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Opthalmology > Gradual vision loss > Flashcards

Gradual vision loss Flashcards

1
Q

ARMD : Anatomy

A
  1. Macula : area of the retina,
    Responsible for central vision
  2. Fovea centralis : a small depression within the macula which contains a high concentration of ‘Cone cells’
  3. Cone cells : Photoreceptor cells responsible for colour vision
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2
Q

ARMD : Layers of the macula

A

Layers of the Macula
1. Photoreceptor cells (cone cells)
2. Retinal pigment epithelium
3. Bruch’s membrane
4. Choroid layer - base which contains the blood vessels that supply the macula

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3
Q

Dry age related macular degeneration : Pathophysiology

A
  1. Drusen accumulation ;
    * Deposit of lipids and potions
    Between the retinal pigment epithelium and Bruch’s membrane
    * Thinning and dysfunction of the Retinal pigment epithelium
  2. Retinal pigment epithelium dysfunction
    * RPE provides support and nourishment for the cone cells
    * Accumulation of Drusen reduces nutrient exchange
  3. Atrophy of Photoreceptor cells
    * Gradual loss leads to decline in central vision
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4
Q

Wet age related macular degeneration: Pathophysiology

A
  1. Over-expression of vascular endothelial growth factor
    * stimulate formation of new abnormal blood vessels from the choroid
  2. Neovascularisation :
    * New vessels develop from choroid layer and travel up to the retina
  3. Increased Permeability:
    * The abnormal blood vessels in wet AMD are very permeable
    * Allow fluids, proteins, and blood to leak into the retinal tissue and the subretinal space
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5
Q

Age related macular degeneration: Complications

A
  1. Macular Edema:
    * Macula swelling caused by the leakage of fluid into the macula * Disrupts the macula, affecting vision
  2. RPE Detachment:
    * The growth of abnormal blood vessels can lead to
    * Detachment of the retinal pigment epithelium (RPE) from the underlying Bruch’s membrane.
  3. Vison loss
    * Photoreceptor Damage
    * The accumulation of fluid, blood, and other materials in the macula can damage the photoreceptor cells, which are essential for vision.
  4. Macular scarring - fibrous tissue can develop in advanced stages
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6
Q

Age related macular degeneration: Risk factors

A
  • Older age > 75 years
  • Smoking > 2x
  • Family history
  • Cardiovascular disease (e.g., hypertension)
  • Obesity
  • Poor diet (low in vitamins and high in fat)
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7
Q

ARMD : Clinical features

A
  1. Unilateral
  2. Onset : Gradual loss of Central vision - macula has high metabolic demand thus accumulates more oxidative stress
  3. Reduced visual acuity :
  • Deterioration of vision at night, worsening ability to read small text
  • Crooked or wavy appearance to straight lines (metamorphopsia) - cones are responsible for detailed vision
  • Flickering lights
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8
Q

Wet ARMD : Clinical features

A

Onset : More acutely

  • Develops within days - complete loss within 2-3 years
  • Often progresses to bilateral disease.
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9
Q

ARMD : Clinical signs on examination

A
  1. Snellen chart : Reduced visual acuity
    * Scotoma (an enlarged central area of vision loss)*
  2. Amsler grid test : assess for the distortion of straight lines seen in AMD
  3. Fundoscopy :
    * Drusen, yellow areas of pigment deposition
    * Wet ARMD : show red patches of sub retinal haemorrhage*
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10
Q

ARMD : Investigations

A

Initial investigation
1 . Slit lamp examination
* gives a detailed view of the retina and macula.

2 . Optical coherence tomography
* gives 3D view of the layers of the retina and is used for diagnosing and monitoring AMD.

3 . Fluorescein angiography
* if wet ARMD is suspected
fluorescein contrast and photographing the retina to assess the blood supply,
* showing oedema and neovascularisation in wet AMD.

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11
Q

ARMD : Management

A
  1. General advice : Avoid smoking, control BP
  2. First line : combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third
  • Wet ARMD
    1. Intravitral injection of anti-VEGF medications : Ranibizumab
    2. Laser photocoagulation : slows progression of ARMD when there is a new vessel formation
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12
Q

Diabetic retinopathy : Definition

A

Diabetic retinopathy involves damage to the retinal blood vessels due to prolonged high blood sugar levels.

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13
Q

Diabetic retinopathy : Pathophysiology

A

1 . Hyperglycaemia :
High blood sugar damages the retinal small vessels and endothelial cells.

2 . Increased vascular permeability :
* leads to leaking blood vessels
* Leaking of blood, lipid and proteins : Blot haemorrhages and hard exudates

3 . Blood vessel damage
* Microaneurysms are small bulges in the blood vessel walls.
* Venous beading veins become tortuous

4 . Damage to nerve fibres
Cotton wool spots : fluffy white patches on the retina

5 . Neovascularisation
involves the release of growth factors in the retina, stimulating new blood vessel development.

