Opthalmology Flashcards

1
Q

What is glaucoma and what are the two types?

A

Optic nerve damage caused by a significant rise in intraocular pressure
The raised intraocular pressure is caused by a blockage in aqueous humour trying to leave the eye

Open angle glaucoma and closed angle glaucoma

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2
Q

Describe the two chambers of the eye

A

Vitrous chamber - contains vitreous humour

Anterior chamber - between cornea and iris

Posterior humour - between lens and iris

Both anterior and posterior chambers contain aqueous humour which is produced by the ciliary bodies

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3
Q

What is the function of the aqueous humour

A

Supply nutrients to the cornea

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4
Q

Describe the journey of the aqueous humour from production to exiting the eye

A

Produced in the ciliary body
Flows around the lens and under the iris through the anterior chamber, through the trabecular meshwork and into the canal of schlemm m from the canal of schlemm it eventually enters the general circulation

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5
Q

What is the normal introcular pressure

A

10-21mmHg

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6
Q

What causes increased intraocular pressure in open angle glaucoma

A

Gradual increased resistance to flow through the trabecular meshwork into the canal of schlemm

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7
Q

What happens in acute angle closure glaucoma

A

The iris bulges forward and seals off the trabecular meshwork from the anterior chamber and prevents aqueous humour being able to drain away
This leads to a continual build up of pressure especially in the posterior chamber which causes pressure behind the iris and worsens the closure of the angle

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8
Q

What is seen on fundoscopy in cases of increased intraocular pressure

A

Cupping of the optic disc

Optic cup greater than 0.5 the size of the optic disc is abnormal

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9
Q

List some risk factors for open angle glaucoma

A

Increasing age
Black
Myopia - near sightedness
FH

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10
Q

How does open angle glaucoma present

A

Asymptomatic
Peripheral vision loss - tunnel vision
Fluctuating pain, headaches, blurred vision
Haloes around lights at night time

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11
Q

How is open angle glaucoma diagnosed

A

Non-contact tonometry - puff of air, not much response is positive for glaucoma

Goldmann applanation tonometry - gold standard, machine with slit lamp that apples different pressures to cornea

Fundoscopy - cupping

Visual field assessment - peripheral field loss

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12
Q

How is open angle glaucoma managed

A

Reduced IO pressure

Prostaglandin analogue eye drops (latanoprost) - increase uveoscleral outflow

Beta blockers (timolol) - reduce the production of aqueous humour

Carbonic anhydrase inhibitors (dorzolamide) - reduce production of aqueous humour

Sympathomimetics (brimonidine) - reduce the production of aqueous humour and increase uveoscleral outflow

Trabeculectomy - create a new channel from anterior chamber through the sclera to a location under the conjunctiva it causes a bleb and the conjunctiva where the aqueous humour drains and is then reabsorbed into general circulation

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13
Q

Give the side effects of prostaglandin analogue eye drops such as latanoprost

A

Eyelash growth, eyelid pigmentation and iris pigmentation (browning)

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14
Q

What are some risk factors of acute angle closure glaucoma

A

Increasing age
Females (4X more often than males)
FH
Chinese and east Asian ethnic origin
Shallow anterior chamber - long sightedness
Medication - adrenergic (noradrenalin), anticholinergic (oxybutynin and Solifenacin), tricyclic antidepressants (amitriptyline)

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15
Q

How do patients with acute angle closure glaucoma present

A

Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting

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16
Q

Describe the examination of acute angle closure glaucoma

A
Red eye 
Teary
Hazy cornea
Decreased visual acuity 
Dilation of the affected pupil 
Fixed pupil size
Firm eyeball on palpation
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17
Q

Describe the management of acute angle closure glaucoma

A

Lie patient on back without pillow
Pilocarpine eye drops
Acetazolamide 500mg PO
Give analgesia and antiemetic if required
Hyperosmotic agents - glycerol and mannitol
Timolol (beta blocker) - reduce production of aqueous humour
Brimonidine
Laser iridotomy - definitive treatment - laser to make a hole in the iris and allow the aqueous humour to flow from the posterior chamber into the anterior chamber - relieves pressure that was pushing the iris against the cornea and allows the humour to drain

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18
Q

How does pilocarpine work

A

Acts on antimuscarinic receptors in the sphincter muscles in the iris and causes constriction of the pupil - Miotic agent
Causes ciliary muscle contraction
Cause pathway for flow of aqueous humour from ciliary body around iris and into trabecular meshwork to open up.

