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Ophthalmology > Retinal Disorders > Flashcards

Retinal Disorders Flashcards

1
Q

What kind of tests can we do to inspect the retina? [6]

A
  • Direct Ophthalmoscope
  • Optical Coherence Tomography (OCT)
  • Fundus Fluorescein Angiography (FFA)
  • Electrical Physiology including Electroretinogram (ERG), Electroculogram (EOG) and Visually Evoked Potentials (VEP)
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2
Q

What is Optical Coherence Tomography? [1]

A

A cross sectional scan of the Fovea Centralis (Macula)

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3
Q

How does a Fundus Fluorescein Angiography work?

A

Fluorescein dye injected

  • > Binds to blood proteins
  • > Blue light shone in and excites the fluorescein
  • > Light returns and the yellow-green light is isolated with a filter
  • > Yellow-green light shows shines on a film
  • > Fluorescein filled vessels appear white

This will help you spot any blockages or bleeds from an optical artery

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4
Q

Name 3 of the 9 retinal layers

A

Layers 1,2 & 9
1 - Retinal Pigment Layer
2 - Layer of rods and cones
9 = Inner cell fiber layer

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5
Q

What is electrical physiology? [1]

Give 3 examples

A

Series of investigations recording electrical signals from the eye, optic nerve or brain in response to visual sitmuli [1]

Includes:

  • Electroretinogram (ERG)
  • Electrooculogram (EOG)
  • Visually Evoked Potentials (VEP)
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6
Q

What does an electroretinogram test? [3]

A

Action Potentials in the retina in order to measure retinal function

An A wave ERG tests photoreceptors
A B wave ERG tests Muller’s Cells (Retinal Glial cells)

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7
Q

What does an Electrooculogram test?

What does it measure? [2]

A

Function of retinal pigment epithelium and photoreceptors (Layers 9 & 8). [2]

It measures the Resting Potential in both layers and forms a ratio called the Arden Ratio (1.85 is normal)

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8
Q

What does a Visually Evoked Potentials (VEP) Test measure? [2]

A

They record optic nerve function [1] by measuring electrical activity in the visual cortex [1] in response to stimuli. (if optic nerve isnt working the visual cortex wont be active)

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9
Q

VEP test: state the clinical significance of each of these pathological signs:

  • Reduced amplitude [2]
  • Latency in signal [2]
A

A reduced amplitude in the signals means theres a reduced cell number. Most often due to Ischaemic or Traumatic Optic Neuropathy.

Latency in the signal means the cell function is reduced. Most often due to Optic Neuritis causing demyelination.

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10
Q

List some retinal disorders

A
  • Central Retinal Vein Occlusion
  • Central Retinal Artery Occlusion
  • Ischaemic Optic Neuropathy
  • Optic Neuritis
  • Retinal Detachment
  • Age Related Macular Degeneration
  • Diabetic Retinopathy
  • Hypertensive Retinopathy
  • Inherited Retinal Dystrophies
  • Drug Induced Retinopathy
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11
Q

What retinal disorders cause a gradual visual loss [4] and which a sudden visual loss [4]?

A

Gradual:

  • Age-related Macular Degeneration
  • Diabetic Retinopathy
  • Inherited Retinal Dystrophies
  • Drug Induced Retinopathy

Sudden:

  • Retinal Detachment
  • Optic Neuritis
  • Ischaemic Optic Neuropathy
  • Central Retinal Artery or Vein Occlusion
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12
Q

What causes Central Retinal Vein Occlusion [4]

What causes Central Retinal Arterial Occlusion [2]

A

CRVO:

  • Hypertension
  • Glaucoma
  • Hyperviscosity eg polycythemia
  • Inflammation eg DM

CRAO:

  • Emboli from atheromatous plaque, valve, dental abscess
  • Inflammation eg SLE, IVDU
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13
Q

How does the retina appear on Central Retinal Vein [3] /Artery Occlusions?

