Ophthalmology_16_10_14 Flashcards

1
Q

What is the most common elective surgical Rx in the UK.

A

Cataract removal - about 330,000 in 2008-9.

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2
Q

What is the aetiology of cataract formation through natural ageing?

A

A disturbance in the structure of the lens and an accumulation of pigment. The normal clarity is arranged through a precise structure of fibres and balanced chemical constituents - cataracts form as these go awry.

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3
Q

What is a cataract?

A

The development of an opacity within the lens.

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4
Q

What is the usual role of the lens?

A

It focuses light passing through it (along with the cornea) and focuses it on the retina.

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5
Q

What is is important that a GP correctly diagnosis and assess the severity of a corneal abrasion?

A

Getting the diagnosis is important - to exclude other causes that require more urgent referral, e.g., acute angle closure glaucoma or acute uveitis.Note that they can all cause acutely painful red eye.

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6
Q

What are the tidal symptoms of a cataract?

A

-gradually become aware of symptoms slowly, over months or years.-sight disturbance, blurring/clouding.-halos and glares are often discribed, e.g., at night around car headlights.-sometimes patients may be unaware of them, and may be referred by an optometrist or optician.-might present as deteriorating ability to read fine print and/or needing more light to see by.-sometimes there is an alteration of colour perception, lack of contrast, and yellowish distortion. (Especially noticeable in patients with unilateral cataract).

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7
Q

Left on its own, will a cataract repair itself?What is the definition of a cataract on a Snellen chart?

A

No! The just get worse!Defined by vision of less than 6/12 on Snellen chart.

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8
Q

What are the broad categories that cause cataract formation? (Name 8; 18 are listed!)

A

Age.Female sex (slightly higher risk).Diabetes.Atopic disorders.Acute extreme dehydration.Eye surgery.Penetrating eye injury.Irradiation or electrocution of the eye.Contusion of the eye.Glaucoma.Retinitis pigmentosa.Extreme myopia.Drug-induced.Smoking.UV radiation.(?alcohol - less robust evidence).

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9
Q

What drugs can cause cataract formation?

A

Ocular steroids (especially prolonged courses) - 15mg day for > 1 yr. other forms of steroid (e.g., oral, nasal) are much less likely to cause cataracts, but occasionally do.Statins!Topical agents used in glaucoma treatment (bit annoying really).Some other drugs have less robust evidence - amiodarone, phenothiazides, TCA, and anti hypertensives (especially diuretics and beta blockers).

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10
Q

What is the medical condition most likely to cause cataracts?

A

Diabetes. Duration of disease and how tightly it is controlled relate to the risk. Mainly causes cortical and posterior capsular cataracts.

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11
Q

What are the different types of cataract? And their typical presenting symptoms?

A

1) nuclear - yellowing and sclerosis of nucleus of lens - reduced contrast and colour intensity; difficulty recognising faces or reading number plates; reading vision is typically preserved more than might be expected.2) cortical -gradually develops from the outside of the lens into the centre - typically presents with glare when driving at night, difficulty with reading. Developed by patients with diabetes.3) subcapsular - occupies the posterior capsular area, begins at the back of the lens. Difficulty in daytime driving (cf cortical), difficulty in reading, often in diabetics, patients with extreme long-sightedness, or retinitis pigmentosa, or in high doses of steroids.4) a small waterfall- no further explanation required.

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12
Q

How should assessment of patient with cataract be made?

A

Focused Hx: visual symptoms (including near and distance vision), past visual problems, binocular vision, amblyopia. Ask about other risk factors. Determine the effect on the person: driving, reading falling, how their quality of life has been affected, any restrictions on work or leisure pursuits.Medication should also be reviewed. (Alpha-agonists raise risk of floppy iris syndrome, and warfarin obviously increased bleeding risk - both make surgery more hazardous).Examination should include Snellen chart used both with and without corrective lenses. General eye examination also should be performed. Look for the red reflex (absent in most cataracts).Comorbidities that make surgery difficult.Obviously- the patients wish for surgery!

