DIS - Diseases of the Vasculature II: Ocular Vessel Disease - Week 9

Question 1

Is the majority of hypertension insidious? What is it referred to as (2)? What is the mechanism and is the pressure rise generally acute or chronic?

Answer 1

Majority of hypertension is insidious (95%)
Referred to as essential or benign hypertension
Mechanisms poorly understood
Pressure rise is chronic

Question 2

What percentage of hypertension is malignant/secondary? What is the pressure rise like and is it acute or chronic?

Answer 2

5% is malignant
Pressure rise is large and acute

Question 3

In which does extensive retinopathy occur early, benign or malignant hypertension?

Answer 3

Malignant

Question 4

What is hypertension defined as, both systolic and diastolic?

Answer 4

Systolic ≥160mmHg
Or diastolic ≥95mmHg

Question 5

Arterial blood pressure is a product of what (2)?

Answer 5

Cardiac output and peripheral vascular resistance
Increase in either increases blood pressure

Question 6

What is arteriosclerosis and why does it happen? What does it increase (2)? Can it lead to hypertension?

Answer 6

Stiffening of the arterial wall with age
-collagen deposition and smooth muscle cell hypertrophy
Increases peripheral resistance
Arteriosclerosis can lead to hypertension

Question 7

Describe how fluid volume in blood may increase due to kidney function, what this causes (3) and what it may accelerate.

Answer 7

Fluid volume in blood increases due to decreased kidney function
-salt, diet, genes, etc
This causes increased cardiac output and peripheral vasospasm and sclerosis
Hypertension accelerates arteriosclerosis

Question 8

What is the relationship between hypertension and arteriosclerosis?

Answer 8

Arteriosclerosis can lead to hypertension
Hypertension can accelerate arteriosclerosis

Question 9

Are arterio/arteriolosclerosis associated with atheroma formation and vessel dissection?

Answer 9

Yes

Question 10

What is the result of arterio/arteriolosclerosis (7)?

Answer 10

Stiffened/thickened wall
Narrow arteriolar lumen
Raised BP
Vascular SM hypertrophy
Collagen deposition
Breakdown of elastin
Endothelial dysfunction

Question 11

What effect does increased blood pressure have on the endothelium (2) and how does this affect blood flow? What risk does this give (3)?

Answer 11

Endothelial damage and proliferation
Causes turbulent blood flow
-thrombus risk
-local haemorrhage
-local ischaemia

Question 12

What effect does increased blood pressure have on gaseous exchange? Name one other factor that also contributes to this. What can this lead to?

Answer 12

Poorer gaseous exchange
-also thickened vascular wall (a consequence of increased blood pressure)
-can cause local ischaemia

Question 13

What can happen to the vascular smooth muscle with increased blood pressure and what are four consequences of this?

Answer 13

Necrosis
Leads to local macrophage invasion, increasing the risk of thrombus formation
Can lead to lumen occlusion, resulting in localised/general ischaemia

Question 14

Does high blood pressure cause poor capillary perfusion?

Answer 14

Yes

Question 15

Are hypertension and arteriolosclerosis often clinically coincident or are they most seen in isolation?

Answer 15

Clinically coincident

Question 16

List four clinical changes that can happen to the arteries in the retina with hypertension/arteriolosclerosis.

Answer 16

Arteriolar narrowing
-general or focal
Increased tortuosity of the vascular tree
Increased prominence of arteriolar reflex
Arteriolovenular crossing changes

Question 17

List 5 stages of malignant hypertension by clinical appearance.

Answer 17

Haemorrhage
Hard exudates
Oedema
Cotton wool spots
Collaterals

Question 18

Explain how increased systemic blood pressure may cause vessel tortuosity (2).

Answer 18

Arterioles and capillaries constrict and spasm, if it is locally uneven or stiff (arteriosclerosis), it may result in tortuosity

Question 19

What four things can vascular endothelial damage cause?

Answer 19

Haemorrhage
Exudates
Oedema
Ischaemia

Question 20

What is meant by the hosepipe effect?

Answer 20

Straightening of the vascular tree due to hypertension

Question 21

How does blood from a haemorrhage tend to pool at the GCL/NFL? What about at the INL/OPL? What are these haemorrhages called? Hypertensive haemorrhages are usually which of these two?

Answer 21

GCL/NFL - pools laterally - flame/splinter haemorrhage
INL/OPL - pools up and down - dot/blot haemorrhages
Hypertensive haemorrhages are usually splinter/flame

Question 22

Aside from retinal vascular changes, what other vessel changes can be seen with hypertension (2) and what two things lead to this response exactly? Mainly which hype of typertension causes these changes? Do similar changes happen to the optic nerve head or is it spared?

