Ophthalmology Flashcards

1
Q

When do cataracts occur ?

A

When the lens in the eye become cloudy and opaque. This reduces visual acuity by reducing the light that enters the eye.

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2
Q

What is the job of the lens ?

A

To focus light coming in to the eye on to the retina at the back of the eye.

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3
Q

What holds the lens in place ?

A

The suspensory ligaments attached to the ciliary body..

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4
Q

How does the lens focus ?

A

By contraction and relaxation of the ciliary body

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5
Q

What other function do the ciliary bodies have ?

A

Produce aqueous humour into the anterior chamber

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6
Q

What happens to the lens when the ciliary bodies contracts and relaxes ?

A

Contract = It releases tension on the suspensory ligaments and the lens thickens.

Relaxes = It increases tension in the suspensory ligaments and the lens narrows.

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7
Q

Fill in the blanks. The lens is nourished by the ___ fluid. It doesn’t have a ___ supply. It ___ and ___ throughout life.

A

Surrounding fluid, blood supply, grows and develops.

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8
Q

When do congenital cataracts occur and how are the screened for ?

A

They occur before birth and are screening for using the red reflex during the neonatal examination.

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9
Q

Name 6 risk factors for cataracts ?

A
  • Increasing age
  • Smoking
  • Alcohol
  • Diabetes
  • Steroids
  • Hypocalcaemia
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10
Q

Are the symptoms in cataracts asymmetrical or symmetrical + why? Name 4 symptoms ?

A

Usually asymmetrical as both eyes are affected separately. It presents with:

  • Very slow reduction in vision
  • Progressive blurring of vision
  • Change in colour vision with colours becoming more brown or yellow
  • “Starbursts” can appear around lights, particularly at night time
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11
Q

Key sign for cataracts ?

A

Loss of the red reflex. The lens can appear grey or white when testing the red reflex. This might show up on photographs taken with a flash.

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12
Q

TOM TIP

A

It is useful in exams to distinguish the causes of visual problems based on the symptoms. Cataracts cause a generalised reduction in visual acuity with starbursts around lights. Glaucoma causes a peripheral loss of vision with halos around lights. Macular degeneration causes a central loss of vision with a crooked or wavy appearance to straight lines.

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13
Q

Management of cataracts ?

A

If the symptoms are manageable no intervention may be necessary.

Cataracts surgery involves drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens into the eye. This is usually done as a day case under local anaesthetic. It generally gives good results.

It is worth noting that cataracts can prevent the detection of other pathology such as macular degeneration or diabetic retinopathy. Once cataract surgery is performed these conditions may be detected. Therefore, the surgery may treat the cataract but they may still have poor visual acuity due to other problems.

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14
Q

What is endopthalmitis, what causes it, how can it be treated and what can it lead to ?

A

It is a rare but serious complication of cataract surgery. It is inflammation of the inner contents of the eye, usually caused by infection. It can be treated with intravitreal antibiotics, injected directly into the eye. Endopthalmitis can lead to loss of vision and loss of the eye itself.

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15
Q

What is glaucoma ?

A

Optic nerve damage caused by a significant rise in intraocular pressure

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16
Q

What causes a raised intraocular pressure ?

A

A blockage in aqueous humour trying to escape the eye.

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17
Q

Pathophysiology of open angle glaucoma ?

A

There is a gradual increase in resistance through the trabecular meshwork. This makes it more difficult for aqueous humour to flow through the meshwork and exit the eye. Therefore, the pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma.

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18
Q

What is the optic cup ? Increased pressure in the eye causes cupping of the optic disc, what is this ?

A

In the centre of a normal optic disc is the optic cup. It is a small indent in the optic disc where there is no nerve fibres or blood vessels. It is usually less than half the size of the optic disc

When there is raised intraocular pressure the indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper. This is called “cupping”. An optic cup greater than 0.5 the size of the optic disc is abnormal.

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19
Q

4 risk factors for open angle glaucoma ?

A
  • Increasing age
  • Family history
  • Black ethnic origin
  • Nearsightedness (myopia)
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20
Q

Presentation of open angle glaucoma ?

A

Often the rise in intraocular pressure is asymptomatic for a long period of time. It is diagnosed by routine screening when attending optometry for an eye check.

Glaucoma affects the peripheral vision first. Gradually the peripheral vision closes in until they experience tunnel vision.

It can present with a gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.

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21
Q

Gold standard way to measure intraocular pressure ?

A

Goldmann applanation tonometry

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22
Q

Diagnosis of open angle glaucoma (three components) ?

A
  • Goldmann applanation tonometry - can be used to check the intraocular pressure
  • Fundoscopy - assessment to check for optic disc cupping and optic nerve health
  • Visual field assessment - to check for peripheral vision
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23
Q

Management of glaucoma (include aims of management, first line, other options, any surgical options) ?