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13
Q

What treatments, other than surgery, are there for cataracts?

A

None! The ONLY true treatment is surgery.However, progression can be slowed by:Avoiding UV light.Discontinuing other risk factors, e.g., drugs that can cause cataracts (risk vs benefit).Reducing glare (e.g. Sunglasses, tinted glasses, hat).Optimising refractive correction.Increasing light levels.Stopping smoking!Consolation of visual aids and supports to reduce disability.

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14
Q

Do GP’s make the decision (with the patient, obviously!) to go for cataract surgery?

A

No! The GP has the role of referring to secondary care - these are the guys who decide whether to offer surgery or not.

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15
Q

Most cataract operations are day-cases; when might they be inpatient operations?

A

If other eye conditions co-exist, as they need extra observation overnight, or for those with significant co-morbidity.Day cases are done with local anaesthetic, overnight class with general anaesthetic.

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16
Q

When considering cataract operation, how does the presence of other eye conditions (e.g., ARMD, diabetic retinopathy, glaucoma) affect decision for surgery or not?

A

Actually, these diseases INCREASE the need for surgery, as the cataract gets in the way of monitoring and treating tho other conditions. E.g., photographic screening for diabetic retinopathy is compromised by cataracts.

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17
Q

How long does a cataract operation take, and how is it done?

A

10-40minutes.Typically, phaecoemulsification is used; the lens capsule remains in place, while the lens itself is broken down by an ultrasonic tip and then suctioned out. Only a small incision is required, which preserves the corneal shape.An alternative is conventional extracapsular cataract extraction (ECCE) but this requires a larger incision, and is usually reserved for more difficult cases.A replacement lens is then inserted.

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18
Q

What are the effects of replacing a lens with an artificial one after a cataract is operated on?

A

The artificial lens is usually designed for optimal distance vision, so patients are typically in need of reading glasses afterwards.Multi focal lenses are being developed but are not typically available on the NHS.Another option (in bilateral cataract operation) is to replace one lens with zero refraction (to give distance vision) and the other with refraction for myopia for near vision. However, this does not result in normal binocular vision or depth perception.

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19
Q

What advice is given to patients following cataract surgery?

A

Likely to experience mild discomfort (can be managed with simple analgesia), itching, bruising, light sensitivity, and some discharge.Swimming, strenuous exercise, and heavy lifting should be avoided, as above, for 7-10 days.The patient should avoid rubbing the eye and exposing it to irritants.Improvement in vision is not always immediate - should take about a week.It might be wise to avoid the patient against straining (e.g., on the loo! Use laxatives!) as this increases the risk of choroidal/suprachoriodal haemorrhage, which is very nasty.Vision should be checked by optometrist in 4-6 weeks;new glasses may be required.

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20
Q

If a patient requires cataract operations on both eyes, should they be carried out at the same time?

A

No, not usually. There are advantages (may aid visual rehabilitation and reduce cost to both patient and society). But……the risk of bilateral endophthalmos has to be borne in mind - this has potentially catastrophic consequences.

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21
Q

What medicines are patients typically discharged on after cataract operation?

A

Antibiotic and steroid eye drops - reduces inflammation and chance of post operative infection.

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22
Q

What complications post cataract surgery should alert the GP to consider re-referral to secondary care?

A

Increasing pain.Worsening vision.Increasing swelling.Excessive discharge.

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23
Q

What is the most common complication 5 years post cataract surgery and how is it managed?

A

Posterior capsular opacification (which has been left in place). Occurs in 28% 5yrs after the operation, and is simply treated with lasers.

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24
Q

What are significant post-cataract operation complications that require immediate referral back to the ophthalmologists? (There are 8; can you name 5?)

A

Raised ICP.Acute post operative infective endophthalmos.Delayed post operative infective endophthalmos.Retinal detachment.Macular oedema.Intra-ocular lens dislocation.Choriodal/suprachoriodal haemorrhage.Toxic anterior segment syndrome.

