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OD3 (S1&2) > DIS - Diseases of the Vasculature IV: Diabetes I - Week 11 > Flashcards

DIS - Diseases of the Vasculature IV: Diabetes I - Week 11 Flashcards

1
Q

What is diabetes mellitus?

A

Sustained hyperglycaemia

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2
Q

List the two types of diabetes and whether they are insulin dependent or independent.

A

Type 1 - insulin dependent
Type 2 - insulin independent

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3
Q

What onset do type 1 and 2 diabetes typically have?

A

1 - juvenile
2 - adult

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4
Q

Can non-insulin dependent diabetes develop into insulin dependent?

A

Yes

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5
Q

What three things related to insulin can diabetes be due to?

A

Lack of endogenous insulin
Reduced efficacy of endogenous insulin
Both

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6
Q

What is the typical random blood glucose level with diabetes? What about fasting?

A

Random - >11mmol/L
Fasting - >7mmol/L

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7
Q

What does the glucose tolerance test measure?

A

Glucose clearance from the blood

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8
Q

What is HbA1c with diabetes?

A

> 6.5%

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9
Q

Describe how a glucose tolerance test is carried out and what the prerequisite is.

A

Prerequisite - eat/drink adequate carbohydrates for 3 days (150g/d)
Fast for 8h before the test
Take fasting blood glucose test
Ingest 75g of glucose (with 2L of fluid)
Blood glucose measured after 1 and 2h

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10
Q

List three early systemic signs of diabetes. What is this related to?

A

Excessive thirst
Excessive urine production
Loss of appetite and weight
-all related to osmosis

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11
Q

What is a late systemic sign of diabetes? Describe why it occurs.

A

Ketoacidosis
-insufficient insulin leads to the body burning fat for energy
-ketones accumulate in blood and urine

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12
Q

Describe the association between insulin and nerves and what the evidence is like.

A

Some evidence suggests insulin is a neurotrophic factor
-neurons need insulin to sustain them

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13
Q

What is the proportion of type 1 and 2 diabetes?

A

1 - 15%
2 - 85%

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14
Q

List the two classifications of diabetic retinopathy and what they are characterised by (1, 2).

A

Non-proliferative
-microangiopathy
Proliferative
-formation of new vessels on the vitreo-retinal interface and in the vitreous
-proliferation of fibrovascular tissue on the retina/disc

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15
Q

What two factors correlate strongest with the presence of diabetic retinopathy?

A

Duration of diabetes
Quality/degree of glycaemic control of diabetes

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16
Q

What is thought to directly link to development and progression of diabetic retinopathy? What are the two major effects of this?

A

Altered glucose metabolism
-increased blood retinal barrier permeability - leakage
-alterations in retinal blood flow (hypoxia)

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17
Q

Describe how hyperglycaemia can lead to changes in vessels (4). Explain what these changes are (2) and what it can lead to (2) and how (1).

A

Causes the production of advanced glycation end products and increased diacylglycerol levels
These activate protein kinase C and overexpression of VEGF
PKC activation lead to capillary leakage and neovascularisation
Capillary occlusion leads to increased expression of insulin-like growth factor (IGF-1)
This leads to the development of pre-retinal and iris neovascularisation

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18
Q

What two things do all diabetics need?

A

Regular retinal examination
Dilated pupil exam

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19
Q

Should newly diagnosed diabetics have a retinal exam?

A

Yes

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20
Q

What happens to the basement membrane of retinal capillaries with diabetes? What is a consequence of this?

A

Thickens
-decreased O2

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21
Q

What happens to pericytes and endothelial cells in retinal capillaries with diabetes? What are two consequences of this?

A

Loss of pericytes
Endothelial enlargement
-microaneurysm formation
-capillary leakage and eventual drop out

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22
Q

What are three early signs of non-proliferative diabetic retinopathy?

A

Microaneurysms
Dot/blot haemorrhages
Lipid exudates

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23
Q

What are five signs of more advanced non-proliferative diabetic retinopathy?

A

More of the three early signs plus
Cotton wool spots
Intraretinal microvascular abnormalities
Flame haemorrhages
Venous beading

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24
Q

What are four signs of proliferative diabetic retinopathy?

A

Signs of non-proliferative DR (usually more advanced) plus
New vessels - NVI, NVE, NVD
Vitreous haemorrhage
Tractional retinal detachment

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25
Q

How do microaneurysms appear? What about with angiography? Are they isolated or clustered?

