Ophthal Flashcards
Q: What is glaucoma?
A: Glaucoma is a group of disorders characterized by optic neuropathy, primarily due to raised intraocular pressure (IOP). However, a minority of patients with raised IOP do not have glaucoma, and vice versa.
Q: What is acute angle-closure glaucoma (AACG)?
A: AACG is a condition where there is a rise in IOP secondary to impairment of aqueous outflow.
Q: What are the factors predisposing to acute angle-closure glaucoma (AACG)?
A: Factors include hypermetropia (long-sightedness), pupillary dilatation, and lens growth associated with age.
Q: What are the common features of acute angle-closure glaucoma (AACG)?
A: Features include severe ocular pain or headache, decreased visual acuity, symptoms worsened by mydriasis (e.g. watching TV in a dark room), hard, red eye, haloes around lights, semi-dilated non-reacting pupil, corneal oedema resulting in a dull or hazy cornea, and systemic upset such as nausea, vomiting, and abdominal pain.
Q: What investigations are used for acute angle-closure glaucoma (AACG)?
A: Tonometry to assess elevated IOP and gonioscopy to visualize the angle using a special slit lamp lens.
Q: What is the management for acute angle-closure glaucoma (AACG)?
A: AACG is an emergency requiring urgent referral to an ophthalmologist, with medical treatment to lower IOP followed by definitive surgical treatment once the acute attack settles.
Q: What is the definitive management for acute angle-closure glaucoma (AACG)?
A: The definitive treatment is laser peripheral iridotomy, which creates a tiny hole in the peripheral iris to allow aqueous humour to flow to the angle.
Q: What is age-related macular degeneration (ARMD)?
A: ARMD is the most common cause of blindness in the UK, characterized by degeneration of the central retina (macula), often bilateral. It involves degeneration of retinal photoreceptors and the formation of drusen visible on fundoscopy and retinal photography.
Q: What are the risk factors for age-related macular degeneration (ARMD)?
A: Risk factors include advancing age, smoking, family history (especially first-degree relatives), hypertension, dyslipidaemia, and diabetes mellitus.
Q: What is the greatest risk factor for developing ARMD?
A: Advancing age is the greatest risk factor, with the risk increasing threefold in patients over 75 years compared to those aged 65-74.
Q: What are the two traditional classifications of macular degeneration?
A: The two traditional forms are dry macular degeneration (90% of cases) and wet macular degeneration (10% of cases). Dry ARMD is characterized by drusen, while wet ARMD involves choroidal neovascularization and fluid leakage.
Q: What are the clinical features of age-related macular degeneration (ARMD)?
A: Clinical features include subacute onset of visual loss (gradual in dry ARMD and subacute in wet ARMD), difficulties with dark adaptation, fluctuating visual disturbances, photopsia (flickering or flashing lights), glare around objects, and visual hallucinations (Charles-Bonnet syndrome).
Q: How is ARMD detected on fundoscopy?
A: On fundoscopy, drusen (yellow areas of pigment deposition) may be seen in the macular area, which may coalesce to form a macular scar in late-stage disease. In wet ARMD, red patches indicating fluid leakage or hemorrhage may be visible.
Q: What investigations are used to diagnose ARMD?
A: Investigations include slit-lamp microscopy, color fundus photography, fluorescein angiography, indocyanine green angiography, and optical coherence tomography (OCT) for detailed 3D visualization of the retina.
Q: What are the treatment options for dry ARMD?
A: The AREDS trial showed that a combination of zinc and antioxidants (vitamins A, C, and E) reduces disease progression by around one-third in dry ARMD, especially in patients with more extensive drusen.
Q: What is the treatment for wet ARMD?
A: Anti-vascular endothelial growth factor (VEGF) agents like ranibizumab, bevacizumab, and pegaptanib are used to limit progression, stabilize, or reverse visual loss. These agents are typically administered via injection every four weeks.
Q: What role does laser photocoagulation play in ARMD treatment?
A: Laser photocoagulation can slow the progression of wet ARMD where new vessel formation is present but carries a risk of acute visual loss, particularly in sub-foveal ARMD, so anti-VEGF therapies are preferred.
Q: What is allergic conjunctivitis?
A: Allergic conjunctivitis is an eye condition often associated with hay fever, characterized by conjunctival erythema, conjunctival swelling (chemosis), and itchiness.
Q: What are the common features of allergic conjunctivitis?
A: Features include bilateral conjunctival erythema, conjunctival swelling, prominent itching, swollen eyelids, and a possible history of atopy. It may be seasonal (due to pollen) or perennial (due to dust mites, washing powder, or other allergens).
Q: What are the possible causes of seasonal and perennial allergic conjunctivitis?
A: Seasonal allergic conjunctivitis is typically triggered by pollen, while perennial allergic conjunctivitis can be caused by dust mites, washing powder, or other allergens.
Q: What is the first-line treatment for allergic conjunctivitis?
A: The first-line treatment for allergic conjunctivitis is topical or systemic antihistamines.
Q: What is the second-line treatment for allergic conjunctivitis?
A: Second-line treatment includes topical mast-cell stabilizers like Sodium cromoglicate and nedocromil.
Q: What is anterior uveitis (iritis)?
A: Anterior uveitis is inflammation of the anterior portion of the uvea (iris and ciliary body), often referred to as iritis. It is an important differential diagnosis for a red eye and is associated with HLA-B27.
