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Ocular Pathophysiology > Diabetes > Flashcards

Diabetes Flashcards

1
Q

Review
Type I Diabetes Mellitus

Pathology & treatments

A
  • Autoimmune reaction: destruction of beta cells that produce insulin
  • Peak incidence at puberty
  • Treatment: insulin, diet, exercise
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2
Q

Review
Type II Diabetes Mellitus

Pathology & treatments

A
  • Strong genetic disposition
  • Usually occurs after 30 years
  • Causes:
  • Cell receptor defect that prevents glucose uptake (! insulin receptors ineffective)
  • Decrease in insulin production from pancreas
  • Excessive glucose production from liver
  • Increased prevalence in African A, Hispanics, Native A.
  • Frequently obese
  • Treatment: diet, exercise, hypertension, oral medication
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3
Q

What questions should you ask EVERY diabetic EVERYTIME?

A
  • Last blood sugar (LBS), fasting blood sugar
  • Glycated hemoglobin (‘HbA1c’)
  • Disease duration
  • Medications (oral vs. injection)
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4
Q

What is a glycated hemoglobin test (HbA1c)

A

A blood test that indicates your average blood sugar level for the past 2-3 months. It measures the % of blood sugar attached to hemoglobin, the oxygen-carrying protein in red blood cells. The higher your blood sugar levels, the more hemoglobin you’ll have with sugar attached.

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5
Q

Values for fasting blood sugar (FBS)

A

Normal: <100mg/dl

Pre-diabetes: 100-125mg/dl

Diabetes: > or equal to 126mg/dl

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6
Q

Values for blood sugar 2 hours after meal

A

Normal: <140mg/dl

Pre-diabetes: 140-199mg/dl

Diabetes: > or equal to 200mg/dl

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7
Q

Values for HbA1c

A

Normal: <5.7%
Pre-diabetes: 5.7 - 6.4%
Diabetes: > or equal to 6.5%

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8
Q

For a person with diabetes, what is the goal fasting blood sugar (BS)?

A

80 - 130 mg/dL

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9
Q

For a person with diabetes, what is the goal blood sugar 2 hours after meals?

A

<180 mg/dL

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10
Q

For a person with diabetes, what is the goal HbA1c?

A

Less than or equal to 7.0%

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11
Q

Describe the effect diabetes has on the ocular vasculature.

A

It primarily affects microvasculature circulation. There are minimal or no changes seen in major vessels.

Remember: HTN affected large blood vessels.

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12
Q

Where are the earliest changes in vasculature noted with diabetes?

A

Capillaries

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13
Q

Describe the pathology of blood vessels that occurs with diabetes.

A
  • There is a thickening of basement membrane
  • Endothelial growth
  • Endothelium lost causing nonperfusion and loss of capillary beds
  • Damage to pericytes
  • End result is decreased oxygenation to surrounding tissue
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14
Q

What does capillary loss lead to?

A
  • Retinal ischemia

* Neovascularization

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15
Q

What are some ophthalmic changes seen with diabetes?

A
  • ** Large fluctuations in refraction
  • ** Retinopathy
  • Cranial nerve III, IV or VI palsy due to ischemia (can be seen with HTN, also)
  • Premature cataracts
  • Corneal curvature changes
  • Chronic conjunctival injection
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16
Q

What is the quintessential ophthalmic finding in undiagnosed diabetes?

A

Fluctuating refractive error

17
Q

Hyperglycemia results to lenticular changes which leads to:

A. Myopic shifts
B. Hyperopic shifts
C. A and B are correct
D. Astigmatism
E. A, B, and C are correct
A

C. Both myopic and hyperopic shifts.

  • The majority of studies show a myopic shift
18
Q

List the mechanisms that result in refractive error due to diabetes

A
  • Changes in regional refractive index
  • Lens curvature
  • Hydration
19
Q

How does myopic shift occur?

