Diabetic Retinopathy Flashcards

1
Q

Explain the pathology of microvascular complications.

A

Thickening of the capillary and arteriole basement membrane is the cardianl feature of microvascular complications.

The small vessels become progressively narrower and they will eventually become blocked.
This leads to ischaemia and tissue dysfunction.

The tissues that are damaged by hyperglycaemia are those that have high blood flow and cannot down-regulate glucose uptake.

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2
Q

Explain the formation of advanced glycation end products (AGE).

A

When some proteins are exposed to increased glucose the glucose will bind irreversibly and cause an advanced glycation end product called AGE.

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3
Q

Give an example of AGE.

A

HbA1c.

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4
Q

Consequences of formation of AGEs.

A

They cause tissue injury and inflammation via stimulation of pro-inflammatory factors, such as complement and cytokines.

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5
Q

Explain hyperglycaemia and the sorbitol-polyol pathway.

A

When there is excess glucose, the glucose is metabolised to sorbitol via the polyol pathway.

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6
Q

Issues with increased orbitol and fructose via the sorbitol-polyol pathway.

A

The accumulation of sorbitol and fructose causes changes in vascular permeability, cell proliferation and capillary structure.

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7
Q

Explain abnormal microvascular blood flow in hyperglycaemia.

A

Along with hypertension endothelial damage occurs and vasoconstrictors such as endothelins and thrombogenesis can lead to microvascular occlusions.

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8
Q

Growth factors and cytokines in diabetes.

A

Due to the increased expression of protein kinase C mitogenic cytokines and growth factors including TGF-beta, tumour necrosis factor and vascular endothelial growth factor (VEGF) are upregulated.

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9
Q

Explain the growth hormone-insulin-like growth factor axis in diabetes.

A

Reduction in portal insulin concentrations impairs the ability of growth hormone to generate IGF-1 in the liver.

This leads to growth hormone hypersecretion by the pituitary gland.

Which in its turn can cause microvascular complications.

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10
Q

What is the most common diagnosed diabetes-related complication?

A

Diabetic retinopathy

Affects around one third of all people with diabetes.

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11
Q

What are the earliest changes in the retina in diabetic retinopathy called?

A

Non-proliferative or background retinopathy.

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12
Q

What are the retinopathy grades of the peripheral retina?

A

Non-proliferative (R1)

Pre-proliferative (R2)

Proliferative (R3)

Advanced retinopathy

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13
Q

What is central retinopathy called?

A

Maculopathy

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14
Q

What retinal abnormalities can be seen in non-proliferative/background retinopathy (R1)?

A

Dot haemorrhages (microaneurysms)

Blot haemorrhages

Hard exudates (lipid deposits)

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15
Q

Expain dot aneurysms/haemorrhages.

A

Damage to the wall of small vessels causes microaneurysms within the retina.

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16
Q

Explain blot haemorrhages.

A

When the vessel walls are breached, superficial (blot) haemorrhages occur in the ganglion cell and outer plexiform layers.

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17
Q

Explain the hard exudates.

A

When the fluid is cleared into the retinal vessels from the blot haemorrhages, proteins and lipid deposits are left, they are seen as hard exudates.

They will eventually be removed by macrophages.

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18
Q

Explain cotton wool spots.

A

Micro-infarcts within the retina due to occluded vessels cause cotton wool spots.

It is actually a swelling of the retinal nerve fibres.

This leads to accumulation of axoplasmic debris.

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19
Q

Explain cytoid bodies.

A

The axoplasmic debris from the cotton wool spots are cleared by macrophages.

White dots will appear at the previous cotton wool spots which are called cytoid bodies.

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20
Q

Can the retinal abnormalities seen in R1 heal?

A

Yes, they can all heal.

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21
Q

What retinal abnormalities can be seen in pre-proliferative retinopathy (R2)?

A

Cotton-wool spots (infarcts)

Cytoid bodies

Venous beading/loops

Intraretinal microvascular abnormalities (IRMAs)

Multiple deep and round haemorrhages.

Refer to specialist

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22
Q

Explain venous beading and loops.

A

Damage to the walls of veins causes their calibre to vary. This is called venous beading.

Elongation also occurs due to the damage, causing elongation aka venous loops.

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23
Q

Retinal abnormalities in proliferative (R3) retinopathy.

A

New blood-vessel formation/neovascularisatio

Preretinal or subhyaloid haemorrhage

Vitreous haemorrhage

Needs urgent referral

24
Q

Explain the neovascularisation.

A

Blockage of blood vessels -> ischaemia. The ischaemia leads to VEGF to be released.

25
Q

Outcomes of neovascularisation.

A

Some are inside the retina and are helpful.

Some emerge through the retina and lie on its surface.

26
Q

Explain IRMAs.

A

The new intraretinal vessels and other vessels that are damaged and dilated will give the appearnce of intraretinal microvascular abnormalities.

(They are a feature of R2)

27
Q

Explain preretinal/subhyaloid haemorrhage.

