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Neurology and special senses (Y4) > 4- Ophthalmology (Gradual deterioration of vision) > Flashcards

4- Ophthalmology (Gradual deterioration of vision) Flashcards

1
Q

causes of gradual loss of vision

A

Front of the eye problems

  • Cataract
    o Age related
    o Pre- senile (steroid, diabetes, trauma, uveitis)
  • Primary open angle glaucoma

Back of the eye problems

  • Age related macula degeneration
  • Diabetic eye disease
    o Retinopathy (nonproliferative, proliferative)
    o Maculopathy (oedematous, ischaemic)
  • Hypertensive retinopathy
  • Thyroid eye
  • Presbyopia
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2
Q

Types of glaucoma summary

A
  • Open-angle
  • Closed-angle (acute angle closure)
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3
Q

Open-angle summary

A
  • Gradual increase in resistance through trabecular meshwork
  • Makes it more difficult for aqueous humour to flow through the meshwork and exist the eye
  • Pressure slowly build within the eye
  • Slow and chronic onset of glaucoma
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4
Q

Closed-angle (acute angle closure)

A

Emergency
- Iris has bulged forward and sealed off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away -> continual build up of pressure
- Ophthalmology emergency

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5
Q

Open angle glaucoma
Background

A
  • Glaucoma refers to optic nerve damage that is caused by significant rise in intraocular pressure
  • Raised intraocular pressure is caused by blockage in aqueous humour trying to escape the eye
  • Gradual
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6
Q

Risk factor/causes
open angle glaucoma

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Near-sightedness (myopia)
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7
Q

Pathophysiology open angle glaucoma

A
  • Gradual increase in resistance through trabecular meshwork
  • Makes it more difficult for aqueous humour to flow through the meshwork and exist the eye
  • Pressure slowly build within the eye
  • Slow and chronic onset of glaucoma
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8
Q

presentation of open angle glaucoma

A
  • Rise in intraocular pressure is asymptomatic from a long period of time
  • Diagnosed often by routine screening
  • Affects peripheral vision first -> the peripheral vision closes in until they experience tunnel vision
  • Other
    o Fluctuating pain
    o Headaches
    o Blurred vision
    o Halos appearing around lights in the evening
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9
Q

open angle glaucoma and peripheral vision

A
  • Peripheral vision goes first
  • Later stages tunnel vision
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10
Q

investigations for open angle glaucoma

A
  • measuring intraocular pressure
  • Fundoscopy
  • Visual field assessment (peripheral vision loss)
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11
Q

measuring intraocular pressure

A

Non- contact tonometry(more crude method)
- For estimating – less accurate
- Puff of air shot at cornea and corneal response to air measured

Goldmann applanation tonometry(gold standard)
- Special device mounted on a slip lamp that makes contact with the cornea and applies different pressures to the front of the cornea to get an accurate measurement of the intraocular pressure

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12
Q

goldman applantion tonometry findings

A
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13
Q

fundoscopy and open angle glaucoma

A

look for optic disc cupping and optic nerve health

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14
Q

aim of management of open angle glaucoma

A

Aim is to reduce intraocular pressure.

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15
Q

when is treatment started with open angle glaucoma

A

Treatment commenced if pressure of 24mmHg or above

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16
Q

first line management of open angle glaucoma

A

First line: Prostaglandin analogue eye drops e.g. latanoprost

  • Increase uveoscleral outflow
  • Side effects: eyelash growth, eyelid pigmentation
  • Iris pigmentation (browning)

Other options

  • Beta-blockers (e.g. timolol) reduce production of aqueous humours
  • Carbonic anhydrase inhibitors e.g. dorzolamide to reduce production of aqueous humour
  • Sympathomimetics e.g. brimonidine, reduce the production of the aqueous fluid and increase uveoscleral outflow
17
Q

surgical management of open angle glaucoma

A

Trabeculectomy – if eye drops ineffective
- Creating new channels from the anterior chamber, through the sclera to a location under the conjunctiva -> causes a ‘bleb’ under the conjunctiva where aqueous humour drains- it then reabsorbed from this bled into general circulation

