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Posterior Segment > Diabetic Retinopathy > Flashcards

Diabetic Retinopathy Flashcards

1
Q

What does increased blood glucose (Diabetes) cause insulin to do? (2 things)

A

Insulin production defects
Impaired insulin action
Both

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2
Q

Who changed the criteria for diagnosis, classifications, and control guidelines of diabetes? When were the revisions published?

A

1997 International Expert Committee on Diabetes Mellitus.
Revision published in 2003

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3
Q

What are the 2 main categories of Diabetes?

A

Type 1 Diabetes: Insulin not produced at all
Type 2 Diabetes: Insulin production impaired

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4
Q

What are Islets of Langerhans? What kind of cells do they contain? What do those cells produce? How does this help us?

A

Islets of Langerhans are pancreatic cells that contain 30% alpha and 60% beta cells, and 10% other cells.

Alpha cells produce glucagon that stimulates the liver to break down glycogen into glucose and release it into the blood stream. This occurs in times of fasting when our body needs energy.

Beta cells create insulin which goes into bloodstream and helps the glucose be absorbed into the body. This occurs in times of eating.

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5
Q

What happens to in Type 1 diabetes?

A

The body’s immune system mistakes the beta cells and completely destroys them (autoimmune response). Since the beta cells are responsible for producing insulin, there will be a complete absence of insulin in the body. This can result in losing weight easily, frequent urination, and intense hunger or thirst.

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6
Q

What percent of diagnosed cases of Diabetes is Type 1 Diabetes?

A

about 5%-10%

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7
Q

What are 3 clinical symptoms for a patient who has Type 1 Diabetes?

A

1)Lose Weight easily (body isn’t able to absorb)
2)Urinate frequently (glucose needs flushed out by kidneys since its not absorbed)
3) Intense hunger or thirst (the glucose draws water out of body and is extorted)

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8
Q

What happens to in Type 2 diabetes?

A

The tissues inside your body get desensitized by the amount of insulin in the blood stream. This causes the B cells to not produce as much because they have less of a response to glucose.
“pancreatic beta cell insufficiency or insulin resistance”

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9
Q

In type 2 diabetes, is there enough insulin to prevent ketosis?

A

Yes, there is enough insulin production to prevent ketosis.

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10
Q

If an elderly patient has uncontrolled Type 2 diabetes, what is something severe that could happen?

A

Hyperosmolar non-ketotic diabetic coma.
It is caused by hyperglycemia in the blood stream, resulting in severe dehydration occasional neurological signs, lethargy, and absence of ketosis

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11
Q

For type 1 diabetes, what 2 general factors may have caused it? What are the percents?

A

Environmental (2/3)
Genetic (1/3)
T1DM is more commonly due to environmental factors.

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12
Q

What are the 3 clinical symptoms for a patient who has type 2 diabetes?

A

Frequent Urination
Intense thirst
Gaining of weight (its are usually overweight)

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13
Q

What is pre-diabetes formally known as?

A

Impaired glucose tolerance

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14
Q

Of all pregnancies, what percent of mothers acquire gestational diabetes?

A

2-10% of mothers

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15
Q

What percent of mothers will have diabetes immediately after pregnancy/postpartum?

A

5-10% of mothers

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16
Q

What percent of mothers will develop diabetes within 10-20 years after gestational diabetes?

A

35-60% of mothers

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17
Q

What does MODY stand for? What percent of cases does this make up?

A

MODY stands for “Maturity-Onset Diabetes of the Young”
It acts like type 2 diabetes but in young patients.
Makes up 1-5% of cases

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18
Q

What are 4 tests to measure a patients blood-glucose level? What 2 are we able to perform in clinic?

A

1) Random blood glucose test
2) Hemoglobin A1C
3) Fasting plasma glucose (FPG)
4) Oral Glucose Tolerance Testing (OGTT)

Random blood-glucose tests and Hemoglobin A1C tests are both able to be performed in clinic.

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19
Q

When measuring fasting plasma glucose (FPG), when are you able to make a diagnosis? How long do you have to not eat or drink before the test?

A

After two readings on separate occasions, or if the FPG reading was off the charts.
Must not eat or drink(unless its water) for at least 12 hours before the test.

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20
Q

What are the criteria for diagnosing Diabetes Mellitus? (using FPG or OGTTT)

A

1) FPG > 126 mg/dL
2) Two- hour plasma glucose > 200 mg/dl when given the OGTT after 75g glucose load.