Q: What are the common features of anterior uveitis?
A: Features include acute onset, ocular discomfort and pain (which may increase with use), small and possibly irregular pupil, photophobia (often intense), blurred vision, red eye, lacrimation, ciliary flush (a ring of red spreading outwards), hypopyon (pus and inflammatory cells in the anterior chamber), and initially normal visual acuity that may become impaired.
Q: What is hypopyon?
A: Hypopyon refers to the presence of pus and inflammatory cells in the anterior chamber of the eye, often forming a visible fluid level.
Q: What conditions are associated with anterior uveitis?
A: Anterior uveitis is commonly associated with HLA-B27-linked conditions such as ankylosing spondylitis, reactive arthritis, ulcerative colitis, Crohn’s disease, Behcet’s disease, and sarcoidosis (which may cause bilateral disease).
Q: What is the management for anterior uveitis?
A: Management involves urgent referral to ophthalmology, use of cycloplegics (e.g. atropine, cyclopentolate) to relieve pain and photophobia by dilating the pupil, and steroid eye drops.
Q: What is the Argyll-Robertson pupil (ARP)?
A: The Argyll-Robertson pupil is a classic pupillary syndrome, often seen in neurosyphilis, characterized by small, irregular pupils that do not respond to light but do respond to accommodation.
Q: What is a mnemonic for remembering the characteristics of the Argyll-Robertson pupil?
A: The mnemonic is “Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA),” which highlights the response to accommodation but absence of the pupillary light reflex.
Q: What are the key features of Argyll-Robertson pupil?
A: Features include small, irregular pupils with no response to light but a response to accommodation.
Q: What are the common causes of Argyll-Robertson pupil?
A: Common causes include diabetes mellitus and syphilis.
Q: What is blepharitis?
A: Blepharitis is inflammation of the eyelid margins, caused by either meibomian gland dysfunction (posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (anterior blepharitis). It is more common in patients with rosacea.
Q: What are the common features of blepharitis?
A: Features include bilateral grittiness and discomfort around the eyelid margins, eyes being sticky in the morning, red eyelid margins, swollen eyelids (in staphylococcal blepharitis), increased occurrence of styes and chalazions, and possible secondary conjunctivitis.
Q: What is the management for blepharitis?
Softening the lid margin with hot compresses twice a day.
‘Lid hygiene’ to mechanically remove debris from lid margins, using cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo, or sodium bicarbonate in cooled boiled water.
Artificial tears for symptom relief in patients with dry eyes or abnormal tear film.
Q: What is blurred vision?
A: Blurred vision is defined as a loss of clarity or sharpness of vision. It can be caused by various conditions, and it is important to assess for associated symptoms such as visual loss, double vision, and floaters.
Q: What are the most common causes of blurred vision?
A: The most common causes of blurred vision include refractive error, cataracts, retinal detachment, age-related macular degeneration, acute angle-closure glaucoma, optic neuritis, and amaurosis fugax.
Q: How is blurred vision assessed?
Visual acuity testing with a Snellen chart.
Use of a pinhole occluder to check if the blurred vision improves (indicating a refractive error).
Visual field testing.
Fundoscopy to assess the retina and other structures.
Q: What is the significance of a pinhole occluder in blurred vision assessment?
A: A pinhole occluder is used to check if the blurred vision improves, which would suggest that the cause is likely a refractive error. If it does not improve, other causes should be considered.
Q: What is the management of blurred vision?
If there is gradual onset, improvement with a pinhole occluder, and no associated symptoms, an optician review is recommended.
If there are associated symptoms like visual loss or pain, the patient should be referred urgently to ophthalmology.
Q: What is a cataract?
A: A cataract is a condition where the lens of the eye becomes cloudy, which makes it difficult for light to reach the retina, causing reduced or blurred vision. It is the leading cause of curable blindness worldwide.
Q: What are the common causes of cataracts?
A: The most common cause of cataracts is the normal ageing process. Other possible causes include smoking, increased alcohol consumption, trauma, diabetes mellitus, long-term corticosteroid use, radiation exposure, myotonic dystrophy, and metabolic disorders like hypocalcaemia.
Q: What are the typical symptoms of cataracts?
A: Symptoms include gradual onset of reduced vision, faded color vision, glare (brighter lights), and halos around lights.
Q: What is the significance of a red reflex defect in cataracts?
A: A red reflex defect occurs when cataracts prevent light from reaching the retina, making it impossible to see the normal reddish-orange reflection during ophthalmoscopy.
Q: What are the main types of cataracts?
Nuclear: Common in old age, changes the lens refractive index.
Polar: Localized, inherited, lies in the visual axis.
Subcapsular: Due to steroid use, located just deep to the lens capsule in the visual axis.
Dot opacities: Common in normal lenses, seen in diabetes and myotonic dystrophy.
Q: What is the management for cataracts?
A: Early management involves prescribing stronger glasses/contact lenses and encouraging the use of brighter lighting. Surgery is the only effective treatment, involving removal of the cloudy lens and replacement with an artificial lens.
Q: What factors should be considered before cataract surgery?
A: Prior to surgery, factors such as the presence of visual impairment, the impact on quality of life, patient choice, whether both eyes are affected, and the potential risks and benefits should be considered.
Q: What are the complications following cataract surgery?
A: Complications include posterior capsule opacification (thickening of the lens capsule), retinal detachment, posterior capsule rupture, and endophthalmitis (inflammation of the aqueous and/or vitreous humor).
