Aoc Internal Eye Diseases

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Back 1

4 stages of Age Related Macula Degeneration (AMD)

Early AMD: several small drusen, few medium sized drusen

Intermediate AMD: many medium drusen, at least one large drusen

Advanced Non-Neovascular AMD:

Many drusen and atrophy into macula

Advanced Neovascular AMD: Choroidal neovascularisation

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Pathogenesis of Non-exudative (Dry) AMD

Back 2

RPE is responsible for waste removal from the outer segments of the rods and cones

Extra cellular lipid deposits build up in RPE, excess material transferred to Bruchs membrane in the choroid

Oxidative stress from aging causes changes in Bruchs membrane and choriocapillaris

Drusen begins to appear

RPE shows degenerative changes that are not being replaced

The photoreceptors then degenerate

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Pathogenesis of Exudative (Wet) AMD

Back 3

New blood vessels formed in the choroid grow through Bruchs Membrane into sub retinal space

As the RPE bulges away from the choroid, blood supply is reduced causing the new vessels to grow.

These vessels are poor and tend to leak causing a sudden, profound vision loss

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Aetiology of AMD

Back 4

Age

Smoking

Poor diet

Obesity

UV exposure

Light irides

Genetic factors

Hypertension

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Symptoms of AMD

Back 5

Near Va gets worse quicker than distance va

Central scotoma

Contrast sensitivity

Loss of colour perception

Dark adaption issues

Glare

Visual hallucinations

Photopsia

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AMD treatment

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None currently for dry AMD, so monitor progression and provide support. Always check the amslar chart for signs of distortion. Dietary and lifestyle advice.

For wet, need anti-VEGF injections to prevent new blood vessels growing and HES monitoring appointments

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Diabetes Types

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Type 1:

Approx 10% of diabetics

Not related to lifestyle or diet

Pancreas does not produce insulin

Insulin allows glucose to enter our cells for use

Glucose builds up in bloodstream

Managed by insulin replacement injections

Type 2:

Approx 90% of diabetics

Insulin resistance, either insufficient pancreatic or bodies inability to effectively use insulin

Increased blood glucose levels

Associated with obesity, physical activity, Hypertension or disturbed blood lipid levels

Controlled by lifestyle changes and eventually medicine

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Associated ocular events with diabetes

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Diabetic Retinopathy

'Snowflake' cataract

Extraocular muscle Palsy

Dry eye

Diabetic keratopathy

Retinal vein occlusion

Optic disc swelling

Optic neuropathy

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Back 9

Diabetic Retinopathy

Risk factors:

The longer a patient has been Diabetic, the more at risk they are of Retinopathy

50% have it after 10 years

80% have it after 20 years

Hypertension

Smoking

Pregnancy

Poor metabolic control

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Pathogenesis of Diabetic Retinopathy

Back 10

A micro vascular disease

Caused changes in blood chemistry with excess amounts of glucose

Leads to hyper-glycaemia induced vascular damage

Loss of pericytes, causing microanuersym, occlusion and ischaemia

Results in a range of damage to retinal cells

Increased VEGF

Causes exudative events such as haemorrhages

New vessels leak causing further damage

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Background Retinopathy

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No treatment

Managed with annual screening

Lifestyle and health advice

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Pre-proliferative Retinopathy

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Regular monitoring

4-6 months depending on severity

Severe cases 50% risk of developing into proliferative

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Proliferative Retinopathy

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Full Pan retinal photocoagulation

treatment for new vessels

Laser to 'burn' retina which destroys weak or leaking blood vessels

Side effects:

Mild pain

Va loss

Reduction in scotopic and colour vision

Reduction in contrast

Choroidal effusions

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Back 14

Glaucoma

A group of diseases that result in changes to the optic nerve head and retinal nerve Fibre Layer and the leading cause of preventable sight loss in the world

2% of adults in the UK over 40 have it

10% adults over 75 have it

Black/afro-carribean pxs 4 times more likely to suffer from it

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Open Angle Glaucoma

Back 15

A reduction of drainage of aqueous, or extracellular material in the trabecula meshwork

Production of aqueous is greater than drainage and IOPs become raised

This causes mechanical stress on posterior eye structures

Deforms the Lamina cribrosa

Optic cup deepens and enlarges

Eventually results in visual field loss or tunnel vision and eventually, blindness

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Risk factors of open angle glaucoma

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Increased IOPs

Family history

Race

Diabetes

Steroid use

Hypertension

High myopia

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Treatment options for Open angle glaucoma

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PGA, reducing outflow resistance

Beta blockers, reduce aqueous production

Trabeculoplasty: series of laser burns to trabecular meshwork

Trabeculectomy, creates a new channel for aqueous to flow

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Back 18

Cataract

An opacification of the crystalline lens, which causes light scatter in the eye

3 types:

Corticol

Nuclear sclerosis

Posterior subcapsular

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Pathogenesis of cataract

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Compaction and stiffening of Central lens material

Ongoing proliferation of cortical fibres

Abnormal changes in lens proteins

Pigmentation of proteins becoming yellow/brown

Changes in ionic components

Stress damage to fibres

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Cataract risk factors

Back 20

Steroid use

Trauma

High myopia

Congenital

Following internal eye inflammation

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Cataract surgey and complications

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Phaco-emulsification

PCO: Posterior Capsule opacification

Retinal detachment

Internal Eye inflammation

Vitreous loss

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Back 22

Retinal detachment

A separation of the neural retina from the Retinal Pigment Epithelium

Vitreous enters the sub Retinal space

Follows a Retinal tear, hole or break

Risk factors:

High myopia

Cataract surgery

Pxs who have had a previous detachment

Eye trauma

Family history

Scleritis or Retinopathy

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Posterior Vitreous Detachment

Back 23

Usually the first stage before a retinal detachment. The separation of the Vitreous from the neurosensory retina

Increase in flashes and floaters and blurred or hazy vision

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Back 24

Retinitis Pigmentosa Causes cells in the retina to break down over time leading to vision loss

Affects both rods and cones of retina

Affects both rods and cones of retina

Affects both rods and cones of retina

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Posterior Capsule Opacification

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Residual cells left after cataract surgery proliferate and produce symptoms of blurring and glare.

Treatment is YAG laser to create aperture in Capsule