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Finals > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

Define glaucoma

A

optic nerve damage due to a rise in intraocular pressure

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2
Q

What is raised intraocular pressure caused by?

A

blockage in aqueous humour trying to escape the eye

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3
Q

Name the types of glaucoma

A

open angle glaucoma
acute angle-closure glaucoma

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4
Q

what is the vitreous chamber of the eye filled with

A

vitreous humour

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5
Q

what is the anterior chamber filled with

A

(between iris and cornea) aqueous humour

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6
Q

what is the posterior chamber filled with

A

(between iris and lens) aqueous humour

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7
Q

what does the aqueous humour do

A

supplies nutrients to the cornea. It is produced by the ciliary body. It flows through the posterior chamber and around the iris to the anterior chamber.

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8
Q

Explain drainage of the aqueous humour

A
  • Drains through the trabecular meshwork to the canal of Schlemm at the angle between the cornea and the iris.
  • From the canal of Schlemm, it eventually enters the general circulation
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9
Q

what is normal intraocular pressure

A

10-24mmHg created by resistance to flow through the trabecular meshwork.

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10
Q

Describe open angle glaucoma

A

Gradual increase in resistance to flow through the trabecular meshwork. Pressure slowly builds within the eye

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11
Q

Describe acute angle closure glaucoma

A
  • The iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining. - There is a continual build-up of pressure and an acute onset of symptoms.
  • Acute angle-closure glaucoma is an ophthalmological emergency.
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12
Q

What does raised intraocular pressure cause

A
  • Cupping of optic disc.
  • Optic cup in the centre of optic disc grows wider and deeper.
  • Cup disk ratio >0.5 is abnormal
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13
Q

RFs for open angle glaucoma

A
  • increasing age
  • FH
  • black ethnicity
  • myopia (nearsightedness)
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14
Q

Presentation of open angle glaucoma

A

can be asymptomatic for a long time
- affects peripheral vision first: gradual onset of peripheral vision loss (tunnel vision)

It can also cause:
- Fluctuating pain
- Headaches
- Blurred vision
- Halos around lights, particularly at night

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15
Q

How to measure intraocular pressure

A

Non-contact tonometry for screening (puff of air)
Goldmann applanation tonometry (gold standard)-

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16
Q

How to diagnose open angle glaucoma

A
  • Goldmann applanation tonometry for the intraocular pressure
  • Slit lamp assessment for the cup-disk ratio and optic nerve health
  • Visual field assessment for peripheral vision loss
  • Gonioscopy to assess the angle between the iris and cornea
  • Central corneal thickness assessment
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17
Q

Mx of open angle glaucoma

A

Treat when pressure is 24mmHg or >
- 360° selective laser trabeculoplasty
- Prostaglandin analogue eye drops (e.g. latanoprost). They increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning)

2nd line eye drop drops:
- Beta-blockers (e.g., timolol) reduce the production of aqueous humour. Avoid in asthma and heart block
- Carbonic anhydrase inhibitors (e.g., dorzolamide) reduce the production of aqueous humour
- Sympathomimetics (e.g., brimonidine) reduce the production of aqueous fluid and increase the uveoscleral outflow. avoid if on TCAs or MAOIs

Trabeculectomy surgery may be required where other treatments are ineffective.

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18
Q

Risk factors for acute angle-closure glaucoma

A

Increasing age
Family history
Female (4x F>M)
Chinese and East Asian ethnic origin
Shallow anterior chamber
hypermetropia

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19
Q

Medications that precipitate acute angle-closure glaucoma

A
  • Adrenergic medications (e.g., noradrenaline)
  • Anticholinergic medications (e.g., oxybutynin and solifenacin)
  • Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
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20
Q

Presentation of acute angle-closure glaucoma

A

Generally unwell, with:
- Severely painful red eye
- Blurred vision
- Halos around lights
- Associated headache, nausea and vomiting

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21
Q

Examination signs in acute angle-closure glaucoma

A
  • Red eye
  • Hazy cornea
  • Decreased visual acuity
  • Mid-dilated pupil
  • Fixed-size pupil
  • Hard eyeball on gentle palpation
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22
Q

Initial management for acute angle-closure glaucoma

A

immediate admission/call ambulance
- lie on back, no pillow
- Pilocarpine eye drops (2% for blue and 4% for brown eyes)
- Acetazolamide 500 mg orally
- Analgesia and an antiemetic, if required

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23
Q

Secondary care mx for acute angle-closure glaucoma

A
  • Pilocarpine eye drops
  • Acetazolamide (oral or intravenous)
  • Hyperosmotic agents (e.g., intravenous mannitol) increase the osmotic gradient between the blood and the eye
  • Timolol is a beta blocker that reduces the production of aqueous humour
  • Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
  • Brimonidine is a sympathomimetics that reduces aqueous humour production and increases uveoscleral outflow
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24
Q

How does pilocarpine work

A

Acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent).
It also causes ciliary muscle contraction.
These two effects open up the pathway for the flow of aqueous humour from the ciliary body, around the iris and into the trabecular meshwork.