A

The new vessels which lie on the surface of the retina can become damaged due to normal shearing stresses.

These small haemorrhages give rise to pre-retinal haemorrhages.

28
Q

Explain vitreous haemorrhage.

A

Further bleeding of the pre-retinal haemorrhages gives rise to vitreous haemorrhages.

Vitreous may occur with sudden vision loss.

29
Q

Retinal abnormalities of advanced retinopathy.

A

Retinal fibrosis

Traction retinal detachment

30
Q

Explain retinal fibrosis.

A

Later on in retinopathy collagen tissue will grow along the margins of the new vessels.

This gives rise to fibrotic bands.

31
Q

Explain traction retinal detachment.

A

The fibrotic bands from retinal fibrosis may contract and pull on the retina.

This leads to further haemorrhages but also retinal detachment.

32
Q

What is rubeosis?

A

Vessels may be induced to grow on the pupil margin

This is called rubeosis.

33
Q

What is rubeotic glaucoma?

A

The vessels may also grow in the angle of the anterior chamber.

This gives rise to a rapid increase in intraocular pressure.

34
Q

What might be needed to define the extent of potentially sight-threatening diabetic retinopathy?

A

Fluorescein angiography.

Makes it way thorugh the retinal vessels.

35
Q

Explain retinal abnormalities in maculopathy.

A

Hard exudates within 1 disc-width of macula.

Lines or circles of hard exudates within 2 disc-widths of macula.

Microaneurysms or retinal haemorrhages within 1 disc-width of macula.

It is essentially non-proliferative retinopathy but close to the macula. It is a problem because fluid from leaking vessels are poorly cleared in this area.

36
Q

Why is maculopathy worse than R1?

A

Because maculopathy may affect vision.

37
Q

Retinopathy is usually detected via an ophthalmoscope or with retinal photography.

This is not possible in maculopathy.

How do you check for macular oedema?

A

Ocular coherence tomography.

38
Q

Action needed for R1.

A

Annual screening

39
Q

Action needed for R2.

A

Non-urgent referral to an ophthalmologist.

40
Q

Action needed for R3.

A

Urgent referral to an ophthalmologist.

41
Q

Action needed for advanced retinopathy.

A

Urgent referral to an ophthalmologist.

However much vision is already lost at this point.

42
Q

Action needed for maculopathy.

A

Prompt referral to an ophthalmologist.

43
Q

Management of diabetic retinopathy.

A

Best way is…

Prevention:

Risk of development and reduction of progression can be reduced by tight control of both glucose and blood pressure.

Smoking cessation.

Fenofibrates have been shown to slow progression.

Intravitreal injection

Laser photocoagulation

Vitreoretinal surgery

44
Q

When might short-term deterioration of retinopathy occur?

A

After rapid improvement of glycaemic control.

During pregnancy and by nephropathy.

45
Q

Explain intravitreal injections.

A

Repeated injections of anti-VEGF drugs such as bevacizumab aflibercept and ranibizumab.

This can control the proliferative grade of diabetic retinopathy (R3) and sight-threatening maculopathy.

46
Q

Side effects of intravitreal injections.

A

Infection

Glaucoma

Cataract

Retinal detachment

47
Q

Other possible medication for sight-threatening maculopathy due to macular oedema.

A

Corticosteroid triamcinolone.

48
Q

Explain laser photocoagulation.

A

Used to treat the new vessels of proliferative (R3) retinopathy.

This is because the new vessels on the disc carry the worst prognosis and warrants urgent laser therapy.

49
Q

What kind of laser photocoagulation is performed if vesseles grow on the optic disc?

A

Panretinal photocoagulation.

50
Q

Treatment of rubeosis.

A

Panretinal photocoagulation.

51
Q

Adverse effects of laser photocoagulation.

A

Destruction of retinal tissue.

This means that the visual field becomes permanently smaller and reduction of dark adaptation.

Peripheral vision is sacrificed to maintain central vision.

52
Q

Explain vitreoretinal surgery.

A

If the bleeding is recurrent and preventing laser therapy surgery can be done instead.

It can also treat fibrotic traction retinal detachment in advanced retinopathy.

53
Q

Explain other eye problems due to diabetes.

A

Cataract

Refractory defects

External ocular palsies

Glaucoma

Blindness

54
Q

Predispositions of cataracts in diabetes.

A

Poor diabetes control and degrees of ketosis can cause an acute cataract called snowflake cataract.

55
Q

What nerve palsies are most common in diabetes?

A

CN VI

CN III

Usually resolve spontaneously within 3-6 months.

56
Q

Clinical examination of eye in diabetes.

A

Visual acuity by pinhole and distance spectaces worn.

Ocular movements

Iris examination for rubeosis and for cataract.

All four quadrants of the retina are examined.

The macula is the systematically examined.

57
Q

What should every person with diabetes undergo to prevent diabetic retinopathy?

A

Annual eye screening