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Ophthalmology Flashcards

1
Q

Glaucoma

A

refers to the optic nerve damage that is caused by a significant rise in intraocular pressure.
The raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye. There are two types

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2
Q

Most common form of glaucoma

A

Open- angle

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3
Q

open-angle glaucoma

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

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4
Q

cupping of the optic disc

A

happens due to increased pressure
it is a small dent in the centre of a normal optic disc,usually less than half the size of the optic disc
when pressure increased, this indent becomes larger as the pressure in the eye puts pressure on that indent making it wider and deeper
optic cup greater than 0.5 the size of the optic disc is abnormal.

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5
Q

Risk Factors open angle glaucoma

A

Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)
hypertension
diabetes mellitus
corticosteroids

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6
Q

Clinical features of open-angle glaucoma

A
  1. asymptomatic at first
  2. affects peripheral vision
  3. peripheral vision closes in ( scotomata) until they experience tunnel vision
  4. Gradual onset of fluctuating pain, headaches, blurred vision, haloes around lights, particularly at night time
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7
Q

Ix for glaucoma

A

Goldmann applanation tonometry is the gold standard for intraocular pressure
Fundoscopy assessment to check for optic disc cupping and optic nerve health
Visual field assessment to check for peripheral vision loss

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8
Q

Management of Open-Angle Glaucoma

A

Treatment is usually started at an intraocular pressure of 24 mmHg or above
1. Prostaglandin analogue eye drops (e.g. latanoprost) are first line (increase uveoscleral outflow)
2. Beta-blockers (e.g. timolol) reduce the production of aqueous humour
3. Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
4. Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow
Trabeculectomy surgery may be required where eye drops are ineffective

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9
Q

side effects Prostaglandin analogue eye drops (e.g. latanoprost)

A

eyelash growth, eyelid pigmentation and iris pigmentation (browning)

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10
Q

Pathophysiology of acute angle-closure glaucoma

A

iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away.pressure builds up particularly in the posterior chamber

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11
Q

risk factors Acute angle closure

A

Increasing age
Females
Family history
Chinese and East Asian ethnic origin
Shallow anterior chamber
Hypermetropia

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12
Q

Which medications precipitate acute angle-closure glaucoma

A

Adrenergic medications such as noradrenalin
Anticholinergic medications such as oxybutynin and solifenacin
Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects

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13
Q

Clinical presentation of acute angle-closure glaucoma

A

patient will generally appear unwell
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
Symptoms may worsen at night as the pupil dilates, closing the iridio-corneal angle even more.

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14
Q

Acute angle closure O/E

A

Red-eye
Teary
Hazy/cloudy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size, mid dilated
Firm eyeball on palpation

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15
Q

Management of acute angle closure glaucoma in primary care

A

Lie patient on their back without a pillow
Give pilocarpine eye drops (2% for blue, 4% for brown eyes) miotic /constrictive agent
Give acetazolamide 500 mg orally
Given analgesia and an antiemetic if required

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16
Q

Management of acute angle closure glaucoma in secondary care

A

Pilocarpine
Acetazolamide (oral or IV)
Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in 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 sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow

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17
Q

definitive treatment of acute angle-closure glaucoma

A

Laser iridectomy

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18
Q

Myopia

A

(Nearsightedness)
you can see objects near to you clearly,but objects farther away are blurry.
It occurs when the shape of your eye causes light rays to bend (refract) incorrectly, focusing images in front of your retina instead of on your retina

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19
Q

Hypermetropia

A

(long-sightedness)
nearby objects appear blurred, but your vision is clearer when looking at things further away.

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20
Q

Amaurosis Fugax symptoms

A

Monocular visual loss that usually lasts seconds to minutes, but may last 1-2 hours.
Vision returns to normal. It is most commonly a negative visual phenomenon, described as a blackout, or ‘greying out’ of vision

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21
Q

Mx Amaurosis Fugax

A

Start 300g aspirin, referral to neurology/cardiology or vascular surgery as appropriate

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22
Q

Migraine with aura symptoms

A

bilateral
when eyes are closed
flickering, scintillating, or bright geometric shapes
last 10-60 mins
associated/followed by headache

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23
Q

Vitreous haemorrhage

A

occurs as a result of bleeding into the vitreous humour, most often from unstable retinal neo-vasculature. Therefore, any condition which risks the formation of retinal neo-vasculature is a risk factor for vitreous haemorrhage

