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OD3 - Clinical Optometry Practice > DIS - Diseases of the Vasculature II: Ocular Vessel Disease - Week 9 > Flashcards

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

1
Q

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?

A

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

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2
Q

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

A

5% is malignant

Pressure rise is large and acute

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3
Q

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

A

Malignant

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4
Q

What is hypertension defined as, both systolic and diastolic?

A

Systolic ≥160mmHg

Or diastolic ≥95mmHg

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5
Q

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

A

Cardiac output and peripheral vascular resistance

Increase in either increases blood pressure

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6
Q

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

A

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

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7
Q

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

A

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

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8
Q

What is the relationship between hypertension and arteriosclerosis?

A

Arteriosclerosis can lead to hypertension

Hypertension can accelerate arteriosclerosis

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9
Q

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

A

Yes

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10
Q

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

A 
Stiffened/thickened wall
Narrow arteriolar lumen
Raised BP
Vascular SM hypertrophy
Collagen deposition
Breakdown of elastin
Endothelial dysfunction
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11
Q

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

A 
Endothelial damage and proliferation
Causes turbulent blood flow
-thrombus risk
-local haemorrhage
-local ischaemia
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12
Q

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

A

Poorer gaseous exchange

  • also thickened vascular wall (a consequence of increased blood pressure)
  • can cause local ischaemia
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13
Q

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

A

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

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14
Q

Does high blood pressure cause poor capillary perfusion?

A

Yes

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15
Q

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

A

Clinically coincident

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16
Q

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

A

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

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17
Q

List 5 stages of malignant hypertension by clinical appearance.

A 
Haemorrhage
Hard exudates
Oedema
Cotton wool spots
Collaterals
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18
Q

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

A

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

19
Q

What four things can vascular endothelial damage cause?

A

Haemorrhage
Exudates
Oedema
Ischaemia

20
Q

What is meant by the hosepipe effect?

A

Straightening of the vascular tree due to hypertension

21
Q

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?

A

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

22
Q

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?

A

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

23
Q

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

A

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

24
Q

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

A

No, they are usually seen together

25
Q

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

A

Vessel narrowing

-this implies that hypertension usually accelerates arteriolosclerosis

26
Q

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

A

Hypertensive vascular spasm followed by arteriolosclerosis

27
Q

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

A

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

28
Q

What does the profile of a retinal haemorrhage indicate?

A

Its position within the nerve pathway

29
Q

Define vasculitis.

A

General term for vascular inflammation

30
Q

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

A

Immune mediation
Respond to immune suppressants
Cause usually unknown

31
Q

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

A

One or more of the classic hypersensitivity reactions

32
Q

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

A 
Giant cell arteritis (most common)
Phlebitis
Polyarteritis nodosa
Systemic lupus erthyematosus
Sjogrens syndrome
Behcets disease
33
Q

List four main clinical signs of giant cell arteritis.

A

AION
Vision loss
Jaw/scalp tenderness
CRAO

34
Q

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?

A

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

35
Q

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?

A

Raised CRP levels
Blood blecomes sticky
Causes raised ESR

36
Q

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

A

Yes it is, risk of cardiac failure

37
Q

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?

A

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

38
Q

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

A

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

39
Q

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

A

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

40
Q

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

A

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

41
Q

What vessels does giant cell arteritis tend to affect?

A

Large muscular and elastic arteries

42
Q

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

A

Secondary

43
Q

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?

A

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
44
Q

Is GCA usually chronic or acute?

A

Chronic

OD3 - Clinical Optometry Practice (114 decks)

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