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OD3 - Clinical Optometry Practice > DIS - Diseases of the Vasculature I: Systemic Cardiovascular Disease and Ocular Blood Flow - Week 9 > Flashcards

DIS - Diseases of the Vasculature I: Systemic Cardiovascular Disease and Ocular Blood Flow - Week 9 Flashcards

1
Q

List three things that can cause an unwanted platelet response. What ends up forming and what happens if it breaks?

A

Primary atheroma
Lodged embolus
Vascular wall anomalies
A thrombus forms, slowing down blood flow
Parts can break off and cause downstream blockage - embolus

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2
Q

What is atheromatosis mainly a disease of? What is it a consequence of? give two common causes. What can turbulent blood flow lead to? Can it cause an embolism?

A

Mainly a disease of large and elastic muscular arteries
Consequence of chronic endothelial injury
-smoking
-hypertension
Turbulent blood flow may lead to secondary thrombus formation
Pieces of plaque may become an embolus

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3
Q

What is a hollenhurst plaque?

A

ICA (or other major vessel) atheroma

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4
Q

What is endocarditis?

A

Endocardium infection

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5
Q

List 7 important sources of embolisms to the eye.

A 
Hollenhurst plaque
Endocarditis
ICA stenosis
Mitral valve/aortic stenosis
ICA thrombus
IV drug use
Bone trauma - neutral fat
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6
Q

Why can drug use cause eye embolisms (2)?

A

They may contain talc/cornstarch

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7
Q

List 7 things that can cause blood flow abnormality.

A 
Dissection/aneurysm
Blood dyscrasia (like sickle cell)
Hypertension
Vessel disease
Tumour
Arterial vasospasm
Mechanical pressure from neighbouring vessels
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8
Q

List three vessel diseases that can cause blood flow abnormalities.

A

Arteriosclerosis
Arteriolosclerosis
Giant cell arteritis

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9
Q

Describe how a tumour can case abnormal blood flow (2).

A

New vasculature competes with normal supply or pressure/occlusion

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10
Q

In which age population is arterial vasospasm more common?

A

Younger

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11
Q

Define ischaemia. How is it different to hypoxia?

A

State when tissue has arterial perfusion lowered relative to its metabolic requirement
Ischaemia relates to blood flow
Hypoxia relates to oxygen availability

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12
Q

What is an infarction and what causes it?

A

Extensive but localised area of necrotic tissue brought about by ischaemia

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13
Q

Does ischaemia affect local tissue only? Explain.

A

Both the local tissue and the vessel walls

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14
Q

What are haemorrhages due to, slowed blood flow or back pressure buildup?

A

Slowed blood flow, not due to back pressure buildup

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15
Q

What does blood stasis lead to? Particularly in which type of blood vessel?

A

Leads to vessel wall ischaemia

-particularly venous, but can be arterial

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16
Q

What happens with vascular endothelial damage? What happens as a result?

A

Breakdown of tight junctions

-blood products leak onto tissue

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17
Q

What two things exacerbate local tissue ischaemia?

A

Stagnant blood and reduced capillary perfusion

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18
Q

What is a consequence of arterial obstruction?

A

Deprives tissue of oxygenated blood

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19
Q

What is a consequence of venous obstruction (2)?

A

Slows arterial flow

Deprives tissue of oxygenated blood

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20
Q

Does reduced blood flow cause ischaemia of the vascular endothelium? Explain (2). Does it promote thrombosis?

A

Causes ischaemia of the vascular endothelium
Also causes oedema and haemorrhage as a consequence
Promotes thrombosis

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21
Q

What does tissue ischaemia cause the release of? What do they exacerbate?

A

Inflammatory mediator release

-exacerbates oedema and haemorrhage

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22
Q

What does haemorrhage stimulate and what is a consequence of this?

A

Stimulates clotting, interrupting blood flow

  • causes further ischaemia
  • vicious circle
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23
Q

Is haemorrhage usually a result of ischaemia? Do haemorrhages indicate ischaemia?

A

Haemorrhages are usually a result (and indicative) of ischaemia

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24
Q

How does retinal artery occlusion affect vision? Is pain involved?

A

Sudden painless loss of vision

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25
Q

How does the retina appear with retinal artery occlusion? What about the macula? What about the arterioles?

A

White/opacified retina
Cherry red spot at the macula
Attenuated artioles

26
Q

List 5 important causes of retinal artery occlusion.

A 
Embolisms
ICA dissection
Vasospasm
GCA
Hypercoabulable state
27
Q

Are primary atheromas common or rare in the central retinal artery?

A

Rare

28
Q

How do cholesterol emboli appear on histology? Why? What may you see of note with the vessel wall? What surrounds the plaque? What are they?

A

Cigar shaped holes - fixation dissolved cholesterol
May see vascular wall reaction to the embolus
Giant cells surround the plaque
-fusion of lipomacrophages

29
Q

How do thrombic emboli appear on histology? What colour does it stain? What may you see of note in blue staining and what does it indicate?

A

Red staining plug of erythrocytes and platelets

Blue staining regions in the thrombus indicate the connective tissue of atheromatous material

30
Q

Why do fat emboli tend to occur? what are its underlying emchanisms? how does it appear on histology?

A

Secondary to bone fractures, mechanisms uncertain

Appears grey/bue homogenous stain

31
Q

How do calcium emboli appear on histology? What compound is it? What is their origin (2)?

A

White, crystalline - calcium hydroxide

Origin in heart valves and ICA

32
Q

What protects the outer retinal structures and is the mechanism behind the cherry red spot with retinal ischaemia?

