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Ophthalmology > 5. Diabetic Retinopathy and AMD > Flashcards

5. Diabetic Retinopathy and AMD Flashcards

1
Q

What percentage of the diabetic population has Diabetic Retinopathy?

A

40.00%

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2
Q

In which type of diabetes is DR more common?

A

Type 1

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3
Q

What percentage of the diabetic population has sight threatening disease?

A

10.00%

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4
Q

What percentage of the diabetic population has Proliferative Diabetic Retinopathy?

A

10.00%

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5
Q

What are the risk factor for the development of DR?

A 
Duration of Diabetes
Poor Control of Blood Glucose Levels
Pregnancy
Hypertension
Nephropathy
Other (Anaemia, hyperlipidaemia, smoking)
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6
Q

Describe the pathogenesis of DR.

A
  1. Cellular damage (due to sorbitol accumulation & oxidative stress)
  2. Capillaropathy (death of pericytes, thickening of capillary basement membrane & endothelial cell proliferation = Leakage of fluid+Microaneurysm
  3. Haematological changes as increased platelet stickiness = Capillary occlusion+ Ischaemia
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7
Q

What is the difference between proliferative and non-proliferative DR?

A

Neovascularization in Proliferative DR

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8
Q

What causes neovascularisation in DR?

A

Capillary non-perfusion = retinal hypoxia = stimulate angiogenesis = neovascularization (PDR Proliferative Diabetic retinopathy)

There are many angiogenic stimulators: Vascular Endothelial Growth Factor VEGF

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9
Q

Outline how DR is classified?

A

Background Diabtetic Retinopathy (BDR)
Diabetic Maculopathy
Proliferative Diabetic Retinopathy
Advanced Diabetic Eye Disease

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10
Q

What are the characteristics of Background DR

A

Microaneurysms

Blot & dot haemorrhages

Exodates (Hard Exudate (Flame - lipoprotein), Soft Exudate (Spots – ischemia)

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11
Q

What is Diabetic Maculopathy?

A

Oedomatous and ischaemic damage of the macula which threatens vision

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12
Q

Describe the different types of Proliferative Diabetic Retinopathy?

A 
Neovascularization at the disc (NVD)
Neovascularization elsewhere (NVE)
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13
Q

What constitutes advanced diabetic eye disease?

A

Retinal Detachment
Vitreous haemorrhage
Neovascular Glaucoma

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14
Q

Describe the optical coherence tomography?

A

Non-invasive, non-contact imaging system

Provides high resolution cross sectional imaging of the retina

Analogous to B-scan (light hits area of different refractive index it bounces back) ultrasonography but uses near-infrared light rather than sound waves

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15
Q

What is the OCT principle?

A

The various layers,they’re thickness and they’re relative density are represented in a cross sectional image.

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16
Q

Describe Fundus Fluorescein Angiography (FFA)

A

Fluorecein is an orange water-soluble dye

When injected IV, remains mainly intravascular

Disruption of the inner blood retinal barrier will permit leakage of fluorescein

S/E: Anaphylactic (she said epilieptic shock have epi on hand)

17
Q

Which type of DR does not require treatment? What does it require though?

A

Background Diabetic Retinopathy does not require treatment, observation only

18
Q

What is the Tx for Macular Oedema?

A

Intravitreal anti-VEGF agents (usually has to be repeated as effects wear off)
Laser photocoagulation to leaking areas in FFA
Not always successful (70% will have stable vision, 15% better, 15% worse)
See floaters
Risk of Infection
Risk of Uvitits
2/3 sessions 4-6 weeks apart
4 weeks later repeat OCT
Use fluorescence to find leaks

19
Q

What is the Tx for proliferative diabetic retinopathy?

A

Laser/ Panretinal photocoagulation PRP

If we burn out these area stop advance

20
Q

Describe Laser photocoagulation use in PDR?

A

Aim is to induce the involution of new vessels, thereby preventing visual loss
It photocoagulate/burns the retinal tissue
This would reduce the overall oxygen demand of the retina
Less stimulation for neovascularization
Laser is a permanent treatment
May reduce peripheral vision

21
Q

What is the Tx for Vitreous Haemorrhage?

A

Vitreous haemorrhage: wait 6 months to clear by itself, then do vitrectomy if still not absorbed
Vitrectomy

Opening up to remove the vitreus and insert fluid which would be replaced eventually with fluid from the body.
Also trying to resolve/limit any retinal detachment by removing fibrous tissue

Worst Outcomes
May loose peripheral vision
Wont be able to drive (minimum 120 degree vision)
Laser may reduce peripheral vision

22
Q

What is ARMD?

A

Is a degenerative disorder affecting the macula

23
Q

What are the symptoms of ARMD?

A

Loss of central vision
Metamorphopsia

Early clinical findings including drusen & RPE changes
Will be hyper and hypo pigmentation
Patient 40/50yo losses central vision since disease affects the macula
Will see wavy lines since there are waves formed inside the retina

24
Q

What are the risk factors for ARMD

A

Age
Race, more common in Caucasians
Heredity
Smoking
Hypertension
Dietary factors, high fat intake & obesity may promote AMD.
Antioxidant intake have protective effect

25
Q

Describe the histopathology behind ARMD?

A

Drusen: extracellular deposits located at the interface between RPE and Bruch membrane

Drusen may enlarge and cause pigment epithelial detachment

26
Q

How is ARMD classified?

A

Wet and Dry AMD

27
Q

Which is the most common type of ARMD?

A

Dry

28
Q

What constitutes the advanced stage of dry AMD?

A

Geographic atrophy is the advanced stage of dry AMD

29
Q

What are the characteristic of Wet AMD?

A

Less common
Rapid progression & sight loss

The main findings are choroidal neovascular membrane CNV & pigment epithelial detachment PED

30
Q

What are the main findings in Wet AMD?

A

The main findings are

  1. Choroidal neovascular membrane (CNV) (new vasc beneath retina)
  2. Pigment epithelial detachment (PED)
31
Q

At what point is Wet AMD no longer amenable to treatment?

A

Once there is fibrosis there is no treatment

32
Q

What investigation should be performed for AMD?

A

OCT

FFA

33
Q

What is the Tx for AMD?

A

Prophylactic use of antioxidant in patients with unilateral advanced AMD to save the second eye

Treatable risk factors should be addressed: smoking, HT, dietary consideration (BROCCOLI,VITAMENS)

Amsler grid should be provided

Low vision aids (Magnifying Glass etc)

34
Q

What is the Tx for CNV in wet AMD?

A

Treatment with Anti-VEGF
The predominant means of treating the CNV

Intravitreal injection is the method of administration

Notable risks include RD, damage to the lens, endophthalmitis

Elevated intraocular pressure & uveitis may occur

Ophthalmology (10 decks)

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