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19
Q

What is age related macular degeneration and give the two types

A

Degeneration of the macula causing a progressive deterioration in vision
Most common cause of blindness in the UK
Wet and dry AMD

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20
Q

Which AMD has the worse prognosis

A

Wet

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21
Q

Describe the layers of the macular

A

Photoreceptors at top
Retinal pigment epithelium
Bruchs membrane
Choroid layer - blood vessels

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22
Q

Give some features seen in both wet and dry AMD

A

Drusen - yellow deposits of protein and lipids that appear between the retinal pigment epithelium and Bruchs membrane
Atrophy of the retinal pigment epithelium
Degeneration of photoreceptors

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23
Q

What is a key feature of wet AMD

A

New vessel growing from choroid layer into the retina

The vessels can cause oedema and more rapid vision loss

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24
Q

Which chemical stimulates development of new blood vessels

A

Vascular endothelial growth factor (VEGF)

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25
List some risk factors for age related macular degeneration
``` Age Smoking White or Chinese FH CVD ```
26
Describe the presentation of AMD
Gradual worsening central visual field loss Reduced visual acuity Crooked or wavy appearance to straight lines Wet AMD presents more acutely - loss of vision over days
27
What is seen on examination in AMD
Reduced acuity on Snellen chart Scotoma - central patch vision loss Amsler grid test - wavy lines Fundoscopy - drusen Slit lamp fundus examination Optic coherence tomography (OCT) - layers of the retina - wet AMD Fluorescein angiography - fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina - oedema and neovascularisation - used second line to diagnose wet AMD if OCT does not exclude it
28
How is dry age related macular degeneration managed
No specific treatment - lifestyle Stop smoking Reduce BP Vitamin supplementation
29
How is wet age related macular degeneration managed
Anti-VEGF medication Ranibizumab, bevacizumab and pegaptanib Injected into vitreous chamber once a month Typically need to be started within 3 months to be beneficial
30
What is the pathophysiology of diabetic retinopathy
Hyperglycaemia leads to damage to retinal small vessels and endothelial cells. Leakage from vessels causes blot haemorrhages and formation of hard exudates Damage to blood vessel walls leads to microaneurysms and venous beading Damage to nerve fibres in the retina cause cotton wool spots Intraretinal microvascular abnormalities (IMA) shunt between arterial and venous vessels in the retina Neovascularisation - growth factors into the retina causing development of new blood vessels
31
Describe the classification of diabetic retinopathy
Non-proliferative diabetic retinopathy Proliferative diabetic retinopathy Diabetic maculopathy
32
Describe non-proliferative (pre-proliferative/background) diabetic retinopathy
Mild - microaneurysms Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots and venous beading Severe - blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants or Intraretinal microvascular abnormality in any quadrant
33
Describe proliferative retinopathy
Neovascularisation | Vitreous haemorrhage
34
Describe diabetic maculopathy
Macular oedema | Ischaemic maculopathy
35
List the complications of diabetic retinopathy
``` Retinal detachment Vitreous haemorrhage Rebeosis iridis - vessel development in iris Optic neuropathy Cataracts ```
36
How is diabetic retinopathy managed
Laser photocoagulation Anti-VEGF medication - ranibizumab and bevacizumab Vitreoretinal surgery
37
Describe hypertensive retinopathy and its features
Damage to the retina as a result of hypertension (either chronic or malignant) Silver/copper wiring - sclerosed and thickened arterioles AV nipping - where arterioles cause compression of the veins where they cross - sclerosis Cotton wool spots - ischaemia and infarction causing nerve fibre damage Hard exudates - lipids leaking into the retina Retinal haemorrhages- damaged vessels rupturing and releasing blood into the retina Papilloedema - ischaemia to the optic nerve - swelling and blurring of the disc margins
38
Describe the Keith Wagener classification for hypertensive retinopathy
Stage 1 - mild narrowing of arterioles Stage 2 - focal constriction and AV nipping Stage 3 - cotton wool patches, exudates and haemorrhages Stage 4 - papillooedema
39
How is hypertensive retinopathy managed
Control BP | Modify RF - smoking and blood lipids
40
What are cataracts
Where the lens becomes cloudy and opaque | Loss of visual acuity by reducing the light entering the eye
