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(2) Introductory ocular disease > Retinal Vasculature > Flashcards

Retinal Vasculature Flashcards

1
Q

What are some common leakage/depositions defects in the retina?

A

• Haemorrhages in and around the retina
• Oedema
• Exudates
• Drusen
• Cotton wool spots

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2
Q

Types of haemorrhage:

A

• Retinal haemorrhages
- Flame shaped haemorrhages
- Dot-blot haemorrhages
• Sub-retinal haemorrhages
• Pre-retinal haemorrhages
- Subhyaloid haemorrhages
- Vitreous hemorrhages

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3
Q

Retinal haemorrhages:

A

• Flame shaped haemorrhages
- from superficial pre-capillary arterioles
- in NFL
• Dot-blot haemorrhages
- from venous end of capillaries
- in middle retinal layers

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4
Q

Sub retinal haemorrhages: describe

A

• Dark colour
• Retinal vessels clearly visible above
• Blood can spread in this area so these harmorrhages can have an arbitrary shape
• Can be associated with an RPE detachment

• Causes include:
- wet ARMD (by far most common)
- choroidal tumors
- trauma

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5
Q

Sub-hyaloid haemorrhages: describe

A

• Level of subhyaloid space between posterior vitreous face and retina OR under internal limiting membrane

• May get localised vitreous detachment
• Characteristically have a boat-shaped (horizontal blood level) appearance

• Obscures underlying retina

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6
Q

Vitreous Haemorrhages: Describe

A

• Spread of subhyaloid haemorrhage into vitreous itself
• Often blurry appearance
• Obscures underlying retina

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7
Q

Vitreous Haemorrhages: causes

A

• Abnormal blood vessels
- Don’t have endothelial tight junctions, predisposing them to spontaneous bleeding
• Rupture of normal blood vessels
- Something pulling on blood vessel and causes it to rupture
- Trauma

• Blood from adjacent source
- Haemorrhages from retinal haemorrhages, tumours, wet ARMD can extend into vitreous

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8
Q

Oedema: Describe

A

• Diffuse: caused by extensive leakage

• Localised: focal leakage

• Between OPL and INL, may later involve IPL and NFL

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9
Q

Exudates: Describe

A

• Chronic localised oedema
• Located at junction of normal and oedematous tissue
• Lipoprotein and macrophages
• Mainly in OPL
• Get spontaneously absorbed

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10
Q

Drusen: Describe

A

• RPE hyperpigmentation

• Deposition of Lipofuscin between Bruch’s membrane and the RE; metabolically active cells
- Deficient metabolism of the photoreceptor outer segments by the RE

• Increase in number and size causing damage to photoreceptors reduction in vision

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11
Q

Cotton wool spots: Describe

A

• Accumulation of neuronal debris in NFL
• Disruption of axial flow of neurons

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12
Q

Hypertensive retinopathy: symptoms

A

• Most often patient is asymptomatic
• Blurred/distorted vision if at later stage and it affects the macula

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13
Q

Hypertensive retinopathy: signs
(Venous/arterial)

A

• Venous changes:
- dilation
- tortuosity

• Arterial changes:
- AV nipping
- generalised narrowing
- localised narrowing
- copper wiring
- silver-wiring

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14
Q

Hypertensive retinopathy: Signs

A

• Retinal haemorrhages (dot blot and flame)
• Hard exudates, macular star
• Cotton wool spots
• Disc swelling

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15
Q

Hypertensive retinopathy: Management

A

• Get BP checked
• If severe send to ophthalmologist

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16
Q

Retinal artery occlusion: Describe and types

A

• Most commonly caused by atherosclerosis related embolism and thrombosis
• Causes sudden, profound, painless, loss of vision affecting the retinal area that the artery supplies

Types:
• Amaurosis fugax
• Branch retinal artery occlusion
• Central retinal artery occlusion
• Cilioretinal artery occlusion

17
Q

Amaurosis fugax: Symptoms

A

• Transient monocular loss of vision due to an embolus
• ‘Curtain over vision’
• Complete or incomplete loss of vision
• Typically lasts a few minutes

18
Q

Amaurosis fugax: Signs

A

• Usually no retinal signs evident

19
Q

Retinal artery occlusion: Signs

A

• Fundus:
- Attenuation of arteries
- Cloudy white oedematous retina in affected are
- Visible emboli
- CRAO: cherry red spot which disappears gradually over days/weeks

• VA variable, dependent upon location of occlusion, e.g. CRAO VA severely reduced, if branch not affecting macula VA could be ok