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25
Q

What is toxic anterior segment syndrome?

A

Passage of exogenous material into the anterior chamber causing inflammatory reaction. Presentation is usually with sudden reduction in vision and mild eye pain, with eyelid selling, conjunctival redness, hypopyon, or diminished red reflex. (I.e., similar to those of acute post operative endophthalmic infection, but with only mild or minimal pain, and occurring more swiftly, usually with the first 24hrs of surgery.

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26
Q

What is acute post operative infective endophthalmitis?

A

Develops within days of surgery. Presentation is usually with sudden reduction in vision and increasing eye pain, with eyelid selling, conjunctival redness, hypopyon, or diminished red reflex.

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27
Q

What is delayed post-operative infective endophthalmitis?

A

This develops weeks to months after surgery (average 9 months). Visual loss is insidious, but it occurs with minimal pain. Examination may show hypopyon, inflammatory clumps in the anterior chamber, and corneal oedema.

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28
Q

What is amblyopia?

A

Reduction in visual acuity in the absence of detectable organic disease, affecting one or both eyes. Visual acuity is usually better when letters are viewed singly rather than in series.Note that the reduced visual acuity is not reduced further by reducing illumination (unlike in many organic diseases).There is also usually a disorder of pursuit movement. Often as symptomatic and picked up by chance when the eyes are detected separately.In some individuals it can be corrected.

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29
Q

What is a hypopyon?

A

This is an ophthalmological emergency.There are pus cells in the anterior chamber. On examination thee is the characteristic picture of a congested eye with a white/yellow fluid level of pus in the anterior chamber.It is caused by severe infection of the eye or in severe iritis, e.g. Behçet’s disease.There may be a recent Hx of steroid drop use to treat sore red eyes, or of immunosuppression.

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30
Q

What is macular oedema and what does it cause?

A

Blurred central vision. The presentation is usually a little delayed, but it is the commonest cause of unexpected visual loss following cataract surgery.

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31
Q

Retinal detachment can occur following cataract surgery. How common is this?

A

It is rare, though over ten years the risk excess is 5.5; the presentation is as with any other cause of retinal detachment.

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32
Q

Does raised intraocular pressure occur following cataract surgery?

A

Some risk in pressure is common and self limiting. However, sometimes rapid elevations present as as an acute glaucoma with an acutely painful red eye; this is usually inflammatory in origin.

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33
Q

Following cataract surgery, how does intraocular lens dislocTion present?

A

Reduced vision, ghosting of images, halos, diplopia. If there is pain and/or a red eye, then anterior capsule dislocation is more likely - this would be caused by mechanical injury or an inflammatory response to the displaced lens.

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34
Q

What is choroidal/suprachoriodal haemorrhage?

A

Sudden excruciating throbbing pain with an immediate loss of vision. The risk is increased by straining.

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35
Q

What is the usual postoperative vision in those after cataract operation?

A

At best 6/12.The problem is, the disease progresses non-linearly, and will up ultimately result in severe disability if not treated; thus the question is often not whether to operate, but when to operate.

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36
Q

How common is infantile cataract, and what are they caused by?

A

They are diagnosed in around 3 in 10,000 children under the age of one.They can be an inherited trait, but can also be due to a harmful event in utero, the most usual being infections in pregnancy (varicella or rubella in particular), Down’s syndrome, myotonic dystrophy, and intrauterine/neonatal hypocalcaemia.

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37
Q

If an infant is found to have bilateral cataracts and no Fx, what conditions is it prudent to exclude (one more than the other)?

A

Primarily, galactosaemea, but also galactokinase deficiency.

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38
Q

In infantile cataracts, what do long term visual problems typically develop from?

