Common eye disorders Flashcards

1
Q

Briefly describe trachoma

A
  • Most common infective cause of blindness
  • Is still occurring in some remote areas in Australia, but has declined from 14% (2009) to 4% (2014)
  • Approx. 4% of blindness worldwide
  • Chlamydia trachomatis (serotype A-C)
  • Chronic conjunctivitis
  • Transmitted by flies or close contact
  • Poor socio-economic communities; hygiene
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2
Q

Describe the four key features of trachoma

A

I. Follicular conjunctivitis – active repeated episodes over years

II. Tarsal conjunctival scarring

III. Trichiasis

IV. Corneal opacity

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3
Q

Describe the condition of trachoma in Au

A

The bad news
Australia is the only developed country in the world to still have cases of trachoma.

(as per previous slide) rates in some Communities can be as high at 5% which is considered endemic levels.

Trachoma was eradicated from mainstream Australia 100 yrs ago.

In 1975 $1.4m was committed to the National Trachoma and Eye Health Program (under Fred Hollow’s Foundation).

The good news

Of 200 “at risk” Communities, 150 no longer have trachoma.

According to the National Indigenous Eye health Survey (NIEHS) and the National Eye Health Survey (NEHS) the level of blindness has decreased from 2.8% (2008) to 0.3% (2016).

2017 – Commonwealth Government committed $20.6m over 4yrs to support trachoma eradication targets.

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4
Q

Describe the management and prevention of trachoma

A

Surgery for trichiasis

Antibiotics - azithromycin p.o., even a single dose can last for 2 years; topically tetracycline or polymixin

Facial cleanliness and hygiene

Environmental improvements - water and sewage system

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5
Q

Describe the burden of eye disease in Australia

A

The health costs of treating eye disease are extremely large -&raquo_space; $5 billion in 2009.

This is more than the combined cost of
- coronary heart disease
- stroke
- arthritis
- depression

More than the health spending on diabetes and asthma - two ‘National Health Priority Areas’ – combined

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6
Q

Define vision impairment

A
  • Vision impairment is any diagnosed condition of the eye or visual system that cannot be corrected to within normal limits.
  • Disease, damage or injury causing vision impairment can occur to any part of the visual system - the eye, the visual pathways, to the brain and/or visual cortex.

Severe vision impairment: 6/60 - 3/60 - otherwise known as legal blindness

Blindness fro 3/60 to 1/60

Blindness is 1/60 with light perception

Blindness with no light perception

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7
Q

List some causes of reading difficulties

A
  • macular degeneration (10%)
  • glaucoma (3%)
  • diabetic eye disease (2%)
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8
Q

List some causes of blindness in all ages

A
  • cataract (12%),
  • glaucoma (14%)
  • refractive error (4%)
  • all other (11%)
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9
Q

Describe cataracts broadly

A
  • cataract is the most common eye disease
  • increasing prevalence with age
  • 70% Australians > 80 yrs have cataracts, or have had cataract surgery
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10
Q

Describe the three types of cataracts

A

Cataract is loss of lens transparency

Nuclear Cataract

  • hardening of the core of the lens (hence ‘nuclear’ as in ‘nucleus’) that expands through the layers
  • associated with yellowing/ ‘brunessence’ of the lens (due to accumulation of glutathione-3-hydroxy kynurenine glycoside)
  • causes reduced transmittance of light (especially blue), increased scatter, and increased fluorescence. Things appear more reddish, and ‘blurry’.
  • Associated with aging.
    ![[Pasted image 20240308195927.png]]

Cortical Cataract

  • changes to lens proteins that start at the margin of the lens, and spread through the more superficial layers towards the optic axis

Capsular Cataract

  • modification of the lens capsule, anteriorly or posteriorly
  • often occur subsequent to eye surgery, or trauma
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11
Q

Discuss the prevalence of cataracts in Indigenous populations,causes of cataracts and potential barriers to accessing care

A

Aboriginal and Torres Strait Islander people are 3x more likely than non-Indigenous Australians to be affected by vision loss due to cataracts.

It is the second leading cause of blindness in Aboriginal and Torres Strait Islander peoples (2016).

Causes include high UV exposure.

Barriers to cataract surgery exist at health-service, community and individual levels:

  • lack of access to optometrists and ophthalmologists,
  • isolation, transport
  • complexity of the system / clinical pathways
  • infrastructure
  • interpreters
  • cost
  • Community and individual factors include ignorance of cause, fear of surgery

In the ACT today it is difficult to access cataract surgery as a public patient… this affects all people on low income, and has a disproportionate impact on people of Aboriginal and Torres Strait Islander backgrounds.

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12
Q

Describe glaucoma

A

Second leading cause of blindness worldwide ~70 million people affected / impairs the vision of about 2% of persons over the age of 50 years and 12% over 85. ~50% of those affected are unaware (and 50% of these have been to an ophthalmologist)

‘Glaucoma’ is a spectrum of related disorders characterized by progressive death of ganglion cells (GC) and axon loss (optic nerve).

It is an ‘anterior segment’ disorder that has its impact in the posterior segment, causing death of ganglion cells.