A

For a healthy lens, we need hexokinase. For a person with uncontrolled diabetes, hexokinase is not really around. Another enzyme called aldose reductase kicks in and creates sorbitol. Sorbitol pulls water into the lens, causing swelling of the lens. This tends to produce a myopic shift. It also causes a refractive index in the lens itself.

20
Q

In step form, myopic shift is caused by:

A
  1. Increase in blood sugar level
  2. Hyperglycemia
  3. Increase in osmotic pressure of the lens
  4. Increase in refractive index of the lens
21
Q

A patient with uncontrolled diabetes comes into the office. What is the long-term plan with this patient?

A
  • Educate the patient that their correction will be changing as their blood sugar level stabilizes.
  • Re-refract in 2-4 weeks AFTER stabilization
  • Refract 2-3x over a 6 week period

Temporary correction may need to be considered (e.g., contact lenses)

  • Stress the need for follow up
22
Q

Describe the pathogenesis of diabetic retinopathy

A

Note: This happens at the capillary level

  • Basement membrane thickening
  • Pericyte loss

With the above, the tight junctions allow leakage

  • Smooth muscle cell depletion
  • Vascular endothelial cell loss
  • Vascular occlusion and recanalization
  • **Neovascularization
23
Q

Name the clinical classifications of diabetic retinopathy

A

Nonproliferative diabetic retinopathy (NPDR)

Proliferative diabetic retinopathy (PDR)

24
Q

What is CSME?

A

Clinically significant macular edema.

In diabetes, this is diabetic macular edema (DME).

This can happen at any point at both NPDR or PDR.

25
Q

What is the very first sign of non-proliferative diabetic retinopathy?

A

Microaneurysms

26
Q

What are characteristic findings of non-proliferative diabetic retinopathy (NPDR)?

A
  1. Microaneurysms
    - Leaky vessels
    - Appear as focal red dots
    - Though they’re tiny, they can cause a lot of damage because they leak
  2. Intraretinal hemorrhages
    - Dot/blot type (larger than microaneurysms)
    - Found in deep retinal layers
    - Capillary damage
  3. Hard exudates
    - Lipoproteins related to elevated serum lipids
    - Vessel leakage
    - Circular “circinate” pattern
  4. Edema
    - Not necessarily at the macula
    - Retinal thickening
    - Breakdown of tight junctions between retinal vessels and RPE
  5. Cotton wool spots
    - Not as common in diabetic retinopathy (more common in HTN)
    - Due to localized ischemia
27
Q

What characterizes proliferative diabetic retinopathy?

A
  1. Neovascularization
    - Fine, new blood vessels that can develop in the:
    * Disc (NVD - neovascularization disc)
    * Elsewhere (NVE)
    * Iris (NVI)
    * Angle (NVA)
  2. Pre-retinal vitreous hemorrhage
28
Q

What is maculopathy?

A

Swelling in the macula

29
Q

What can maculopathy cause?

A

Decreased visual acuity

30
Q

What is clinically significant macular edema (CSME), a form of maculopathy, characterized by?

A
  1. Edema
    - The most common loss of vision
    - Can be measured with OCT
    - Can be reversible
  2. Ischemia and capillary damage
  3. Damage to photoreceptors
    - Damage can often be permanent
31
Q

At what point does CSME occur during diabetic retinopathy?

A. During NPDR
B. During PDR
C. At any time during DR

A

C. At any time during DR

32
Q

Name the ways diabetic retinopathy can be recorded

A
  • NPDR w/ macular edema
  • NPDR w/o macular edema
  • PDR w/ macular edema
  • PDR w/o macular edema
33
Q

Retinopathy pathophysiology: What is occurring?

A

PKC beta becomes over-activated in diabetics causing changes:

  1. Vessel leakage
  2. Endothelial damage
  3. Capillary damage
  4. Edema
34
Q

What causes microaneurysms in NPDR?

A

The pressure inside the blood vessel is too much, causing engorgement of vessels early in disease and ‘out-pouching’

Ocular Pathophysiology (4 decks)

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