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

Question 1

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

Answer 1

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

Question 2

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?

Answer 2

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

Question 3

What is a hollenhurst plaque?

Answer 3

ICA (or other major vessel) atheroma

Question 4

What is endocarditis?

Answer 4

Endocardium infection

Question 5

List 7 important sources of embolisms to the eye.

Answer 5

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

Question 6

Why can drug use cause eye embolisms (2)?

Answer 6

They may contain talc/cornstarch

Question 7

List 7 things that can cause blood flow abnormality.

Answer 7

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

Question 8

List three vessel diseases that can cause blood flow abnormalities.

Answer 8

Arteriosclerosis
Arteriolosclerosis
Giant cell arteritis

Question 9

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

Answer 9

New vasculature competes with normal supply or pressure/occlusion

Question 10

In which age population is arterial vasospasm more common?

Answer 10

Younger

Question 11

Define ischaemia. How is it different to hypoxia?

Answer 11

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

Question 12

What is an infarction and what causes it?

Answer 12

Extensive but localised area of necrotic tissue brought about by ischaemia

Question 13

Does ischaemia affect local tissue only? Explain.

Answer 13

Both the local tissue and the vessel walls

Question 14

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

Answer 14

Slowed blood flow, not due to back pressure buildup

Question 15

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

Answer 15

Leads to vessel wall ischaemia
-particularly venous, but can be arterial

Question 16

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

Answer 16

Breakdown of tight junctions
-blood products leak onto tissue

Question 17

What two things exacerbate local tissue ischaemia?

Answer 17

Stagnant blood and reduced capillary perfusion

Question 18

What is a consequence of arterial obstruction?

Answer 18

Deprives tissue of oxygenated blood

Question 19

What is a consequence of venous obstruction (2)?

Answer 19

Slows arterial flow
Deprives tissue of oxygenated blood

Question 20

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

Answer 20

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

Question 21

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

Answer 21

Inflammatory mediator release
-exacerbates oedema and haemorrhage

Question 22

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

Answer 22

Stimulates clotting, interrupting blood flow
-causes further ischaemia
-vicious circle

Question 23

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

Answer 23

Haemorrhages are usually a result (and indicative) of ischaemia

Question 24

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

Answer 24

Sudden painless loss of vision

Question 25

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

Answer 25

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

Question 26

List 5 important causes of retinal artery occlusion.

Answer 26

Embolisms ICA dissection Vasospasm GCA Hypercoabulable state

Question 27

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

Answer 27

Rare

Question 28

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?

Answer 28

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

Question 29

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?

Answer 29

Red staining plug of erythrocytes and platelets Blue staining regions in the thrombus indicate the connective tissue of atheromatous material

Question 30

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

Answer 30

Secondary to bone fractures, mechanisms uncertain Appears grey/bue homogenous stain

Question 31

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

Answer 31

White, crystalline - calcium hydroxide Origin in heart valves and ICA

Question 32

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

Answer 32

Choroidal blood supply

Question 33

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

Answer 33

Retinal ischaemia is immediate Cell function shut down is rapid

Question 34

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

Answer 34

4-6 weeks - indicative of necrotic changes taking over

Question 35

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

Answer 35

Few vasoformative factors released Retinal neovascularisation is rare

Question 36

Is gliosis present with retinal ischaemia? Why?

Answer 36

Glial cells die - no gliosis

Question 37

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

Answer 37

Cant survive more than a few hours without oxygen Rescue is possible but reperfusion injury may be significant

Question 38

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

Answer 38

Initial effects cause oedema of the NFL, GCL, IPL, and INL Rarely, if ever, see haemorrhages - uncertain why

Question 39

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

Answer 39

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

Question 40

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

Answer 40

Arterial system

Question 41

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

Answer 41

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

Question 42

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

Answer 42

They share a sheath, as do AV crossings

Question 43

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?

Answer 43

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

Question 44

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

Answer 44

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

Question 45

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

Answer 45

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

Question 46

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

Answer 46

The position (i.e. pre/retrolaminar)

Question 47

Do haemorrhages spread within the NFL? Explain.

Answer 47

Yes, usually not past the ILM

Question 48

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

Answer 48

Residual waxy deposits -serum breakdown products in the OPL

Question 49

What are exudates after retinal haemorrhages?

Answer 49

Muller cells constrain lipoproteins with lipid filled macrophages

Question 50

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

Answer 50

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

Question 51

What drains circum-macular fluid to the fovea?

Answer 51

Perifoveal henle fibre orientation

Question 52

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

Answer 52

Localised - cotton wool spots

Question 53

What are cotton wool spots exactly?

Answer 53

Local microinfarcts knownas cytoid bodies

Question 54

What are cytoid bodies?

Answer 54

Swollen axons

Question 55

What happens following necrotic tissue resorption in cotton wool spots?

Answer 55

Gliosis

Question 56

List three things that may become neovascularised with later ischaemia.

Answer 56

Iris Retina ONH

Question 57

With ischaemia, what may aid blood drainage and how?

Answer 57

Arteriovenular shunts - bypassing closed capillary networks

Question 58

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

Answer 58

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

Question 59

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

Answer 59

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

Question 60

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)?

Answer 60

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

Question 61

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

Answer 61

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

Question 62

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

Answer 62

Iron deposition -RBC remnants in macrophages