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25
Q

How does acetazolamide work

A

Carbonic anhydrase inhibitor that reduces the production of aqueous humour.

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26
Q

definitive treatment for acute angle-closure glaucoma

A

Laser iridotomy
This involves making a hole in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber. This relieves the pressure pushing the iris forward against the cornea and opens the pathway for the aqueous humour to drain.

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27
Q

Define age-related macular degeneration

A

Progressive condition affecting the macula. It is the most common cause of blindness in the UK. It is often unilateral but may be bilateral.

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28
Q

Name the types of AMD

A
  • Wet (neovascular), accounting for 10% of cases
  • Dry (non-neovascular), accounting for 90% of cases
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29
Q

Describe the layers of the macula

A

The macula is in the centre of the retina. It generates high-definition colour vision in the central visual field.

It has four layers:
- Choroid layer (at the base), which contains the blood vessels that supply the macula
- Bruch’s membrane
- Retinal pigment epithelium
- Photoreceptors (towards the surface)

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30
Q

What is Drusen

A

Important finding with AMD.
They are yellowish deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane. A few small drusen can be normal in older patients. Frequent and larger drusen can be an early sign of macular degeneration.

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31
Q

Features common to wet and dry AMD

A
  • Atrophy of the retinal pigment epithelium
  • Degeneration of the photoreceptors
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32
Q

What happens in wet AMD

A
  • New vessels develop from the choroid layer and grow into the retina (neovascularisation).
  • These vessels can leak fluid or blood, causing oedema and faster vision loss.
  • 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.
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33
Q

RFs for AMD

A
  • older age
  • smoking
  • FH
  • CVD
  • obesity
  • poor diet
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34
Q

Presentation of AMD

A

Visual changes associated with AMD tend to be unilateral, with:

  • Gradual loss of central vision
  • Reduced visual acuity
  • Crooked or wavy appearance to straight lines (metamorphopsia)
  • Worsening ability to read small text

Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years. It often progresses to bilateral disease.

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35
Q

What is the difference between presentation of glaucoma and AMD

A
  • Glaucoma is associated with peripheral vision loss and halos around lights.
  • AMD is associated with central vision loss and a wavy appearance to straight lines.
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36
Q

Examination findings of AMD

A
  • Reduced visual acuity using a Snellen chart
  • Scotoma (an enlarged central area of vision loss)
  • Amsler grid test can be used to assess for the distortion of straight lines seen in AMD
  • Drusen may be seen during fundoscopy
  • Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
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37
Q

Mx of AMD

A

Dry AMD:
Monitor and reduce the risk of progression by:

  • Avoiding smoking
  • Controlling BP
  • Vitamin supplementation

Wet AMD:
- Anti-VEGF medications (e.g., ranibizumab, aflibercept and bevacizumab) block VEGF and slow the development of new vessels. They are injected directly into the vitreous chamber of the eye (intravitreal), usually about once a month.

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38
Q

Define diabetic retinopathy

A

damage to the retinal blood vessels due to prolonged high blood sugar levels

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39
Q

Different findings on fundoscopy in proliferative diabetic retinopathy

A
  • cotton wool spots
  • microaneurysms
  • hard exudates
  • blot haemorrhages
  • neovascularisation
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40
Q

Types of diabetic retinopathy

A
  • background
  • pre-proliferative
  • proliferative
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41
Q

What is diabetic maculopathy

A
  • Exudates within the macula
  • Macular oedema
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42
Q

How to distinguish between non-proliferative and proliferative diabetic retinopathy

A

proliferative diabetic retinopathy is the development of new blood vessels (neovascularisation).

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43
Q

Complications of diabetic retinopathy

A
  • Vision loss
  • Retinal detachment
  • Vitreous haemorrhage (bleeding into the vitreous humour)
  • Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
  • Optic neuropathy
  • Cataracts
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44
Q

Mx of diabetic retinopathy

A

Non-proliferative diabetic retinopathy: close monitoring and careful diabetic control.

Proliferative diabetic retinopathy:
- Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels
- Anti-VEGF medications by intravitreal injection
- Surgery (e.g., vitrectomy) may be required in severe disease

An intravitreal implant containing dexamethasone is an option for macular oedema.

