Ocular Abnormality- Hypertension & Haematological Disease

Front 1

Cardiovascular disease CVD affects what percentage of the population?

Back 1

50%

Front 2

50% of over 65s suffer from what?

Back 2

Hypertension

Front 3

Recap- what are arteries, veins and capillaries?

Back 3

• Artery: muscular (pump, resist pressure)- 25% blood vol. (pressure reservoir)

• Capillary: highly permeable

• Vein: lower pressure, valves- 75% blood vol. (volume reservoir)

Front 4

What happens to arteries with age?

Back 4

• Vessels stiffen with age

• Less elastic

• ↑ damage by sheer stress

• Lumen ↓

• Atherosclerosis- “fatty streak” – fibrosis (protrusion)

• Same blood volume

Front 5

Blood is ejected at....?

Back 5

...high pressure

Front 6

What do arteries do with this high pressure blood flow?

Back 6

Arteries smooth pressure changes – more constant in periphery (heartbeat fluctuations)

Front 7

What happens to elastin fibres with age?

Back 7

Elasticity decreases with age, which increases pressure changes

Front 8

Where is reverse pressure wave more prominent?

Back 8

More prominent in periphery (smaller vessel and proximity)

Front 9

What affect does the ripple effect have?

Back 9

absorbed when young

• summative with vessel stiffness

(∴ further ↑ in BP)

Front 10

What is sphygmomanometry?

Back 10

Measuring blood pressure

Front 11

How is blood pressure measured?

Back 11

Should be performed by optometrists!

• Restrict blood flow (supra-pressure)

• Gradually reduce

• First blood through (systolic)

• Flow normalised (diastolic)

Front 12

What can affects the blood pressure reading?

Back 12

• Cuff size (too small ↑10-40mmHg)

• Clothing (↑ 10-50mmHg)

• Rest (seated for 5 minutes)

• Posture (back supported, legs uncrossed, arm on desk)

• Stress (white-coat hypertension)

• Talking

• Smoking, alcohol, caffeine (30 minutes before)

• Temperature (cold office can increase blood pressure)

• Exercise

Front 13

Blood pressure stages

Back 13

Front 14

What is Arteriosclerosis?

Back 14

Thickening of vessel wall

Hyalinisation

Hypertrophy

Hyperplasia

Front 15

What is Hyalinisation?

Back 15

Reduced flexibility

Front 16

What is Hypertrophy?

Back 16

Thickening= constriction

Front 17

What is Hyperplasia?

Back 17

Cell proliferation

Front 18

Why does hypertensive retinopathy develop?

Back 18

as the vascular anatomy is gradually degraded by persistent increase(s) in blood pressure

Front 19

What are the stages of hypertensive retinopathy?

Back 19

• Vasoconstrictive phase

• Sclerotic phase

• Exudative phase

• Malignant Hypertension

Front 20

What is the Vasoconstrictive phase of hypertensive retinopathy?

Back 20

• vasospasm and arteriole narrowing

• ↓ A:V ratio (veins unchanged)

• Some damaged vascular segments can’t undergo narrowing ∴ focal arteriolar narrowing (esp. older Px)

Front 21

What is the Sclerotic phase of hypertensive retinopathy?

Back 21

• Intimal thickening

• Medial hyperplasia

• Hyaline degeneration of vessel wall

• Severe narrowing, compression of underlying veins, broad and brighter reflex.

Front 22

What is the Exudative phase of hypertensive retinopathy?

Back 22

• Retinal haemorrhages (dot, blot, flame)

• Hard exudates (macular star)

• Necrosis of smooth muscle and retinal ischemia (cotton wool spots)

Front 23

What is Malignant Hypertension?

Back 23

Severely raised intracranial BP causes optic nerve ischemia and oedema:

• Papilloedema

Front 24

State the 4 stages of hypertensive retinopathy.

Back 24

1. Arteriosclerosis (thickening of vessel wall)

2. Arterial narrowing (general / focal)

3. Cotton-wool spots (ischemia)

4. Haemorrhages (vascular leakage)

Front 25

What is this?

Back 25

Arteriosclerosis

Front 26

What is this?

Back 26

Arterial narrowing

Front 27

What is this?

Back 27

Cotton-wool spots (ischemia)

Front 28

What is Grade I of the Keith-Wagner-Barker grading scale?

