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Specialties > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Name three risk factors for cataracts

A

Diabetes
Metabolic abnormalities - hypocalcaemia
Drugs - chlorpromazine and steroids
UV radiation

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2
Q

Name the hallmark finding on fundoscopy for cataract

A

Black opacities

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3
Q

How does Endophthalmitis present?

A

Painful red eye
Reduced VA
Hypopyon

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4
Q

How do you treat Endophthalmitis?

A

Intraocular ABx

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5
Q

What is the hallmark symptom for Chronic open angle glaucoma?

A

Tunnel vision

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6
Q

Name which drugs are used to treat chronic open angle glaucoma, their mechanism of action and common side effects

A
  1. Prostaglandin analogues - latanoprost (encourage drainage through uveoscleral) brown pigmentation of iris
  2. Beta blockers (inhibit secretion of aqeous) - bradycardia and bronchospasm
  3. Miotics - pilocarpine (uveoscleral) - constrict pupil
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7
Q

What is the laser and surgical management of chronic angle glaucoma?

A

Trabeculoplasty and Trabeculectomy

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8
Q

What does a tonometer measure

A

IOP

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9
Q

What does gonioscopy do

A

Allows us to see if the angle is open

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10
Q

What is the hallmark finding on fundoscopy for chronic open angle glaucoma?

A

Pathological cupping (>0.3)

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11
Q

What is a big risk factor for primary angle closure glaucoma?

A

Family history of hypermetropia

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12
Q

How does primary angle closure glaucoma present?

A
  • Red painful eye - leading to ocular pain and headaches
  • Watery eye
  • Blurred vision leading to rapid visual loss
  • Haloes
  • Nausea and Vomiting
  • Fixed, non-reactive, mid-dilated pupil
  • Hazy, cloudy cornea
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13
Q

How do we treat primary angle closure glaucoma?

A

Medically - bring IOP pressure down.
1. Acetozolamide (carbonic anhydrase inhibitor - reduces aqeuous secretion) - IV and orally
2. All other drugs that we use in open angle glaucoma
3. Pilocarpine causes pupil constriction so will draw the peripheral iris out of the angle
Surgically -
- Peripheral iridotomy done in BOTH eyes

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14
Q

What can cause secondary glaucoma?

A

Retinal vein occlusion, intraocular tumours, long term retinal detachment, corticosteroids

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15
Q

What are the risk factors for ARMD?

A
  1. Increasing age (>60)
  2. Smoking
  3. Family history
  4. Obesity
  5. Caucasian
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16
Q

What are the symptoms of ARMD?

A

Gradual loss of central vision - central scotoma
Sudden L.O.V - can be due to vitreous haemhorrage
Reduced visual acuity
Metamorphopsia
Photopsia
Macropsia and micropsia
Charles Bonnet syndrome - visual hallucinations

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17
Q

What is the difference between dry and wet AMD on fundoscopy

A

Dry AMD - Drusen in Bruch’s membrane

Wet AMD - choroidal neovascularisation

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18
Q

How do we treat dry ARMD

A

Dry - no medical treatment but we can control risk factors ie. stop smoking, change diet (eat more vitamin C, E and beta carotene) and refractive clinics to maximise what vision they have.
Also safety net for wet ARMD

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19
Q

How do we treat wet ARMD?

A
  1. Control risk factors and safety net
  2. Intra-vitreal ranibizumab - anti VEGF (3 month treatment)
  3. Surgical - photocoagulation or photodynamic therapy
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20
Q

How quickly should we refer someone to opthalmology when we suspect ARMD?

A

1 week referral

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21
Q

Name 3 risk factors for diabetic retinopathy

A
  1. Duration of disease
  2. Poor glycaemic control
  3. Comorbidities e.g HTN
  4. Smoking
  5. Complications of diabetes e.g renal disease
  6. Pregnancy and diabetes
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22
Q

What are the stages of diabetic retinopathy and how do each of them appear on fundoscopy?