41
What is the function of the lens
To focus the light onto the retina
42
Describe the anatomy of the lens
Held by suspensory ligmanets attached to the ciliary body The ciliary body contracts and relaxes to focus the lens When the ciliary body contracts it releases tension on the suspensory ligament and the lens thickens When the ciliary body relaxes, it increases tension on the suspensory ligaments causing the lens to narrow The lens does not have a blood supply so it grows and develops throughout life
43
List some risk factors for cataracts
``` Age Smoking Alcohol Diabetes Steroids Hypocalcaemia ```
44
Describe the presentation of cataracts
Very slow reduction in vision Progressive blurring of the vision Change in colour vision with colours becoming more brown or yellow Starbursts can appear around lights - at night time
45
What is a sign of a cataracts on examination
Loss of the red light reflex - lens appears grey/white
46
What causes a generalised loss of vision with starbursts around light
Cataracts
47
What causes a peripheral loss of vision and halos round light
Glaucoma
48
What causes a central loss of vision with crooked appearance to straight lines
Age related macular degeneration
49
Describe the management of cataracts
None if asymptomatic Surgery if wanting to detect other eye pathology or patient wants the cataract removed - pseudophakia (artificial lens) implanted
50
Name one important complication of cataracts surgery and give its management and complications
Endophthalmitis Inflammation of the inner contents of eye usually due to infection Treated with Intravitreal antibiotics injected into the eye Can lead to loss of vision or loss of the eye
51
Describe how pupil constriction and dilation occur
Constriction - Circular muscles of iris stimulated by acetylcholine of parasympathetic nervous system travelling along the oculomotor nerve Dilation - dilator muscles travel from inside to outside of the iris and stimulated by adrenalin by the sympathetic nervous system
52
List some causes of abnormal pupil shape
Trauma to sphincter muscles - surgery Adhesions - anterior uveitis Vertical oval - acute angle closure glaucoma - ischaemic damage to muscles of iris Rubeosis iridis - neovascularisation of the iris in DR Coloboma - congenital malformation - hole in iris Tadpole pupil - spasm in a segment of iris associated with migraines
53
List the causes of mydriasis (pupil dilation)
``` 3rd nerve palsy Holmes Adie syndrome Stimulants - cocaine Congenital Raised ICP Trauma Anticholinergic drugs ```
54
List the causes of miosis (pupil constriction)
``` Horner's syndrome Cluster headache Argyll-Robertson pupil (neurosyphilis) Opiates Nicotine Pilocarpine ```
55
Describe a third nerve palsy
Ptosis - CN3 innervates levator palpabrae superioris Mydriasis (dilation) and non reactive pupil -CN3 contains parasympathetic supply which normally constricts pupil so palsy causes dilatation Divergent strabismus (squint) and Down and out position of the eye - CN3 innervates all the extraocular muscles except lateral rectus and superior oblique so palsy causes down and out as lateral rectus and superior oblique still functioning
56
Which nerve innervates lateral rectus
Abducens (6)
57
Which nerve innervates superior oblique
Trochlear (4)
58
What does a third nerve palsy with pupil sparing suggest
Sparing of parasympathetic fibres so the cause is microvascular - DM - HTN - Ischaemia
59
List the causes of a full third nerve palsy
Compression of the nerve including parasympathetic fibres - surgical third - Idiopathic - Trauma - Tumour - Cavernous sinus thrombosis - Posterior communicating artery aneurysm - Raised ICP
60
Which two brain structures does the third cranial nerve travel close to
Cavernous sinus | Posterior communicating artery
61
Describe Horner's syndrome
Ptosis Miosis Anhidrosis (loss of sweating) May have enopthalmos - sunken eye
62
What causes Horner's syndrome
Damage to the sympathetic nerves supplying the face Congenital - heterochromia (difference in eye colour on affected eye) Central - Stroke - MS - Swelling/tumour - Syringomyelia (cysts in the spinal cord) Pre-ganglionic - Tumour - Pancoasts tumour - Trauma - Thyroidectomy - Cervical rib Post-ganglionic - Carotid artery dissection - Cavernous sinus thrombosis - Cluster headache
63
Describe the journey of the sympathetic nerves to the head
Arise from spinal cord in the chest (pre-ganglionic nerves) They enter the sympathetic ganglion on at the base of the neck and exit as post ganglionic nerves They then travel to head alongside internal carotid artery
64
How can the location of the Horner syndrome be determined
If there is anhidrosis Central lesions cause anhidrosis of the arm and trunk and face Pre-ganglionic lesions cause anhidrosis of the face Post-ganglionic lesions do not cause anhidrosis