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24
Q

Risk factors for Vitreous haemorrhage

A

diabetic retinopathy and hypertensive retinopathy. anti-coagulant use and trauma,posterior vitreous detachment

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25
Vitreous haemorrhage symptoms
dark spots obscuring vision/ complete loss of vision if the bleed is large enough. The bleed can also cause a red hue and potentially loss of red reflex if large enough This condition will resolve with time.
26
Posterior vitreous detachment symptoms
Painless Spots of vision loss Floaters (Weiss ring) Flashing lights
27
Central Retinal Occlusion symptoms
Sudden and painless loss of vision.
28
Central Retinal Vein Occlusion signs
Flame and blot haemorrhages Optic disc oedema Macula oedema dilated tortuous veins, cotton wool spots
29
Management of Central Retinal Vein Occlusion
Management in secondary care aims to treat macular oedema and prevent complications such as neovascularisation of the retina and iris and glaucoma Laser photocoagulation Intravitreal steroids (e.g. a dexamethasone intravitreal implant) Anti-VEGF therapies (e.g. ranibizumab, aflibercept or bevacizumab)
30
Central Retinal Artery Occlusion
where something blocks the flow of blood through the central retinal artery which supplies the blood to the retina. most common cause is atherosclerosis, also giant cell arteritis far less common than retinal vein occlusion, and vision deteriorates faster
31
Central retinal artery occlusion signs
Relative Afferent Pupillary Defect (RAPD) pale retinal (abnormal and asymmetrical red reflex) cherry red spot-area of cilioretinal sparing - 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
32
Management Central Retinal Artery Occlusion
Urgent (same day) ESR and CRP to exclude Giant Cell Arteritis,and temporal artery biopsy Ocular massage Removing fluid from the anterior chamber to reduce intraocular pressure. Inhaling carbogen (a mixture of 5% carbon dioxide and 95% oxygen) to dilate the artery Sublingual isosorbide dinitrate to dilate the artery
33
Retinal detachment
separation of sensory retina from the retinal pigment epithelium often due to predisposing retinal hole tear – often associated with myopia but may follow trauma Tear allows vitreous fluid to get under the retina and fill the space between the retina and the choroid. It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.
34
Retinal detachment symptoms
painless loss of vision/ Blurred or distorted vision ecent history of increased number of visual floaters and/ or visual flashes. dark shadow/ curtain coming down in the vision of the affected eye/ Peripheral vision loss.
35
Retinal detachment signs
grey area of retina which is where it is detached, vision reduced if retina detaches and involves the macula
36
Mx retinal detachment
urgent (same day) referral to ophthalmologist.Requires urgent fixation usually with laser. It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.
37
Optic neuritis
presenting feature of multiple sclerosis,can also be linked to diabetes and syphilis most common in women between 18-50 years old and in Caucasian populations.
38
Optic neuritis symptoms
Painless unilateral loss of vision over hours to days. Orbital pain usually associated with eye movement Impaired colour vision in the affected eye, typically red desaturation, Central scotoma. This is an enlarged blind spot
39
Optic neuritis signs
reduced visual acuity and colour vision RAPD on affected side Visual field defects: commonly central but can be any pattern, central scotoma, optic disc may look normal (retrobulbar neuritis) or be swollen
40
Mx optic neuritis
urgent (same day) referral to ophthalmologist may be indicated for further MRI investigation and intravenous steroid treatment may be required. Vision starts to recover within a month without treatment. Following recovery ,clinical findings such as RAPD, red desaturation, and optic nerve pallor (atrophy) commonly persist and there is Gradual loss vision
41
Cataract
lens in the eye becomes cloudy and opaque. This reduces visual acuity by reducing the light that enters the eye.
42
Cataract risk factors
Increasing age Smoking Alcohol Diabetes Steroids Hypocalcaemia
43
Cataract symptoms
usually asymmetrical Very slow reduction in vision Progressive blurring of vision Change of colour of vision with colours becoming more brown or yellow “Starbursts” can appear around lights, particularly at night time myopic shift : patient becomes more short sighted due to the increased refractive index of the cataract.
44
Cataract key sign
loss of the red reflex. The lens can appear grey or white
45
Mx cataracts
If the symptoms are manageable then no intervention may be necessary. Cataract surgery involves drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens into the eye.
46