A

Amblyopia. The deprivation of visual stimuli causes structural changes in the brain. However, in the first 6 weeks of life, the visual systems are sufficiently immature that these changes do not take place. These first six weeks are referred to as ‘the latent period’, but if the cataract is removed after this time then theses structural changes in the brain and subsequent amblyopia tend to develop. (Note that in bilateral infantile cataract, the latent period is closer to ten weeks).

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39
Q

Why does this latent period exist? How can a baby see at all if it is not exposing the higher cortical structures to visual input?

A

During the latent period, vision is predominantly via sub cortical pathways.

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40
Q

If a child with infantile cataract has it removed before the latent period is up, what future consequences to sight will there be? What if it is left later? However, what reason MIT there be to delay a cataract operation?

A

If the cataract is removed in the latent period, it is thought that there will be no lasting impact on sight. If it is left until after the latent period, there will be a progressively worse outcome in terms of final visual abilities depending on how long it is left.On the other hand, there is an argument that cataract removal in the first year of life increases the risk of subsequent glaucoma development.

41
Q

What further treatments to infantile cataracts require after the operation? What is a recognised complication?

A

Occlusion (patching) is often required after the surgery, and is frequently only a useful vision of 6/60 or better.A frequent complication is nystagmus, even with patching; it typically develops 3 months after the surgery and persists indefinitely.

42
Q

What is a recognised complication of repair of bilateral infantile cataracts? How is it managed?

A

Strabismus. It is managed with lower intensity occlusion.

43
Q

What is strabismus?

A

A squint. A condition where the visual axes of the eyes are not directed simultaneously at the same object.

44
Q

The absence of a red reflex in a child may represent an infantile cataract, however it is not pathognomic for this condition. What else could it represent?

A

Retinoblastoma.Retrolental fibroplasia (a consequence of retinopathy of prematurity).Ocular toxocariasis (ocular infection by a nematode parasite found in cats and dogs).Because all these differentials (including infantile cataract) are potentially serious, finding them is a red flag, and demands urgent specialist referral.

45
Q

What are the symptoms of a corneal abrasion? What do they result from?

A

Symptoms of pain, sensation of something in eye, redness of eye, decreased acuity, blurring, epiphora (increased watering).Caused by superficial trauma to the most anterior aspect of the eye, the corneal epithelium.

46
Q

What is the function of the cornea?

A

Refract light (before further refraction through the lens) to focus it on retina.Perhaps an element of protection/a barrier to infection.

47
Q

How long do corneal abrasions take to heal?

A

Most are self limiting, and heal within a few days. Deeper cuts and slices take longer, and there is the danger of, e.g., infection.

48
Q

What elements of a history make corneal abrasion a differential?

A

Hx of trauma to the eye.Pain.Feeling of something in eye.Blurriness/loss of acuity.Epiphora.Redness.Photophobia.

49
Q

What is it always important to determine about a patient if a corneal abrasion is suspected?

A

Do they wear contact lenses! Can complicate the situation and make specialist referral more likely to be required.

50
Q

Why is it important to examine a patient if you suspect a corneal abrasion even if the patient does not recall a trauma?

A

Because it might have happened anyway! An examination might find evidence of this!

51
Q

Before examining for corneal abrasion, what is the patient given and why? Why are they not given this to take away?

A

A topical ophthalmic anaesthetic, eg., tetracaine 0.5%, to put the patient at ease and allow a more thorough examination.But the patient should not be sent away with this! They are easy for patients to over use, delay wound healing, and can promote corneal ulcer formation.

52
Q

When examining for corneal abrasion, the exam should be systematic. After I stilling the topical anaesthetic, what next?

A

1) Assess visual acuity in each eye.2) Examine the eyelids and adnexa for signs of inflammation and trauma.3) Evert the upper eyelid to look for foreign body-if found, remove if possible.4) Examine pupils for size and reactivity, comparing the two.5) Visualise the the cornea with a cobalt blue light after staining with fluorescein. (Abrasions are usually seen in green over the corneal surface).