65
What affect do cocaine eye drops have on a pupil in Horner's syndrome
No affect
66
What affect do adrenaline eye drops have on a Horner's syndrome pupil
Dilation
67
Describe a Holme's-Adie pupil
Unilateral dilated pupil which is sluggish to react to light with slow dilation after constriction Damage to post-ganglionic parasympathetic fibres probably viral
68
What is Holmes-Adie syndrome
Holmes Adie pupil with absent ankle and knee reflexes
69
What causes an Argyll Robertson pupil
Neurosyphilis
70
Describe argyll-robertson pupil
Irregularly shaped Constricted pupil Accommodates but does not react
71
Describe blepharitis
Inflammation of eyelid margins Causes dry, itchy, gritty sensation Dysfunction of Meibomian glands (secrete oil onto eye) leading to styes and chalazions
72
How is blepharitis managed
Hot compress Gentle cleaning of eye - baby shampoo and sterile water Lubricating eye drops - hypromellose, polyvinyl alcohol (start with these - middle viscous) and carbomer (most viscous lasting 30-60 mins)
73
Describe styes and their management
Hordeolum externum - infection of glands of zeis (sebaceous glands ) and glands of moll (sweat glands) at base of eyelashes Tender red lump that may contain pus Hordeolum internum - infection of Meibomian glands, deeper and more painful and may point inwards under the eyelid Managed with hot compress and analgesia, may require topical antibiotic (chloramphenicol) if associated conjunctivitis or persistent
74
What are chalazions and how are they managed
Blocked Meibomian glands - cyst, typically non-tender but can be Managed with hot compress and possible topical antibiotics May require drainage
75
What is entropion and its treatment
Eyelid inward with lashes against eyeball Lashes may cause corneal ulceration and damage Initial management - taping down of eyelid and regular lubricating eye drops Definitive management - surgery
76
What is ectropion and its treatment
Eyelid turned outward with inner aspect of eyelid exposed Exposure keratopathy Management - if mild no treatment, lubricating drops, more severe require surgery
77
What is periorbital cellulitis and its management
Infection in front of the orbital septum - swelling, redness and hot skin around eyelid CT to differentiate from orbital cellulitis Treat with systemic antibiotics as risk of developing orbital cellulitis
78
What is orbital cellulitis and its management
Infection around eyeball involving tissues behind orbital septum Pain on eye movement, change in vision, abnormal pupil reaction, forward movement of eyeball Medical emergency - admission and IV antibiotics - may require surgical drainage if an abscess forms
79
What is conjunctivitis
Inflammation of the conjunctiva - thin layer of tissue that covers the inside of the eyelids and the sclera of the eye
80
List and describe the three types of conjunctivitis
Bacterial - purulent discharge Viral - clear discharge and other signs of viral infection such as dry cough, sore throat, blocked nose and tender periauricular lymph nodes Allergic - lots of watery discharge
81
What are the symptoms of conjunctivitis
Discharge Itch Gritty sensation Red eye Not painful or photophobia or reduced visual acuity Blurring may be due to discharge but resolves when discharge clears Unilateral/bilateral
82
What is the differential for an acutely red painful eye
``` Glaucoma Anterior uveitis Corneal abrasions/ulcers Scleritis Keratitis Foreign body Traumatic or chemical injury ```
83
What is the differential for an acutely red painless eye
Conjunctivitis Episcleritis Subconjunctival haemorrhage
84
How is conjunctivitis managed
Usually resolves without treatment within 1-2weeks Good hygiene to avoid spreading and avoid the use of contact lenses. Clean the eyes with cooled boiled water and cotton wool to help clear the discharge Bacterial conjunctivitis - topical antibiotic eye drops - chloramphenicol and fusidic acid Allergic conjunctivitis - antihistamines (topical or oral) and topical mast cell stabilisers in patients with chronic seasonal symptoms - preventing mast cells releasing histamine - require use for several weeks before showing benefit
85
What is anterior uveitis
Inflammation in the anterior part of the uvea Uvea involves the iris, ciliary body and choroid (layer between the retina and sclera) Inflammation and immune cells in the anterior part of the eye - becomes infiltrated by neutrophils, lymphocytes and macrophages Can be acute or chronic
86
What is acute anterior uveitis associated with
HLAB27 related conditions Ankylosing spondylitis Inflammatory bowel disease Reactive arthritis
87
What is chronic anterior uveitis associated with
``` More granulomatous diseases Sarcoidosis TB Lyme disease Herpes virus Syphylis ```
88
Describe chronic anterior uveitis
>3 months | Less severe
