Gradual Loss Of Vision Flashcards

0
Q

Cataract

A

Loss of transparency in the lens - most common disorder of the lens and of treatable blindness in the world
Usually due to age and common in the over 70s
Presents with gradual blurring of vision, increasing myopia and glare

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1
Q

Lens anatomy

A

Behind the iris, in front of the vitreous humour
Suspended on spoke-like zonules
Composed of a capsule - thin, elastic, outer basement membrane
Cortex - outer layer of lens epithelial cells
Nucleus - central lens fibres

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2
Q

Assessment of cataracts

A

Measure acuity

On ophthalmoscopy - diminished red reflex and difficult view of the fundus

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3
Q

Causes of cataracts

A

Age-related - most common, degeneration of the lens due to age, UV and smoking
Congenital - rare, 1/3 inherited autosomal dominant, 1/3 due to birth trauma/rubella/toxoplasmosis infection from mother, detected as loss of red reflex in newborns
Early onset - due to systemic disease (diabetes), trauma, steroids or ocular disorders (uveitis)

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4
Q

Presentation of age-related cataracts

A

Can be:
nuclear - central
Posterior sub-capsular - small at the back of the lens
Cortical - wedge shaped segments coming in from the outside
My present as a combination of types

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5
Q

Cataract surgery

A

Benefits of surgery - low risk, quick, cost effective
Risks - rarely complications such as rupture of posterior lens capsule
1/500 may suffer - suprachoroidal (intraocular) haemorrhage or endophalmitis

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6
Q

Procedure of cataract surgery

A

LA - self-sealing corneal incision into anterior chamber
Circular opening in the anterior lens capsule (capsulorhexus)
Break-up (phakoemulsification) and aspiration of lens material
Insertion of intraocular lens with correct power

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7
Q

Outcomes of cataract surgery

A

90% achieve visual acuity of 6/12 or better
May develop posterior capsular opacification where lens cells proliferate and opacify the capsule - this can be treated with lasers (YAG laser capsulotomy)

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8
Q

Age related macula degeneration (AMD)

A

Leading cause of blindness in the western world
Associated with increasing age
Affects central vision - peripheral vision unaffected, so pts often live independently
Can be wet or dry AMD

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9
Q

Anatomy of the macula

A

Located at the posterior pole of the eye and includes the fovea
Cones are concentrated in the macula which is responsible for colour and acuity of vision
Rods are distributed throughout the retina and are responsible for low light vision and movement detection

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10
Q

Symptoms of AMD

A

Dry - gradual loss of central vision

Wet - acute or semi-acute loss of central vision
Distorted central vision
Both will have reduced acuity and require dilated fundoscopy

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11
Q

Signs of dry AMD

A

Drusen - tiny yellow accumulations of extra cellular waste from photoreceptors. They accumulate under the neuro-retina
Mottled appearing macula - patches of hyper- and hypo- pigmentation
In advanced disease there is marked central atrophy

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12
Q

Signs of wet AMD

A

Choroidal neovacularization - grey/green lesions of new vessels

Yellow exudates

Retinal haemorrhage

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13
Q

Fluorescein angiography

A

a technique to identify areas of micro- vascular leakage
Can identify the extent of the lesion
Required for wet AMD but not AMD

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14
Q

Optical coherence tomography

A

Laser scanner used to capture a detailed cross-sectional image of the macula
Shows intra-retinal fluid in wet AMD

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15
Q

Amsler chart

A

Essentially graph paper which displays any central vision distortion in wet AMD

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16
Q

Management of AMD

A

In unilateral disease use ambler chart to monitor the other eye
dietary supplements may reduce the risk of other eye involvement
Counselling/low vision aids/registration as sight impaired
No treatment for dry AMD but wet AMD can be treated with intravitreal injections of anti-VEGF drugs
Stop smoking

17
Q

Prognosis of AMD

A

Dry AMD - a slow deterioration in vision but may progress to wet AMD
Wet AMD - without treatment 75% have marked vision loss over 3 years, 60% have fellow eye involvement within 5 years
With anti-VEGF treatment most maintain vision with slight reductions over time

18
Q

Primary open angle glaucoma

A

A progressive optic neuropathy associated with optic head damage and visual field loss, typically with raised intraocular pressure (IOP)
Most common type - incidence 2% >40yro and 10% >80yro
A progressive disease if untreated

19
Q

Types of glaucoma

A

Primary open angle (POAG)
Closed/narrow angle -usually presents acutely with a red painful eye
Congential glaucoma (rare)