53
Q

What are the steps in everything the upper eyelid to look for a foreign body?

A

1) Ensure patient is sitting comfortably and ask them to look down.2) Using thumb and forefinger gently pull on upper eyelashes.3) Use a cotton but to gently press down on the central part of the upper eyelid.4) Gently evert the eyelid, and thoroughly examine the area for any foreign body.5) Using a clean, sterile cotton bud, sweep the palperbral conjunctiva to remove any foreign body.

54
Q

What are the basic treatments for a corneal abrasion?

A

Topical antibiotics.Topical antinflamatories.Removal of any foreign body.Advice for patient.Follow up as required.

55
Q

What topical antibiotics should be prescribed in corneal abrasion? What choice might be used in contact lens wearers and why?

A

Can give chloramphenicol 1% ointment or 0.5% drops qds for 5-7 days.Ciprofloxacin 0.3% or ofloxacin 0.3% may also be used.The latter should be considered in contact lens wearers as it has activity against pseudomonas (which can grow under contact lenses).

56
Q

Should topical NSAIDS be given to patients with corneal abrasions?If not topical, then can you give oral NSAIDS?

A

Although not commonly me given currently in primary care, recent research says yes! A systemic review showed decreased pain and quicker return to normal activities, with no delay in healing rates or significant side effects.E.g. diclofenac 0.1%, ketorolac 0.5%, and indomethacin 0.1%.Oral analgesics can be used, but don’t work very well as the cornea is an avascular structure-hence very little of these compounds find their way to the cornea!

57
Q

Where are foreign bodies most commonly found in corneal abrasion? If you find one and yet cannot remove it, what must you do?

A

They are generally found lodged on either the corneal surface or underneath the upper eyelid (subtarsal).If you cannot remove the foreign body yourself, you must admit defeat and refer them urgently to an ophthalmology service for review!

58
Q

What advice should you give patients who have presented with a corneal abrasion? Should follow up be advised?

A

Advice that most corneal abrasions are self limiting and settle down within 48-72 hours. If the symptoms persist longer than this, or especially if they worsen, then they must be reviewed. This may be by a GP, but may involve referral to eye casualty or ophthalmology; the worry is the development of a corneal ulcer.Routine follow up is not the rule, and should only be suggested for patients with large corneal abrasions as they may take a long time to heal and are therefore at higher risk of secondary infection.

59
Q

In treating someone with a corneal abrasion, are there treatments to avoid?

A

Yes!1) Topical anaesthetics - delay wound healing increase chance of corneal ulcer formation.2) Topical mydriatics (they used to be used, the thinking being that hey would relax the ciliary muscle and ease the pain, but this thinking has been disproven).3) Eye patches. These were used in the past, but a Cochrane review looked at lots of studies and concluded the main effect of patches was to marginally delay healing times! Furthermore, patching means loss of binocular vision which gets in the way of driving, work, and other activities.

60
Q

Why are contact lens wearers especially at risk of corneal ulcer?

A

If they fit tightly, they may pull off some of the epithelium on removal.This is especially true in people with dry eyes.Edges of microscopically torn contact lenses can rub against the cornea and cause abrasions.Pseudomonas can grow beneath contact lenses, so this should be taken into account when considering a topical antibiotic (ofloxacin 0.3%).Corneal abrasions in contact lens wearers have a higher chance of developing into corneal ulcers and secondary keratitis.It is very important to emphasise the non-use of contact lens while the abrasion is treated (including the topical antibiotic).Have a low threshold for referring these patients for specialist ophthalmology review if diagnosis unclear or symptoms fail to improve as expected.

61
Q

Which patients with corneal abrasion should be referred for urgent specialist ophthalmology review? (Or at least consider doing so!)Answer 4.

A

1) Unable to remove foreign body.2) Abrasion to only functioning eye.3) Contact lens wearer with worsening symptoms.4) No improvement after 48 hours.5) Dry eyes.6) Recent eye surgery.7) Recurrent corneal abrasion.8) History of previous herpatic keratitis (which may present with reduced acuity and a red eye in the absence of pain).