Q: What is central retinal artery occlusion (CRAO)?
A: CRAO is a rare cause of sudden unilateral visual loss, often caused by thromboembolism (from atherosclerosis) or arteritis (such as temporal arteritis).
Q: What are the key features of central retinal artery occlusion?
A: Features include sudden, painless unilateral visual loss, relative afferent pupillary defect, and a “cherry red” spot on a pale retina.
Q: What is the management for central retinal artery occlusion?
A: Management is difficult, and the prognosis is poor. Any underlying conditions (e.g., temporal arteritis) should be treated, such as with intravenous steroids. In acute cases, intra-arterial thrombolysis may be attempted, but trial results are mixed.
Q: What is central retinal vein occlusion (CRVO)?
A: CRVO is a condition that causes sudden painless loss of vision and is considered a differential diagnosis for such cases.
Q: What are the risk factors for central retinal vein occlusion?
A: Risk factors include increasing age, hypertension, cardiovascular disease, glaucoma, and polycythaemia.
Q: What are the key features of central retinal vein occlusion?
A: Features include sudden, painless reduction or loss of visual acuity (usually unilateral), widespread hyperaemia on fundoscopy, and severe retinal haemorrhages, often described as “stormy sunset.”
Q: What is the difference between central retinal vein occlusion and branch retinal vein occlusion (BRVO)?
A: BRVO occurs when a vein in the distal retinal venous system is occluded due to blockage at arteriovenous crossings, leading to a more limited area of the fundus being affected, unlike the widespread impact seen in CRVO.
Q: What is the management for central retinal vein occlusion?
A: Most patients are managed conservatively. Treatment is indicated in cases of macular oedema (treated with intravitreal anti-VEGF agents) and retinal neovascularization (treated with laser photocoagulation).
Q: What is a corneal abrasion?
A: A corneal abrasion is any defect in the corneal epithelium, commonly caused by trauma such as fingernails or branches.
Q: What are the key features of a corneal abrasion?
A: Features include eye pain, lacrimation, photophobia, foreign body sensation, conjunctival injection, and decreased visual acuity in the affected eye.
Q: How is a corneal abrasion investigated?
A: Investigation involves fluorescein staining, which reveals a yellow-stained abrasion. This can typically be seen with the naked eye and is enhanced with a cobalt blue filter or a Wood’s lamp.
Q: What is the management for a corneal abrasion?
A: Management involves using a topical antibiotic to prevent secondary bacterial infection.
Q: What are the key features of a corneal foreign body?
A: Features include eye pain, foreign body sensation, photophobia, watering eye, and red eye.
Q: When should a patient with a corneal foreign body be referred to ophthalmology?
A: Referral is indicated for suspected penetrating eye injury (from high-velocity injuries or sharp objects), significant orbital or peri-ocular trauma, chemical injuries (after irrigation), foreign bodies made of organic material (such as seeds or soil), foreign bodies near the center of the cornea, or any red flags such as severe pain, irregular or non-reactive pupils, or significant reduction in visual acuity.
Q: What is a corneal ulcer?
A: A corneal ulcer is a defect in the cornea, typically secondary to an infectious cause. Corneal abrasions refer to corneal defects caused by physical trauma.
Q: What are the risk factors for corneal ulcer?
A: Risk factors include contact lens use and vitamin A deficiency (especially in the developing world).
Q: What are the different types of keratitis that can lead to corneal ulcers?
A: Types include bacterial keratitis, fungal keratitis, viral keratitis (such as herpes simplex and herpes zoster, which may lead to a dendritic ulcer), and Acanthamoeba keratitis (associated with contact lens use).
Q: What are the key features of a corneal ulcer?
A: Features include eye pain, photophobia, watering of the eye, and focal fluorescein staining of the cornea.
Q: What is diabetic retinopathy?
A: Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years and results from hyperglycaemia causing retinal damage.
Q: What is the pathophysiology of diabetic retinopathy?
A: Hyperglycaemia causes increased retinal blood flow and abnormal metabolism in retinal vessels, leading to endothelial dysfunction, increased vascular permeability, and microaneurysms. Neovascularisation occurs in response to retinal ischaemia.
Q: How is diabetic retinopathy classified?
A: It is classified into non-proliferative diabetic retinopathy (NPDR), proliferative diabetic retinopathy (PDR), and maculopathy.
Q: What are the stages of non-proliferative diabetic retinopathy (NPDR)?
Mild NPDR: 1 or more microaneurysms
Moderate NPDR: Microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading, and intraretinal microvascular abnormalities (IRMA)
Severe NPDR: Blot haemorrhages and microaneurysms in 4 quadrants, venous beading in 2 quadrants, IRMA in 1 quadrant
Q: What are the features of proliferative diabetic retinopathy (PDR)?
A: PDR features retinal neovascularisation, fibrous tissue forming anterior to the retinal disc, and a higher risk of vitreous haemorrhage. It is more common in Type 1 diabetes and can cause blindness in 50% of patients within 5 years.
Q: What are the key features of maculopathy in diabetic retinopathy?
A: Maculopathy is based on location, often involving hard exudates and background changes on the macula. It is more common in Type II diabetes.
Q: What is the management of diabetic retinopathy?
Optimise glycaemic control, blood pressure, and hyperlipidemia.
Regular ophthalmology reviews.