A 
CRVO:
- The retina is darker
- Tortuous dilated and engorged veins
- Macular & Optic Disc Oedema
- Cheesy pizza! Flame shaped hemorrhages
All because of the back up of blood

CRAO:

  • Pale retina, cherry red spot at macula
  • Conspicuously lacking blood
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14
Q

What are the types of Ischaemic Optic Neuropathy? [3]

A

Arteritic (AION) - Usually caused by giant cell arteritis

Non-Arteritic (NAION) - Unknown cause

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15
Q

AION

  • Definition [2]
  • GCA presentation [6]
  • GCA investigations [2]
  • Treatment [2]
A 
Optic nerve damage [1] when posterior ciliary arteries are blocked [1] by inflammation or atheroma
GCA presentation
- Headache
- Scalp Tenderness
- Jaw Claudication
- Neck Pain
- Nausea/Anorexia
- Visual Loss/Diplopia

Test for inflammatory markers & a Temporal Artery Biopsy
Carry out ix before steroids

Treatment

  • Prednisolone 80mg for 24h PO
  • Taper steroids as ESR and symptoms settle, may take >1y
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16
Q

What are the symptoms of optic neuritis [4] and its cause [1]?

A
  • Pain on eye movements
    • acute onset Loss of vision (central scotoma)
  • Relevant Afferent Pupil Defect
  • Swollen Optic Disc

MS!

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17
Q

Define scotoma

A

Loss of visual acuity [1] in a specific area of vision [1]

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18
Q

What are the risk factors for age related macular degeneration? [3]
ARMD nature of vision loss [3]

What are the types of Age Related Macular Degeneration and explain differences in pattern of vision loss?

A

Age
Smoking
Poor Diet (B12 def)

Progressive loss of the central vision with distortion (metamorphopsia). Quiet eye.

Wet (20%) - sudden
Dry (80%)- slow onset, gradual

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19
Q

Wet AMD pathogenesis [2]
Dry ARMD description [2]
Fundal signs [4]

A

Wet AMD occurs when aberrant vessels grow from the choroid into neuro-sensory retina and leak

Dry ARMD- drusen and degenerative changes at the macula

Ophthalmoscope:

  • Optic disc edge is made irregular by lumpy, yellow matter
  • Optic cup absent
  • Vessels show abnormal branching patterns
  • Disciform scar - as blood vessels grow subretinally and bleed, blood reabsorbs with subsequent fibrosis and raised sub retinal scar is left
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20
Q

Diabetic retinopathy
What is the main first step in microvascular disease of diabetes in the eye?
Ocular changes can be classified into 2
Ocular changes can also be staged into 2

A

Microvascular disease leads to ocular ischemia and hypoxia, increased VEGF

Ocular changes can be classified into

  • Structural changes
  • Retinopathy

Stages:

  1. Non-proliferative diabetic retinopathy
  2. Proliferative diabetic retinopathy
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21
Q

What are Retinal Dystrophies? [3]

A

A large number of inherited disorders [1] which affect photoreceptor function [1] leading to Progressive Visual Loss [1]

22
Q

What are the types of retinal Dystrophies? [4]

A

Photoreceptor Dystrophies e.g. Retinitis Pigmentosa
RPE-Dystrophies (Retinal Pigment Epithelium) e.g. Stargardt Macular Dystrophy
Choroidal Dystrophies
Vitreoretinal Dystrophies

23
Q

What is retinitis Pigmentosa [2] and its inheritance [1]

Symptoms [2]

A

Causes severe degeneration [1] of the Rod photoreceptors [1]

Can be Autosomal dominant, recessive or x-linked. [1]

Night blindness
Tunnel vision loss (loss of peripheral retina)

24
Q

Name some drugs that cause drug-induced retinopathy? [3]

Pattern of loss of vision in drug-induced retinopathy [1]

A

Antimalarials
Phenothiazines
Tamoxifen

All can lead to gradual loss of vision

25
Q

List some modern treatments for retinal diseases? [2]

A

Gene Therapy

Bionic Eye

26
Q

How does Gene Therapy work for retinal disorders? [3]

A
  • Disorder due to a defective or missing gene (E.g. Choroideraemia)
  • Viral vector inserts replacement gene
  • Replacement gene synthesises protein
27
Q

CRAO
Presentation [2]
Signs [3]

A

Presentation

  • Dramatic visual loss within seconds of occlusion
  • Episodes of amaurosis fugax

Signs:

  • Afferent pupil defect + cherry red spot (fovea)
  • retina appears pale
  • may see emboli inside arteries
28
Q

CRVO
Compare pattern of visual loss to CRAO and explain this difference [2]

State 2 types of CRVO

A

Pattern of visual loss

  • Sudden painless visual loss
  • Less sudden than CRAO why?
  • Mechanism of visual loss due to development of ischemia and macular edema

