1-12 RVD - Hypertension + Prematurity Flashcards

1
Q
  • 3 characteristic cellular features of aterioles in Hypertensive Retinopathy
  • Complications of HTR?
A
  • Vasoconstriction (Caused by high BP)
  • Sclerotic (Induced arteriolosclerosis)
  • Exudative (Inner BRB disrupted, blood and fluid leaks causing oedema)

Can complicate to:
- other retinal vascular disorders e.g. RVOs, RAOs
- Hypertensive optic neuropathy and choroidopathy
Can be presenting sign of hypertensive emergency

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2
Q

Signs of HTR

A

Ateriole narrowing:
- Constricted + tortuous arterioles
- Focal or generalised.
Arteriosclerosis:
- Presents as copper or silver wiring. This is because the “BVs” seen in fundus imaging is actually just the blood w/ a light reflex down the middle of it. When wall thickens, the red part becomes smaller whilst the light reflex becomes broader and duller.
AV crossing abnormalities present too (since artery is big, it bends the veins around it)

Vascular leakage
- Retinal haemorrhages (flame mostly)
- CWS
- Hard exudates, macular star
- Retinal oedema (ONH maybe too)

If malignant, can affect choroid
- Siegrist streak = Hypopigmented streaks follow choroidal vessel. Later progression leads to hyperpigmented
- Elschnig spots = Concentrated RPE death areas. Hyperpigmented spot w/ paler ring around it.

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3
Q

HTR Retinal arteriosclerosis grading?

A

Scheie classification
Grade:
0 = No abnormalities
1 =
- Subtle light reflex
- Mild arteriolar attenuation
- Vein concealment
2 =
- Obvious broadening of arteriolar light reflex
- Salus’ sign (Defelction of veins at AV crossings)
3 =
- Copper wiring
- Bonnet sign (Banking of veins distal to AV crossings)
- Gunn sign (tapering of veins either side of AV crossing)
- Right angled vein deflection
4 =
- Silver wiring + grade 3

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4
Q

Scheie grading system for HTR

A

Schieie:
0 = HTN w/o HTR
1 =
- diffuse uniform narrowing
2 =
- Pronounced narrowing
- w/ focal constriction
3 =
- Obvious + severe narrowing
- Obvious + severe focal constriction
- Retinal haemorrhages
4 =
- Above
- Retinal oedema
- ONH oedema
- Hard exudates

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5
Q

Keith Wagner Barker grading system for HTR

A

Keith:
1 = A/V ratio >= 1/2
2 = A/V ratio =< 1/2
3 =
- A/V ratio =< 1/2
- Retinal oedema
- Retinal haemorrhages
- Hard exudates
- CWS
4 =
- Above
- ONH oedema

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6
Q

Define ROP:
- What is it?
- Describe vascularisation process normally

A

Retinopathy of prematurity:
Incomplete development of retinal vasculature due to premature birth.
Because retinal vasculature complete just before birth.
- at 14-16 weeks, avascular retina w/ vascularisation starting at ONH and slowly growing outwards.
- at 32 weeks, vasculogenic wave reaches nasal ora serrata
- at 40-42 weeks, reaches temporal ora serrata

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7
Q

ROP
- Risk factors (4 things)

A
  • Short gestational age
  • Low birth weight
  • High unregulated O2 supplements post-birth
  • Systemic illness
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8
Q

Pathogenesis of ROP

A

Phase 1:
- Hyperoxic state after birth in contrast to in utero
- Relatively high O2 reduces VEGF synthesis
- Peripheral BVs stop growing
Phase 2:
- Higher O2 demand as baby grows
- Higher HIF-1-alpha upregulates VEGF expression
- Uncontrolled, anomalous proliferation of BVs -> fibrous, bursting, haemorrhages, tractional…

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9
Q

How is ROP classified?

A

Active stages divided into zones. Zone:
I = within 2x ONH to macula distance
II = within same distance between ONH to nasal ora serrata
III = Every other part not covered by zones I or II.
Stages describe severity. Stage:
0 = Before ROP develops, vascularisation is incomplete
1 = Sharp, flat demarcation line separates vascular vs avascular
2 = Lines extends towards vitreous, elevated ridge
3 = Extraretinal fibrovascular proliferations + neovascularization from ridge, into vitreous
4 = Partial RD
5 = Total RD
Extent recorded in clock hours.

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10
Q

ROP prognosis

A

Weeks to days.
- 75% cases milder ROP, sponteanous regression w/o treatment
Increased risk of
- strabismus, high Rx, and cataract -> amblyopia
- Cicatricial sequelae (Vitreoretinal fibrosis, macula + disc dragging, late RD)
- Secondary glaucoma (neovasc spreads to AC or just because they’re preterm)

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11
Q

ROP Tx?

A
  • Ablation of avascular peripheral retina to minimis TRD risk (laser photocoagulation)
  • Intravitreal anti-VEGF stops BV growth
  • Pars planar vitrectomy
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12
Q

Describe Coat’s disease
- What is it?
- Appearance?
- Tx?

A

Primary developmental retinal telangiectasia (abnormally shaped BVs at the far end so capillaries mostly).
- Seen as dilatation and tortuosity.
- Unilateral, mostly in men, likely within 10 years of age
- Intra- and subretinal exudate accumulation, esp. beneathe macula. Often leads to CMO or exudative RD, or later on cause iris NV.
- Treated w/ anti-VEGF, laser photocoagulation, or pars planar virectomy. If neovasc glaucoma, can remove entire eye if too painful and eye not working anyway.

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13
Q

Two variants of Coat’s disease?

A

Leber’s miliary aneurysms
- Milder
- Resembles millet seeds
- Later presentation in life, localised
- Better prognosis
Type 1 idiopathic macular telangiectasia
- Idiopathic aneurysmal telangiectasia
- Adult onset at middle age, at macula, affects males.

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