62
Q

What’s the leading cause of visual impairment in the uk’s working age population?

A

Diabetic retinopathy.

63
Q

In broad terms, what is the aetiology of diabetic retinopathy?

A

Chronic hyperglycaemia –> vascular injury –> leakage and occlusion of small vessels in the eye –> new (abnormal) vessel formation, an attempt at revascularisation –> causes loss of sight through multiple measures including occlusion.

64
Q

How many stages of diabetic retinopathy are there and what are they called?

A

1) Background retinopathy.2) Pre-proliferative retinopathy.3) Proliferative diabetic retinopathy.(Also Macular oedema…but is this a stage? Ask Sam!)

65
Q

What are the features of background diabetic retinopathy?

A

Early changes found in fundus.Micro-aneurysms - dialatation of the capillary wall where it has been damaged or weakened.Retinal haemorrhages - small dot or larger blot-shaped lesions that form following rupture of vessels within deep retinal layers. (If rupture more superficially, form flame-shaped haemorrhages).Exudates - white lesions with vague margins (AKA cotton wool spots or soft exudates) due to rupture in superficial layers. (ASK SAM - DOESNT IT JUST SAY THAT SUPERFICIAL LAYER RUPTURE IS A FLAME HAEMORRHAGE??)

66
Q

What are the features of pre-proliferative diabetic retinopathy?

A

Features of increasing retinal ischaemia.Dot or blot haemorrhages.Venous bleeding - localised increase in calibre and often length of a vein, an initial attempt at revascularisation of a ischaemia zone.Intra-retinal microvascular abnormalities (IRMA). This is an abnormally dilated capillary, which may present intra-retinal neovascularisation which is yet to breach the internal limiting membrane of the retina.

67
Q

What is the role of the early treatment diabetic retinopathy study (ETDRS)?

A

To identify multiple retinal haemorrhages, venous calibre changes, and IRMA as signs indicative of progression to proliferative diabetic retinopathy.

68
Q

What is proliferative diabetic retinopathy, and what are the signs of this?

A

Prolonged retinal ischaemia up-regulates the production of endothelial growth factors and insulin-like growth factor, which induces new vessel growth.A new vessel disk - a vessel that grows at the disk or within one disk diameter of the disk.If a new vessel grows further out from the disk, this is referred to as “new vessels elsewhere”.In severe cases, the vessels grow forward to the vitreous cavity. Because they are fragile, they can bleed easily resulting in vitreous haemorrhage..

69
Q

How can proliferative diabetic retinopathy result in tractional detachment? (ASK SAM WHAT THIS IS.??!)

A

Fibrovascular proliferation of of established new vessels on the retina can cause tractional detachment

70
Q

What is rubeosis iridis?

A

In proliferative diabetic retinopathy, if the ischaemia drive extends into the anterior chamber, new vessel growth can occur at the iris and in the angle of the anterior chamber - this is rubeosis iridis. It tends to occur with more established severe diabetic retinopathy for many years.

71
Q

Why is history so important for a GP when assessing the presence of or level of diabetic retinopathy?

A

They lack specialist ophthalmic equipment! They therefore have to rely heavily on patients describing their ocular symptoms, and then the doctor understanding their significance.

72
Q

What is macular oedema?

A

Retinal oedema and the associated hard-lipid deposits called exudates.Can cause a serious impact on visual function.It is the result of leakage from the broken blood-retinal barriers, and can actually occur early on in the disease process.Exudates are often found encircling damaged vessels (‘circinates’) and Re associated with ischamic areas.

73
Q

What is macular oedema called when it is detected and it is affecting the vision? What is the definition of this?

A

This is called clinically significant macular oedema (CSMO).Defined as exudate within 500 microns of the fovea OR retinal thickening within 500 microns associated with exudates OR an area of thickening greater than one disk diameter OR within one disk diameter of the fovea.