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45
Q

Define hypertensive retinopathy

A

damage to the small blood vessels in the retina relating to hypertension
Can happen due to chronic or malignant hypertension

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46
Q

Features of hypertensive retinopathy

A
  • Silver/copper wiring (walls of the arterioles become thickened and sclerosed and reflect more light on examination)
  • Arteriovenous nipping (AV nipping) (arterioles cause compression of the veins where they cross due to sclerosis and hardening of the arterioles)
  • Cotton wool spots (ischaemia and infarction in the retina, causing damage to nerve fibres)
  • Hard exudates (damaged vessels leaking lipids onto the retina)
  • Retinal haemorrhages (damaged vessels rupturing and releasing blood in the retina. Dot and blot haemorrhages occur deeper, in the inner nuclear layer or outer plexiform layer. Flame haemorrhages occur in the nerve fiber layer)
  • Papilloedema (ischaemia to the optic nerve, resulting in optic nerve swelling)
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47
Q

Keith-Wagener Classification in hypertensive retinopathy

A

Stage 1: Mild narrowing of the arterioles
Stage 2: Focal constriction of blood vessels and AV nicking
Stage 3: Cotton-wool patches, exudates and haemorrhages
Stage 4: Papilloedema

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48
Q

Define cataracts

A

Progressively opaque eye lens, which reduces the light entering the eye and visual acuity.

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49
Q

Test for congenital cataracts

A

negative neonate red light reflex

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50
Q

RFs for cataracts

A
  • increasing age
  • smoking
  • diabetes
  • alcohol
  • steroids
  • hypocalcaemia
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51
Q

presentation of cataracts

A
  • asymmetrical
  • Slow reduction in visual acuity
  • Progressive blurring of the vision
  • Colours becoming more faded, brown or yellow
  • Starbursts can appear around lights, particularly at night
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52
Q

Mx of cataracts

A

cataract surgery

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53
Q

Complication of cataract surgery

A

endophthalmitis: inflammation of inner eye contents caused by infection. Can lead to vision loss. Treat with intravitreal antibiotics

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54
Q

what muscles in the iris are responsible for pupil constriction

A

circular muscles
stimulated by parasympathetic nervous system using ACh

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55
Q

what muscles in the iris are responsible for pupil dilation

A

dilator muscles
stimulated by sympathetic nervous system using adrenaline

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56
Q

Causes of abnormal pupil shape

A
  • Trauma to the sphincter muscles in the iris (e.g., during cataract surgery)
  • Anterior uveitis can cause adhesions in the iris
  • Acute angle-closure glaucoma can cause ischaemic damage to the muscles of the iris and an abnormal pupil shape, usually a vertical oval
  • Rubeosis iridis (neovascularisation in the iris) can distort the shape of the iris and pupil. This is usually associated with poorly controlled diabetes and diabetic retinopathy
  • Coloboma is a congenital malformation that can cause a hole in the iris and an irregular shape.
  • Tadpole pupil involves muscle spasm in part of the dilator muscle of the iris, causing a misshapen pupil. It is a temporary condition and may be associated with migraines and Horner syndrome.
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57
Q

Causes of mydriasis (dilated pupil)

A
  • Congenital
  • Stimulants (e.g., cocaine)
  • Anticholinergics (e.g., oxybutynin)
  • Trauma
  • Third nerve palsy
  • Holmes-Adie syndrome
  • Raised intracranial pressure
  • Acute angle-closure glaucoma
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58
Q

Causes of Miosis (Constricted Pupil)

A
  • Horner syndrome
  • Cluster headaches
  • Argyll-Robertson pupil (neurosyphilis)
  • Opiates
  • Nicotine
  • Pilocarpine
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59
Q

What is third nerve palsy

A

oculomotor nerve (CN3)
- Ptosis (drooping upper eyelid)
- Dilated non-reactive pupil
- Divergent strabismus (squint) in the affected eye, with a “down and out” position of the affected eye

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60
Q

what muscles does CN3 supply

A
  • Oculomotor nerve.
  • Supplies all the extraocular muscles except the lateral rectus and superior oblique. Therefore, when the oculomotor nerve stops working, most of the extraocular muscles stop working, and the lateral rectus and superior oblique (which are still working) pull the eye downward and outward.

The oculomotor nerve also supplies the levator palpebrae superioris, which is responsible for lifting the upper eyelid. Therefore, a third nerve palsy causes ptosis (drooping of the upper eyelid).