Maculopathy: Intravitreal VEGF inhibitors if visual acuity changes.
Non-proliferative retinopathy: Regular observation; consider panretinal laser photocoagulation for severe/very severe cases.
Proliferative retinopathy: Panretinal laser photocoagulation, intravitreal VEGF inhibitors (e.g., ranibizumab), and vitreoretinal surgery for severe cases or vitreous haemorrhage.
Q: What is episcleritis?
A: Episcleritis is the acute onset of inflammation in the episclera of one or both eyes, with the majority of cases being idiopathic.
Q: What conditions are associated with episcleritis?
A: Episcleritis is associated with inflammatory bowel disease and rheumatoid arthritis.
Q: What are the key features of episcleritis?
Red eye
Typically not painful (mild irritation or discomfort may occur)
Mild watering and photophobia
The injected vessels are mobile with gentle pressure, differentiating it from scleritis.
Phenylephrine drops can be used to differentiate episcleritis from scleritis. The redness improves with phenylephrine in episcleritis.
Q: How can episcleritis be differentiated from scleritis using phenylephrine?
A: Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine, the diagnosis is episcleritis.
Q: What is the management of episcleritis?
A: The management is typically conservative. Artificial tears may sometimes be used to relieve symptoms.
Q: What are common eyelid problems?
A: Common eyelid problems include blepharitis, stye, chalazion (Meibomian cyst), entropion, and ectropion.
Q: What is a stye (hordeolum)?
A stye is an infection of the glands of the eyelids, and there are two types:
External (hordeolum externum): infection of the glands of Zeis (sebaceous) or glands of Moll (sweat glands).
Internal (hordeolum internum): infection of the Meibomian glands, which may lead to a residual chalazion (Meibomian cyst).
Q: How is a stye managed?
A: Management includes hot compresses and analgesia. Topical antibiotics are only recommended if there is an associated conjunctivitis.
Q: What is a chalazion (Meibomian cyst)?
A: A chalazion is a retention cyst of the Meibomian gland. It presents as a firm, painless lump in the eyelid. Most cases resolve spontaneously, but some require surgical drainage.
Q: What are entropion and ectropion?
Entropion: in-turning of the eyelids.
Ectropion: out-turning of the eyelids.
Q: What is the most common presentation of Herpes simplex keratitis?
A: The most common presentation is a dendritic corneal ulcer.
Q: What are the features of Herpes simplex keratitis?
Red, painful eye
Photophobia
Epiphora (excessive tearing)
Decreased visual acuity
Fluorescein staining may show an epithelial ulcer.
Q: How is Herpes simplex keratitis managed?
Immediate referral to an ophthalmologist
Topical aciclovir.
Q: What is Herpes zoster ophthalmicus (HZO)?
A: Herpes zoster ophthalmicus (HZO) is the reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of shingles cases.
Q: What are the features of Herpes zoster ophthalmicus?
Vesicular rash around the eye, which may or may not involve the eye itself
Hutchinson’s sign: Rash on the tip or side of the nose, indicating nasociliary involvement and a strong risk factor for ocular involvement.
Q: How is Herpes zoster ophthalmicus managed?
Oral antiviral treatment for 7-10 days, ideally started within 72 hours
Intravenous antivirals for very severe infection or if the patient is immunocompromised
Topical antiviral treatment is not given in HZO
Topical corticosteroids for secondary inflammation of the eye
Urgent ophthalmology review if ocular involvement occurs.
Q: What are the complications of Herpes zoster ophthalmicus?
Ocular: Conjunctivitis, keratitis, episcleritis, anterior uveitis
Ptosis
Post-herpetic neuralgia.
Q: What is Holmes-Adie pupil?
A: Holmes-Adie pupil is a benign condition most commonly seen in women, characterized by a dilated pupil that remains small for an abnormally long time after constriction. It is slowly reactive to accommodation but poorly reactive to light.
Q: What is the common presentation of Holmes-Adie pupil?
A: Holmes-Adie pupil is typically unilateral in 80% of cases and features a dilated pupil that constricts slowly and remains small for an abnormally long time after constriction. It is poorly reactive to light but slowly reactive to accommodation.
Q: What is Holmes-Adie syndrome?
A: Holmes-Adie syndrome refers to the association of Holmes-Adie pupil with absent ankle and knee reflexes.
Q: What are the features of Horner’s syndrome?
A: Horner’s syndrome is characterized by miosis (small pupil), ptosis, enophthalmos (sunken eye), and anhidrosis (loss of sweating on one side).
Q: How can heterochromia help in diagnosing Horner’s syndrome?
A: Heterochromia (difference in iris color) is seen in congenital Horner’s syndrome.
Q: What pharmacologic test can help confirm Horner’s syndrome?
A: Apraclonidine drops can be used to confirm the diagnosis of Horner’s syndrome and localize the lesion. They cause dilation in Horner’s syndrome due to denervation supersensitivity but cause constriction in normal pupils.
Q: What are the distinguishing features between central, pre-ganglionic, and post-ganglionic lesions in Horner’s syndrome?
Central lesions: Anhidrosis of the face, arm, and trunk (e.g., stroke, syringomyelia, multiple sclerosis).
Pre-ganglionic lesions: Anhidrosis of the face (e.g., Pancoast’s tumour, thyroidectomy, trauma).