74
Q

What is the most common cause of moderate visual loss in all types of diabetic retinopathy?

A

CSMO is the most common cause.

75
Q

When does ischaemia maculopathy occur in the context of diabetic retinopathy?

A

When there is oedema preset;arises due to extensive microvascular occlusion.

76
Q

How is ischaemia maculopathy identified?

A

NOT by fundusoscopy alone - need to diagnose by performing a fluroescein angiogram, which is usually requested when a patient is showing little response to treatment.

77
Q

What is the prognosis of ischaemic maculopathy?

A

Poor!:-(

78
Q

When, in a GP surgery, might CSMO be suspected?

A

When a diabetic with poor vision hat has decreased in acuity, and fundoscopy shows areas of featureless retina surrounded by typical microangiopathy.

79
Q

Does a large degree of diabetic retinopathy need to occur for sighit to be threatened?

A

No! Rubeosis can occur relatively early and is sight threatening.

80
Q

What do you do if you see a patient with CSMO or rubeosis?

A

Refer them URGENTLY to ophthalmology for laser treatment

81
Q

Why is screening for diabetic retinopathy vital?

A

Because the disease is largely often asymptomatic until the advanced stages, and the treatment (laser therapy) is effective at preventing rather than reversing diabetic eye damage.

82
Q

When was the NHS diabetic eye screening program introduced, and how does it work?

A

Introduced in 2003.All people with DM1 or 2 over the age of 12 are offered annual screening. In addition, patients with diabetes who become pregnant are offered a retinal screening after their first antenatal check, and then again at regular stages through the pregnancy.Note, though, that non-diabetic mothers who develop gestational diabetes are NOT offered screening.Patients with newly diagnosed diabetes should be referred for initial assessment screening.Appointments take 30-40 minutes

83
Q

What does diabetic retinal screening involve?

A

Check visual acuity.Dilation and photography of retina (these images are then reviewed by an ophthalmologist). Patients are recalled if indicated.Two field mydriatic digital imagining of the fundus is deemed the most effective tool to accurately stage diabetic retinopathy.

84
Q

What is the definition of glaucoma?

A

Progressive optic neuropathy characterised by structural optic nerve head changes, with corresponding loss of visual field.There are both structural and function deficits.NOT always a raised intraocular pressure. But all of the treatments are geared towards reducing this.There are lots of other risk factors.

85
Q

What is the structure called where the optic nerve is pinched and thought to be damaged in glaucoma?

A

Lamina cribrosa, behind the eye, sort of the posterior part of the sclera. Fibrous tissue, not bone. It is the destruction of fibres running through this ‘pinch point’ that leads to disk cupping (as the fibres are lost, the ‘hole’ becomes deeper and the cup:disk ratio gets bigger). Although the sight loss in glaucoma is typically peripheral (at least until late in the disease), the thinning of fibres still occurs at the disk, as this is where ALL the fibres run through, from wherever on the retinal layer they originate.

86
Q

Name risk factors /associations for glaucoma (name 5)

A

Raised IOP.Microvascular pathology (Hypertension, diabetes; BUT hypotensive episodes can cause it).Hypoxia damage to the nerve (eg hypotensive episodes)Sleep apnoea (can cause hypoxia episodes)Major blood lossMigraine (causes blood flow abnormalities - the sensitive neurones of the optic nerve can be damaged).Metabolic - B12 deficiencySmokingSteroids (especially in steroid responders who also get increased IOP). This can be by any route, I.e., not just optic steroid drops, but inhalers, nasal sprays, systemic, etc.Highly short sighted (myopic) people (due to the anatomy of the eye).

87
Q

Where is the aqueous humour formed and drained in a healthy eye?

A

Formed in the ciliary body, in the posterior chamber, behind the iris.Drained through the trebecular mesh work (like a sieve), located at the angle of the anterior chamber and the iris. After this, through Schlemm’s canal, then through the venous system.