Risk factors for Age related macular degeneration
Age Smoking White or Chinese ethnic origin Family history Cardiovascular disease
47
Age related macular degeneration symptoms
Gradual worsening central visual field loss Reduced visual acuity Crooked or wavy appearance to straight lines Wet age-related macular degeneration presents more acutely
48
Age related macular degeneration O/E
Reduced acuity using a Snellen chart Scotoma (a central patch of vision loss) Amsler grid test can be used to assess the distortion of straight lines Fundoscopy. Drusen are the key finding. - yellow deposits of proteins and lipids
49
Dx AMD
Slit-lamp biomicroscopic fundus examination Optical coherence tomography 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 to show up any oedema and neovascularisation. It is used second line to Optical coherence tomography
50
Management of wet AMD
Medications such as ranibizumab, bevacizumab and pegaptanib block VEGF and slow the development of new vessels.
51
Management Dry AMD
no specific treatment Management focuses on lifestyle measure that may slow the progression: Avoid smoking Control blood pressure Vitamin supplementation has some evidence in slowing progression
52
Retinitis pigmentosa
primarily affects the peripheral retina resulting in tunnel vision night blindness is often the initial sign fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
53
Red flag eye symptoms
Sudden onset Visual loss Photophobia Fever Recent trauma Vomiting Associated red eye Contact lens wearer History of malignancy History of flashers or floaters
54
Serious and potentially sight-threatening causes of red eye include
Acute glaucoma. Anterior uveitis. Corneal ulcer, contact lens-related red eye and corneal foreign body. Neonatal conjunctivitis. Trauma, such as penetrating eye injury or high-velocity foreign body. Chemical injuries. Scleritis. Endophthalmitis.
55
Blepharitis
Very common non specific generalised inflammation of the eyelids caused by staphylococcal infection, seborrhoeic dermatitis, meibomian gland dysfunction, or all of above It can lead to styes and chalazions.
56
Blepharitis symptoms
sore eyes, itching, burning Eyelids may stick together on waking. crusty appearance at the base of the eyelashes Symptoms are bilateral dry eye syndrome: watery eyes, blurred vision, dry eyes and intolerance of contact lenses. associated seborrhoeic dermatitis: dandruff, oily skin, facial rashes. associated rosacea: facial flushing, redness or telangiectasia.
57
Mx Blepharitis
daily lid hygiene,hot compresses , lubrication as required with routine referral
58
Ectropion
Lid turning outwards with exposure of conjunctival sac. Eye may be sore and watery It usually affects the bottom lid Can cause exposure keratopathy as the eyeball is exposed
59
Entropion
Lids turning inwards and eyelashes may abrade cornea.This results in pain and can result in corneal damage and ulceration
60
Mx entropion
Definitive management is with surgical intervention. When the eyelid is taped down it is essential to prevent the eye drying out by using regular lubricating eye drops. A same-day referral to ophthalmology is required if there is a risk to sight.
61
Trichiasis
Ingrowing eyelashes. This results in pain and can result in corneal damage and ulceration. - epilate eyelash when touching cornea, lubricate with routine referral.Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent the lash regrowing.
62
Stye
infection of the glands of Zeis or glands of Moll (hordeolum externum) or infection of the Meibomian glands (hordeolum internum)
63
Mx stye
treated with hot compresses and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if it is associated with conjunctivitis or persistent.
64
Chalazion/Meibomian cyst
Meibomian gland becomes blocked and swells up presents with a swelling in the eyelid that is typically not tender Treatment is with hot compress and analgesia. Consider topic antibiotics (i.e. chloramphenicol) if acutely inflamed
65
Corneal foreign body and ocular trauma presentation
foreign body sensation, pain, and photophobia Visual acuity and pupil reflexes are usually normal.
66
Mx Chemical burns
ophthalmic emergency and should be immediately irrigated before any steps are taken. Common agents include cement, plaster powder and oven cleaner, all of which are alkaline. Refer once pH has stabilised.
67
Subconjunctival haemorrhage
hx of rf such as straining with coughing or constipation,may be associated with hypertension. usually unilateral, localised and sharply circumscribed. Underlying sclera not visible. No inflammation, pain or discharge. Vision unchanged. Possible association with minor injuries including rubbing. Common with use of antiplatelet agents and anticoagulants. Reassure and routine referral only if condition worsens or pain develops
68
Common causes of corneal abrasion/erosion
