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Flashcards in Opthamology Deck (38):
1

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

2

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.

3

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.

4

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

5

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.

6

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.

7

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)

8

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

9

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.

10

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

11

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

12

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.

13

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.

14

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.

15

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

16

Describe optic neuritis, it's causes, signs, and management

Causes: MS, syphilis, diabetes, vitamin b12 deficiency drugs e.g. Amiodarone, ethambutol, isoniazid

Symptoms:
-Unilateral loss of acuity occurs over hours or days.
-Colour vision is affected, reds appear less red
-pain, eye movement hurts.
-The pupil shows an afferent defect.
-Disc size is normal in 60%, swollen in 23% and blurred or hyperaemic in 18%

Management:
-recovery is usually over 2-6 weeks
-in acute setting methylprednisolone for 3days is recommended
-Lifetime risk of developing MS is 50% if MRI lesion present and 25% otherwise

17

Describe Horner's syndrome, its features, and some causes

Occurs on disrupting sympathetic fibres, so the pupil is miotic (smaller), and there is partial pots is, and the pupil does not dilate in the dark. Unilateral facial anhydrosis is may indicate a lesion proximal to the carotid plexus.

Features: Miosis, partial ptosis, unilateral facial anhydrosis.

Causes may be differentiated by the presence of heterchromia (Congential Horner’s) and the presence and distribution of anhidrosis:

Anhidrosis of the Face, arms, and trunk (Central Lesions S's) : Stroke (posterior inferior cerebellar artery or basilar artery occlusion), Syringomyelia, Multiple Sclerosis, Tumour, Encephalitis

Anhidrosis of the face (Pre-ganglionic lesions T's): Pancoasts tumour, Thyroidectomy, Traume, Cervical Rib

No anhidrosis (Post-ganglionic lesions C's): Carotid artery dissection, Carotid aneurysm, Carvenous sinus thrombosis, Cluster headache.

18

Describe retinitis pigmentosa, its features, and associated diseases.

This is the most prevalent inherited degeneration in the retina. Due to degeneration of rod photoreceptors. Sporadic types are more common (mostly autosomal recessive, though autosomal dominant types has better prognosis, X-linked is rarest but worst prognosis) Through life, 25% retain the ability to read, with reduced visual fields.

Features:
-initially deceased night vision due to loss of rod photoreceptors
-ring scotoma
-loss of peripheral vision first then central vision due to loss of the peripheral retina.
- Fundoscopy show black bone spicule-shaped pigmentation in the peripheral retina, mottling of retinal pigment epithelium.

Associated disease:
-Refsum disease (Cerebellar ataxia, Peripheral neuropathy, Deafness, ichthysosis)
-Usher Syndrome
-Abetalipoproteinaemia
-Lawrence-Moon-Biedl syndrome
-Kearns-Sayre Syndrome
-Alport's syndrome

19

Describe Retinal detachment, its symptoms, and management

May be rhegmatogenous (Greek for break, occur when retinal tear leads to fluid accumulation and separation of retinal layer), or secondary due to fibrous bands in diabetes or melanoma. May also occur by trauma e.g. Cataract surgery. If a retinal break is identified before a detachment, cryo/laser retinopexy may be preventative

Symptoms: The four 'F's, floaters, flashes, field loss, fall in acuity. It presents painless. Ophthalmoscopy shows grey opalescent retina ballooning forward. Note course of venules and retinal fold.

Management:
-urgent referral for surgery, vitrectm and Gas tamponade or silicone oil.
-Cryotherapy/laser coagulation is used to secure the retina.
-Post-op re-detachment occurs in 5-10%

20

Describe episcleritis and it management

Inflammation below the conjuctiva in the episclera is often seen with an inflammatory nodule. Bilateral in 30%. The sclera may look blue below a focal cone-shaped wedge (with the thin end towards the pupil) of engorged vessels which can be moved over the area unlike in scleritis. The eye aches and is tender, visual acuity is OK.

