opthalmology Flashcards
What is the anterior chamber in the eye
area from the cornea to the iris
What is the posterior chamber in the eye?
Narrow space between the iris and the lens
What is the vitreous chamber in the eye?
Big space between the lens and the back of the eye
Which chambers are in the anterior section of the eye?
–> anterior chamber
–> posterior chamber
Which chamber makes up the posterior section of the eye?
vitreous chamber
What fluid is the anterior section of the eye filled with?
aqueous humour
What fluid is the posterior section of the eye filled with?
Vitreous humour
What secretes aqeous humour in the anterior section of the eye?
Cilliary epithelium
Describe the pathway of aqueous fluid in the anterior section of the eye?
–> Cilliary epithelium secretes aqueous humour in the posterior chamber ( narrow space between iris and lens)
–> Aqueous humour flows through the narrow posterior chamber through the pupil into the anterior chamber
–> Fluid flows out of the eye through the trabecular meshwork
–> through canal of Schlemn
–> into aqueous veins (episcleral venous system)
Describe what is meant by glaucoma?
–> optic nerve damage caused by a rise in intraocular pressure.
–> Raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.
There are two types of glaucoma:
Open-angle glaucoma
Acute angle-closure glaucoma
How does acute angle closure glaucoma arise?
–> iris bulges forward
–> seals off trabecular meshwork from anterior chamber
–> Prevents aqueous humour from draining
–> increased IOP (intraocular pressure)
–> Pressure build up in posterior chamber
–> Pushes iris further forward and exacerbates the angle closure
OPTHALMOLOGICAL EMERGENCY
What are the risk factors for acute angle closure glaucoma?
–> hypermetropia (long-sightedness)
–> increasing age (lens growth)
–> family history
–> female
–> chinese and east asian ethnic
–> shallow anterior chamber
Which medications can precipitate acute angle closure glaucoma?
Adrenergic medications (e.g., noradrenaline)
Anticholinergic medications (e.g., oxybutynin and solifenacin)
Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
What are the clinical features of acute angle closure glaucoma?
–> severe pain - could be ocular or headaches
–> Decreased visual acuity
–> symptoms worse with mydriasis (pupil dilation - watching TV in a dark room)
–> hard red eye
–> haloes around lights
–> semi dilated non reacting pupil
–> Corneal oedema results in dull or hazy cornea
–> systemic upset - N+V/ abdo pain
What are the investigations for acute angle closure glaucoma?
Tonometry to assess for elevated IOP
gonioscopy - special lens for the slit lamp that allows you to visualise angle
What is the initial management of acute angle closure glaucoma?
–> emergency - Urgent referral to opthalmologist
–> Lying the patient on their back without a pillow
–> Pilocarpine eye drops (2% for blue and 4% for brown eyes)
–> Acetazolamide 500 mg orally
–> Analgesia and an antiemetic, if required
How do pilocarpine eye drops work?
–> Act on 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.
How does acetazolomide work?
Acetazolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour.
What is the secondary care managment of acute angle closure glaucoma?
–> 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
Laser iridotomy is usually required as a definitive treatment. This involves making a hold 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.
What is the normal intraocular pressure?
10-21 mmHg - created by resistance to flow through the trabecular meshwork
What is the pathophysiology of open angle glaucoma?
–> gradual increase in resistance to flow through the trabecular meshwork
–> pressure slowly builds up in the eye
–> Raised IOP causes cupping of the optic disc
–> centre of the optic disc is an indent called the optic cup.
–> The optic cup usually is less than 50% of the size of the optic disc. –> Raised intraocular pressure causes this indent to become wider and deeper, described as “cupping”.
–> A cup-disk ratio greater than 0.5 is abnormal.
What are the risk factors for open-angle glaucoma?
–> increasing age
–> family history
–> black ethnic origin
–> myopia (nearsightedness)
–> hypertension
–> diabetes mellitus
–> corticosteroids
what is the presentation of open angle glaucoma?
–> may be asymptomatic for a long time and diagnosed by routine eye testing.
–> Glaucoma affects the peripheral vision first, resulting in a gradual onset of peripheral vision loss (tunnel vision). It can also cause:
–> Fluctuating pain
–> Headaches
–> Blurred vision
–> Halos around lights, particularly at night
–> optic disc cupping
What are the investigations for open angle glaucoma?
