Opthamology Flashcards
Describe Acute Closed-angle Glaucoma, its symptoms, its cause, and management
A disease of middle years, in 25% acute uniocular attacks occur with headache, nausea and a painful red eye, often preceded by blurred vision or haloes around lights, at night.
Symptoms: Clouding (dull) of cornea, ciliary injection, large to cup to disc ratio. Unreactive partially dilated pupil
Cause: blocked flow of aqueous fro the anterior chamber via the canal of schlemn. Pupil dilatation at night worsens this. Intra-ocular pressure then rises to over 30mmHg (normal 15-20) the pupil becomes fixed and dilated and axonal death occurs.
Management:
- Pilocarpine 2-4% drops/2h (miosis opens a blocked ‘closed’ drainage angle, + 500mg IV acetazolamide stat then 250mg/8h PO/IV (to decrease aqueous formation).
- analgesia and antiemetics may be used.
- Admit to monitor IOP.
- Peripheral iridectomy is done once IOP is controlled
Describe Age-Related Macular Degeneration, its types, risk factors, features, investigations, and treatment
It is the chief cause of registrable blindness, it occurs in elderly who present with deteriorating central vision. There is pigment, drusen and sometimes bleeding at the macula.
Can be classified into two types:
- Dry ARMD, shows mainly drusen and degenerative changes at the macular and progresses slowly.
- Wet ARMD, occurs when aberrant vessels grow from the choroid into the neuro-sensory retina and leak. Vision detioriates rapidly and visual distortion e.g. straight lines appearing wavy is a key feature.
Risk factors: Age over 60, Smoking, FH, Caucasian, High cumulative sunlight exposure, Female
Features:
- Reduced visual acuity e.g. blurred distorted vision. Central vision affected first. Straight lines appear crooked or wavy
- Central scotomas
- Fundoscopy may show druse or pigmentary changes.
Investigations:
- Optical Coherence Tomography: Provide cross-sectional views of the macula
- If neovascularisation is present fluorescein angiography is performed.
Treatment:
- Patients are advised to stop smoking and have a diet rich in green vegetables.
- Intravitreal vascular endothelia growth factor (VEGF) inhibitors (bevacizumab aka avastin, ranibizumab) may be used in wet ARMD to increase acuity, decrease cell proliferation and formation of new blood vessels.
Describe cataracts, its presentation, treatment, and post-op complications.
Cloudy patches that develop in the lens of the eye. When a cataract is found measure fasting plasma glucose to exclude DM. Immature cataracts red reflex is intact.
Presentation: Blurred vision, unilateral cataracts are often unnoticed, but loss of stereopsis affects distance judgement. Bilateral cataracts cause gradual loss of vision +/- dazzle/glare.
Treatment:
- Mydriatic drops (atropine), sunglasses, but if symptoms are troubling or lifestyle/driving restricted offer surgery.
- Surgery involves ideally local (general if young, squeamish), small-incision surgery and phacoemulsion +/- intraocular lens implant.
- Antibiotic and anti-inflammatory drops 3-6weeks post-op.
Post-op Complications: capsule thickening requiring capsulotomy, astigmatism, eye irritation, anterior evitis, vitreous haemorrhage, retinal detachment, glaucoma.
Describe Orbital Cellulitis, its presentation, causes, and its management.
Spread is typically via paranasal sinus infection (or eyelid, dental injury/infection).
Presentation: A child with inflammation in the orbit, fever, lid swelling, and decrease eye mobility.
Causes: staphs, Strep Pneumoniae, Strep Pyogenes, or Milleri.
Management:
- Admit for prompt, CT, ENT and ophthalmic opinion + antibiotics +/- surgery to prevent extension to meninges or cavernous sinus.
- Blindness is a risk from pressure on the optic nerve or thrombosis of its vessels. Rule out underlying rhabdomyosarcoma
What is the principle behind Panretinal Photocoagulation treatment in proliferative retinopathy?
Reduces the number of hypoxic peripheral retinal cells producing VEGF. This reduces overall oxygen consumption of the retina and the balance between oxygen supply and demand is reestablished. This causes new blood vessels to regress. The main side effects thus is poor peripheral vision and poor night vision due to rod destruction.
What is Presbyopia and briefly describe the mechanism
Age-related reduced near-acuity due to failing accommodation. The ciliary muscle reduces tension in the lens, allowing it to get more convex, for close focusing. Young lenses can go from far to near in 0.4s. With age, the lens stiffens and hence the need for glasses for reading. These changes start in the lens at 40yrs and are complete by 60yrs.
Describe Giant Cell Arteritis, its presentation, tests, and management
Large vessel Vasculitis, common in the elderly (consider takaysu’s if under 55yrs) associated with Polymylagia Rheumatica (PMR).
Presentation: headache, temporal artery and scalp tenderness, jaw claudication, amaurosis fugax or sudden blindness.
Test: increased ESR (typically over 47) + CRP (typically greater than 2.45mg/dL), increased platelets, increased ALP and decreased Hb.
Management:
- Immediate Prednisolone 80mg/d PO due to risk of irreversible blindness.
- Temporal biopsy within 7 days of steroids (beware skip lesions)
Describe Diabetic Retinopathy, pathogenesis, signs, types, and management.
Pathogenesis is through microangiopathy in capillaries, precapillary arterioles and venules which causes occlusion +/- leakage. Diabetics should be regularly screened and assessed for any diabetic retinopathy.
Pathogenesis: vascular occlusion causes ischaemia +/- new vessels in the retina, optic disc, and iris i.e. Proliferative retinopathy. New vessels are leaky and may bleed causing vitreous haemorrhage.
Signs:
- Cotton wool spots which are ischaemic nerve fibres due to occlusion.