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61
Q

Causes of third nerve palsy

A

idiopathic

If pupil not effected (parasympathetic fibres spared):
- diabetes
- hypertension
- ischaemia

full third nerve palsy (CN3 compression):
- trauma
- Tumour
- Cavernous sinus thrombosis
- Posterior communicating artery aneurysm
- Raised ICP

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62
Q

What is horner syndrome

A

ptosis
miosis
anhidrosis
can also have enopthalmos
due to sympathetic fibres affected

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63
Q

Causes of horner syndrome

A

4 Ss, 4 Ts and 4 Cs mnemonic. S for Sentral, T for Torso (pre-ganglionic) and C for Cervical (post-ganglionic).

Central lesions (anhidrosis of arm, trunk and face):
S – Stroke, Multiple Sclerosis, Swelling (tumours), Syringomyelia (cyst in the spinal cord)

Pre-ganglionic lesions (anhidrosis of face):
T – Tumour (Pancoast tumour)
T – Trauma
T – Thyroidectomy
T – Top rib (a cervical rib growing above the first rib and clavicle)

Post-ganglionic lesions (no anhidrosis):
C – Carotid aneurysm
C – Carotid artery dissection
C – Cavernous sinus thrombosis
C – Cluster headache

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64
Q

What is congenital horner syndrome associated with

A

Heterochromia (different iris colour on affected side)

65
Q

Test for horner syndrome

A

cocaine eye drops (dilates in normal, no reaction in horner’s)
low dose adrenalin eye drops (dilates in horner’s)

66
Q

What is Holmes-Adie pupil

A
  • damage to post-ganglionic parasympathetic fibres
  • unknown cause
  • Dilated
  • Sluggish to react to light
  • Responsive to accommodation (the pupils constrict well when focusing on a near object)
  • Slow to dilate following constriction (“tonic” pupil)
67
Q

What is Argyll-Robertson pupil

A
  • in neurosyphylis
  • Constricted pupil that accommodates when focusing on a near object but does not react to light.
  • Irregularly shaped
68
Q

What is blepharitis

A

inflammation of the eyelid margins

69
Q

Presentation of blepharitis

A

gritty, itchy, dry sensation in the eyes. It can be associated with dysfunction of the Meibomian glands, which are responsible for secreting meibum (oil) onto the surface of the eye. It can lead to styes and chalazions.

70
Q

Mx of blepharitis

A

Warm compresses and gentle cleaning of the eyelid margins to remove debris (e.g., using a cotton bud and baby shampoo)

71
Q

What is hordeolum externum (stye)

A

infection of the glands of Zeis (sebaceous glands at base of eyelashes) or glands of Moll (sweat glands at base of eyelashes)

72
Q

What is hordeolum internum (stye)

A

infection of the Meibomian glands. They are deeper, tend to be more painful and may point inwards towards the eyeball underneath the eyelid.

73
Q

Mx of stye

A

Hot compress
Analgesia
Topical antibiotics if assoc with conjunctivitis

74
Q

What is Chalazion

A
  • Meibomian gland blocked and swells. It is often called a Meibomian cyst. It presents with a swelling in the eyelid that is typically not tender (however, it can be tender and red).
  • Mx: warm compresses and gentle massage towards the eyelashes (to encourage drainage). Rarely, surgical drainage may be required.
75
Q

What is Entropion

A
  • Eyelid turns inwards with the lashes pressed against the eye.
  • Pain and can cause corneal damage and ulceration
  • Mx: tape eyelid down and then surgical mx. Use lubricating eye drops when lid taped down
76
Q

What is Ectropion

A
  • Eyelid turns outwards, exposing the inner aspect (usually lower)
  • Most don’t need treatment
  • Can use lubricating eye drops or maybe surgery
77
Q

what is trichiasis

A
  • Inward growth of the eyelashes
  • Results in pain and can cause corneal damage and ulceration.
  • Mx: remove the affected eyelashes. Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent them from regrowing
78
Q

What is periorbital cellulitis

A

eyelid and skin infection in front of the orbital septum (in front of the eye).
It presents with swollen, red, hot skin around the eyelid and eye.
Must be differentiated from orbital cellulitis

79
Q

Mx of periorbtial cellulitis

A

systemic abx (oral/IV)

80
Q

How to distinguish between periorbital and orbital cellulitis

A

CT scan

81
Q

What is orbital cellulitis

A

infection around the eyeball involving the tissues behind the orbital septum.
Symptoms include :
- pain with eye movement
- reduced eye movements
- vision changes
- abnormal pupil reactions
- proptosis (bulging forward of the eyeball).