–> 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
What are the fundoscopy signs of open angle glaucoma?
–> Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
–> Optic disc pallor - indicating optic atrophy
–> Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
–> Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
What is the management of open angle glaucoma?
–> 360° selective laser trabeculoplasty - laser is directed at the trabecular meshwork, improving drainage. It may delay or prevent the need for eye drops. A second procedure may be necessary at a later date.
–> Prostaglandin analogue eye drops (latanoprost) - first line medical management - increases uveoscleral outflow
–> beta-blockers (timolol) - reduce the production of aqueous humour
–> carbonic anhydrase inhibitors (dorzoloamide/ azetazolomaide) - reduces the production of aqueous humour
–> Sympathomimetics (e.g., brimonidine) reduce the production of aqueous fluid and increase the uveoscleral outflow
–> miotics - pilocarpine - increase iveoscral outflow
–> Trabeculectomy surgery may be required where other treatments are ineffective. This involves creating a new channel from the anterior chamber through the sclera to a location under the conjunctiva, causing a bleb on the conjunctiva. From here, it is reabsorbed into the general circulation.
What are the side effects of prostaglandin eyedrops such as latanoprost?
–> eyelash growth
–> eyelid pigmentation
–> iris pigmenetation (browning)
What is age related macular degeneration?
–> progressive condition affecting the macula
–> most common cause of blindness in the UK
–> often unilateral but can be bilateral
–> two types - Wet (also called neovascular), accounting for 10% of cases/ Dry (also called non-neovascular), accounting for 90% of cases
Where is the macula and what does it do?
–> centre of retina
–> generates high-definition colour vision in the central visual field, has four layers
What are the four layers of the macula?
–> Choroid layer (at the base), which contains the blood vessels that supply the macula
–> Bruch’s membrane
–> Retinal pigment epithelium
–> Photoreceptors (towards the surface)
what are Drusen findings in age-related macular degeneration?
–> Drusen are yellowish deposits of protein and lipids
–> between retinal pigment epithelium and Bruch’s membrane
–> few small Drusen normal in elderly, larger and frequent can be an early sign of macular degeenration
What are the risk factors of age-related macular degeneration?
–> older age
–> smoking
–> family history
–> cardiovascular disease (hypertension)
–> obeisty
–> poor diet (low in vitamins and high in fats)
What are the two types of macular degeneration and what are the characteristics of each?
–> Dry macular degeneration
- 90% of cases
- also known as atrophic
- characterised by Drusen - yellow round spots in Bruch’s membrane
–> Wet macular degeneration
- 10% of cases
- also known as exudative or neovascular macular degeneration caused by vascular endothelial growth factor (VEGF)
- characterised by choroidal neovascularisation
- leakage of serous fluid can result in rapid loss of vision
- carries the worst prognosis
What is the presentation of age related macular degeneration?
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)
Patients often present with a gradually 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.
How do you differentiate between glaucoma and age related macular degeneration
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. This helps you tell them apart in exams.
What are the signs seen in age related macular degneration?
–> distortion of line perception may be noted on Amsler grid testing
–> fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
–> in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
What are the investigations for age related macular degeneration?
Key findings on examination are:
–> 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
–> Slit lamp examination gives a detailed view of the retina and macula.
–> Optical coherence tomography gives a cross-sectional view of the layers of the retina and is used for diagnosing and monitoring AMD.
–> Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.
What is the managment of age related macular degeneration?
Patients with suspected AMD require specialist ophthalmology assessment and management.
There is no specific treatment for dry AMD. Management involves monitoring and reducing the risk of progression by:
Avoiding smoking
Controlling blood pressure
Vitamin supplementation has some evidence in slowing progression
Anti-VEGF medications are used to treat wet AMD (not dry AMD). Vascular endothelial growth factor (VEGF) stimulates the development of new blood vessels in the retina. 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.
What is diabetic retinopathy?
damage to the retinal blood vessels due to prolonged high blood sugar levels
What is the pathophysiology of diabetic retinopathy?
Hyperglycaemia (high blood sugar) damages the retinal small vessels and endothelial cells.