A

Tiny red dots like dot haemorrhages
Hyperfluorescent on FA
Sometimes isolated, sometimes clustered

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26
Q

What retinal layer do dot/blot haemorrhages occur (non-specific)?

A

From middle retinal layers
-from microaneurysms/deep capillaries

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27
Q

What colour and shape are intra-retinal lipids?

A

Yellow - often circinate - circular

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28
Q

What two things are generally used for staging diabetic retinopathy?

A

Number of microaneurysms and haemorrhages

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29
Q

What is a cotton wool spot?

A

Ischaemia of the RNFL

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30
Q

What is a flame haemorrhage?

A

Haemorrhage of the superficial capillary layer supplying the RNFL

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31
Q

What is venous beading? What can be seen on fluorescein angiography?

A

Sacular bulges, dilation
Capillary dropout on both sides of the vein on angiography

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32
Q

What are intraretinal microvascular abnormalities? What do they bypass and what do they mimic? What are they often seen with?

A

Dilated abnormal capillaries
Bypass capillaries
Mimic new vessels
Often with venous loops and cotton wool spots

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33
Q

Can capillary compromise/dropout be seen directly?

A

No, only with fluorescein angiography

34
Q

What are venous loops often adjacent to?

A

Areas of ischaemia

35
Q

What causes diabetic macular oedema? At what stage of DR can it develop?

A

Leakage from microaneurysms near the macula/fovea
Can develop at any stage

36
Q

Is diabetic macular oedema reversible?

A

Yes with timely treatment

37
Q

What is the progression of diabetic macular oedema (2)?

A

VA drop from oedema affecting middleretinal layers
Eventual destruction - atrophy
-permanent vision loss

38
Q

What is clinically significant macular a subset of?

A

Subset of diabetic macular oedema close to the fovea

39
Q

How is clinically significant macular oedema defined (3)?

A

Retinal thickening within 500u of the centre of the fovea
Lipid exudate within 500u of the centre of the fovea with adjacent retinal thickening
Retinal thickening of >1,500u which is <1,500u from the centre of the fovea

40
Q

What is 1,500u comparable to?

A

1DD

41
Q

What consequence does diabetic macular oedema have on the blood retinal barrier?

A

It breaks down

42
Q

What 6 overlapping vascular, inflammatory, and neuronal changes occur as a result of diabetic macular oedema?

A

Proinflammatory cytokines
Increased VEGF production
Endothelial tight junction dysfunction
Involvement of leucocytes
Microglial activation
Muller cell dysfunction

43
Q

What happens to the retinal inner layers as a result of diabetic macular oedema? what is this called?

A

DRIL - disorganisation of retinal inner layers
-loss of boundaries

44
Q

Can there be recovery from DRIL?

A

No

45
Q

What is neovascularisation indicative of in diabetic retinopathy (2)? What is it associated with?

A

Proliferative DR
Significant oedema
Associated with capillary dropout/non-perfusion

46
Q

Where does neovascularisation first occur, growing through what layer? What is a vitreous scaffold?

A

Originate in retina, grow through ILM
Vitreous scaffold - on or above retina

47
Q

With neovvascularisation in diabetic retinopathy, where does it often occur in the periphery and what appearance does it have (2)?

A

Often along vascular vessels
-cartwheel appearance
-fine wispy vessels

48
Q

Define NVE, NVD, NVI.

A

New vessels elsewhere
New vessels on disc
New vessels on iris

49
Q

What is often the reason for blindness in diabetes?

A

Uncontrolled neovascularisation

50
Q

What three things does neovascularisation in diabetic retinopathy give significant risk of?

A

Pre-retinal/vitreous haemorrhage
Fibrosis with subsequent shrinkage
Neovascular glaucoma

51
Q

Distinguish between intra-retinal microvascular abnormalities and neovascularisation in diabetic retinopathy.

A

Neovascularisation - vessels grow on the retinal surface and into the vitreous
IRMA - intra-retinal

52
Q

What is tractional retinal detachment in proliferative diabetic retinopathy the end result of (2)?

A

Vitrous haemorrhage and fibrosis on the retinal surface
Contraction of fibrous membrane on the retinal surface

53
Q

What should you beware in patients with longstanding diabetes and apparently mild DR?

A

May have a silent problem
-slow peripheral capillary dropout
-very subtle neovascularisation

54
Q

What is a differential diagnosis for non-proliverative DR? Give nine examples.