82
Q

Mx of orbital cellulitis

A

Emergency admission under ophthalmology
Intravenous antibiotics
Surgical drainage if an abscess forms

83
Q

what is conjunctivitis

A

inflammation of the conjunctiva.
Bacterial, viral or allergic
unilateral/bilateral

84
Q

presentation of conjunctivitis

A
  • Red, bloodshot eye
  • Itchy or gritty sensation
  • Discharge
  • Not painful
  • Bacterial= purulent discharge, morning stuck, highly contagious
  • Viral= clear discharge, pre-auricular LNs, viral sx, contagious
85
Q

Causes of an acute PAINFUL red eye

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury
86
Q

Causes of an acute PAINLESS red eye

A
  • conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
87
Q

Mx of conjunctivitis

A
  • hygiene measures
  • chloramphenicol or fusidic acid for bacterial if necessary
  • In neonates caused by gonococcal infection -> emergency
88
Q

what is allergic conjunctivitis

A

contact with contact allergens
- swelling of the conjunctival sac, eyelid itching and watery discharge
- Mx antihistamines or topical mast cell stabilisers for chronic

89
Q

What is anterior uveitis

A

inflammation of the anterior uvea

90
Q

What is the uvea

A

uvea consists of iris, ciliary body and choroid

91
Q

Causes of anterior uveitis

A

autoimmune process usually causes it, but it can be due to infection, trauma, ischaemia or malignancy.

92
Q

What conditions is anterior uveitis associated with

A
  • Seronegative spondyloarthropathies (e.g., ankylosing spondylitis, psoriatic arthritis and reactive arthritis)
  • Inflammatory bowel disease
  • Sarcoidosis
  • Behçet’s disease
93
Q

Presentation of anterior uveitis

A
  • Painful red eye (typically a dull, aching pain)
  • Reduced visual acuity
  • Photophobia (due to ciliary muscle spasm)
  • Excessive lacrimation (tear production)
94
Q

Examination findings in anterior uveitis

A
  • Ciliary flush (a ring of red spreading from the cornea outwards)
  • Miosis (a constricted pupil due to sphincter muscle contraction)
  • Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes
  • Hypopyon (inflammatory cells collected as a white fluid in the anterior chamber)
95
Q

Mx of anterior uveitis

A
  • Steroids (eye drops, oral or intravenous)
  • Cycloplegics (e.g., cyclopentolate or atropine eye drops)

Cycloplegics dilate the pupil and reduce pain associated with ciliary spasm. Cycloplegic refers to paralysing the ciliary muscles. Cyclopentolate and atropine are antimuscarinic drugs that reduce the action of the iris sphincter muscles and ciliary muscles.

DMARDs and anti-TNF for recurrent cases

96
Q

Define episcleritis

A

Benign and self-limiting inflammation of the episclera, the outermost layer of the sclera, just below the conjunctiva.

97
Q

Episcleritis demographic

A

relatively common
> young/middle aged adults
Associated with inflammatory conditions like:
- RA
- IBD
- SLE

98
Q

Presentation of episcleritis

A

acute onset unilateral features
- Localised or diffuse redness (often a patch of redness in the lateral sclera)
- No pain (or mild pain)
- Dilated episcleral vessels
- normal visual acuity

NO photophobia or discharge –>scleritis

99
Q

what sx would suggest scleritis over episcleritis

A

photophobia and discharge

100
Q

how to differentiate between scleritis and episcleritis

A

Apply phenylephrine eye drops.
It will cause blanching of the episcleral vessels, causing the redness to disappear. It will not affect scleral vessels and will not impact the redness in scleritis.

101
Q

Mx of episcleritis

A

self-limiting (1-2 weeks)
analgesia and lubricating eye drops
steroid eye drops for severe cases

102
Q

what is scleritis

A

inflammation of the sclera (white of eye)

103
Q

what is the most severe type of scleritis

A

necrotising scleritis which can lead to sclera perforation

104
Q

causes of scleritis

A

most- idiopathic
underlying systemic inflammatory condition
less common- staph A/pseudomonas
F>M

105
Q

conditions associated with scleritis

A

RA
vasculitis (particularly granulomatosis with polyangiitis)

106
Q

presentation of scleritis

A

Scleritis usually presents with a more gradual onset. It can be unilateral or bilateral. Features include:

  • Red, inflamed sclera (localised or diffuse)
  • Congested vessels
  • Severe pain (typically a boring pain)
  • Pain with eye movement
  • Photophobia
  • Epiphora (excessive tear production)
  • Reduced visual acuity
  • Tenderness to palpation of the eye
107
Q

Mx of scleritis

A
  • Refer for urgent assessment
  • Assess for an underlying systemic condition (e.g., rheumatoid arthritis or vasculitis).