Increased vascular permeability leads to leaking blood vessels, blot haemorrhages and hard exudates. Hard exudates are yellow-white deposits of lipids and proteins in the retina.
Damage to the blood vessel walls leads to microaneurysms and venous beading. Microaneurysms are small bulges in the blood vessel walls. Venous beading is where the walls of the veins are no longer straight and parallel and look more like a string of beads or sausages.
Damage to nerve fibres in the retina causes fluffy white patches called cotton wool spots to form on the retina.
Intraretinal microvascular abnormalities (IRMA) refer to dilated and tortuous capillaries in the retina. These can act as a shunt between the arterial and venous vessels in the retina.
Neovascularisation involves the release of growth factors in the retina, stimulating new blood vessel development.
How is diabetic retinopathy graded?
Diabetic retinopathy is graded based on the findings on fundus examination:
Background – microaneurysms, retinal haemorrhages, hard exudates and cotton wool spots
Pre-proliferative – venous beading, multiple blot haemorrhages and intraretinal microvascular abnormality (IMRA)
Proliferative – neovascularisation and vitreous haemorrhage
Diabetic maculopathy also exists separately and involves:
Exudates within the macula
Macular oedema
The key feature of proliferative diabetic retinopathy is the development of new blood vessels (neovascularisation).
What are the three main classifications of diabetic retinopathy?
Non-proliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), and maculopathy.
What is the defining feature of mild non-proliferative diabetic retinopathy (NPDR)?
The presence of one or more microaneurysms.
What additional features are seen in moderate NPDR compared to mild NPDR?
Microaneurysms, blot haemorrhages, hard exudates, cotton wool spots (retinal infarction), venous beading/looping, and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR.
What criteria define severe NPDR?
Blot haemorrhages and microaneurysms in 4 quadrants.
Venous beading in at least 2 quadrants.
Intraretinal microvascular abnormalities (IRMA) in at least 1 quadrant.
What is the hallmark feature of proliferative diabetic retinopathy (PDR)?
Retinal neovascularisation, which can lead to vitreous haemorrhage.
What other key features are associated with PDR besides retinal neovascularisation?
Fibrous tissue forming anterior to the retinal disc and a higher prevalence in Type 1 diabetes mellitus, with a 50% chance of blindness within 5 years.
What are the characteristic features of diabetic maculopathy?
Hard exudates and other background changes on the macula, with visual acuity needing to be checked.
Which type of diabetes is maculopathy more commonly associated with?
Type 2 diabetes mellitus.
Why is maculopathy considered potentially serious in diabetic retinopathy?
Because it affects the macula, which is critical for central vision.
What are the complications of diabetic retinopathy?
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
What is the mangement of diabetic retinopathy?
Non-proliferative diabetic retinopathy requires close monitoring and careful diabetic control.
Treatment options for proliferative diabetic retinopathy are:
Pan-retinal photocoagulation (PRP) – extensive laser treatment across the retina to suppress new vessels
Anti-VEGF medications by intravitreal injection e.g., ranibizumab
Surgery (e.g., vitrectomy) may be required in severe disease
An intravitreal implant containing dexamethasone is an option for macular oedema.
What is cataracts?
Cataracts describe a progressively opaque eye lens, which reduces the light entering the eye and visual acuity.
What are the risk factors of cataracts?
Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia
What is the presentation of cataracts?
Patients typically present with a gradual onset of:
Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights
Signs:
A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.
What are the investigations for cataracts?
Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve
Slit-lamp examination. Findings: visible cataract
What is the management of cataracts?
No intervention may be necessary if the symptoms are manageable.
Cataract surgery involves drilling and breaking the lens to pieces, removing the pieces and implanting an artificial lens. It can be performed as a day case under local anaesthetic and generally gives good results.
Cataracts can prevent the detection of other pathology, such as macular degeneration or diabetic retinopathy, which can become apparent after surgery. Therefore, they may still have reduced visual acuity after the cataract is treated.
What are the potential complications after cataracts surgery?
Complications following surgery
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour
What is blepharitis?
inflammation of the eyelid margins
What causes blepharitis?
–> Meibomian gland dysfunction - which secrete oil onto the eye surface to prevent rapid evaporation of the tear film
–> RARE - subhorrhoeic dermatitis
–> RARE - staphylococcal infection