Contact lenses ( can be associated with infection with pseudomonas) Foreign bodies Finger nails Eyelashes Entropion (inward turning eyelid)
69
Signs of Corneal abrasian/erosion
eye red and watery, area where corneal epithelium not intact stains with fluorescein
70
Mx Corneal abrasian/erosion
check no foreign body, topical antibiotics (i.e. chloramphenicol) and can pad the eye although this does not help healing Antibiotics to prevent infection because of the break in corneal epithelium. Ointment provides a barrier so that when they sleep eyelid sticks to ointment and not to healing scab. Uncomplicated corneal abrasions usually heal over 2-3 days.
71
Microbial Keratitis
infection of the cornea that can be caused by a range of non-viral pathogens characterised by an sub/acute onset of pain, conjunctival injection, and corneal ulceration with a stromal inflammatory infiltrate. gritty sensation in the eyes, vision may be impaired depending on location RF include history of contact lens wear, foreign travel, Poor lens hygiene, swimming
72
Herpes simplex keratitis
sore red eye , not sticky abnormal corneal epithelium in dendrite pattern which stain with fluorescein Topical aciclovir
73
Bacterial corneal infection symptoms
eye sore and red , often in contact lens wearer ulcers or infections, monthly disposable lens its most often seen with. Pain, photophobia, vision may be affected Signs: white area on cornea, maybe peripheral or central
74
Viral conjunctivitis symptoms
often recent eye/URT infection Burning sensation and watery discharge rapid spread to the other, often pre-auricular lymphadenopathy, swelling
75
Mx viral conjunctivitis
Will resolve on own and treatment aimed at comfort. Cool compresses, regular lubricants (without preservative). Antibiotic drops if indicated. Resolution may take weeks. Refer if photophobia and decrease in visual acuity, severe disease lasting longer than 3 weeks.
76
Bacterial conjunctivitis symptoms
red sticky eyes with purulent discharge
77
Mx bacterial conjunctivitis
regular hygiene to minimise secretion buildup, topical antibiotics for 5 days. Eg chloramphenicol. Refer if needs
78
Acute Anterior uveitis
inflammation of the anterior segment of the eye. It may be associated with other inflammatory disorders, such as ankylosing spondylitis
79
Acute Anterior uveitis symptoms
Gradual onset, photophobia, eye red and sore, blurred vision, , headache, pain on accommodating, increased lacrimation, ibd history
80
Acute Anterior uveitis signs
VA may be reduced, redness more localised around the corneal edge (ciliary injection), pupils may be constricted or irregular due to adhesions between the lens and iris (termed synechiae). anterior chamber appears cloudy from cells and flare When severe, white cells precipitate on the corneal endothelial surface
81
Scleritis symptoms
severe eye pain which radiates to head or jaw and wakes them at night, purple hue , pain despite adequate analgesia
82
Scleritis signs
Eye is red , may have nodules and necrotic patch, sclera may be discolored and is tender to palpation. Progressive onset of photophobia and visual impairment, gradual decrease in vision
83
Hypopyon
Visible accumulation of white cells inferiorly seen in severe uveitis,located in the anterior chamber. Can be due to inflammation or infection If no recent surgery more likely to be inflammation Urgent (same day) referral for investigatio
84
Hyphaema
Red cells in anterior chamber
85
Management hyphaema
Bed rest,keep patient upright so only bottom of cornea will have rbc and will have better vision than if it was spread over,eye pad. Urgent (same day) assessment by ophthalmologist. Steroids to prevent inflammation Sleep upright too to prevent conrea being stained and to help blood drain away Keep eye on pressure too
86
Endophthalmitis
post-operative infection that occurs within the first 2 weeks of surgery and can rapidly cause blindness
87
Endophthalmitis symptoms
hx eye surgery, reduced vision, significant pain/headache, hypopyon. Red eye, decreasing visual acuity, and pain
88
Mx Endophthalmitis
Urgent/immediate referral for intravitreal and systemic antibiotics reatment is intravitreal vancomycin as the most common causative organisms after surgery are gram positive
89
Periorbital Cellulitis
an eyelid and skin infection in front of the orbital septum (in front of the eye). It presents with swelling, redness and hot skin around the eyelids and eye.CT to make sure it isn't orbital cellulitis
90
Orbital Cellulitis
infection around the eyeball that involves tissues behind the orbital septum. Key features that differentiate this is pain on eye movement, reduced eye movements, changes in vision, abnormal pupil reactions and forward movement of the eyeball (proptosis).
91
Pupil Constriction