Management: Topical or systemic NSAIDs

21

Describe scleritis

Rarely the sclera itself may be inflamed and pain is significant. There is generalised inflammation and oedema of the conjunctiva and scleral thinning tends to be due to vasculitis, refer to specialist.

22

Describe blepharitis, symptoms and management.

+/- style, Lid inflammation e.g. Due to staphs, seborrhoeic dermatitis or rosacea.

Symptoms: eyes having burning itching red margins with scales on the lashes.

Management:
-cleaning eye especially crust of lashes, baby shampoo
-fusidic acid, steroid drops, oral doxycycline have a role
-if style hot compresses

23

Describe chronic simple glaucoma, its symptoms, screening, and treatment.

Can lead to blindness and may be asymptomatic and so screening of at risk groups is necessary. If IOP raised life-long follow up needed.

Symptoms: Asymptomatic, Visual field loss, increased cup to disc ratio, scotomata.

Screening if:
-older than 35 with FHx
-Afro-Caribbean
-Myopia
-Diabetic/thyroid eye disease

Screening entails multiple stimulus static visual field screening, documenting optic disc cupping and increased IOP.

Treatment:
-Reduce IOP by 30% of baseline. Surgery if drugs fail
-Prostaglandin analogues (latanoprost) acts to increased uveoscleral outflow, SEs include red eye, iris colour change, periocular skin pigmentation, eyelash growth
-B-blockers (timolol) to decrease production of aqueous. SEs include bradycardia, bronchospasm, dry eyes
-alpha-adrenergic agonists (brimonidine) decreased production of aqueous and increased uveoscleral outflow SEs include lethargy, dry mouth
-Carbonic Anhydrase inhibitors (acetazolamide) decreased production of aqueous SE include lassitude, dyspepsia, Hypokalaemia,
-Miotics (pilocarpine) decrease resistance to aqueous outflow it cause miosis and reduce acuity and brow ache from ciliary muscle spasm.
-Surgery, trabeculectomy s a filtration surgery that establishes a pressure valve at the limbus so aqueous can flow into a conjunctival bleb.

24

Describe Charles Bonnet Syndrome and its risk factors.

Characterised by persistent or recurrent complex hallucinations (usually visual or auditory) occurring in clear consciousness. This is usually against a background of visual impairment. In sight is usually preserved. Must occur in absent of any other significant neuropsychiatric disturbance.

Risk factors: Advanced age, peripheral visual impairment (ARMD, Glaucoma, cataract), social isolation, sensory deprivation, early cognitive impairment.


25

Describe Oculogyric crisis, it's causes, symptoms, and management.

A dystonias reaction to certain drugs or in medical condition characterised by prolonged involuntary upward deviation of the eyes.

Causes:
-Drugs e.g. Neuroleptics, carbamazepine, cisplatin, levodopa, lithium, Nifedipine, metoclopramide, domperidone, certirizine.
-Tourette's syndrome, MS, Neurosyphilis, Trauma, Parkinson's, Kernicterus.

Symptoms: restlessness, agitation, malaise, extreme sustained upward deviation of the eyes, widely opened mouth with tongue protrusion, ocular pain.

Management:
-IV antimuscarinic e.g. Procyclidine usually effect within 5-30 minutes.

26

Describe Keratoconus, it's symptoms, and management.

The cornea bulges and becomes conical in shape on lateral viewing due to corneal thinning. More common in people with allergic disease, Down's, Connective tissue disorders

Symptoms: visual distortion, causes multiple 'ghost' images, photophobia, Fleischer rings due to haemosiderin deposition.

Management:
-Rigid Gas Permeable contact lenses, to correct vision.
-refer to ophthalmology for monitoring
-if severe deterioration Corneal cross-linking if under 35yrs.

27

Describe Blepharospasm, it's symptoms, and management

Involuntary contraction of the orbicularis oculi. Stress is an important exacerbating factor. May be caused by neuroleptic drugs, Parkinson's disease, progressive supra nuclear palsy, paraneoplastic or idiopathic.

Symptoms: Tight eyes, often preceded by exaggerated blinking. Other dystonias may be present. Usually starts unilaterally becoming bilaterally.