Post-ganglionic lesions: No anhidrosis (e.g., carotid artery dissection, carotid aneurysm, cavernous sinus thrombosis).
Q: What is the cause of enophthalmos in Horner’s syndrome?
A: The appearance of enophthalmos is due to a narrow palpebral aperture rather than true enophthalmos.
Q: What are the features of Stage I hypertensive retinopathy?
A: Stage I features arteriolar narrowing and tortuosity, with an increased light reflex known as silver wiring.
Q: What are the features of Stage II hypertensive retinopathy?
A: Stage II features arteriovenous nipping.
Q: What are the features of Stage III hypertensive retinopathy?
A: Stage III features cotton-wool exudates, flame and blot haemorrhages, which may collect around the fovea, resulting in a “macular star.”
Q: What are the features of Stage IV hypertensive retinopathy?
A: Stage IV features papilloedema.
Q: What is the characteristic discharge in bacterial conjunctivitis?
A: Bacterial conjunctivitis typically presents with a purulent discharge. The eyes may be “stuck together” in the morning.
Q: What is the characteristic discharge in viral conjunctivitis?
A: Viral conjunctivitis typically presents with a serous discharge, often associated with a recent upper respiratory tract infection (URTI) and preauricular lymph nodes.
Q: What is the general management for infective conjunctivitis?
A: Infective conjunctivitis is usually self-limiting and resolves within 1-2 weeks. Topical antibiotic therapy, such as Chloramphenicol drops (2-3 hourly) or ointment (qds), may be offered. Fusidic acid is an alternative, especially for pregnant women (twice daily).
Q: How should contact lens users manage infective conjunctivitis?
A: Contact lens users should avoid wearing lenses during an episode of conjunctivitis. Topical fluorescein can be used to identify corneal staining, and treatment should follow the same guidelines as for other cases.
Q: Is school exclusion necessary for infective conjunctivitis?
A: No, school exclusion is not necessary for infective conjunctivitis.
Q: What is keratitis?
A: Keratitis is inflammation of the cornea, which can be microbial and potentially sight-threatening. It should be urgently evaluated and treated.
Q: What are common bacterial causes of keratitis?
A: Common bacterial causes include Staphylococcus aureus and Pseudomonas aeruginosa (especially in contact lens wearers).
Q: What are some other causes of keratitis?
A: Causes can also include fungal infections, amoebic keratitis (including acanthamoebic keratitis in contact lens users), viral infections (e.g., herpes simplex), environmental factors (e.g., photokeratitis, exposure keratitis), and contact lens-related acute red eye (CLARE).
Q: What are the typical clinical features of keratitis?
A: Clinical features include a red eye, pain and erythema, photophobia, foreign body sensation, gritty feeling, and the presence of hypopyon (pus in the anterior chamber).
Q: What is the management for keratitis in contact lens wearers?
A: Contact lens wearers should stop using lenses until symptoms resolve. Management typically involves topical antibiotics (e.g., quinolones), cycloplegic agents (e.g., cyclopentolate) for pain relief, and urgent referral to an eye specialist for accurate diagnosis.
Q: What are potential complications of keratitis?
A: Potential complications include corneal scarring, perforation, endophthalmitis, and visual loss.
Q: What is mydriasis?
A: Mydriasis refers to the dilation of the pupil (large pupil).
Q: What are common causes of mydriasis?
A: Common causes include third nerve palsy, Holmes-Adie pupil, traumatic iridoplegia, pheochromocytoma, and congenital factors.
Q: What drug causes can lead to mydriasis?
A: Drug causes of mydriasis include topical mydriatics (e.g., tropicamide, atropine), sympathomimetic drugs (e.g., amphetamines, cocaine), and anticholinergic drugs (e.g., tricyclic antidepressants).
Q: What is anisocoria?
A: Anisocoria refers to a condition where there is a difference in size between the two pupils, which may cause apparent mydriasis in one pupil.
Q: What is nasolacrimal duct obstruction?
A: Nasolacrimal duct obstruction is the most common cause of a persistent watery eye in an infant, usually caused by an imperforate membrane at the lower end of the lacrimal duct.
Q: When do symptoms of nasolacrimal duct obstruction typically appear in infants?
A: Symptoms usually appear around one month of age.
Q: How is nasolacrimal duct obstruction managed?
A: Management involves teaching parents to massage the lacrimal duct. Symptoms resolve in 95% of cases by the age of one year.
Q: What should be done if symptoms of nasolacrimal duct obstruction do not resolve by one year?
A: Unresolved cases should be referred to an ophthalmologist for consideration of probing, which is done under a light general anaesthetic.
Q: What is hyphema in the context of ocular trauma?
A: Hyphema is the presence of blood in the anterior chamber of the eye, often due to trauma, and it requires urgent referral to an ophthalmic specialist for assessment and management.
Q: What is the main risk to sight in hyphema?
A: The main risk is raised intraocular pressure, which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes.
Q: What is the management for hyphema?
A: Strict bed rest is required to prevent the redistribution of blood. High-risk cases may need to be admitted. Even isolated hyphema requires daily ophthalmic review and pressure checks initially as an outpatient.
Q: What should be assessed in cases of ocular trauma besides hyphema?
A: Orbital compartment syndrome, such as secondary to retrobulbar hemorrhage, should also be assessed.
Q: What are the features of orbital compartment syndrome?
A: Eye pain/swelling, proptosis, “rock hard” eyelids, and relevant afferent pupillary defect.