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21
Q

What is the criteria for diagnosing Gestational Diabetes Mellitus? (using PG and glucose load)

A

When plasma glucose is greater than 2 of 4 values with OGTT after 100g load:

1) Fasting, 105 mg/dL
2) 1 hour, 190 mg?dL
3) 2 hour, 165 mg/dL
4) 3 hour, 145mg/dL

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22
Q

What is the criteria for diagnosing Pre-Diabetes? (using PG and 2-hour load)

A

1) Plasma glucose is 100-125 mg/dL after over night fast (impaired fasting glucose)

2) Two hour plasma glucose is 140-199mg/dL with the OGTT after 75g load of glucose. (Impaired glucose tolerance)

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23
Q

What is :control” of diabetes defined by?

A

Control will be defined by daily and random blood glucose monitoring.

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24
Q

What is Hemoglobin A1c used for? Is it used to make a diagnosis?

A

Hemoglobin A1c is NOT used to make a diagnosis. It is used to see how well the patient is controlled.

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25
Q

When does a patients hemoglobin A1C become problematic?

A

It becomes problematic when it is above 6%

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26
Q

When should you typically perform hemoglobin A1C on patient?

A

At least 2 hours after last meal

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27
Q

As an optometrist, when would you order an hemoglobin A1C? Who might you order it for?

A

1) when patient is showing signs of diabetic retinopathy
2) for undiagnosed diabetes

May order it for patients who arent as engaged with their care or if a diabetic patient isnt feeling well.

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28
Q

About what percent of people in the United States have pre-diabetes? What does this trend show?

A

38% or 96 million people.

This trend shows that there will be about 1/3rd of the population in the United States that has diabetes

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29
Q

Where does Diabetes rank in cause of death?

A

7th leading cause of death

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30
Q

What are 8 severe complications people may have with Diabetes Mellitus? Which of these is the leading cause of death in diabetic patients?

A

1) Heart disease - #1 LEADING CAUSE of death in diabetic patients (68%)
2) Stroke
3) Hypertension
4) Blindness
5) Kidney Disease
6) Nervous Disease
7) Amputations
8) Complications during pregnancy

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31
Q

What is the leading cause of new blindness among adults aged 20-74?

A

Diabetes Mellitus

32
Q

What percent of diabetes patients also have hypertension?

A

75% of diabetes patients also have hypertension. Caused by scarring of the kidneys which raises salt and water retention which raises BP. Also damages blood vessels which causes them to stiffen.

33
Q

Diabetes increases the chances of infection and acute complications. Why does this refer to us?

A

If the diabetic patient has something like a corneal ulcer or cataract surgery, they will have a more difficult and longer time healing than what a normal patient would have. So we must monitor them more closely.

34
Q

What signs might optometrists see in patients who have Diabetic Retinopathy? (11)

A

1) Microaneurysms
2) Dot-blot hemorrhages
3) Flame-shaped hemorrhage
4) Cotton Wool Spots
5) Edema
6) Exudate
7) Intraretinal Microvascular Abnormalities (IRMA)
8) Neovascularization

9) “Sausaging” and “loops” of veins (dilation and tortuosity like sausage)
10) Arterial narrowing (looks like silver wiring)
11) Dark dot-blot hemorrhages (larger than traditional dot-blot heme)

35
Q

When doing a fluorescein angiography on a diabetic patient, you see patches of hypoflourescent and hyperflourescent areas. What does this signify? What is hyperflourescence associated with and what can it elevate to?

A

HYPOfluorescent: Ischemic
HYPERfluorescent: leakage of blood

Since hyperfluorescence is leakage, it is associated with neovascularization. Since the patient has diabetes and now having neovascularization, it is now considered Proliferative Diabetic Retinopathy (PDR).

36
Q

What is the likely cause of visual impairment for a patient with diabetes?

A

Diabetic Maculopathy

37
Q

What are 2 ways the macula is affected by diabetes?

A

1) Edematous - swelling of macula
2) Ischemic - not receiving blood supply

38
Q

What are the 3 types of Diabetic Maculopathy?

A

1) Focal maculopathy
2) Diffuse Maculopathy
3) Ischemic Maculopathy

39
Q

What kind of maculopathy shows as well-circumscribed retinal thickening?

A

Focal maculopathy

40
Q

What is diffuse maculopathy? What is it associated with? What affect does this have when looking at the fovea?