Strongly associated with increased intraocular pressure (IOP). However, about 50% of diagnosed glaucoma occurs in the absence of increased IOP

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13
Q

Describe the pathophysiology of glaucoma

A

Pressure on the posterior aspect of the iris causes the iris to buckle, compressing the trabecular meshwork and restricting the drainage of aqueous. Alternatively, the trabecular meshwork and drainage network can become ‘clogged’ and restrict the passage of aqueous…this is open angle glaucoma

Increased IOP in the anterior segment is transferred posteriorly through the vitreous. Pressure distorts the sclera at the lamina cribrosa, compressing GC axons leading the GC death.

Mechanism of GC loss involves:
- Decline in the retrograde supply of neurotrophins to GC from their axon terminals
- Release of excitotoxic amino acids by damaged GC, 2-8 fold.
- Apoptotic cell death of GC

Note that it tends to affect peripheral vision so frequently not noticed until quite late

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14
Q

Describe glaucoma diagnosis

A

Initial finding, and raising suspicion is based on assessment of the optic disc (OD).

ODs are normally mirror images of each other. This underlies importance of comparison

Normal disc has a distinct, reddish neural margin, where the majority of axons are located. The centre is paler (‘pallid’)

In glaucoma
- the margin appears eroded, often inferiorly

  • the disc appears enlarged, and the area of ‘pallor’ increases
  • the normally shallow ‘cupping’ of the disc increases over time, with progression of the disease

Bundles of axons tend to be affected, resulting in loss of GC input to brain from specific sectors / regions of the retina

Changes seen at the disc and in the fundus are associated with progressive visual field loss, due to death of ganglion cells, resulting from compression of their axons

Typically losses are patchy, begin in peripheral visual field, and progress centrally < losses compensated for by eye movements and may not be registered

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15
Q

Describe advanced glaucoma course and management

A

Management of intraocular pressure is most efficacious strategy - but if IOP is not raised, options are limited.

Animal models show large diameter axons affected before smaller ones (ie., parasol system ahead of midget) ß hence effects in periphery rather than central retina

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16
Q

Describe AMD broadly

A

AMD is an insidious disease, that develops over decades

Clinical diagnosis of AMD is recognition of end-stage degeneration of neural tissue - it cannot be repaired

We are ALL at risk of AMD - some more than others

Risk can be reduced by adopting a healthy lifestyle - best to start young!

Smoking is a highly significant, avoidable risk-factor

17
Q

Describe pathophysiology of AMD broadly

A

Multi-factorial disease characterized by the loss of central (macular) vision

Vision loss due to degeneration of the photoreceptors, specifically those in the macular region

The causes of this photoreceptor loss are not clear, but is associated with degeneration of the RPE and/or neovascularization of the outer retina.

18
Q

Describe AMD epidemiology

A

Worldwide, there are no populations free of AMD; incidence does vary and is slightly lower in heavily pigmented groups

Early stages of the disease affect 1 in 4 people >60 years, in Australia

In Australia, 1.9% of the population have ‘end stage’ disease and are legally blind as a result.

The cost of AMD to the Australian economy is estimated at $5 billion per annum (Access Economics, 2011)

19
Q

Describe AMD pathophysiology specifically

A

Central 2 mm is the source of 25% of visual input to the brain – mostly from midget GC

If you lose macular vision you become legally blind.

Drusen / ‘white spots’ are one of the earliest signs of AMD

Area of cell loss, centered on the macula.

Principal cell types affected are light- sensitive photoreceptors, and their supporting pigmented epithelial cells.

Principal cell types affected are light- sensitive photoreceptors, and their supporting pigmented epithelial cells.

20
Q

Describe signs of dry AMD

A
  • Thickening of Bruch’s membrane
  • Subretinal Deposits Drusen (D). Most retinas have some drusen. Drusen are classified into ‘soft’ and ‘hard’; small or confluent; the type, size and distribution of drusen is used in clinical diagnosis of early AMD.
  • Pigmentary Disturbance

Histopathology of active AMD

  1. Dry / Non-exudative AMD
    - loss of photoreceptors and RPE cells in the macular region
    - accumulation of leukocytes in teh choriocapillaris
    - sharp transition into histologically ‘normal’ photoreceptors
  2. Wet / Neovascular AMD
    - Breakdown of Bruch’s membrane (BM) by phagocytic cells
    - Sprouting of choroidal vessels which (i) breach BM and (ii) often the RPE
    - choroidal neovascularization of the retina - choroidal vessels are normally ‘leaky’. This facilitates diffusion of O2 and nutrients to photoreceptors
    - new choroidal vessels leak (exude) serum constituents and blood cells into the outer retina, promoting retinal dysfunction and loss of vision
21
Q

Describe AMD risk factors of detail

A
  • Age
    • risk increases with age
    • risk increases 5% per decade after 55
    • 30% of population over 75 years are affected although many undiagnosed
  • Environmental factors
    • smoking
      • increases chance of developing drusen
      • increases risk of dry and wet AMD
    • diet
      • high intake of saturated fat and cholesterol increases early AMD by 80%
      • high intake of fatty acids decreases risk of early AMD
      • eating fish 1/week decreases risk of early AMD by 40%