Non-ischemic, ischemic CRVO

29
Q 
CRVO
Investigation
What is the treatment given and why [2]
Prognosis [2]
What should you aim to prevent long term [1] and how [4]
A

Fundus fluorescein angiogram
- Determines degree of ischemia

Treatment

  • Pan-retinal photocoagulation [1] prevents and treats neovascularisation [1]
  • Aim to prevent rubeotic glaucoma and painful eye
  • Give beracizumab for macular edema
  • dexamethasone intravitreal implants

Prognosis - visual prognosis is poor [1] even if macular edema resolves anatomically [1]

30
Q

BRVO

  • presentation [1]
  • explain difference [2]
A

Presentation

  • Asymptomatic if macula not affected
  • Unilateral visual loss
  • Visual field defect corresponds to affected area

Only a portion of retina is affected as opposed to the whole retina in central retinal a/v occlusion
But otherwise same predisposing factors as CRVO

31
Q

Explain how retinal ischemia can cause macular edema [4]

A
  • Retinal ischemia leads to release of VEGF [1]
  • neovascularisation [1]
  • fragile and leaky blood vessels [1]
  • prone to hemorrhage [1]
  • macular edema
32
Q

Explain how drusen is formed in pathogenesis of dry ARMD [4]

A

Drusen signify optic nerve head axonal degenration [1]
Abnormal axonal metabolism leads to intracellular mitochondrial calcification [1]
Some axons rupture and mitochondria are extruded [1] into extra-cellular space
Calcium is deposited here and drusen form [1]
This causes the optic disc head to become irregular and lumpy and the optic cup to become absent with abnormal branching vessels

33
Q

AMD risk factors [4]
Symptoms [5]
Signs [3]

A

RF:
- increasing age, smoking, CV RFs, FHx
Sy:
- initially no deterioration in visual acuity but difficulty making out images
- difficulty reading and making out faces
- difficulty with night vision and changing light conditions (specifically changes in Amsler grid self-evaluation and trouble with reading)
- visual fluctuation, metamorphsia (distortion of central vision)
- central vision loss

Si:

  • poor visual acuity (especially near vision early in disease)
  • full peripheral field
  • quiet eye
34
Q 
Diabetic retinopathy Classification
Mild NPDR
Moderate NPDR [5]
Severe NPDR [3]
Proliferative diabetic retinopathy features

Structural changes

  • Age-related cataracts (AGE)
  • Ocular ischemia causing neovasculargenesis (rubeosis)
  • Glaucoma
A

Mild NPDR
- 1 or more microaneurysm

Moderate NPDR

  • microaneurysms
  • blot haemorrhages
  • hard exudates
  • cotton wool spots, venous beading/looping
  • intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR:

  • blot haemorrhages and microaneurysms in 4 quadrants
  • venous beading in at least 2 quadrants
  • IRMA in at least 1 quadrant

Stage 1: hyperglycemia damages pericytes but eye exam normal
Proliferative:
- hypoxia causes increased VEGF > neovascularisation
- fragile leaky capillaries are prone to bleeding
- Vitreous hemorrhage > increased risk of RD due to fibrosis causing traction
- Maculopathy - leakage from vessels near macula cause edema

35
Q

Name 3 types of hemorrhages you would see on PDR
Name 3 conditions that accelerate development of DM retinopathy
Treatment modalities [4]

A

Types of hemorrhages: blot, flame shaped, vitreous

Conditions that accelerate DM retinopathy:

  • Pregnancy
  • Dyslipidemia, high BP
  • Renal disease, smoking, anemia

Treatment

  • Good glycemic control
  • Laser photocoagulation for maculopathy and proliferative retinopathy
  • Triamcinolone, anti-VEGF (intravitreal)
  • Vitrectomy if big VH
36
Q

Describe the outcomes laser photocoagulation [2]

A

Outcome of laser photocoagulation:

  • Will not improve vision
  • Aim to prevent blindness
37
Q

CRAO Ax [3]

A

Ax:
• Carotids: atheromatous disease causes fibrin-platelet emboli; often gives rise to amaurosis fugax
• Heart: calcifications from aortic valves, endocarditis or SLE vegetation, mural thrombus (AF), atrial myxoma
• Vasculitis: vaso-occlusion due to GCA, PAN or SLE

38
Q

CRAO Mx [5]