20
Q

Presentation of primary open angle glaucoma

A

Optic nerve head damage (cupping,or increased cup to disc ratio)
Loss of peripheral visual field
Usually raised IOP (above 21mmHg is abnormal)
Usually bilateral but often asymmetric

21
Q

Pathogenesis of primary open angle glaucoma

A

With age or idiopathically the trabecular meshwork may not drain as effectively causing IOP to rise
This can damage the nerve fibres in the optic disc producing a field defect, or may be asymptomatic (ocular hypertension)

22
Q

Normal pressure glaucoma

A

Some people have disc cupping and field loss with normal IOP

23
Q

Risk factors for glaucoma

A

IOP - most important and modifiable
Family history of glaucoma - also being black
Age / Diabetes / Myopia
Early disease is often asymptomatic, picked up in routine eye screens - by the symptomatic late stage vision can’t be restored

24
Q

Signs of POAG

A

Raised IOP
Cupped optic nerve head - cup-to-disc ratio should be 0.2/3, greater than 0.6 is suspicious
Progressive peripheral visual field defects

25
Q

Non contact tonometry

A

Also known as air-puff tonometry
A rapid air pulse is used to flatten (applanate) the cornea, detected by an electro-optical system
The IOP is estimated by the force of air at the time of applanation
This has historically been considered only and estimate and is useful for children/non-complient patients

26
Q

Goldman tonometry

A

Most widely accepted and gold standard of IOP measurement
A disinfected prism is placed on the cornea and a colbalt blue filter is used to view 2 green semi-circles
Force is applied until they meet and when 3.06mm of cornea is flattened corneal rigidity and tear film cancel out and IOP is determined from the force applied

27
Q

Visual field testing

A

Confrontation testing is not sensitive enough
Humphrey visual field testing is used
Classical field defect is ‘arcuate scotoma’ which extends from the enlarged blind spot around the macula

28
Q

Treatment of POAG

A

1st - suppress aqueous humor production using beta-blockers, carbonic anhydrase inhibitors or alpha-agonists
2nd - increase aqueous outflow using prostaglandin analogues
If unresponsive - surgery - trabecular meshwork can be layered to open drainage, or trabeculectomy to open alternative drainage

29
Q

Trachoma

A

A bilateral follicular, non-purulent conjunctivitis due to chlamydia trachomatis infection

30
Q

Progression of trachoma infection

A

Follicles on superior tarsal conjunctiva and superior limbus leading to conjunctival cicatrisation (scarring) - this can cause Entropian (inversion of the eyelid)
Trachomatis (eyelashes growing towards the cornea)
Dry eyes - this all leads to scarring, opacification and blindness

31
Q

Diagnosis of trachoma

A

Conjunctival scrappings

32
Q

Treatment of trachoma

A

Oral antibiotics (azithromycin)

33
Q

The WHO SAFE strategy

A

Surgery to treat trichiasis
Antibiotics to treat infection
Facial cleanliness
Environmental improvement

34
Q

Onchocerciasis

A

‘River blindness’ due to infection by onchocerca volvulus
It is transmitted by black fly and has an incubation of 1year
Endemic to equatorial Africa and central/south America

35
Q

Progression of onchocerca infection

A

Black fly bites form subcutaneous nodules
Adult female worm sheds microfilariae which migrate through the skin
Eye symptoms occur when chronic infection reaches the conjunctiva

36
Q

Ocular signs/complications of onchocerciasis

A

Lid nodules/depigmentation
Chronic conjunctivitis with punctuate keratitis
Corneal opacification, iritis and cataract
Glaucoma and optic neuritis

37
Q

Treatment of onchocerciasis

A

Ivermectin

38
Q

Xerophthalmia

A

Gradual blindness due to vitamin A deficiency
Vit A is required for synthesis of rhodopsin
Major cause of blindness in children in developing countries

39
Q

Complications of vitamin A deficiency

A

Initially Night blindness
Corneal/conjunctival dryness and keratinisation
Corneal ulcers which can lead to perforation - advanced disease can show progressive corneal necrosis

40
Q

Treatment of Xerophthalmia

A

Oral vitamin A
Ocular lubrication
Infective keratitis can be treated with antibiotics

41
Q

Prevention of Xerophthalmia

A

Diet with enough vitamin A - fat soluble form (dairy, eggs, fish liver oil) or pro-vitamin form (fruit and veg)
Supplementation may be needed for vulnerable populations