Genetic factors
1. Complement Factor H (CFH)
- SNP resulting in a histidine substituting for a tyrosine
- interferes with the normal inhibitory effects of CFH on activation of the ‘innate’ immune system
- results in increased susceptibility for AMD (OR 2.5)
- deletions in CFH-related genes CFHR1 and R3 are associated with decreased risk (OR 0.4)
2. Other complement-related genes
- some deletions in CFH-related genes (CFHR1 and R3) are associated with decreased risk (OR 0.4)
- overall, variants of complement related genes (including CFB, C3 and C2) account for ~70% risk for developing AMD (most of this from CFH Y402H)
3. Chromosome 10q26 - ARMS2 and HTRA1
- identified from gene linkage screens - precise polymorphisms not yet agreed
- variations most strongly linked with AMD in the Japanese population (> CFH)
- both genes strongly associated with AMD by GWAS; function of the protein encoded by ARMS2 is not known

22
Q

Describe diabetic retinopathy,prognostic markers and risk factors

A
  • The total number of people with diabetes is projected to rise from 285 million in 2010 to 439 million in 2030.
  • Diabetic retinopathy is responsible for 1.8 million of the 37 million cases of blindness throughout the world.
  • Diabetic retinopathy (DR) is the leading cause of blindness in people of working age in industrialized countries.
  • Progressive dysfunction of the retinal blood vessels caused by chronic hyperglycemia.
  • DR can be a complication of diabetes type 1 or diabetes type 2.
  • Initially, DR is asymptomatic, if not treated though it can cause low vision and blindness.
  • The best predictor of diabetic retinopathy is the duration of the disease
  • After 20 years of diabetes, nearly 99% of patients with type 1 diabetes and 60% with type 2 have some degree on diabetic retinopathy; 33% of patients with diabetes have signs of diabetic retinopathy
  • People with diabetes are 25 times more likely to become blind than the general population.

RISK FACTORS

  • Duration of diabetes
  • Poor Blood Sugar control
  • Hypertension
  • Hyperlipidemia
  • Barriers to care
23
Q

Descrieb DR pathophysiology

A

Microvascular occlusion is caused by:

  • Thickening of capillary basement membranes
  • Abnormal proliferation of capillary endothelium
  • Increased platelet adhesion
  • Increased blood viscosity
  • Defective fibrinolysis

Microvascular leakage is caused by:

  • Impairment of endothelial tight junctions
  • Loss of pericytes
  • Weakening of capillary walls
  • Elevated levels of vascular endothelial growth factor (VEGF)
24
Q

Describe prevention measures for DR

A

Primary prevention

  • Strict glycemic control
  • Blood pressure control

Secondary prevention
- Annual eye exams

*Tertiary prevention

  • Retinal Laser photocoagulation
  • Vitrectomy
  • anti- VEGF antibody treatment
25
Q

Distinguish between closed and open angle

A

Closed Angle Glaucoma – pressure on the posterior aspect of the iris causes the iris to buckle,
compressing the trabecular meshwork and restricting the drainage of aqueous humour. Passage
for outflow too small, rapid pressure build-up. Abrupt onset of severe eye pain, redness, blurry
vision, headaches, nausea and visual halos.
Open angle glaucoma (most common) – trabecular meshwork and drainage network can
become clogged and restrict the passage of aqueous humour. Drainage system clogged over
time, resulting in a gradual pressure increase – starts as outer rim atrophy (decreasing peripheral
vision)
Abnormal drainage of anterior segment causes intra-ocular pressure (IOP) to increase which
damages the optic nerve via compressing the GC axons.

26
Q

Describe the mechanism of GC loss

A

Mechanism of ganglion cell (GC) loss
-Decline in the retrograde blood supply of neurotrophins to GC from their axon terminals
-Release of excitotoxic amino acids by damaged GC
-Apoptotic cell death of GC
Initial diagnosis based on assessment of the optic disc (OD)
Normal disc – distinct, reddish neural margin with paler centre
In glaucoma – margin eroded, disc appears enlarged, disc cupping
Bundles of axons tend to be affected, resulting in loss of GC input to brain from
specific sectors of the retina

27
Q

Distinguish between dry and wet AMD

A

Dry (atrophic) AMD – drusen / white spots are early sign.
Area of cell loss visible on macula. Principle cell types
affected are light-sensitive photoreceptors and supporting
pigmented epithelial cells
Accumulation of leucocytes in the choriocapillaris. Sharp
transition into histologically normal photoreceptors.
Wet (exudative/neovascular) AMD – blood vessels leak fluid or
blood into the macula.
Breakdown of Bruch’s membrane (BM) by phagocytic cells.
Sprouting of choroidal vessels which breach BM and often the RPE
Choroidal neovascularisation – vessels are ‘leaky’ (for nutrient
transport), new vessels exude serum constituents and blood cells
into the outer retina, promoting retinal dysfunction and vision loss.

28
Q

List signs of emergent AMD

A

-Subretinal depots (drusen)
-Basal laminar deposit (BLD)
-Pigmentary disturbance