Q: How is orbital compartment syndrome managed?
A: Urgent lateral canthotomy should be performed to decompress the orbit before diagnostic imaging.
Q: What is the most common associated disease with optic neuritis?
A: Multiple sclerosis.
Q: What are some other causes of optic neuritis?
A: Diabetes and syphilis.
Q: What are the key features of optic neuritis?
A: Unilateral decrease in visual acuity over hours or days, poor discrimination of colors (“red desaturation”), pain worse on eye movement, relative afferent pupillary defect, and central scotoma.
Q: What is the diagnostic investigation for optic neuritis?
A: MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases.
Q: What is the management for optic neuritis?
A: High-dose steroids, with recovery usually taking 4-6 weeks.
Q: What is orbital cellulitis?
A: Orbital cellulitis is an infection affecting the fat and muscles posterior to the orbital septum, within the orbit but not involving the globe. It is usually caused by a spreading upper respiratory tract infection from the sinuses.
Q: What is the difference between orbital cellulitis and periorbital (preseptal) cellulitis?
A: Orbital cellulitis is more serious, affecting deeper tissues within the orbit, while periorbital cellulitis is a less severe superficial infection anterior to the orbital septum.
Q: What are the main risk factors for orbital cellulitis?
A: Childhood (mean age of hospitalization 7-12 years), previous sinus infection, lack of Haemophilus influenzae type b (Hib) vaccination, recent eyelid infection or insect bite, ear or facial infection.
Q: What are the key features of orbital cellulitis?
A: Redness and swelling around the eye, severe ocular pain, visual disturbance, proptosis, ophthalmoplegia/pain with eye movements, eyelid edema and ptosis, drowsiness, and nausea/vomiting in severe cases with meningeal involvement.
Q: How can orbital cellulitis be differentiated from preseptal cellulitis?
A: Reduced visual acuity, proptosis, and ophthalmoplegia/pain with eye movements are not consistent with preseptal cellulitis.
Q: What investigations are required for orbital cellulitis?
A: Full blood count (elevated WBC and inflammatory markers), clinical ophthalmological examination (decreased vision, afferent pupillary defect, proptosis), CT with contrast (inflammation of orbital tissues and sinusitis), and blood cultures/microbiological swabs.
Q: What are the most common bacterial causes of orbital cellulitis?
A: Streptococcus, Staphylococcus aureus, and Haemophilus influenzae B.
Q: What is the management for orbital cellulitis?
A: Admission to hospital for IV antibiotics.
Q: What is papilloedema?
A: Papilloedema describes optic disc swelling caused by increased intracranial pressure, and it is almost always bilateral.
Q: What are the key features observed during fundoscopy in papilloedema?
A: Venous engorgement (usually the first sign), loss of venous pulsation, blurring of the optic disc margin, elevation of optic disc, loss of the optic cup, and Paton’s lines (concentric/radial retinal lines cascading from the optic disc).
Q: What is venous engorgement in the context of papilloedema?
A: Venous engorgement is the first sign of papilloedema, seen as dilated retinal veins due to increased pressure in the optic disc.
Q: What are Paton’s lines in papilloedema?
A: Paton’s lines are concentric or radial retinal lines cascading from the optic disc, often seen in papilloedema.
Q: What are the common causes of papilloedema?
A: Space-occupying lesions (neoplastic, vascular), malignant hypertension, idiopathic intracranial hypertension, hydrocephalus, and hypercapnia.
Q: What is posterior vitreous detachment?
A: Posterior vitreous detachment is the separation of the vitreous membrane from the retina, typically due to natural changes in the vitreous fluid with ageing.
Q: What is the epidemiology of posterior vitreous detachment?
A: It occurs in over 75% of people over the age of 65 and is more common in females.
Q: What are the risk factors for posterior vitreous detachment?
A: Aging (as vitreous fluid becomes less viscous) and being highly myopic (near-sighted) due to the longer axial length of the eye.
Q: What are the common symptoms of posterior vitreous detachment?
A: Sudden appearance of floaters, flashes of light, blurred vision, cobweb across vision, and the appearance of a dark curtain descending down vision (indicating possible retinal detachment).
Q: What are the signs of posterior vitreous detachment?
A: Weiss ring (a ring-shaped floater due to detachment of the vitreous membrane around the optic nerve).
Q: How should posterior vitreous detachment be investigated?
A: All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24 hours to rule out retinal tears or detachment.
Q: What is the management for posterior vitreous detachment?
A: It typically does not cause permanent vision loss and symptoms improve over 6 months without treatment. If there is a retinal tear or detachment, surgery may be required.
Q: What is preseptal cellulitis?
A: Preseptal cellulitis is an infection of the soft tissues anterior to the orbital septum, involving the eyelids, skin, and subcutaneous tissue, but not the contents of the orbit.
Q: How is preseptal cellulitis different from orbital cellulitis?
A: Preseptal cellulitis affects the soft tissues in front of the orbital septum, while orbital cellulitis affects the tissues behind the orbital septum and is a much more serious infection.
Q: What is the most common cause of preseptal cellulitis?
A: The infection usually spreads from other nearby sites such as breaks in the skin or local infections (e.g., sinusitis, respiratory tract infections). Common causative organisms include Staphylococcus aureus, Staphylococcus epidermidis, streptococci, and anaerobic bacteria.
Q: What is the typical epidemiology of preseptal cellulitis?