Management in secondary care:
- NSAIDs (oral)
- Steroids (topical or systemic)
- Immunosuppression appropriate to the underlying systemic condition (e.g., methotrexate in rheumatoid arthritis)
- Antimicrobial treatment for infectious scleritis.

108
Q

What are corneal abrasions

A

Scratches or damage to the cornea. They cause a red, painful eye and photophobia

109
Q

Causes of corneal abrasion

A
  • Damaged contact lenses (assoc with pseudomonas infection)
  • Fingernails
  • Foreign bodies (e.g., metal fragments)
  • Tree branches
  • Makeup brushes
  • Entropion (inward turning eyelid)
  • Chemical abrasions (e.g., from acid) can cause severe damage and vision loss, requiring immediate extensive irrigation.
110
Q

presentation of corneal abrasion

A

Painful red eye
Photophobia
Foreign body sensation
Epiphora (excessive tear production)
Blurred vision

111
Q

how to diagnose corneal abrasion

A

A fluorescein stain can be applied to the eye.
This is a yellow-orange colour and collects in abrasions or ulcers, highlighting them, particularly when viewed under cobalt blue light.

112
Q

Mx of corneal abrasion

A

Mild, uncomplicated abrasions may be managed in primary care where there is appropriate experience and skill. Uncomplicated corneal abrasions usually heal over 2-3 days. More complicated cases require assessment and management by ophthalmology.

Management options include:
- Removing foreign bodies
- Simple analgesia (e.g., paracetamol)
- Lubricating eye drops
- Antibiotic eye drops (e.g., chloramphenicol)
- Close follow-up

Lubricating eye drops vary in their viscosity:
- Hypromellose drops are the least viscous (the effects last around 10 minutes)
- Polyvinyl alcohol drops are the middle viscous choice
- Carbomer drops are the most viscous (the effects last about 30-60 minutes)

113
Q

what is herpes keratitis

A

inflammation of the cornea. most common cause of keratitis.
Can be primary or recurrent. Recurrent is in trigeminal ganglion and can lie latent

114
Q

causes of keratitis

A
  • Viral infection (e.g., herpes simplex)
  • Bacterial infection (e.g., Pseudomonas or Staphylococcus)
  • Fungal infection (e.g., Candida or Aspergillus)
  • Contact lens-induced acute red eye (CLARE)
  • Exposure keratitis, caused by inadequate eyelid coverage (e.g., ectropion)
115
Q

What layer of cornea does herpes keratitis effect

A

Usually affects only the epithelial layer of the cornea.
Inflammation of the stroma (the layer between the epithelium and endothelium) is called stromal keratitis. This is associated with complications such as stromal necrosis, vascularisation and scarring and can lead to corneal blindness.

116
Q

presentation of herpes keratitis

A

Primary infection- mild symptoms of blepharoconjunctivitis (inflammation of the eyelid margins and conjunctiva).

Recurrent infection may present with:
- Painful red eye
- Photophobia
- Vesicles (fluid-filled blisters)
- Foreign body sensation
- Watery discharge
- Reduced visual acuity

117
Q

how to diagnose keratitis

A

Slit lamp examination.
Fluorescein staining shows a dendritic corneal ulcer. Dendritic describes the branching appearance of the ulcer.
Corneal scrapings can be used for viral testing.

118
Q

Mx of herpes keratitis

A

Refer for urgent assessment
Specialist management involves topical or oral antivirals (e.g., aciclovir or ganciclovir).

Corneal transplant is an option to treat permanent scarring and vision loss after keratitis.

119
Q

What is subconjunctival haemorrhage

A

Small blood vessel within the conjunctiva ruptures, releasing blood into the space between the sclera and the conjunctiva.
They often appear after episodes of strenuous activity, such as heavy coughing, weight lifting or straining when constipated. They can also be caused by trauma to the eye.

120
Q

Causes of subconjunctival haemorrhage

A
  • most idiopathic
  • Hypertension
  • Bleeding disorders (e.g., thrombocytopenia)
  • Whooping cough
  • Medications (e.g., antiplatelets, DOACs or warfarin)
  • Non-accidental injury
121
Q

presentation of subconjunctival haemorrhages

A

patch of bright red blood underneath the conjunctiva. It covers the white of the eye
painless, does not affect vision.