88
Q

Where is the posterior chamber in the eye?

A

Behind the iris, in front of the lens.NOT the vitreous chamber.The anterior chamber is in front of the iris.

89
Q

What is the hole in the iris called?

A

Pupil.

90
Q

Why is acute glaucoma ususally actually a misnomer?

A

Because if is is treated quickly and properly there is no nerve damage - no neuropathy.

91
Q

What time of day can people typically present with acute angle closure and why?

A

Time of day that it starts to get dark! Because pupil dilates and this can cause an angle closure in susceptible people.

92
Q

What is the presentation of acute angle closure?

A

Red, very painful eye.Fixed mid-dilated pupil.Vomiting.Reduced, blurry vision.Cornea becomes hazy/opaque. (Which is what causes the above).Always unilateral, but likely that the other eye would be susceptible due to a narrow angle. (Usually a narrow angle is a bilaterally inherited phenotypical trait).

93
Q

What is the Treatment for acute angle closure?

A

Ophthalmic emergency.Eye drops to lower pressure (either by reducing aqueous humour production or by increasing it’s drainage). IV acetazolamide (carbonic anhydride inhibitor). Give IV as the patient is often vomiting! Also will act fast. This reduces aqueous secretion.Pilocarpine to constrict the pupil. A miotic. (An alpha agonist).Topical anti hypertensives (especially beta blockers, usually timolone).Ultimate Rx is a laser iridotomy (a hole is made in the iris, can actually be done by surgery not just lasers). After the acute event is treated, the other eye is often treated prophylactically, as bilateral anatomy makes a similar attack on the other eye likely at some point.

94
Q

What is the most common form of glaucoma?

A

Chronic/primary open angle glaucoma - caused by increased resistance to aqueous outflow through trabecular mesh work.

95
Q

What is the treatment for open angle glaucoma?

A

Prostaglandin analogue - latanoprost for e.g., works by increasing outflow through uveo-scleal outflow (which usually would account for about 20% of outflow). Usually taken once at night as eye drop. (S/e - can make eyelashes grow).Topical (eye) beta blocker (timolol) - reduces aqueous formation. Very effective, but has systemic s/e, so is contraindicated in anyone who beta blockers would usually be contraindicated in, e.g., asthmatics.Carbonic anhydride inhibitors eg brinzolamide - again reduces aqueous formation.Also, get combinations eg beta blocker + prostaglandin analogue together.Surgical - trebeculectomy (traditional) effective, but there are risks, so tend to use only when the drops not working/neuropathy still progressing. The tendency is to make a trap door that will spring open when pressures get too high. (On examination, these patients will have a blob of conjunctiva). This lets the high-pressure aqueous drain out of the anterior chamber.Laser treatment - selective laser trebeculoplasty. Makes trebecular meshwork more permeable. Tends to work for a few years, but then may need re-doing.

96
Q

What is the role of mitomycin C? (MMC)What eye condition is it used in?

A

It is used in chronic open angle glaucoma.This drug is given at the time of the trebeculectomy, after the cut is made in the eye to make the “trapdoor”, to stop an inflammatory reaction and scarring happening.Could also be used a few months following an op if suspicious that a inflammatory reaction is starting to occur.

97
Q

If someone presents with an acute red eye and reduced visual acuity in the absence of pain, what should you suspect?How do you treat them?

A

Suspect previous herpatic keratitis of that eye. Treat by urgen ophthalmological referral!

98
Q

What is floppy iris syndrome? What can cause or predispose towards it?

A

It is usually found in cataract surgery as a complication, where the iris becomes floppy and flaccid and billows in response to ordinary inraocular fluid currents. It tends to prolapse towards the area of cataract extraction, and there is progressive intra-operative pupil constriction.It is associated with alpha blockers, e.g., tamsulosin. Even taking these drugs once in your life makes it more likely to occur! Also associated with finasteride, which is also associated with cataract formation!