Answer 22

Choroidal vascular changes, mainly due to malignant hypertension
RPE ischaemia and neovascular responses lead to focal RPE changes and serous detachment
Similar changes happen to the ONH

Question 23

Is there any association between conjunctival haemorrhage and hypertension or arteriolosclerosis? Is there any evidence of microvascular changes to conjunctival vasculature?

Answer 23

Subconjunctival haemorrhage associated with hypertension and arteriolosclerosis but there is little evidence of microvascular changes

Question 24

Is it easy to determine if arteriolosclerosis causes hypertension or vice versa?

Answer 24

No, they are usually seen together

Question 25

What is the most common presenting sign of hypertension/arteriolosclerosis in ocular tissue? What does this imply?

Answer 25

Vessel narrowing
-this implies that hypertension usually accelerates arteriolosclerosis

Question 26

What causes AV ratio change and crossing changes in ocular tissue (2)?

Answer 26

Hypertensive vascular spasm followed by arteriolosclerosis

Question 27

What can happen if hypertension is not treated (3) and why (2)?

Answer 27

Turbulent blood flow and thickened vessel walls can lead to vessel and tissue ischaemia, oedema, and haemorrhage

Question 28

What does the profile of a retinal haemorrhage indicate?

Answer 28

Its position within the nerve pathway

Question 29

Define vasculitis.

Answer 29

General term for vascular inflammation

Question 30

What do nearly all types of vasculitis show systemic signs of? Do they respond to immunosuppressants? What is the cause?

Answer 30

Immune mediation
Respond to immune suppressants
Cause usually unknown

Question 31

Vasculitis will usually show all histopathological hallmarks of what other condition(s)?

Answer 31

One or more of the classic hypersensitivity reactions

Question 32

What is the most common type of vasculitis? List 5 other types that can affect the eye.

Answer 32

Giant cell arteritis (most common)
Phlebitis
Polyarteritis nodosa
Systemic lupus erthyematosus
Sjogrens syndrome
Behcets disease

Question 33

List four main clinical signs of giant cell arteritis.

Answer 33

AION
Vision loss
Jaw/scalp tenderness
CRAO

Question 34

What does biopsy of the temporal artery with giant cell arteritis show? What is seen with the internal elastic lamina? What cell structure can be seen throughout?

Answer 34

Vasculitis in all layers
Ruptured internal elastic lamina
Giant cell formation (granuloma)

Question 35

What happens to blood C-reactive protein levels in blood with giant cell arteritis? What happens to the bloods consistency as a result? What blood test can this be seen in?

Answer 35

Raised CRP levels
Blood blecomes sticky
Causes raised ESR

Question 36

Is giant cell arteritis life-threatening? What is there a risk of?

Answer 36

Yes it is, risk of cardiac failure

Question 37

What percent of patients permanently lose their vision with giant cell arteritis? What is this loss of vision due to (3)? Are retinal arterioles affected?

Answer 37

15%
Due to axon ischaemia at the ONH, choroidal non-perfusion (inflammed PCA) or CRA inflammation (well behind the ONH)
-retinal arterioles unaffected

Question 38

Describe the classic acute granulomatous giant cell arteritis histology on a temporal artery biopsy (4).

Answer 38

Multinucleated giant cell clusters near the intima/edia boundary
Extensive infiltration of lymphocytes, plasma cells, and macrophages
IEL ruptured with breaks
Remnants of the tunica media

Question 39

Describe the atypical non-granulomatous giant cell arteritis histology on a temporal artery biopsy (2).

Answer 39

Extensive infiltration of lymphocytes, plasma cells, and macrophages
IEL ruptured with breaks

Question 40

Describe how a healed giant cell arteritis histology appears on a temporal artery biopsy (4).

Answer 40

Little evidence of cellular infiltrates
Prominent thickening of the intima
No evidence of media inflammation but scarring present
Linking of intima with media through ruptured IEL

Question 41

What vessels does giant cell arteritis tend to affect?

Answer 41

Large muscular and elastic arteries

Question 42

Are any retinal or optic nerve arteriolar problems with giant cell arteritis directly due to GCA or secondary?

Answer 42

Secondary

Question 43

What kind of disease is GCA and what does it structure is targetted? What does this suggest of central retinal artery involvement? What ocular structure can it affect?

Answer 43

It is often an autoimmune disease targetting the IEL
-will therefore rarely affect the CRA within the eye
-can affect the SPCA within the choroid

Question 44

Is GCA usually chronic or acute?

Answer 44

Chronic