122
Q

Mx of subconjunctival haemorrhages

A

Dagnosis based on a history and examination. Underlying causes should be considered, for example:

  • Check BP
  • Checking INR in patients taking warfarin

Self-limiting (2 weeks).
Lubricating eye drops may be helpful if there is mild irritation

123
Q

what is Posterior vitreous detachment

A

When the vitreous body comes away from the retina. It is common in older age.

124
Q

presentation of posterior vitreous detachment

A

Painless condition
It may be completely asymptomatic. The key symptoms are:

Floaters
Flashing lights
Blurred vision

125
Q

Mx of posterior vitreous detachment

A

No treatment is necessary. Over time, the symptoms will improve as the brain adjusts.

Can predispose patients to develop retinal tears and retinal detachment. These conditions can present similarly with flashes, floaters and vision loss. It is essential to exclude a retinal tear or retinal detachment with a thorough assessment of the retina, usually by an optometrist or ophthalmologist.

126
Q

what is retinal detachment

A

Involves the neurosensory layer of the retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (the base layer attached to the choroid).
This is usually due to a retinal tear, allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
The neurosensory retina relies on the blood vessels of the choroid for its blood supply. Therefore, retinal detachment can disrupt the blood supply and cause permanent damage to the photoreceptors, making it sight-threatening.

127
Q

RFs for retinal detachment

A
  • Lattice degeneration (thinning of the retina)
  • Posterior vitreous detachment
  • Trauma
  • Diabetic retinopathy
  • Retinal malignancy
  • Family history
  • myopia
128
Q

Presentation of retinal detachment

A
  • Painless
  • Peripheral vision loss (often sudden and described as a shadow coming across the vision)
  • Blurred or distorted vision
  • Flashes and floaters
129
Q

Mx of retinal detachment

A

Create adhesions between the retina and the choroid:
- Laser therapy
- Cryotherapy

Aim to reattach the retina and reduce any traction/pressure that may cause it to detach again. The options for reattaching the retina are vitrectomy, scleral buckle or pneumatic retinopexy.
- Vitrectomy= keyhole surgery removing the vitreous fluid, fixing the tear, and then inserting gas/oil to hold the retina in place.
- Scleral buckling= a silicone “buckle” to put pressure on the sclera from outside, squashing the eye inwards to reconnect the layers of the retina.
- Pneumatic retinopexy= injecting a gas bubble into the vitreous body and positioning the patient so the gas bubble presses the separated layer back into place.

130
Q

Define retinal vein occlusion

A

When a blood clot forms in the retinal veins, blocking the drainage of blood from the retina. The thrombus may form in the central retinal vein or branch retinal veins.
Central blockage affects whole retina

131
Q

Categories of retinal vein occlusion

A

ischaemic or non-ischaemic. Retinal ischaemia leads to the release of vascular endothelial growth factor (VEGF), resulting in new blood vessel development (neovascularisation).

132
Q

Describe path of retinal vein occlusion

A

Blockage of a retinal vein causes venous congestion in the retina. Increased pressure in the retinal veins results in fluid and blood leaking into the retina, causing macular oedema and retinal haemorrhages. This results in retinal damage and vision loss.

133
Q

RFs for retinal vein occlusion

A
  • Hypertension
  • High cholesterol
  • Diabetes
  • Smoking
  • High plasma viscosity (e.g., myeloma)
  • Myeloproliferative disorders
  • Inflammatory conditions (e.g., SLE)
134
Q

Presentation of retinal vein occlusion

A
  • painless blurred vision or vision loss. In branch retinal vein occlusion, the vision loss corresponds to the affected area of the retina. When it involves the branch draining the macula, central vision is lost.
135
Q

Fundoscopy findings in retinal vein occlusion

A

Dilated tortuous retinal veins
Flame and blot haemorrhages
Retinal oedema
Cotton wool spots
Hard exudates
“stormy thunder” appearance

136
Q

Mx of retinal vein occlusion

A

Refer
Aim to treat macular oedema and prevent neovascularisation:

  • Anti-VEGF therapies (e.g., ranibizumab and aflibercept)
  • Dexamethasone intravitreal implant (to treat macular oedema)
  • Laser photocoagulation (to treat new vessels)
137
Q

Define Central retinal artery occlusion

A

obstruction to blood flow through the central retinal artery. The central retinal artery is a branch of the ophthalmic artery, which is a branch of the internal carotid artery.

138
Q

Cause of central retinal artery occlusion

A

atherosclerosis- most common
GCA

139
Q

RFs for central retinal artery occlusion

A

CVD RFs (smoking, hypertension, diabetes and raised cholesterol)
GCA RFs (white ethnicity, older age, female and polymyalgia rheumatica)

140
Q

Presentation of central retinal artery occlusion

A
  • sudden painless loss of vision
  • “curtain coming down” over the vision
  • relative afferent pupillary defect
  • Fundoscopy will show a pale retina with a cherry red spot
141
Q

Mx of central retinal artery occlusion

A

vision-threatening emergency, refer immediately.