Management:
-Botulinum neurotoxin

28

Describe One and a Half syndrome and its causes.

A movement weakness in both eyes in which one cannot move laterally at all and the other can move in only one lateral direction, more formally a conjugate horizontal gaze palsy in one direction and an internuclear ophthalmoplegia in the other.

Causes: Pontine haemorrhage, ischaemia, tumours, infective mass lesions such as tuberculomas and MS.

29

What the features of Vitamin A deficiency?

1. Night blindness
2. Tunnel vision
3. Poor acuity
4. Dry conjunctivae (xerosis)
5. Bitot spots (small foamy plaques)

30

Describe optic atrophy and its causes.

Seen as pale, well demarcated disc on fundoscopy. It is usually bilateral and causes a gradual loss of vision.

Acquired Causes:
-Multiple Sclerosis
-longstanding papilloedema
-raised intraocular pressure (e.g. Glaucoma, tumour)
-retinal damage (e.g. Choroidits, retinitis pigmentosa)
-Ischaemia
-Toxins e.g. Tobacco amblyopia, quinine, methanol, arsenic, lead
-nutritional e.g. Vitamin B1,B2,B6 and B12 defiency

Congenital Causes:
-Friedreich's ataxia
-Mitochondrial disorders e.g. Leber's optic atrophy
-DIDMOAD (cranial Diabetes Insipidus, Diabetes Mellitus, Optic Atrophy and Deafness) aka Wolfram's Syndrome

31

Describe Angioid Retinal Streaks and their causes.

Seen on fundoscopy as irregular dark red streak radiating from the optic nerve head. They are caused by degeneration, calcification and breaks in Bruch's membrane.

Causes:
-Pseudoxanthoma elasticum
-Ehler-Danlos syndrome
-Paget's disease
-Sickle-cell anaemia
-acromegaly

32

What is pseudophakia?

The term refers to having an artificial lens implanted after the natural eye lens has been removed e.g. Cataract surgery

33

Describe Cornea Verticillata and its associations

A condition characterised by corneal despots at the level of the basal epithelium forming a faint golden-brown whorl pattern.

Associations:
It is seen in Fabry disease or incase of prolonged amiodarone intake.

34

Describe Usher Syndrome and its features

A rare autosomal recessive disorder caused by a mutation in any one of at least 11 genes resulting in a combination of hearing loss and visual impairment. It is a leading cause of deaf blindness.

35

Describe Vitreous Haemorrhage, its features, and management.

One of the most common causes of sudden painless visual loss. Degree of visual loss varies from haziness and floaters to complete obscuration. Most commonly underlying causes are proliferative diabetic retinopathy, posterior vitreous detachment, ocular trauma.

Features: Sudden painless visual loss, red hue, floaters and cobwebs, symptoms may be worse in the morning.

Management:
-Emergency referral to ophthalmologist
-Ofter clears in days to weeks to allow evaluation of retina.
-Ultrasonography to r/o retinal detachment.
-Laser photocoagulation in proliferative vasculopathies.
-Anterior retinal cryotherapy has been used in fresh vitreous haemorrhage to cause break down of blood-retinal barrier which interns leads to clearance of liquefied blood.
-Vitrectomy if underlying pathology is likely to progress fast. e.g. retinal tears or when the retina can't be visualised.
-Intravitreal anti-VEGF agents are used in proliferative vasculopathies particularly if there is no view allowing photocoagulation.

36

Describe Ocular Ischaemic syndrome and its features.

A rare constellation of ocular signs and symptoms secondary to severe, chronic arterial hypoperfusion to the eye. Usually caused by severe ipsilateral or bilateral carotid artery stenosis, also associated with Takyasu’s, GCA.

Features: Vision Loss, dull ache.

37

Describe Holmes-Adie Pupil.

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.

38

Describe Rubeosis Iridis, its features.

Aka Neovascularisation of the iris. Associated with the disease processes of the retina, which involve ischaemia and release of VEGF.

Can be treated wit panretinal photocoagulation, or infection of anti-VEGF medications.