Ophthalmology Flashcards
What is glaucoma?
Optic nerve damage caused by rise in intraocular pressure caused by blockage in aqueous humour
Where would you find vitreous humour?
In vitreous chamber of eye
Where would you find aqueous humour?
In the anterior chamber (between cornea and iris) and posterior chamber (between lens and iris) of eye
What is the role of the aqueous humour, where is it produced, and where does it drain?
Supplies nutrients to cornea
Produced by ciliary body
Drains through trabecular mesh work to canal of Schlemm at angle between cornea and iris
What is normal intraocular pressure?
10-21mmHg
Created by resistance to flow through trabecular meshwork
What is the pathophysiology of open angle glaucoma?
Gradual increased in resistance to flow through trabecular moshwork
What is the pathophysiology of acute angle closure glaucoma?
Iris bulges forwards and seals off trabecular mesh work from anterior chamber preventing aqueous humour from draining
Continual build up of pressure and acute onset of symptoms
EMERGENCY
What happens to the optic disc with raised intraocular pressure?
Cupping of optic disc
What are the risk factors for open angle glaucoma?
Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Outline presentation of open angle glaucoma
Affects peripheral vision first, resulting in gradual onset tunnel vision
Fluctuating pain
Headaches
Blurred vision
Halos around lights (particularly at night)
How do you measure intraocular pressure?
Non-contact tonometry- Puff of air at cornea and measures response
Goldmann applanation tonometry (gold standard)- Lamp applies pressure to cornea
How is open angle glaucoma diagnosed?
Goldmann applanation tonometry
Slit lamp to assess cup-disc ratio and optic nerve health
Visual field assessment
Gonioscopy (assess angle between iris and cornea)
Central corneal thickness
Outline management of open angle glaucoma
Started at IO pressure >24mmHg
360 degree selective trabeculoplasty
Prostaglandin analogue eye drops (latanoprost)- Increase uveoscleral outflow
BB eye drops (timolol)- Reduce production of aqueous humour
Carbonic anhydride inhibitors (dorzolamide)- Reduce production of aqueous humour
Sympathomimetics (brimonidine)- Reduce production of aqueous fluid and increase uveoscleral outflow
Trabeculectomy- If other treatment ineffective- Creates bleb
What are the side effects of prostaglandin analogue eye drops (latanoprost)?
Eyelash growth
Eyelid pigmentation
Iris pigmentation (browning)
What is acute angle closure glaucoma?
Iris bulges forward and seals off trabecular mesh work from anterior chamber, preventing aqueous humour draining, leading to continual increase in IO pressure
Pressure builds in posterior chamber, pushing iris forward and exacerbating angle closure
EMERGENCY
What are the risk factors for acute angle closure glaucoma?
Increasing age
Family history
Female (4x more likely)
Chinese and East Asian ethnic origin
Shallow anterior chamber
Which medications can precipitate acute angle closure glaucoma?
Adrenergic meds (noradrenaline)
Anticholinergic meds (oxybutynin and solifenacin)
TCAs (amitriptyline)
How does acute angle closure glaucoma present?
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
List signs on examination of acute angle closure glaucoma
Red eye
Hazy cornea
Decreased visual acuity
Mid dilated pupil
Fixed size pupil
Hard eyeball on gentle palpation
What is the initial management of acute angle closure glaucoma?
Lie patient on back without pillow
Pilocarpine eye drops (2% for blue, 4% for brown)
Acetazolamide 500mg orally
Analgesia and antiemetic if required
How does pilocarpine work?
Acts on Muscarinic receptors in sphincter muscles in iris and causes pupil constriction (miosis) and ciliary muscle contraction
Opens pathway for flow of aqueous humour from ciliary body around iris and into trabecular meshwork
How does Acetazolamide work?
Carbonic anhydride inhibitor
Reduces production of aqueous humour
What is the definitive treatment of acute angle closure glaucoma?
Laser iridotomy
Hole in iris with laser
What is age-related macular degeneration?
Progressive condition affecting macula
Most common cause of blindness
2 types- Wet and dry
What is the most common type of age related macular degeneration?
Dry
What is the difference between wet and dry AMD?
Dry- No Neovascularisation (90%)
Wet- Neovascularisation (10%)
What is the function of the macula?
Found in centre of retina
Generates high definition colour vision in central visual field
What are the 4 layers of the macula?
Choroid- Base layer, contains blood vessels that supply the macula
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors
Which condition are Drusen associated with?
AMD
Deposits of proteins and lipids between retinal pigment epithelium and Bruchs membrane
What are frequent and large Drusen a sign of?
Early sign of AMD
What features are common on ophthalmoscope of AMD?
Atrophy of retinal pigment epithelium
Degeneration of photoreceptors
Drusen
What is the chemical that stimulates development of new vessels?
Vascular endothelial growth factor (VEGF)
What are the risk factors for AMD?
Old age
Smoking
FHx
CVD (eg: HTN)
Obesity
Poor diet (low in vitamins, high in fat)
Outline presentation of AMD
Unilateral
Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphosia)
Gradually worsening ability to read small text
What is the difference in presentation of wet and dry AMD?
Wet- More acute presentation- Vision loss can develop within days and progress to complete vision loss in 2-3y- Often progresses to bilateral disease
What are the examination findings in AMD?
Reduced visual acuity on snellen chart
Scotoma (enlarged central area of vision loss)
Amsler grid test (assesses distortion on straight lines)
Drusen on fundoscopy
What is used to diagnose AMD?
Slit lamp- Detailed view of retina and macula
Optical coherence tomography- Cross section of layers of retina- Used for diagnosis and monitoring
Fluorescein angiography- Photographs retina to assess blood supply- Shows oedema and Neovascularisation in wet AMD
Outline management of dry AMD
Avoid smoking
Control BP
Vit supplements
Outline management of wet AMD
Anti-VEGF meds- Ranibizumab, aflibercept, bevacizumab- Block VEGF and slow development of new vessels
Inject directly into vitreous chamber once a month
What is diabetic retinopathy?
Damage to retinal blood vessels due to prolonged high blood sugar levels
Outline the management of non-proliferative diabetic retinopathy
Close monitoring
Diabetic control
Outline management of proliferative diabetic retinopathy
Pan-retinal photocoagulation- Extensive laser treatment to suppress new vessels
Anti-VEGF
Virectomy
What is a treatment option for macular oedema?
Intravitreal implant containing dexamethasone
List complications of diabetic retinopathy
Vision loss
Retinal detachment
Vitreous haemorrhage
Rubeosis iridis (new blood vessel formation in iris)- Can lead to Neovascular glaucoma
Optic neuropathy
Cataracts
What is diabetic maculopathy?
Exudates within macula
Macular oedema
Outline grading of diabetic retinopathy
Background- Microaneurysms, retinal haemorrhages, hard exudates, cotton wool spots
Pre-proliferative- Venous bleeding, multiple blot haemorrhages, intraretinal micro vascular abnormality (IMRA)
Proliferative- Neovascularisation and vitrous haemorrhage
Outline pathophysiology of diabetic retinopathy
Hyperglycaemia damages retina, small vessels and endothelial cells
Increased vascular permeability = Leaky blood vessels, blot haemorrhages and hard exudates (yellow/white deposits of lipids and proteins in retina)
Damage to blood vessels leads to Microaneurysms and venous beading
Damage to nerve fibres in retina= Cotton wool spots
IMRA- Dilated and tortuous capillaries in retina- Act as shunt between arterial and venous vessels in retina
Neovascularisation- Release of growth factors into retina, new blood vessel development
What is management of hypertensive retinopathy?
Control BP and manage risk factors