Back 28

Generalised arterial narrowing (+ mild increase in reflex)

Front 29

What is Grade II of the Keith-Wagner-Barker grading scale?

Back 29

• Obvious ↑ arterial light reflex

• Salus’ sign – S-deflection of veins at A:V crossing (no tapering)

Front 30

What is Grade III of the Keith-Wagner-Barker grading scale?

Back 30

• Copper wiring

• Bonnet’s sign – vein deflected away from A:V crossing

• Gunn’s sign – tapering of vein either side of A:V crossing (“nipping”)

Front 31

What is Grade IV of the Keith-Wagner-Barker grading scale?

Back 31

G III and silver wiring (NOT occlusion)

Front 32

What are the issues with the KWB grading scale?

Back 32

• Subjective

• Out-dated

• Subtle cases

• Longitudinal changes

Front 33

KWB grading scale

Back 33

KWB grading scale

Front 34

Scheie grading scale

Back 34

Comparison

Front 35

What is the underlying mechanism to vessel tortuosity?

Back 35

veins less muscular, less able to adjust to ↑ pressure

Front 36

What is this?

Back 36

Macular star

Front 37

What is macular star?

Back 37

• Seen in severe cases of hypertensive retinopathy

• Hard exudates deposited around macula

• Associated with macular oedema

Front 38

What is the management for hypertensive?

Back 38

• Some GPs – newly-diagnosed hypertensive scheme

• Measure BP?

• Advise Px

• See GP

• Lifestyle

• Family Hx

Front 39

How would you record vessel appearance?

Back 39

• Tortuosity

• Branching angles

• Fractal dimension

Front 40

What is Malignant Hypertension?

Back 40

• Sudden, rapid, severe increase in blood pressure (aka accelerated hypertension)

• BP: >220/120mmHg (syst./diast.)

• Papilloedema

• ASx (h/a?)

Front 41

How do you manage Malignant Hypertension?

Back 41

• Emergency – require specialised anti-hypertensive therapy

• At risk of further damage

Front 42

What is Hypertensive Choroidopathy?

Back 42

• Rare

• Acute hypertensive crisis (young adults, pre-eclampsia)

• Non-perfusion (lobular – anatomy of vasculature)

Front 43

Name some haematological pathologies.

Back 43

• Sickle-cell anaemia

• Leukaemia

• Hyperviscosity

• Valsalva manoeuvre

Front 44

What is Sickle-cell anaemia?

Back 44

• Genetic condition (African, Caribbean, Middle Eastern, Asian)

• Unusual shaped RBCs (esp. in hypoxia & acidosis)

• short life span

• ↑ rigidity - prone to block blood vessels

Front 45

What are the steps of proliferative sickle cell retinopathy?

Back 45

1. Peripheral arterial occlusion

2. Peripheral AV anastomoses – pre-existing capillaries

3. Neovascularisation from anastomoses – sea-fan

4. Proliferation continues → vitreous haemorrhage

5. Fibrovascular proliferation → tractional RD

Front 46

What is Leukaemia?

Back 46

Cancer of WBC

• Acute / Chronic:

1. Lymphocytes (NB – attack virus cells)

2. Myeloid cells (NB – protect cell, fight bacteria)

Front 47

What are the secondary changes with Leukaemia?

Back 47

• Haemorrhage

• Infection

• Occlusion

• Non-retinal (iritis, CN palsies, hyphaema …)

Front 48

What is Acute leukaemia?

Back 48

• Haemorrhages, CW spots, Roth spots (haemorrhage with white centre)

• Haemorrhage →WBC adhesion to damaged endothelium → coagulate

Front 49

What is Chronic leukaemia?

Back 49

• Peripheral neovascularisation

• Choroidal deposits (leopard-print retina)

Front 50

What is Hyperviscosity?

Back 50

“Sticky blood”

• Secondary to underlying pathology

• Polycythaemia

• Proliferation of RBCs

Front 51

What is Valsalva retinopathy?

Back 51

• ↑ intrathoracic pressure

• ↑ in BP, baroreceptors in aorta: ↓ cardiac output, ∴can feel dizzy

• ‘Pop’ ears with a cold

Front 52

What can happen with Valsalva retinopathy?

Back 52

• Spontaneous haemorrhage of capillaries:

- Pre-retinal haemorrhage

- Subconjunctival haemorrhage

• ASx

• Vision affected depending on location of haemorrhage

• Resolve (if serious, refer)