A: It is most common in children, with 80% of patients being under 10 years old and the median age of presentation being 21 months. It is more common in winter due to increased respiratory infections.
Q: What are the common symptoms of preseptal cellulitis?
A: The patient presents with a red, swollen, painful eye of acute onset, often accompanied by fever.
Q: What are the key signs of preseptal cellulitis?
A: Erythema and oedema of the eyelids, partial or complete ptosis, but no orbital signs (such as pain on movement of the eye, proptosis, or visual disturbance) which would suggest orbital cellulitis.
Q: What are the significant differentials for preseptal cellulitis?
A: Orbital cellulitis and allergic reactions.
Q: How is preseptal cellulitis investigated?
A: Blood tests may show raised inflammatory markers, and a swab of any discharge may be taken. Contrast CT of the orbit may be used to differentiate from orbital cellulitis.
Q: How is preseptal cellulitis managed?
A: All cases should be referred to secondary care. Oral antibiotics, typically co-amoxiclav, are often sufficient. Children may require admission for observation.
Q: What complications can arise from preseptal cellulitis?
A: Bacterial infection may spread into the orbit, evolving into orbital cellulitis.
Q: What is the aim of treatment for primary open-angle glaucoma?
A: The aim is to lower intraocular pressure (IOP) to prevent progressive loss of visual field.
Q: What is the first-line treatment for primary open-angle glaucoma according to NICE guidelines?
A: 360° selective laser trabeculoplasty (SLT) for people with an IOP of ≥ 24 mmHg.
Q: How does 360° SLT affect treatment?
A: 360° SLT can delay the need for eye drops and reduce but not completely remove the chance that eye drops will be needed later.
Q: What is the next-line treatment for primary open-angle glaucoma after SLT?
A: Prostaglandin analogue (PGA) eye drops.
Q: What are the other treatments used for primary open-angle glaucoma?
A: Beta-blocker eye drops, carbonic anhydrase inhibitor eye drops, sympathomimetic eye drops, and trabeculectomy for refractory cases.
Q: What is the mode of action of prostaglandin analogues (e.g., latanoprost)?
A: Prostaglandin analogues increase uveoscleral outflow and are administered once daily.
Q: What are the adverse effects of prostaglandin analogues?
A: Brown pigmentation of the iris and increased eyelash length.
Q: What is the mode of action of beta-blockers (e.g., timolol, betaxolol)?
A: Beta-blockers reduce aqueous production.
Q: What are the considerations for beta-blockers in glaucoma treatment?
A: Beta-blockers should be avoided in asthmatics and patients with heart block.
Q: What is the mode of action of sympathomimetics (e.g., brimonidine)?
A: Sympathomimetics reduce aqueous production and increase outflow.
Q: What are the adverse effects and considerations for sympathomimetics?
A: Avoid sympathomimetics if taking MAOIs or tricyclic antidepressants. Adverse effects include hyperaemia.
Q: What is the mode of action of carbonic anhydrase inhibitors (e.g., dorzolamide)?
A: Carbonic anhydrase inhibitors reduce aqueous production.
Q: What are the adverse effects of carbonic anhydrase inhibitors?
A: Systemic absorption may cause sulphonamide-like reactions.
Q: What is the mode of action of miotics (e.g., pilocarpine)?
A: Miotics increase uveoscleral outflow.
Q: What are the adverse effects of miotics?
A: A constricted pupil, headache, and blurred vision.
Q: What are the risk factors for primary open-angle glaucoma (POAG)?
A: Increasing age, genetics (first-degree relatives), Afro-Caribbean ethnicity, myopia, hypertension, diabetes mellitus, and corticosteroids.
Q: At what age does primary open-angle glaucoma (POAG) typically affect individuals?
A: POAG affects <1.5% of individuals under 55 years of age, but up to 10% of individuals over the age of 80 years.
Q: How does primary open-angle glaucoma (POAG) typically present?
A: POAG may present insidiously with features such as peripheral visual field loss (nasal scotomas progressing to tunnel vision), decreased visual acuity, and optic disc cupping.
Q: What are the key features seen in fundoscopy in primary open-angle glaucoma (POAG)?
A: Optic disc cupping (cup-to-disc ratio >0.7), optic disc pallor (optic atrophy), bayonetting of vessels (vessels disappear into the deep cup and re-appear), cup notching (usually inferior), and disc haemorrhages.
Q: How is primary open-angle glaucoma (POAG) diagnosed?
A: Diagnosis is made through investigations such as automated perimetry (visual field testing), slit lamp examination with pupil dilatation, applanation tonometry (IOP measurement), central corneal thickness measurement, and gonioscopy (assessing peripheral anterior chamber configuration).
Q: What is the role of automated perimetry in diagnosing primary open-angle glaucoma (POAG)?
A: Automated perimetry is used to assess visual field and detect peripheral visual field loss, such as nasal scotomas.
Q: What is applanation tonometry used for in diagnosing primary open-angle glaucoma (POAG)?
A: Applanation tonometry is used to measure intraocular pressure (IOP).
Q: Why is central corneal thickness (CCT) measured in primary open-angle glaucoma (POAG)?
A: Central corneal thickness is measured as part of assessing the risk of glaucoma and future visual impairment.
Q: What is gonioscopy used for in diagnosing primary open-angle glaucoma (POAG)?