89
Describe the presentation of anterior uveitis
Unilateral symptoms that start spontaenously without history of trauma/precipitating event May occur with a flare of the associated disease Dull, aching, painful red eye Ciliary flush - red ring spreading from the cornea outward Reduced visual acuity Floaters and flashes Sphincter muscle contraction - miosis Photophobia due to ciliary muscle spasm Pain on movement Excess tear production Abnormally shaped pupil - posterior synechiae (adhesions) Hypopyon - collection of white cells in anterior chamber - yellowish fluid settled in front of the lower iris
90
Describe the management of anterior uveitis
Urgent ophthalmology review - slit lamp and intraocular pressure assessment Steroids - oral, topical, IV Cycloplegic-mydriatic medication - cyclopentolate or atropine - dilates the pupils and relaxes the ciliary bodies to reduce pain associated with ciliary body spasm Immunosuppressants - DMARDs and TNF inhibitors Laser therapy, cryotherapy or surgery
91
What is episcleritis
Inflammation of the episclera (layer under the conjunctiva) Common in young and middle aged adults Associated with IBD and RA
92
How does episcleritis present
``` Not painful Segmental redness - lateral sclera Foreign body sensation Dilated episcleral vessels Watering of the eye No discharge ```
93
Describe the management of episcleritis
``` Self limiting - 1-4 weeks Cold compress Lubricating eye drops can help Simple analgesia Safety net advice More severe cases may benefit from systemic NSAIDs and topical steroid eye drops ```
94
Describe scleritis
Inflammation of the full thickness of the sclera
95
What are the complications of scleritis
Visual impairment - Necrotising scleritis and perforation of the sclera
96
What conditions are associated with scleritis
``` IBD RA SLE Sarcoidosis Granulomatosis with polyangitis ```
97
Describe the presentation of scleritis
``` Severe pain Pain with eye movement Photophobia Eye watering Reduced visual acuity Abnormal pupil reaction to light Tenderness to palpation of the eye 50% bilateral ```
98
How is scleritis managed
``` Urgent ophthalmology referral - same day Consider underlying systemic condition NSAIDs Steroids Immunosuppression ```
99
List some causes of corneal abrasions
``` Contact lenses Foreign bodies Finger nails Eyelashes Entropion ```
100
Which bacteria may infect the eye if abrasion associated with contact lenses
Pseudomonas
101
What is an important differential to consider in corneal abrasions
Herpes keratitis
102
Describe the presentation of corneal abrasions
``` Painful red eye Foreign body sensation Watering eye History of contact lens use Blurring of vision Photophobia ```
103
How is a corneal abrasion diagnosed
Fluorescein stain - yellow/orange colour which collects in abrasions and ulcers Slit lamp examination - more significant
104
How are abrasions managed
``` Slit lamp assessment Remove foreign bodies Simple analgesia Lubricating eye drops Chloramphenicol Follow up after 24hrs Chemical abrasions require immediate irrigation for 25-30 mins and urgent referral to ophthalmology Uncomplicated abrasions heal over 2-3 days ```
105
List some causes of keratitis
``` Viral - herpes simplex Bacterial - pseudomonas and staphylococcus Fungal - candida or aspergillus Contact lens acute red eye Exposure keratitis ```
106
What is the most common cause of keratitis
Herpes simplex virus
107
Describe herpes simplex keratitis
Primary or recurrent Affects the epithelial layer of the cornea If there is stromal inflammation risk of - stromal necrosis, vascularisation and corneal blindness ``` Painful red eye Photophobia Vesicles around the eye Foreign body sensation Watering eye Reduced visual acuity ```
108
How is herpes keratitis diagnosed
Fluorescein stain - dendritic (branching) corneal ulcer Slit lamp examination Corneal swabs or scrapings - isolate the virus using viral culture or PCR
109
Describe the management of herpes keratitis
Aciclovir - topical or oral Ganciclovir eye gel Topical steroids - alongside antivirals to treat stromal keratitis Corneal transplant - may be required after the infection has resolved to treat corneal scarring caused by stromal keratitis
110
What is a subconjunctival haemorrhage, how does it present, what causes it and how is it managed?
Blood vessel in conjunctiva ruptures causing a patch of blood between the sclera and conjunctiva Does not affect vision Occurs after heavy lifting, coughing or straining af with consitpation HTN and bleeding disorders or medications (warfarin, DOACs and antiplatelets may lead to this) Resolves spontaneously over 2 weeks Investigate if underlying cause suspected If foreign body sensation - give lubricating eye drops
111
What is the vitreous body