• RAPD often present in branch, profound in CRAO

20
Q

Retinal artery occlusion: management

A

• Emergency referral to hospital and 1st aid measures at hospital if within 24-48hrs of occlusion
• Otherwise urgent referral to hospital

21
Q

Describe Retinal Vein occlusion:

A

• Typically, atherosclerotic hardening of an artery compresses the vein at the arteriovenous crossing point where they share a sheath

22
Q

Retinal Vein occlusion: Signs

A

• Increased arteriolar light reflex (copper wiring - silver wiring)
• tortuosity
• AV nipping

23
Q

Retinal Vein occlusion: Predisposing factors

A

• Age
• HBP
• High cholesterol
• Diabetes
• Oral contraceptive o Increased IOP
• Smoking

24
Q

Retinal Vein occlusion: Types

A

• Branch retinal vein occlusion
• Central retinal vein occlusion
- Impending (partial; mild non-ischaemic)
- Non-ischaemic
- Ischaemic
• Hemi-retinal (may be ischaemic or non-ischaemic as above)

25
Q

Retinal Vein occlusion: Symptoms

A

• Sudden painless onset of reduced/blurred vision

26
Q

Retinal Vein occlusion: Signs
(Fundus; Acute)

A

• Dilation and tortuosity of affected venous segment
• Flame-shaped and dot blot haemorrhages in retinal area drained by the vein
• Cotton wool spots and disc swelling if CRVO
• Resolve within 6-12 months

27
Q

Retinal Vein occlusion: Signs
(Fundus; Long term)

A

• Collateral vessels (aka AV shunts, aka optociliary shunts) after weeks-months (good prognosis due to improved blood supply and reduction in possibility of neovascularisation)

• Chronic macular oedema

• Neovascularisation: retinal and in iris after approx 2-4months

28
Q

Retinal Vein occlusion: Signs
(VA)

A

• VA is dependent on severity/location
- e.g. CF or less if ischaemic CRVO, 6/12 or could be better if branch or non-ischaemic

• RAPD is dependent on severity
e.g. CRVO: profound RAPD, non-ischaemic or branch: mild/absent

29
Q

Retinal Vein occlusion: Signs
(Management)

A

• Urgent referral to ophthalmologist
• Detection and management of associated systemic disease

• Ophthalmological follow-up:
- CRVO: Monthly follow-up for 1st 6/12, gonioscopy to check angles
- BRVO: Follow-up 6-12 weeks to check resolution
- Treat macular oedema or neovascularisation

30
Q

Diabetic retinopathy: Symptoms

A

• Often asymptomatic (unless it affects the macula)
• Blurred/distorted vision
• Sudden onset reduced vision

31
Q

Diabetic retinopathy: Investigations

A

• VA o Retinal examination
• Visual fields (? if see something?)
• IOP (? for a baseline?)
• Slit lamp

32
Q

Diabetic retinopathy: Signs

A

• Caused by leakage:
- Microaneurysms, Retinal haemorrhages (dot-blot and flame-shaped), Oedema, Hard exudates
• Signs caused by retinal ischaemia:
- Cotton wool spots, IRMA
• Venous changes: dilation, tortuosity, looping, beading, sausage-like segmentation
• Arterial changes: narrowing (esp periphery), silver-wiring
• Signs caused by hypoxia: new blood vessels

33
Q

Diabetic retinopathy: Management

A

• Monitor during milder stages (either optometrist or vision screening or by ophthalmologist if a bit more advanced)
• Laser surgery to stop growth of blood vessels

34
Q

What are the types of abnormal blood vessels at level of retina:

A

• IRMA aka A-V shunts
- Dilated capillaries
- collateral vessels (maintain blood flow to a structure when main blood supply blocked)
- telangiectasis
• New blood vessels

35
Q

Intra-Retinal Microvascular Abnormalities (IRM)

A

• A-V shunts running between arterioles and venules

• New vessels or dilated capillaries??
• IRMA tend not to leak on fluorescein angiography therefore more likely to be dilated capillaries

36
Q

New blood vessels: Describe

A

• New vessels at the disc (NVD)
• New vessels elsewhere (NVE)
• New vessels in the iris (NVI)

• New vessels:
- Cross major blood vessels
- Leak in fluorescein angiography (FA)

37
Q

How can Blood vessels change:

A

• Microaneurysms
• Venous changes: dilation, tortuosity, looping, beading, sausage-like segmentation
• Arterial changes: narrowing (esp periphery), silver-wiring
• AN nipping

38
Q

Micro-aneurysms: Describe

A

• dilation of capillary wall
• endothelial cell proliferation

(2) Introductory ocular disease (16 decks)

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