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14
Q

Diabetic retinopathy : Grading

A
  • Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots
  • Pre-proliferative – venous beading, multiple blot haemorrhages, cotton wool spots
    • Proliferative – neovascularisation

Diabetic maculopathy may show
* Exudates within the macula
* Macular oedema

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15
Q

Diabetic retinopathy : Complications

A
  • Vision loss
  • Retinal detachment
  • Vitreous haemorrhage (bleeding into the vitreous humour)
  • Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
  • Optic neuropathy
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16
Q

Diabetic retinopathy : Management

A
  1. Maculopathy - If changes in visual acuity - ANTIVGEF inhibitor
  2. Non-proliferative
    * diabetic retinopathy requires close monitoring and careful diabetic control.

3 . Proliferative diabetic retinopathy :
* Pan-retinal photocoagulation– extensive laser treatment across the retina to suppress new vessels
* Anti-VEGF medications by intravitreal injection
* Surgery (e.g., vitrectomy) may be required in severe disease

17
Q

Hypertensive Retinopathy : Definition

A
  • Hypertensive retinopathy involves damage to the small blood vessels in the retina relating to hypertension (high blood pressure).
  • Changes can happen slowly with chronic hypertension or develop quickly in response to malignant hypertension.
18
Q

Hypertensive Retinopathy : Clinical features

A

1 . Copper wiring
* walls of the arterioles become thickened and sclerosed and reflect more light on examination.

2 . Arteriovenous nipping (AV nipping)
* arterioles cause compression of the veins where they cross due to sclerosis and hardening of the arterioles.

3 . Cotton wool spots
* are caused by ischaemia and infarction in the retina, causing damage to nerve fibres.

4 . Hard exudates
* caused by damaged vessels leaking lipids onto the retina.

5 . Retinal haemorrhages
* caused by damaged vessels rupturing and releasing blood in the retina.

6 . Papilloedema :
* caused by ischaemia to the optic nerve, resulting in optic nerve swelling (oedema).

19
Q

Hypertensive Retinopathy : Classification

A
  • Stage 1: Mild narrowing of the arterioles, + light reflex - silver wiring
  • Stage 2: AV nicking
  • Stage 3: Cotton-wool patches, exudates and haemorrhages
  • Stage 4: Papilloedema
20
Q

Hypertensive Retinopathy : Management

A

Management is focused on controlling blood pressure and managing risk factors (e.g., smoking and blood lipids).

21
Q

Cataracts : Definition

A

Cataracts describe a progressively opaque eye lens, which reduces the light entering the eye and visual acuity.

22
Q

Cataracts : Anatomy of lens

A
  1. Role : lens is to focus light on the retina.
  2. Supply : no blood supply and is nourished by the aqueous humour.

3. It is held in place by suspensory ligaments

4. Suspensory ligaments attached to the ciliary body.

5. Ciliary body contracts -> releases tension on the suspensory ligaments ->
lens thickens

6. Ciliary body relaxes -> the suspensory ligaments tension -> lens narrow

23
Q

Cataracts : Pathophysiology

A

1 . Aggregations of lens protein
* Due to ageing, proteins clump together interfering with the normal arrangement of lung fibres

2 . Changes in Lens fiber cells
* Changes in the structure of organised elongated fibre cells - disrupts transparency of the lens

24
Q

Cataracts : Risk factors

A
  1. Increasing age
  2. Smoking
  3. Alcohol
  4. Diabetes
  5. Steroids
  6. Hypocalcaemia
25
Q

Cataracts : Clinical presentation

A

Asymmetrical
Onset: Slow reduction in visual acuity
1. Progressive blurring of the vision
2. Colours becoming more faded, brown or yellow
3. Starbursts can appear around lights, particularly at night

26
Q

Cataracts : Clinical signs

A
  1. Loss of the red reflex is a key examination finding.
    * The lens can appear grey or white using an ophthalmoscope
27
Q

Cataracts : Management

A
  • Cataract surgery : involves drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens
28
Q

Retinitis Pigmentosa : Definition

A

A genetic condition causing degeneration of the photoreceptors in the retina, particularly the rods cells > cone cells

*Rod cells : peripheral retina, low light and non colour perception

29
Q

Retinitis Pigmentosa : Clinical presentation

A

Rods degenerate more than the cones.
Rods are responsible for night vision and peripheral vision. Therefore, there is:

  • Night blindness (often the first symptom)
  • Peripheral vision loss (before the central vision is affected)
30
Q

Retinitis Pigmentosa : Fundoscopy

A

‘Bone-Spicule appearance : sharp pointed appearance similar to bone matrix
* Concentrated at ‘Peripheral retina’

Opthalmology (5 decks)

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