Long term plan

A
  • form of stroke; mx according to local stroke protocols*
  • If seen within 6h of onset, aim is to increase retinal blood flow by reducing IOP by ocular massage
  • Hyperbaric oxygen, inhaled carbon
  • Identify and treat CV risk factors
  • Surgical: Anterior chamber paracentesis (of aqueous humor)
  • Infusion of tPA in opthalmic artery

o Long term: primary prevention of CVS RFs to minimise further events

39
Q

CRVO RF [5]

A
  • increasing age, HTN, DM
  • open angled glaucoma
  • hypercholesterolemia
  • hyper viscosity (polycythaemia, leukaemia, Waldenstrom’s macroglobulinaemia)
  • inflammatory (sarcoidosis, Bechet’s disease)
40
Q

CRVO Mx

3 modalities

A

Manage 3 areas:

  • Vision loss
  • Retinal neovascularisation: photocoagulation
  • Prevent rubeotic glaucoma and painful eye
41
Q

CRVO Rx
Vision loss [2]
Prevent rubeotic glaucoma and pain fun eye [2]

A

• Vision loss:

  • intra-vitreal anti-VEGF
  • DEXAMETHASONE implants or intravitreal TRIAMCINOLONE ACETONIDE

• Prevention of rubeotic glaucoma and painful eye:

  • RANIBUZUMAB for macular oedema, lasers
  • intravitreal DEXAMETHASONE implants
42
Q

Retinitis pigmentosa
Fundoscopy [2]
Ix [4]

A

Fundoscopy:

  • black bone spicule shaped pigmentation in peripheral retinal
  • mottling of retinal pigment epithelium

Ix:

  • slit lamp examination
  • genetic testing
  • electro retinopathy
  • visual field perimetry
  • optical coherence tomography
43
Q

Retinitis pigmentosa

Mx [2]

A

Mx:

  • incurable but vitamin A
  • mx of any co-existing cataracts or glaucoma can help slow progression
44
Q

Vitreous haemorrhage

Ax [8]

A
  • proliferative diabetic retinopathy (50%)
  • branch or central retinal vein occlusion
  • sickle cell anaemia
  • retinal hole or retinal tear formation
  • wet disciform macular degeneration
  • posterior vitreous detachment
  • Valsalva phenomenon
  • posterior uveitis
45
Q

Vitreous haemorrhage
Symptoms [4]
Signs apparent on large hemorrhage [4]

A
  • sudden, painless loss of vision or haze
  • red hue in vision
  • floater
  • shadows or dark spots in vision
    Signs:
  • reduced visual acuity, absent red reflex
  • retina cannot be seen
  • visual field defect
46
Q

Vitreous haemorrhage
Ix [3]
Prognosis

A

Ix:

  • dilated fundscopy (vitreous haemorrhage)
  • slit-lamp (RBC in anterior vitreous)
  • B-scan USS to identify cause

Prognosis: usually spontaneously absorbs

47
Q

Vitreous haemorrhage Mx

  • Dense VH [1]
  • DM patients with previous photocoagulation and recurrent VH
A

Vitrectomy to remove blood for dense VH

DM patients with previous photocoagulation and recurrent VH: acceptable to wait 3m for resolution

48
Q

Mx of AMD
Dry [3]
Wet [3]

A

Dry AMD:
• Glasses and visual aids - magnifiers
• Social support including blind registration if required
- zinc and anti-oxidant vitamins A, C and E may reduce progression

Wet AMD:
• Argon laser photocoagulation may be helpful in early neovascular macular degeneration,
to ablate membrane of new vessels and prevent bleeding
• Intravitreal anti-VEGF (Avastine, Lucentis) monoclonal antibodies treatment
• Cold laser + Verteporfin to ablate membrane of new vessels and prevent bleeding

49
Q

Fundoscopy of AMD features of:
Dry [3]
Wet [3]
2 other investigations

A

o Dry:
- drusen (colloid bodies)
- retina appears dry with areas of hyperpigmentation
- prominent choroidal vessels
o Wet:
- fluid exudates
- localised detachment of pigment
- disciform scar (subretinal blood vessels grow and bleed and blood is reabsorbed with subsequent fibrosis and a raised subretinal scar)
Ix: slit lamp, fluorescein angiography (if considering laser)

50
Q

AMD prognosis

A

wet carries worse prognosis (progresses more rapidly) but dry is less treatable

Ophthalmology (10 decks)

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