A
  1. Normal
  2. Background retinopathy - few haemorrhages, microaneurysms (dots) and exudates generally on retina
  3. Maculopathy - above findings but on the macula
  4. Pre-proliferative retinopathy - above + cotton wool spots, venous looping and beading, deeper haemorrhages
  5. Proliferative - neovascularisation of retina and larger haemorrhages (may lead to vitreal haemmorhage)
  6. Advanced - above + may get retinal detachment
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23
Q

How do we treat pre-proliferative diabetic retinopathy?

A

Laser photocoagulation

24
Q

How does diabetic retinopathy present?

A

painless, gradual loss of vision
may have sudden LOV due to vitreous haemmorhage
may get some dark floaters from microaneurysms that disappear after a few minutes

25
Q

What is the gold standard for diagnosing diabetic retinopathy?

A

Dilated retinal photography

26
Q

How do we treat diabetic retinopathy?

A
  1. Primary prevention - glycaemic control, stop smoking, lose weight etc.
  2. Refer anyone from maculopathy upwards to an opthalmologist along with anyone with vitreous haemmorhage
  3. Laser photocoagulation - inhibits neovascularisation of retina
  4. Surgery - vitrectomy if vitreous haemorrhage
27
Q

What are the complications of diabetic retinopathy?

A

Macular oedema, macular ischaemia, vitreous haemmorhage and tractional retinal detachment

28
Q

Describe the stages of hypertensive retinopathy

A
  1. Mild hypertension - some arterial narrowing generalised
  2. More marked HTN - focal arterial narrowing and AV nipping
  3. Mild angiospastic hypertension (symptomatic) - above + lipid exudates, flame haemmorhages, cotton wool spots
  4. Sever HTVe retinopathy - all of above plus papilloedoma
29
Q

Name 3 causes of papilloedema

A

Malignant hypertension
Hydrocephalus
SOL
Hypercapnia

30
Q

What are the hallmark features of papilloedema on fundoscopy?

A
  1. Venous engorgment

2. Optic disc - loss of cup, blurred margins, bulging disc

31
Q

What are the causes of Keratitis?

A

Viral - herpes simplex

Bacterial - step and staph. Pseudomonas in contact lens wearers. Acanthamoeba and onchocoecal (river)

32
Q

What are the risk factors of keratitis?

A

Dry eyes, abrasion, any compromisation of the corneal membrane e.g. surgery or trauma, use of contact lenses, prolongued use of steroids

33
Q

How does keratitis present?

A 
Painful eye
Purulent discharge
Gritty feeling
Hypopyon
Corneal ulcer
34
Q

How do we treat keratitis?

A

Abx to be used hourly every day for a few days usually concentrated broad spectrum such as ciprofloxacin

35
Q

How do we write down someones vision

A

6(metres)/ what ever line they can read

36
Q

What happens if someone can’t read the snellen chart from 6M?

A

Move them closer until they can and if they still cant then we use counting fingers

37
Q

How does central retinal artery occlusion (CRAO) present?

A

Sudden, painless loss of vision unilaterally

May be a history of Amaurosis Fugax

38
Q

What are the causes of CRAO?

A

Caused by atherosclerotic emboli - HTN + Diabetes
Thrombophilic disorders
VASCULITIS! (SUSPECT IN ANYONE OVER 50)

39
Q

What are the hallmark features of CRAO on fundoscopy?

A

Cherry red spot - red fovea (choroid can be seen through the very pale and thin ischaemic retina)
Pale optic disc
Attenuated arterioles

40
Q

What do we examine in someone with CRAO?

A

Cardiovascular system

Check for carotic stenoses with doppler USS - carotid endarterectomy may be required if stenosis >70%

41
Q

What is important to rule out in a patient over 50 with CRAO and how shall we manage them?