A

Choroidal blood supply

33
Q

Is retinal iscahemia progressive or immediate? Do cells shut down immediately?

A

Retinal ischaemia is immediate

Cell function shut down is rapid

34
Q

Clinically, how long does it take for the white/grey appearance to disappear and what is it indicative of?

A

4-6 weeks - indicative of necrotic changes taking over

35
Q

Are vasoformative factors released with retinal ischaemia? Is retinal neovascularisation common or rare in artery occlusion?

A

Few vasoformative factors released

Retinal neovascularisation is rare

36
Q

Is gliosis present with retinal ischaemia? Why?

A

Glial cells die - no gliosis

37
Q

How long can retinal tissue survive without oxygen? Is rescue possible after this time? What is a possible consequence?

A

Cant survive more than a few hours without oxygen

Rescue is possible but reperfusion injury may be significant

38
Q

What do the initial effects of ischaemia due to retinal artery occlusion cause (to the retinal layers, 4)? Are haemorrhages commonly seen? Why?

A

Initial effects cause oedema of the NFL, GCL, IPL, and INL

Rarely, if ever, see haemorrhages - uncertain why

39
Q

What does the absolute nature (cell death) of retinal ischaemia (from retinal artery occlusion) prevent? Explain why (3).

A

Cell death is very rapid and necrotic - absolute nature prevents much inflammation

  • tissue doesnt release chemotactic signals
  • inflammatory cells cant pass the blockage
  • glia affected as well
40
Q

What system are most theories of retinal vein occlusion linked to?

A

Arterial system

41
Q

Compare the cross section of the central retinal vein at its lamina cribrosa bore vs the prelaminar and retrolaminar regions.

A

At the lamina cribrosa bore, it is 50% that of the prelaminar portion and much smaller than retrolaminar

42
Q

Do the central retinal artery and vein have separate connective tissue sheaths or do they share one? What about AV crossings throughout the retina?

A

They share a sheath, as do AV crossings

43
Q

Explain how the proximity of the central retinal artery and vein may be a possible mechanism for retinal vein occlusion (2). Where can this particular event happen? Can it cause a thrombus?

A

Increased pressure on the central retinal vein if blood pressure elevates or arterial wall thickenes
Can happen at branch A/V corssings
-can cause thrombus

44
Q

Explain how the cross section of the central retinal vein may be a possible mechanism for retinal vein occlusion.

A

Physiological narrowing of the CRV at the lamina - predisposes to bloof flow turbulence and thrombus formation

45
Q

Explain how the reduced arterial blood flowmay be a possible mechanism for retinal vein occlusion. Is it a true occlusion?

A

Causes venous stasis resulting in ischaemic changes and haemorrhage
-not a true occlusion

46
Q

What may determine if retinal vein occlusion is haemorrhagic or not?

A

The position (i.e. pre/retrolaminar)

47
Q

Do haemorrhages spread within the NFL? Explain.

A

Yes, usually not past the ILM

48
Q

What is left behind with resorption of blood/fluid after haemorrage? What is it?

A

Residual waxy deposits

-serum breakdown products in the OPL

49
Q

What are exudates after retinal haemorrhages?

A

Muller cells constrain lipoproteins with lipid filled macrophages

50
Q

What is the mechanism behind oedema following retinal haemorrhage? Can this happen anywhere?

A

Haemorrhagic fluid taken up by muller cells cause them to coalesce and rupture, and form fluid filled cysts
Can affect any retinal area

51
Q

What drains circum-macular fluid to the fovea?

A

Perifoveal henle fibre orientation

52
Q

Are early ischaemic effects localised or generalised? What is this called?

A

Localised - cotton wool spots

53
Q

What are cotton wool spots exactly?

A

Local microinfarcts knownas cytoid bodies

54
Q

What are cytoid bodies?

A

Swollen axons

55
Q

What happens following necrotic tissue resorption in cotton wool spots?

A

Gliosis

56
Q

List three things that may become neovascularised with later ischaemia.

A

Iris
Retina
ONH

57
Q

With ischaemia, what may aid blood drainage and how?

A

Arteriovenular shunts - bypassing closed capillary networks

58
Q

What do collaterals provide? Are they normal vascular structures? What stimulates development?

A

Provide a capillary bed bypass
Normal vascular structure
-blood flow changes stimulate development

59
Q

What happens if a capillary bed closes? What is released and what does this cause? What is it called? Is it a good thing?

A

If a bed closes, blood is diverted through developing collaterals
Vasoformative factors are released and cause proliferation of normal vascular walls
-arteriogenesis, a good thing

60
Q

What is neovascularisation? Describe the number of pericytes seen in new vessels, as well as their tight junction and basement membrane quality. What are they supported by? What are they prone to (2)?

A

Proliferation of new retinal vessels from compromised/patent capillary networks
Have few (if any) pericytes
Poor tight junctions and basement membrane
Supported by fibroelastic tissue
Prone to leaks and subject to contraction

61
Q

What happens at the endstage of retinal vein occlusion? what forms and what happens to the ILM? What may it have possible links to?

A

Glial cell proliferation in the inner layers
Forms an epiretinal membrane
-wrinkles the ILM
-possible links with the vitreous

62
Q

What does blue staining of gial cell proliferation in the endstages of retinal vein occlusion show? What is it?

A

Iron deposition

-RBC remnants in macrophages

OD3 - Clinical Optometry Practice (114 decks)

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