stimulated by the parasympathetic nervous system using acetylcholine as a neurotransmitter. The fibres of the parasympathetic system innervating the eye travel along the oculomotor (third cranial) nerve.
92
Pupil Dilation
dilator muscles are stimulated by the sympathetic nervous system using adrenalin as a neurotransmitter
93
Causes of Mydriasis (Dilated Pupil)
Third nerve palsy Holmes-Adie syndrome Raised intracranial pressure Congenital Trauma Stimulants such as cocaine Anticholinergics
94
Causes of Miosis (Constricted Pupil)
Horners syndrome Cluster headaches Argyll-Robertson pupil (in neurosyphilis) Opiates Nicotine Pilocarpine
95
Holmes Adie Pupil
unilateral dilated pupil that is sluggish to react to light with slow dilation of the pupil following constriction. Over time the pupil will get smaller. This is caused by damage to the post-ganglionic parasympathetic fibres.
96
Argyll-Robertson Pupil
pecific finding in neurosyphilis. It is a constricted pupil that accommodates when focusing on a near object but does not react to light.ften irregularly shaped
97
mononuclear vision loss
lesion before chiasm
98
Causes of monocular vision loss
optic neuritis, optic atrophy, glaucoma, trauma, central retinal occlusion, retinal detachment
99
bitemporal hemianopia
loss of temporal part of the visual field in both eyes esulting in central tunnel vision. It is usually caused by a lesion in the midline which is exerting pressure effects on the optic chiasm.
100
Causes of bitemporal hemianopia
pituitary tumour craniopharyngoma Meningioma Chiasmatic glioma Aneurysm or ectatic carotid artery Epidermoid cyst Dermoid cyst
101
Homonoymous hemianopia
lesion after chiasm,contralateral optic tract lesion causes by middle cerebral artery occlusion
102
Homonymous inferior quadrantanopia
contralateral pariental upper optic radiation lesion caused by parietal tumour or stroke
103
Homonumous superior quadrantanopia
Contralateral parietal lower optic radiation lesion caused by temporal stroke or tumour
104
Homonymous hemianopia with macular sparing
contralateral occipital visual cortex lesion caused by posterior cerebral artery occlusion
105
Diabetic retinopathy
blood vessels in the retina are damaged by prolonged exposure to high blood sugar levels (hyperglycaemia) causing a progressive deterioration in the health of the retina.
106
Features of Diabetic retinopathy
blot haemorrhages hard exudates microaneurysms and venous beading cotton wool spots Intraretinal microvascular abnormalities (IMRA) is where there are dilated and tortuous capillaries in the retina Neovascularisation
107
Mx diabetic retinopathy
Laser photocoagulation Anti-VEGF medications such as ranibizumab and bevacizumab Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease Primary prevention annual monitoring
108
Signs of hypertensive retinopathy
Silver wiring or copper wiring Arteriovenous nipping Cotton wool spots Hard exudates Retinal haemorrhages Papilloedema
109
Silver wiring or copper wiring
is where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
110
Arteriovenous nipping
is where the arterioles cause compression of the veins where they cross, due to sclerosis and hardening of the arterioles.
111
Cotton wool spots
are caused by ischaemia and infarction in the retina causing damage to nerve fibres.
112
Hard exudates
are caused by damaged vessels leaking lipids into the retina.
113
Retinal haemorrhages
are caused by damaged vessels rupturing and releasing blood into the retina.
114
Papilloedema
is caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
115
Keith-Wagener Classification of hypertensive retinopathy
Stage 1: Mild narrowing of the arterioles Stage 2: Focal constriction of blood vessels and AV arteriovenous nicking Stage 3: Cotton-wool patches, exudates and flame haemorrhages Stage 4: Papilloedema
116
causes of squint
Refractive errors, especially hypermetropia. causes of poor visual acuity in one or both eyes, including occular malformations, optic neuropathy, amblyopia (lazy eye) which can also be a complication of a squint, congenital cataract, and retinoblastoma cerebral palsy and downs syndrome brain tumour
117
Squint is sig after age of
3m Normal binocular coordination is established at about 3 months
118
Squint having underlying cause red flags
Limited abduction. Double vision. Headaches. Nystagmus (involuntary, repetitive, side-to-side oscillation of the eyes).
119
Secondary care treatments for squint
Glasses to correct any refractive error. Occlusion or penalization therapy to treat amblyopia- Surgery (or in some cases injection of botulinum toxin) to correct misalignment of eyes
120
Retinoblastoma presentation
leukocoria (white pupil) deteriorating vision, strabismus or failure to thrive In developing countries, the tumour often presents as eye enlargement.

Medicine (72 decks)

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