A

GCA

  1. Take urgent ESR and CRP
  2. Do coag studies and FBC
  3. Take a temporal artery biopsy
  4. Start on high dose steroids
42
Q

What is the treatment window time for CRAO?

A

90-100 minutes

43
Q

How do we manage CRAO acutely?

A
  1. Ocular massage to try and dislodge the clot
  2. Drugs to reduce IOP i.e. IV acetazolamide
  3. Paracentesis - fluid from ant chamber taken to reduce IOP
  4. Vasodilation using GTN and CO2 rebreathing
44
Q

What is the long term management of CRAO?

A

Treat the underlying cause and also control risk factors as this is an indication of a further ischaemic event!

45
Q

What is the definition of retinal detachment?

A

When the neurosensory layer of the retina detaches from the underlying RPE

46
Q

What is rhegmatogenous retinal detachment?

A

When there is a retinal break preceding the detachement. Usually due to Posterior Vitreous Detachment which happens in old age.

47
Q

What are the two types of non-rhegmatogenous retinal detachment

A
  1. Exudative - where fluid enters the subretinal space from an exudative process such as tumour or toxaemia
  2. Proliferative - where fibres e.g. diabetic retinopathy, contract and pull the retina apart
48
Q

Name me 3 risk factors for retinal detachment

A 
Myopia
Family history
Personal history in one eye
Previous cataract surgery 
Inflammatory and vascular coniditons
49
Q

How does retinal detachment present?

A

Sudden onset of floaters and flashes (which are worse in low light conditions)
Sudden, painless loss of visual fields - the visual loss starts peripherally and works its way inwards like a curtain drawing in
If macula detaches then visual loss is severe.
Pupil - RAPD
Visual fields - lost corresponding to which area of retina becomes detached
Dilated fundal examination with 1% tropicamide
ALWAYS EXAMINE BOTH EYES

50
Q

How do we manage retinal detachment?

A

Aim of treatment is to close break in retina and increase strength between two layers.

  1. Cryotherapy/laser photocoagulation - successful in 95% cases
  2. Vitrectomy - inject air / gas into vitreous space - but poor vision for weeks/months after
  3. Scleral bulking - silicone on sclera under conjunctiva to pressure the eye and force retina to close
  4. Pneumatic Retinopexy - expansile gas into eye
51
Q

What are the main organisms that cause orbital cellulitis

A

Staph and strep in adults

Haemophilus influenzae in children

52
Q

How does orbital cellulitis present?

A 
Painful, red eye
Proptosis 
Visual loss
Periorbital inflammation and swelling
Hot, oedematous area around eye
Diplopia
External ophthalmoplegia
RAPD 
Involvement of optic nerve can cause papilloedema/neuritis
53
Q

How do we investigate orbital cellulitis

A

FBC - Leukocytosis
Swab and culture of any discharge in eye, nose and throat
Children - CT of sinuses and orbit and brain
Adults - CT brain if we suspect cerebral abscess
LP indicated if suspect meningitis

54
Q

How do we manage orbital cellulitis

A

Emergency referral and admission under ophthal and ENT
If >10 abd chronic sinonasal disease - IV Abx + metronidazole
Optic nerve function monitored 4 hourly
If no response to ABX and if theres an orbital collection - surgery indicated.

55
Q

What is preseptal cellulitis

A

less severe and more common than orbital cellulitis

involves the lid structure but eye movements are not affected - can occasionally progress onto orbital cellulitis

56
Q

What are the causes of orbital and preseptal cellulitis

A

Trauma - lacerations to the lid

Spread of infection from the ethmoid sinuses as the anterior wall of the orbit is very thin

57
Q

How do we manage preseptal cellulitis

A

Orbital cellulitis until proven otherwise - ADMIT
Oral co-amoxiclav for both children and adults
Contact ENT if sinusitis is present too.
We can prevent it by prescribing Abx in any case where there is trauma to the eye lid.

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