A

Diffuse maculopathy shows as thickening of the retina due to leakage and is usually associated with Cystoid Macular Edema (CME). Since it has more severe edema, it makes it difficult to observe the macula and are unable to see the foveal light reflex.

41
Q

What happens with ischemic maculopathy? What findings are there?

A

Macula is non-perfused (indicates end-stage diabetic disease)
Expansion of the Foveal avascular zone (ischemic both superficial and deep capillary zones)
Poor VA (likely will lose vision)

Findings: No findings. Macula may look normal, no hemorrhages, CWS, exudate because there is no blood leakage from significant ischemia.

42
Q

What is another name for Clinically Significant Macular Edema (CSME)?

A

Diabetic macular edema (DME)

43
Q

What 3 things would indicate Clinically Significant Macular Edema (CSME) (AKA diabetic macular edema (DME)? What stage of diabetic retinopathy do these occur in?

A

1) Retinal Thickening within 500 micrometers from the center of the fovea

2) Exudate within 500 micrometers from the center of the fovea with adjacent thickening (indicates edema has been there a while)

3) Thickening of at least one disc diameter section that is one disc diameter away from the center of the fovea

Can occur in ANY stage of diabetic retinopathy.

44
Q

Does Clinically significant macular edema (diabetic macular edema) affect vision?

A

Yes it has the potential to cause sever loss of vision, HOWEVER, some patients can also have completely normal vacuity so we are not able to use Acuity as a gauge for Diabetic Macular Edema (DME)

45
Q

What does DCCT stand for?

A

Diabetes Control and Complication Trial

46
Q

Who is more likely to have diabetic retinopathy? Type 1 diabetics or type 2?

A

Type 2 diabetics are more likely because type 1 have been controlling their diabetes from very early in their life so they usually manage it better.

47
Q

According to the DCCT study, What percent of type 1 diabetics will have retinopathy 10 years after their diagnosis?

A

50%

48
Q

According to the DCCT study, What percent of type 2 diabetics will have retinopathy 10 years after their diagnosis?

A

95%

49
Q

The DCCT and EDIC study showed that Intense blood glucose control reduces the risk of eye disease by ____.

A

76%

50
Q

For the DCCT and EDIC study, what was considered “Intense treatment (IT)” for diabetes? What were the results?

A

Intense treatment: check blood sugar 4 times a day, inject insulin 3 times/day, strict diet and exercise program, seeing PCP monthly.

Found to reduce development and progression of all diabetic complications, reduces atherosclerosis and CVD events. Most effective early in disease so the disease doesn’t have a snowball effect.

51
Q

What are the 2 major factors in the pathogenesis of microvascular complications?

A

1) Chronic hyper-glycemia
2) Disease duration

52
Q

What was the Early Treatment Diabetic Retinopathy Study (ETDRS) testing? What things can we take away from this study?

A

Study was focused on the results of photocoagulation (focal and grid) for vision loss due to CSME/diabetic macular edema. Also tested other things like aspirin, timing of laser use, PRP use.

Results:
-photcoagulation stabilizes visual acuity but does NOT improve it
-should be avoided in presence of significant loss of perifoveal capillaries (from ischemia)
-may take months to show resolution of thickening and resolution of exudates (if it ever occurs)
-Aspirin didn’t make it worse, didn’t make it better
-PRP is not helpful, can even make it worse

53
Q

What is the Standard for Care for diabetic macular edema?

A

Laser Photocoagulation

54
Q

What is the treatment of choice for diabetic macular edema in Memphis?

A

Anti-VEGF treatment

55
Q

What does a focal treatment consist of when treating diabetic retinopathy? What is the spot size?

A

Argon laser photocoagulation.
-Applied to active microaneurysms in the center of the circinate rings.
-Be at least 500-3000 microns away from the center of the macula(scar can enlarge, dont want to go into visual axis)
-Burns are only 50-100 microns in size with 0.1 second of exposure.

56
Q

What does a grid treatment consist of when treating diabetic retinopathy? How big is the spot size?

A

Argon laser applied to diffuse retinal thickening 500 microns from the center of the macula and 500 microns from temporal margin of the optic nerve.
Spot size is 100 microns for 0.1 second.

57
Q

What is mild Non-proliferative Diabetic Retinopathy characterized by? (4)

A

1) Micro-aneurysms
2) Occasional hemorrhage (usually dot blot, may only have 1 but still classifies as NPDR)
3) Occasional exudate
4) Possible Clinically Significant Macular Edema (can happen at any stage of diabetic retinopathy)

58
Q

What is different between mild and moderate Non-Proliferative Diabetic Retinopathy?