Giant cell arteritis is a potentially reversible cause. Testing includes an ESR blood test and temporal artery biopsy. Treatment is with high-dose systemic steroids.

Immediate management options attempt to dislodge/resolve the blockage. There is no consensus, guidelines or solid evidence base for these options:

Ocular massage (massaging the eye)
Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure)
Inhaled carbogen (5% carbon dioxide and 95% oxygen) (to dilate the artery)
Sublingual isosorbide dinitrate (to dilate the artery)
Oral pentoxifylline (to dilate the artery)
Intravenous acetazolamide (to reduce the intraocular pressure)
Intravenous mannitol (to reduce the intraocular pressure)
Topical timolol (to reduce the intraocular pressure)

142
Q

Define retinitis pigmentosa

A

genetic condition causing degeneration of the photoreceptors in the retina, particularly the rods

143
Q

Causes of retinitis pigmentosa

A

many different genetic causes. Some causes involve isolated retinitis pigmentosa, while others result in systemic diseases associated with the condition. They vary in age at presentation and prognosis

144
Q

presentation of retinitis pigmentosa

A

Varies depending on the underlying cause.
In most cases, the symptoms start in childhood.

Rods degenerate more than the cones. Rods are responsible for night vision and peripheral vision. Therefore, there is:

  • Night blindness (often the first symptom)
  • Peripheral vision loss (before the central vision is affected)

Fundoscopy shows pigmentation described as “bone-spicule” pigmentation. Spicule describes the sharp, pointed appearance. Bone-spicule refers to the similarity to the networking appearance of the bone matrix. The pigmentation is most concentrated around the mid-peripheral area of the retina.

There can be a narrowing of the arterioles and a waxy or pale appearance to the optic disc.

145
Q

Associated diseases with retinitis pigmentosa

A

Several genetic, systemic diseases involve retinitis pigmentosa. Some examples are:

  • Usher syndrome also causes hearing loss
  • Bassen-Kornzweig syndrome also causes progressive neurological impairments
  • Refsum disease also causes peripheral neuropathy, hearing and ichthyosis (scaly skin)
146
Q

Mx of retinitis pigmentosa

A
  • Referral to an ophthalmologist
  • Genetic counselling
  • Vision aids
  • Sunglasses to protect the retina from accelerated damage
  • Driving limitations and informing the DVLA
147
Q

Most common causes of a sudden painless loss of vision

A
  • Ischaemic/vascular (e.g. thrombosis, embolism, temporal arteritis etc). e.g. occlusion of central retinal vein and occlusion of central retinal artery
  • vitreous haemorrhage
  • retinal detachment
  • retinal migraine
148
Q

Causes of papilloedema

A
  • space-occupying lesion: neoplastic, vascular
  • malignant hypertension
  • idiopathic intracranial hypertension
  • hydrocephalus
  • hypercapnia
149
Q

Causes of tunnel vision

A
  • papilloedema
  • glaucoma
  • retinitis pigmentosa
  • choroidoretinitis
  • optic atrophy secondary to tabes dorsalis
  • hysteria
150
Q

what is optic neuritis

A

inflammation of the optic nerve

151
Q

causes of optic neuritis

A
  • multiple sclerosis: most common
  • diabetes
  • syphilis
152
Q

Presentation of optic neuritis

A
  • unilateral decrease in visual acuity over hours or days
  • poor discrimination of colours, ‘red desaturation’
  • pain worse on eye movement
  • RAPD
  • central scotoma
153
Q

Ix of optic neuritis

A

MRI of the brain and orbits with gadolinium contrast is diagnostic

154
Q

Mx of optic neuritis

A

high-dose steroids
recovery usually takes 4-6 weeks

155
Q

prognosis of optic neuritis

A

MRI: if > 3 white-matter lesions, 5-year risk of developing multiple sclerosis is 50%

156
Q

most common cause of flashes and floaters

A

posterior vitreous detachment
(retinal detachment possible but less common)

157
Q

What is Amaurosis fugax

A

sudden loss of vision due to ischaemia, often due to thromboembolic disease

158
Q

presentation of amaurosis fugax

A
  • Like retinal detachment, altitudinal field defects are commonly seen “curtain coming down”
  • temporary loss of vision
159
Q

Adverse effect of pilocarpine

A

constricted pupil, headache and blurred vision

Finals (10 decks)

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