- microaneurysms, oedema and hard exudate due to pericyte loss causing capillaries to bulge and leak.
- blot haemorrhages due to rupture of microaneurysms at the nerve fibre level causing flame shaped haemorrhages.
Types:
- Non-proliferate diabetic retinopathy e.g. Signs include micro aneurysms, blot haemorrhages, hard exudates (yellow patches), engorged tortuous veins, cotton wool spots, large blot haemorrhages (the late 3 are signs of significant ischaemia)
- preproliferative diabetic retinopathy e.g. Venous beading, venous loops, multiple deep round blot haemorrhages.
- proliferative diabetic retinopathy e.g. Fine new vessels appear on the optic disc, retina and can cause vitreous haemorrhage
- maculopathy e.g. Leakage of vessels close to macula cause oedema and can significantly threaten vision
Management:
- Those with severe NPDR, proliferative, or ,maculopathy need urgent assessment and treatment.
- good control of diabetes is treatment of choice
- pan-retinal photocoagulation is treatment occasionally anti-VEGF may be used in macular oedema.
- vitreous haemorrhage may require vitrectomy if does not clear
Describe the pupillary light reflex and accomodation reflex, and describes some of the eponymous pupillary defects.
Light detection by the retina is passed to the brain via the optic nerve (afferent pathway) and pupil constriction is mediated by the Oculomotor nerve (efferent pathway). The sympathetic nervous system is responsible for pupil dilatation via the ciliary nerves.
Accomodation reflex, pupils focussing on the distance will be dilated and pupils will constrict on near vision.
RAPD (Marcus-Gunn pupil): On beaming a light to the normal eye, both pupils constrict ( direct and consensual reaction) if on swinging the light to the affected eye the pupil dilates as it has an afferent lesion causes include Optic neuritis, optic atrophy and retinal disease.
Holmes-Adie pupil: A benign lesion typically in females, unilateral in 80%. A dilated pupil which constricts to light but remains constricted for longer. Holmes-Adie syndrome is the above with absent knee/ankle reflexes.
Argyll-Robertson: miotic irregular pupils which the Accomodation Reflex is present but light reflex is absent. Causes include neurosyphillis and Diabetes mellitus.
What are some causes of a fixed dilated pupil?
- IIIrd nerve lesion i.e. Cavernous sinus lesion, superior orbital fissure syndrome, diabetes, posterior communicating artery aneurysm
- mydriatics
- trauma e.g. Blow to iris
- acute glaucoma
- coning i.e uncal herniatiom
Describe Central Retinal Vein Occlusion (CRVO), its causes/associations, symptoms, and management.
It is commoner than arterial occlusion. Incidence increases with age.
Causes/associations: Arteriosclerosis, hypertension, diabetes, polycythaemia, glaucoma.
Symptoms: Unilateral painless visual loss, it is less sudden than arterial occlusion. Fundoscopy shows stormy sunset appearance, with swollen optic disc, flame-like haemorrhages.
Management:
- refer within 24hrs to ophthalmology
- if ischaemia anti-VEGF and panretinal photocoagulation may have a role
- monitor non-ischaemic as may progress
Describe Central Retinal Artery Occlusion (CRAO), its symptoms, and management
Occlusion is often thrombo-embolisation i.e. From clot, tumour, infective.
Symptoms: Sudden, unilateral, painless visual loss within seconds of occlusion. In 90% visual acuity is finger-counting or worse. Retina appears white with a cherry red spot at the macula.
Management:
- exclude temporal arteritis
- look for signs of cause
- if seen with 6h aim to increase retinal blood flow by reducing ocular pressure.
Describe blind registration
A person is eligible to register as blind if their acuity is less than 3/60 or higher but with substantial visual field loss i.e. Glaucoma. Those greater than this but less than 6/60 can register as partially sighted.
It is the responsibility of the local authority. Application is made by consultant ophthalmologist and is voluntary, not statutory.
Registering as blind entitles one to extra tax allowances, reduced TV licences, travel concession, access to talking books.
The Royal National Institute for the Blind will advise on aids, such as guide dogs.
Describe Anterior uveitis, it symptoms, causes, tests, and management
The uvea is the pigmented part of the eye (iris, ciliary body, choroid). The iris and ciliary body make up the anterior uvea.
Symptoms: Acute, painful red eye, photophobia, decreased acuity (due to aqueous precipitates), lacrimation (no sticky discharge unlike conjunctivitis), circumcorneal congestion (ciliary congestion), small pupil though may also be irregular or partially dilated.
Causes: Ankylosing spondylitis, stills, sarcoid, behcets, crohns, UC, herpes, TB, syphilis, HIV MS, lymphoma
Tests: Talbot’s test is +ve I.e. Pain increases on convergence as patients watch a finger approach their nose, slit lamp show white precipitates on back of cornea, and anterior chamber cells.
Management:
- Aim to prevent damage from prolonged inflammation as it can lead to disruption of the flow of aqueous and so cause glaucoma +/- adhesions between iris and lens.
- Prednisolone drops 0.5-1%/2h help reduce inflammation
- to prevent adhesions keep dilated wit cyclone tollgate 0.5%/8h unless very mild.
- Intravitreal and biological agents such as anti-TNF show promise adalimumabhas a role.
Describe conjunctivitis, its symptoms, and management.
The conjunctiva (the layer that covers the front of the eye) Is red and inflamed usually due to adenoviruses, bacteria, or allergies.
Symptoms: Red inflamed conjunctiva on palpating of the globe the vessels may be moved over the sclera. Acuity, pupillary responses are unaffected. Eyes itch and burn and lacrimation often with sticky discharge.
Management:
- usually self-limiting
- Chloramphenicol 0.5% drops/4-6h are often used
- try antihistamine drops for allergic conjunctivitis