A

-Moderate has increased number and size of intra-retinal hemorrhages
-Increased evidence of exudate
-Capillary Occlusive Disease (cotton wool spots, neovascularization)
-Clinically significant macular edema still applies here

If you see cotton wool spots, immediately think moderate instead of mild.

59
Q

What is the 4-2-1 rule for Severe Non-proliferative Diabetic Retinopathy? How many must it fulfill?

A
  1. Severe retinal hemorrhage in 4 quadrants
  2. Venous beading in 2 quadrants
  3. IRMA in 1 quadrant

Must fulfill only 1 of these to be considered SEVERE.

60
Q

If a patient has Sever non-proliferative diabetic retinopathy, what are the odds of that patient developing proliferative within a year?

A

50% risk

61
Q

When does non-proliferative become proliferative diabetic retinopathy?

A

When neovascularization occurs. (NVD, NVE, NVI, vitreal hemorrhage)

62
Q

Neovascularization that develops on the optic nerve or within one disc diameter of the optic nerve.

A

Neovascularization of the disc (NVD)

63
Q

Neovascularization anywhere in the fundus that is not NVD, usually around vessels.

A

Neovascularization elsewhere (NVE)

64
Q

Where does neovascularization elsewhere develop?

A

Between perfused and non-perfused retinal tissue

65
Q

What kind of neovascularization development is a threatening sign for Neovascularization glaucoma?

A

Neovascularization of the Iris (NVI)

66
Q

What 2 kinds of neovascularization can cause a vitreal hemorrhage?

A

1) Neovascularization of the disk (NVD)
2) Neovascularization of elsewhere (NVE)

67
Q

How can people with proliferative diabetic retinopathy be at risk for retinal detachment?

A

With neovascularization, the new vessels can become more fibrous, and it can shrink in size which pulls on the retina, possibly causing a vitreal detachment.

68
Q

According to Diabetic Retinopathy Study (DRS), What are the 3 scenarios that would require a patient to have a PRP?

A

1) NVD >1/3 to 1/4 of disc area (2-3 clock hours)
2) Any NVD with associated with Vitreal Hemorrhage
3) Any NVE with associated Vitreal Hemorrhage

69
Q

If you see a virtual hemorrhage in a diabetic, you know it is proliferative because?

A

The neovascularization(NVD and NVE) is most likely what caused the vitreal hemorrhage.

70
Q

High risk characteristics (HRC) treated with PRP had a _____ decrease in severe vision loss.

A

50%

71
Q

Why do we wait until 2-3 clock hours of disk is affected before using PRP? How does PRP work?

A

Because PRP is very destructive so you wouldn’t want to use it unless you had to.
-PRP destroys healthy functioning retina to reduce oxygen demands so VEGF will be reduced thus reducing neovascularization.

72
Q

Does PRP improve visual acuity?

A

No. It may make it worse. If the damage leads to inflammation, it could cause Cystoid macular edema (CME).

73
Q

Possible complications from PRP (4)

A

1) May make vision worse
2) May cause or worsen macular edema/ CME
3) Will likely lose peripheral vision and night vision
4) Will not always cause NVE or NVD to regress

74
Q

In DRCR.net, Protocol B (laser vs. triamcinolone), what worked better over time? What worked better initially?

A

Laser worked better over time and had fewer side effects. Steroid (triamcinolone) worked better initially most likely due to anti-inflammatory components

75
Q

In DRCR.net, Protocol I (Lucentis for DME with delayed laser vs after laser), what worked best?

A

Lucentis worked best when you did it before laser because you still have normally functioning RPE which let it work more.
Also showed that Triamcinolone in pseudophakic (fake lens) was as good as Lucentis.

76
Q

In DRCR.net, Protocol T (Lucentis vs. Avastin vs. Eylea), what worked best? What else did they find?

A

-Eylea worked better in patients that were 20/50 or worse.
-No difference between Lucentis and Eylea after the year 2 mark, but both still better than Avastin.

77
Q

In the READ clinical trial (Ranibizumab(Lucentis) vs Standard of care (photocoagulation) vs Both), what can we conclude? What was the mean gain in letters after 6 months for Ranibizumab only?

A

0.5 mg of Ranibizumab (Lucentis) by itself had better results than photocoagulation and photocoagulation + Ranibizumab.

Mean gain of 7.2 letters after 6 months using Ranibizumab alone.

Posterior Segment (6 decks)

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