A

Management of glaucoma aims to reduce the IOP. Pts are followed up closely to assess the response to treatment.

Prostaglandin analogue eyedrops (e.g. latanoprost) are first line. These increase uveoscleral outflow.

Other options:
-B blockers (e.g. timolol) reduce the production of a
aqueous humour
-Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
-Sympathomimetics (e.g. brimonidine) reduce the proportion of aqueous fluid and increase uveoscleral outflow

Trabeculectomy surgery may be required where eye drops are ineffective. This involves creating a new channel from the anterior chamber, through the sclera to a location under the conjunctiva. It causes a “bleb: under the conjunctiva where the aqueous humour drains. It is then reabsorbed from this bleb into the general circulation.

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24
Q

What is age related macular degeneration ?

A

A condition where there is degeneration in the macular that causes a progressive deterioration in vision.

25
Q

Key finding associated with macular degeneration ?

A

Drusen seen during fundoscopy.

26
Q

What are drusen ?

A

Yellow deposits of protein and lipids that appear between the retinal pigment epithelium and Buch’s membrane. Normal drusen are small and hard. Larger and greater numbers of drusen can be an early sign of macular degeneration.

27
Q

The macular is made of four key layers, what are these layers

A

At the bottom is the choroid layer which contains blood vessels that provide the blood supply to the macula. Above that is Buch’s membrane. Above Buch’s membrane there is the retinal pigment epithelium and above that are the photoreceptors.

28
Q

What are the two types of age related macular degeneration ?

A

90% of cases are dry and 10% are wet. Wet AMD carries a worse prognosis.

29
Q

Name 3 features of dry AMD ?

A
  • Atrophy of the retinal pigment epithelium, choroid and retina
  • The pt develops a central scotoma
  • The pt retains good peripheral vision
30
Q

Name 5 features of wet AMD ?

A

-Choroidal neovascular membrane (CNVM)
-Leaking vessels below retina
-Localised retinal detachment which leads to
distorted central vision and eventually a
central scotoma
-Exudates and haemorrhage seen using the
ophthalmosocope
-Retinal scarring

31
Q

Name 2 features that are common to wet and dry AMD ?

A
  • Atrophy of the RPE

- Degeneration of the photoreceptors

32
Q

Note :

A

In wet AMD there is development of new vessels growing from the choroid layer in to the retina. These vessels can leak fluid or blood and cause oedema and more rapid loss of vision. A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF). This is the target of medications to treat wet AMD.

33
Q

Name 5 risk factors for AMD ?

A
  • Age
  • Smoking
  • White or Chinese ethnic origin
  • Family history
  • Cardiovascular disease
34
Q

Presentation of AMD (include presentation of wet AMD) ?

A

Key visual changes to remember for spotting AMD in exams :

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

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

35
Q

Examination of AMD ?

A
  • Reduced acuity using a Snellen chart
  • Scotoma (a central patch of vision loss)
  • Amsler grid test can be used to assess distortion of straight lines
  • Fundoscopy - drusen are the key finding

Slit-lamp biomicroscopic fundus examination by a specialist can be used to diagnose AMD

Optical coherence tomography is a technique used to gain a cross sectional view of the layers of the retina. It can be used to diagnose wet AMD

Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. It is useful in revealing oedema and neovascularisation. It is used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.

36
Q

Management of AMD (do you refer, dry and wet) ?

A

Refer suspected cases to an ophthalmologist for assessment and management.

Dry AMD:
There is no specific treatment for dry age related macular degeneration. Management focuses on lifestyle measures that may slow the progression:
-Avoid smoking
-Control BP
-Vitamin supplementation has some evidence in slowing progression.

Wet AMD:
-Anti-VEGF medications are used to treat wet AMD. Vascular endothelial growth factor is involvement in the development of new blood vessels in the retina. Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels. They are injected directly into the vitreous chamber of the eye once a month. They slow and even reverse the progression of the disease. They typically need to be started within 3 months to be beneficial.

37
Q

What is retinal detachment ?

A

It is where the retina separates from the choroid underneath

38
Q

What is retinal detachment normally due to ?

A

It is usually due to a retinal tear that allow vitreous fluid to get under the retina and fill the space between the retina and the choroid. The outer retina relies on the blood vessels of the choroid for its blood supply. This makes retinal detachment a sight threatening emergency that needs to be quickly recognised and treatment.

39
Q

Name 6 risk factors for retinal detachment ?

A
  • Posterior vitreous detachment
  • Diabetic retinopathy
  • Trauma to the eye
  • Retinal malignancy
  • Older age
  • Family history
40
Q

Presentation of retinal detachment ?