18
Q

Cataracts
Background

A
  • Where the lens in the eye becomes cloudy and opaque
  • Reduces visual acuity by reducing the light that can enter the eye (Cataracts are thought to increase intraocular light scatter, which can decrease retinal image contrast and adversely affect contrast sensitivity, which is affected far more than visual acuity in patients with cataracts.)
19
Q

Pathophysiology
of cataracts

A

Proteins in the lens of the eye breakdown and aggregrate -> cloudy

20
Q

types of cataract

A

age related

pre-senile

21
Q

age related cataracts risk factors

A

Most develop over years with advanced age in the presence of risk factors
o Smoking
o Alcohol
o Diabetes
o Steroids
o hypocalcaemia

22
Q

pre-senile cataracts risk factors

A
  • Congenital (occurs before birth and are screening for using the red reflex during neonate examination)
     Genetic e.g. galactosaemia
     Infections e.g. rubella
  • Steroids
  • Diabetes
  • Trauma
  • Uveitis
23
Q

presentation of cataracts

A

Presentation
- Asymmetrical
- Slow reduction in vision acuity
- Progressive blurring of vision
- Change of colour of vision with colours becoming more brown or yellow
- ‘starbursts’ can appear around lights

24
Q

examintion for cataracts

A
  • Loss of red reflex
  • Lens appear grey or white when testing red reflex
25
Q

manageemnt of cataracts

A

Management
- Conservative approach if symptoms manageable
- Cataract surgery
o Involves drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens

26
Q

Cataract surgery complication:

A

Endophthalmitis
It is inflammation of the inner contents of the eye, usually caused by infection. It can be treated with intravitreal antibiotics injected into the eye. This can lead to loss of vision and loss of the eye itself.

27
Q

age related macular degeneration

A
  • Condition where degeneration of the macula causes progressive deterioration in vision
  • Most common cause of blindness in the UK
28
Q

types of age related macular degeneration

A

o Dry (90%)
o Wet (10%)- worse prognosis

29
Q

pathophysiology of age related macular degeneration

A

Pathophysiology
The macula is made up of four key layers
- Choroid layer (bottom) -> blood vessels that supply the macula
- Drusen in Bruchs membrane
- Retinal pigment epithelium
- Photoreceptors e.g. rods and cones

Traditionally two forms of macular degeneration are seen:
dry macular degeneration
- 90% of cases
- also known as atrophic
- characterised by drusen - yellow round spots in Bruch’s membrane
wet macular degeneration
- 10% of cases
- also known as exudative or neovascular macular degeneration
- characterised by choroidal neovascularisation
- leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries the worst prognosis
- A key chemical that stimulates the development of new vessels if VEGF -> target of medications that treat wet AMD

30
Q

risk factors for age related macula degeneration

A

Risk factors
- Age
- Smoking
- White or Chinese ethnic origin
- Family history
- CVD disease

31
Q

presentation of age related macula degeneration

A

Presentation
* Gradual worsening central visual field loss
* Reduced visual acuity
* Crooked or wavy appearance to straight lines

Wet age-related macular degeneration presents more acutely. It can present with a loss of vision over days and progress to full loss of vision over 2-3 years. It often progresses to bilateral disease.

32
Q

Examination for age related macula degeneration

A
  • Reduced acuity using Snellen chart
  • Scotoma (central patch of vision loss)
  • Amsler grid test can be used to assess the distortion of straight lines
  • Fundoscopy – Drusen= key finding
33
Q

Investigations
for age related macular degeneration

A
  • Fundoscopy- Drusen
  • Slit lamp biomicroscopic fundus examination
  • Optical coherence tomography
  • Fluorescein angiography
34
Q

age related macular degeneration prevalence

A

leading caus eof severe, irreversible vision loss in people over 55

35
Q

Management
Dry AMD

A
  • No specific treatment
  • Focusses on lifestyle measures that may slow progression
    o Avoid smoking
    o Control blood pressure
    o Vitamin supplementation
36
Q

management wet AMD

A

Anti-VEGF medication e.g. ranibizumab

  • to reduce development of new blood vessels in the retina
  • injected into vitreous chamber once a month
  • can slow down and even reverse progression of disease
  • should be started within 3 months to be beneficial

Neurology and special senses (Y4) (52 decks)

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