A

Any retinal vascular change associated with ischaemia
-hypertension
-CRVO (non-ischaemic)
-radiation retinopathy
-sickle cell disease
-macroaneurysm
-haemoglobinopathies
-carotid artery disease
-vaculitis
-HIV retinopathy

55
Q

What is a differential diagnosis for diabetic macular oedema?

A

Any exudation from capillaries at/near the macula

56
Q

What is a differential diagnosis for proliferative DR?

A

Any retinal vascular change associated with ischaemia, elevated VEGF, and vitreos haemorrhage

57
Q

Describe what you would expect to see with mild non-proliferative DR (1).

A

Microaneurysms only

58
Q

Describe what you would expect to see with moderate non-proliferative DR (1).

A

More microaneurysms, but less than severe NPDR

59
Q

Describe what you would expect to see with severe non-proliferative DR (3).

A

Any of the following:
>20 haemorrhages in each of the four quadrants
Venous beading in 2 or more quadrants
Prominent IRMA in one or more quadrant

60
Q

The presence of what defines proliferative retinopathy (2)?

A

Neovascularisation and/or vitreous/pre-retinal haemorrage

61
Q

Describe mild, moderate, and severe diabetic macular oedema.

A

Mild - some exudate/thickening but not close to the fovea
Moderate - some exudate/thickening, close to, but not involving the macula
Severe - exudate or thickening involving the macula

62
Q

List 5 practitioners that can be involved in the management of diabetes.

A

GP
Ophthalmologist
Endocrinologist
Optometrist
Podiatrist

63
Q

How often should a type 2 diabetic patient be screened for DR? What about if theyre at high risk of DR

A

Every 2 years at least
High risk - every year

64
Q

How often should a type 2 diabetic patient with NPDR have a retinal exam?

A

Every 3-6 months depending on severity

65
Q

How often should pregnant patients with gestational diabetes have an eye exam for DR screening?

A

No need unless it persists

66
Q

How often should pregnant patients have an eye exam for DR screening? What about if they have DR

A

Examine during the first trimester
Any DR - follow through pregnancy

67
Q

Is pan-retinal photocoagulation a viable treatment option for DR? List 4 side effects

A

It is effective in preventing vision loss
-pain
-loss of visual field and some night vision
-increased risk of diabetic macular oedema
-some may still need vitrectomy later

68
Q

does the evidence suggest it is justifiable to treat diabetics with panretinal photocoagulation to prevent proliferative DR?

A

Yes

69
Q

Is anti-VEGF a viable treatment option for PDR?

A

Yes
-standard of care for DMO

70
Q

Can anti-VEGF slow down NPDR progression or does it have no effect?

A

Can slow down all forms of progression, including NPDR to PDR

71
Q

Can anti-VEGF result in regression of PDR to NPDR or is PDR permanent?

A

It can cause regression

72
Q

What is a disadvantage of anti-VEGF when used for DR?

A

Drug effect lost quickly, repeated injections needed

73
Q

In what three cases would you refer to an ophthalmologist with suspected DR?

A

Unexplained VA loss
Suspicion of macular oedema or PDR

74
Q

What stages of DR should you refer (2)?

A

All except mild NPDR
-includes CSMO, vitreous haemorrhaging etc

75
Q

When is vitrectomy indicated for DR (3).

A

Vitreous haemorrhage
Tractional RD
Neovascular glaucoma

76
Q

When is focal and grid photocoagulation used for diabetic macular oedema?

A

Focal - to treat focal CSMO
-directed at microaneurysms
Grid - to treat diffuse CSMO

77
Q

Can ranimizumab improve macular oedema and vision?

A

Yes

78
Q

Are anti-VEGF and ranimizumab superior to laser for DR?

A

Yes, both

79
Q

Aside from anti-VEGF, what is the treatment for DMO?

A

Corticosteroid injection

80
Q

List four mechanisms behind how photocoagulation can treat PDR.

A

Increased oxygenation of inner retinal layers may decrease stimulus for VEGF production
May directly damage or destroy cells that produce angiogenic cytokines
Direct closure of leaky aneurysms
Effects on RPE function

81
Q

When is the optimum time for cataract surgery with DR (3)?

A

If DR advanced, surgery may push retinopathy to disastrous level
Moderate - may cause vision threatening exacerbation
Mild - should be safe

OD3 (S1&2) (114 decks)

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