Gel inside the eye that maintains the eyeball structure and keeps the retina pressed on the choroid Made of collagena and water With age becomes less firm
112
What is posterior vitreous detachment
When the vitreous body comes away from the retina
113
How does posterior vitreous detachment present
``` Painless Spots of vision loss Floaters Flashing lights Brain adjusts till asymptomatic ```
114
What can occur as a result of posterior vitreous detachment
Retinal tears and detachment
115
How is posterior vitreous detachment managed
No management - brain adjusts | Exclude retinal tear/detachment
116
Describe retinal detachment
Retina detaches from the choroid underneath Usually due to retinal tear which allows vitreous fluid to get under the retina and fill the space between the retina and the choroid Retina relies on the choroid for its blood supply - sight threatening- emergency
117
List some risk factors for retinal tears
``` Posterior vitreous detachment Older age Diabetic retinopathy Damage to the eye - trauma Retinal malignancy Family history ```
118
How does retinal detachment present
Peripheral vision loss - sudden and like a shadow coming across vision Blurred or distorted vision Flashes and floaters Painless
119
How are retinal tears managed
Create adhesions between retina and choroid - laser therapy or cryotherapy
120
How is retinal detachment managed
Vitrectomy - remove vittreous body and replace with oil/gas Scleral buckling - silocone buckle to put pressure on outer eye and indent the eye so the choroid touches the retina Pneumatic retinopexy - inject gas bubble into the eye and position patient so bubble creates pressure that flattens the retina against the choroid and close the detachment
121
Describe retinal vein occlusion
Occurs when thrombus blocks the retinal veins from draining the retina Central retinal vein runs through the optic nerve and rains blood from the retina 4 branched veins come together to form the central retinal vein, blockage of a branch leads to problems in the area drained by this branch whereas central retinal vein occlusion leads to problems in the whole retina
122
What does central retinal vein occlusion cause
Macular oedema and retinal haemorrhages Damage in the tissue in the retina and loss of vision Release of VEGF which causes neovascularisation
123
How does central retinal vein occlusion present
Painless loss of vision Flame and blot haemorrhages, optic disc oedema and macula oedema on fundoscopy
124
List the risk factors for central retinal vein occlusion
``` HTN High cholesterol DM Smoking Glaucoma SLE ```
125
Describe the management of central retinal vein occlusion
Laser photocoagulation Intravitreal steroids Anti-VEGF therapy
126
Describe central retinal artery occlusion
Blockage of flow through retinal artery caused by atherosclerosis or giant cell arteritis
127
Describe the formation of the central retinal artery
ICA - opthalmic artery - central retinal artery
128
List some risk factors for central retinal artery occlusion
``` Older age FH Smoking Alcohol HTN DM Poor diet Inactivity Obesity GCA RF - females, white, >50yo, PMR or GCA ```
129
Describe the presentation of central retinal artery occlusion
Sudden painless loss of vision Relative afferent pupillary defect Fundoscopy - pale retina with cherry red spot
130
Describe relative afferent pupillary defect
Pupil in affected eye constricts more when light shone into normal eye due to consensual response whereas light shone into affected eye is not detected by the affected eye/ischaemic retina
131
What is the cherry red spot seen in central retinal artery occlusion on fundoscopy
Macula - thinner surface and shows the red coloured choroid below and contrasts with the pale retina
132
Describe the management of central retinal artery occlusion
GCA - reversible cause - ESR and temporal artery biopsy - high dose steroids - 60mg prednisolone Thrombus - ocular massage, inhale carbogen (5% CO2 and 95% O2), sublingual isosorbide dinitrate to dilate the artery and remove fluid from anterior chamber to reduce intraocular pressure Long term management- modify RF
133
What is retinitis pigmentosa
Inherited congenital condition where there is degeneration of rods and cones. The rods degenerate more than the cones Can occur on its own or part of a disease with hearing (Ushers syndrome), neurological (Bassen-kornzweig syndrome) or skin issues (Refsums disease)
134
Describe the presentation of retinitis pigmentosaq
Peripheral vision loss before central vision loss Night blindness Fundoscopy shows bone-spicule pigmentation in the mid peripheral area of the retina Narrow arterioles Waxy or pale optic disc
135
How is retinitis pigmentosa managed
Ophthalmology genetic counselling Vision aids Sunglasses to protect retina from accelerated damage Driving limitation - inform DVLA Regular follow up to assess for other conditions such as cataracts