A

It is a painless condition that can present with:

  • Peripheral vision loss. This is often sudden and described as a shadow coming across the vision
  • Blurred or distorted vision
  • Flashes and floaters
41
Q

Management of retinal detachment ?

A

Pts presenting with painless flashes and floaters should have a detailed assessment of the retina by someone with the appropriate skill set to detect RETINAL TEARS and RETINAL DETACHMENT. Any suspicion of retinal detachment requires immediate referral to ophthalmology for assessment and management. (I only really need to know this bit)

Management of RETINAL TEARS aims to create adhesions between the retina and choroid to prevent detachment. This can be done using:

  • Laser therapy
  • Cryotherapy

Management of RETINAL DETACHMENT aims to reattach the retina and reduce any traction or pressure that may cause it to detach again. This needs to be followed by treating any retinal tears. Reattaching the retina can be done using one of three options:

  • Virectomy - involves removing the relevant parts of the vitreous body and replacing it with oil or gas
  • Scleral buckling involves using a silicone “buckle” to put pressure on the outside of the eye (the sclera) so that the outer eye indents to bring the choroid inwards and in contact with the detached retina.
  • Pneumatic retinopexy - involves injecting a gas bubble into the vitreous body and positioning the pt so the gas bubble creates pressure that flattens the retina against the choroid and close the detachment.
42
Q

When does central retinal vein occlusion occur ?

A

When a thrombus forms in the retinal veins and blocks the drainage of blood from the retina

43
Q

Where does the central retinal vein run through and what is it responsible for ?

A

It runs through the optic nerve. It is responsible for draining blood form the retina.

44
Q

How many branched veins are there that come together to form the central retinal vein, what happens when a branch is blocked vs the central vein ?

A

4 branched veins. Blockage of one of the branch veins causes problems in the area drained by that branch, whereas blockage in the central vein causes problems with the whole retina.

45
Q

What does blockage of a retinal vein cause and what does this result in ?

A

Pooling of blood in the retina. This results in the leakage of fluid and blood causing macular oedema and retinal haemorrhages. This results in damage to the tissue in the retina and loss of vision. It also leads to the release of VEGF, which stimulates the development of new blood vessels (neovascularisation)

46
Q

Presentation of a retinal vein occlusion ?

A

Sudden painless loss of vision

47
Q

Name 6 RFs for a retinal vein occlusion ?

A
  • HTN
  • High cholesterol
  • Diabetes
  • Smoking
  • Glaucoma
  • Systemic inflammatory conditions such as SLE
48
Q

A fundoscopy examination is diagnostic of a retinal vein occlusion, name 3 characteristic findings ?

A
  • Flame and blot haemorrhages
  • Optic disc oedema
  • Macula oedema
49
Q

Management of a retinal vein occlusion ?

A

Pts with a suspected retinal vein occlusion should be referred immediately to an ophthalmologist for assessment and management.

50
Q

What is the central retinal artery a branch of ?

A

The ophthalmic artery

51
Q

What is the ophthalmic artery a branch of ?

A

The internal carotid artery

52
Q

Most common cause of occlusion of the retinal artery is + what else can cause this ?

A

Atherosclerosis. It can also be caused by GCA, where vasculitis affecting the ophthalmic or central retinal artery causes reduced blood flow.

53
Q

RF’s for central retinal artery occlusion ?

A

Basically the same as for other CVD:

  • Older age
  • Family history
  • Smoking
  • Alcohol consumption
  • HTN
  • Diabetes
  • Poor diet
  • Inactivity
  • Obesity
54
Q

Which pt group is at a higher risk for developing a retinal artery occlusion secondary to GCA ?

A

White pts over 50 yrs of age, particularly females and those already affected by GCA and polymyalgia rheumatica.

55
Q

Presentation of a central retinal artery occlusion ?

A

Sudden painless loss of vision

56
Q

There will be a relative afferent pupillary defect during a central retinal artery occlusion, why is this ?

A

Because the input is not being sensed by the ischaemic retina when testing the direct light reflex but is being sensed by the normal retina during the consensual light reflex

57
Q

What will fundoscopy show during a central retinal artery occlusion and why ?

A

A pale retina with a cherry red spot. The retina is pale due to a lack of perfusion with blood. The cherry red spot is the macula, which has a thinner surface that shows the red coloured choroid below, which contrasts with the pale retina.

58
Q

Management of a central retinal artery occlusion ?

A

Pts suspected of it should be referred immediately to an ophthalmologist for assessment and management.

GCA is an important potentially reversible cause. Therefore older pts are tested and treated for this if suspected. Testing involves an ESR and temporal artery biopsy and treatment is with high dose systemic steroids.

Long term management involves treating reversible risk factors and secondary prevention of CVD