for treatment of CSME, what did the READ-2 Study, RESTORE study, and BOLT study conclude?

A

antiVegF gold standard w/best outcomes or can be combined with laser- only downside is antivegF may need to be repeated more

105
Q

what is an alternative treatment for CSME and what are the potential risks?

A

steroids for edema (for inflammatory component) such as Iluvien intravitreal implant, has risk for increased IOP and secondary glaucoma

106
Q

what do you see on an OCT of CSME

A
  • cystic spaced
  • sub-retinal fluid
  • decrease in reflectivity of RPE
  • hyperreflective exudates
107
Q

what is the difference in appearance between micro and macro aneurysms

A

macro are much larger, thicker, and irregular, has non-homogenous contents and typically surrounding edema and exudates will be present

108
Q

what is the appearance of focal laser scars?

A
  • absence/thinning of the retina
  • photoreceptor/RPE loss
  • increased reflectivity of the choroid and sclera
109
Q

OCT appearance of exudates and

what can exudates lead to?

A
  • hyper-reflective areas at the level of the OPL/ONL
  • isolated and clustered
  • posterior shadowing
  • can eventually lead to fibrotic scarring and loss of retinal structures
110
Q

OCT appearance of neovascularization and where does it start going/ eventually grow to?

A

hyper-reflective, fibrovascular formation along the ILM

-starts developing in the inner retina and will eventually grow into the vitreous (will become elevated)

111
Q

OCT appearance of cotton wool spots

A
  • superficial hyper-reflective nodule at the level of the RNFL
  • can be fusiform
  • posterior shadowing “screen effect”
112
Q

what can cotton wool stops look similar to (but can be differentiated with an OCT)

A

myelnated RNFL

113
Q

OCT appearance of intra-retinal hemorrhages

A

rarely visible on scan due to low reflectivity

114
Q

OCT appearance of pre-retinal hemorrhage

A
  • hyper-reflective

- posterior shadowing

115
Q

FA appearance of dot/blot hemes

A

dark (hypo)

116
Q

FA appearance of micro aneurysms

A

lighted dot with adjacent mild hyper fluorescence (leaky slightly around adjacent tissue)

117
Q

FA appearance of leakage/ neo

A

hyper fluorescence increases (both in size and frequency) as the phases get later

118
Q

FA appearance of cotton wool spots

A

dark areas (hypo) due to non-perfusion

119
Q

FA appearance of capillary non-perfusion/ ischemia

A

dark areas

120
Q

FA appearance of IRMA

A

no leakage or little leakage (not as much as neo)

121
Q

is tractional RD non-rhegmatogenous or rhegmatogenous

A

non

122
Q

list some things fibrovascular tissue can lead to

A
  • dragging.distortion of the macula and optic nerve
  • tractional retinal detachment
  • vitreal hemorrhages
  • macular hole
  • retinal tears
123
Q

pre-retinal hemorrhage (sub-hyaloid):

  • what layer
  • what appearance
  • what type of patient
A
  • in b/w ILM and posterior hyaloid face
  • boat shaped appearance inferiorly or linear streak superiorly
  • usually in younger patients
124
Q

vitreal hemorrhage (intra-vitreal):

  • what causes it
  • what do they look like if old
  • outcomes/ treamtment
A
  • caused by neo growing into vitreous and hemorrhaging
  • old ones turn brown or white and sink to bottom
  • poor vision
  • tx: anti-veg-F, vitrectomy (next option)
125
Q

what are some indications for a vitrectomy?

A
  • non-clearning vitreous heme with anti-VegF treatment
  • tractional RD
  • dense pre-retinal heme
  • severe PDR
  • tractional macular edema
  • progressive neo despite full PRP
  • pre-retinal heme over macula
126
Q

complications and f/u for vitrectomy:

A
  • complications: endophthalmitis, cataract, RD, corneal decompensation
  • f/u: 1 day, 1 week, 1 month, 3 month, and frequent DFEs
127
Q

treatment for angle closure

A
  • cycloplegia 1% BID
  • topical steroids
  • dilate: decrease IOP by increasing outflow through uveo-scleral pathway
  • glaucoma drops (except pilocarpine and prostaglandins)
  • PRP/ anti-Veg-F
  • bleb/shunt
128
Q

what can make macular ischemia worse

A

lots of laser in that area

129
Q

what does capillary non-perfusion look like on OCT

A

-disorganization and thinning of the inner retina
-outer retina typically intact
(dark- areas without capillaries)

130
Q

what is a form of non-AION that is has mild optic nerve head edema, prominent surface vessels with fine hemorrhages on the disc, and with a small APD present

A

diabetic papillopathy

131
Q

what were roth spots believe to be from and what is it believed to be currently

A
  • initially thought to be bacterial emboli or leukocytes
  • white center represents coagulated fibrin thrombus from a ruptured vessel
  • represents more of an acute systemic change
132
Q

what are some systemic causes of roth spots

A
  • bacterial endocarditis
  • leukemia
  • anemia (pernicious usually)
  • HIV (rarely)
  • carbon monoxide poisoning
  • hypertensive retinopathy
  • shaken baby syndrome
  • sickle cell
  • lupus (or other connective tissue disorders)
133
Q

when is diabetic ret involutional

A

“they have it but not active”

  • decrease in the caliber of vessels
  • fibrovascular proliferation
  • ghost vessels

Disease 2B (4 decks)

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