A: Gonioscopy is used to assess the peripheral anterior chamber configuration and depth to rule out angle-closure glaucoma.
Q: How is the risk of future visual impairment assessed in primary open-angle glaucoma (POAG)?
A: The risk is assessed using factors such as IOP, central corneal thickness, family history, and life expectancy.
Q: What are the key features of acute angle closure glaucoma?
A: Severe pain (ocular or headache), decreased visual acuity, haloes, semi-dilated pupil, and hazy cornea.
Q: What are the key features of anterior uveitis?
A: Acute onset, pain, blurred vision, photophobia, small fixed oval pupil, and ciliary flush.
Q: What are the key features of scleritis?
A: Severe pain (worse on movement) and tenderness, often associated with underlying autoimmune diseases like rheumatoid arthritis.
Q: What are the key features of conjunctivitis?
A: Purulent discharge if bacterial, clear discharge if viral.
Q: What are the key features of subconjunctival haemorrhage?
A: History of trauma or coughing bouts.
Q: What are the key features of endophthalmitis?
A: Red eye, pain, and visual loss, typically following intraocular surgery.
Q: How is a relative afferent pupillary defect (RAPD) detected?
A: By the swinging light test.
Q: What is the key finding in RAPD during the swinging light test?
A: The affected and normal eye appear to dilate when light is shone on the affected eye.
Q: What causes a relative afferent pupillary defect (RAPD)?
Lesions anterior to the optic chiasm, including:
Retina: Detachment
Optic nerve: Optic neuritis (e.g., multiple sclerosis)
Q: Describe the afferent pathway of the pupillary light reflex.
A: Retina → Optic nerve → Lateral geniculate body → Midbrain.
Q: Describe the efferent pathway of the pupillary light reflex.
A: Edinger-Westphal nucleus (midbrain) → Oculomotor nerve.
Q: What is retinal detachment?
A: Retinal detachment occurs when the neurosensory retina separates from its underlying pigment epithelium, potentially leading to permanent visual loss if untreated.
Q: What are risk factors for retinal detachment?
Diabetes mellitus (tractional tears from vitreous humour)
Myopia
Age
Previous cataract surgery (accelerates posterior vitreous detachment)
Eye trauma (e.g., boxing)
Q: What are the clinical features of retinal detachment?
New onset floaters (pigment cells in vitreous space)
Flashes of light (retinal traction)
Sudden, painless, progressive visual field loss described as a “curtain” moving centrally
Reduced peripheral and central visual acuity if macula involved
Relative afferent pupillary defect (RAPD) if optic nerve involved
Q: What fundoscopy findings suggest retinal detachment?
Lost red reflex
Retinal folds appearing pale, opaque, or wrinkled
Small breaks may appear normal
Q: What is the management of suspected retinal detachment?
A: Urgent (<24 hours) referral to an ophthalmologist for slit-lamp examination and indirect ophthalmoscopy.
Q: What is retinitis pigmentosa?
A: Retinitis pigmentosa is a group of inherited retinal diseases that primarily affect the peripheral retina, leading to tunnel vision.
Q: What are the clinical features of retinitis pigmentosa?
Night blindness (often the first sign)
Tunnel vision (due to loss of peripheral retina, occasionally referred to as funnel vision)
Fundoscopy: Black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium
Q: What diseases are associated with retinitis pigmentosa?
Refsum disease: cerebellar ataxia, peripheral neuropathy, deafness, ichthyosis
Usher syndrome
Abetalipoproteinemia
Lawrence-Moon-Biedl syndrome
Kearns-Sayre syndrome
Alport’s syndrome
Q: What are the ocular manifestations of rheumatoid arthritis?
Keratoconjunctivitis sicca (most common)
Episcleritis (erythema)
Scleritis (erythema and pain)
Corneal ulceration
Keratitis
Q: What are the iatrogenic ocular complications associated with rheumatoid arthritis treatment?
Steroid-induced cataracts
Chloroquine retinopathy
Q: What is scleritis?
A: Scleritis is a full-thickness inflammation of the sclera, typically non-infective, causing a red, painful eye.
Q: What are the risk factors for scleritis?
Rheumatoid arthritis (most common)
Systemic lupus erythematosus
Sarcoidosis
Granulomatosis with polyangiitis
Q: What are the features of scleritis?
Red eye
Painful eye (more severe than episcleritis)
Watering and photophobia
Gradual decrease in vision
Q: How is scleritis managed?
Same-day ophthalmologist assessment
Oral NSAIDs (first-line)
Oral glucocorticoids for severe cases
Immunosuppressive drugs for resistant cases or associated systemic disease
Q: What is a squint (strabismus)?
A: Squint (strabismus) is a misalignment of the visual axes, leading to improper coordination between the eyes.
Q: How are squints classified?
Concomitant squint: Due to imbalance in extraocular muscles, with convergent squint being more common than divergent.
Paralytic squint: Due to paralysis of extraocular muscles.
Q: How is a squint detected?
Corneal light reflection test: A light source is held 30cm from the child’s face to check for symmetrical light reflection on the pupils.
Cover test: Child focuses on an object while one eye is covered to observe movement of the uncovered eye.
Q: What is the management for squint?
Referral to secondary care.
Eye patches may help prevent amblyopia by encouraging use of the weaker eye.
Q: What is transient monocular visual loss (TMVL)?
A: TMVL refers to a sudden, transient loss of vision lasting less than 24 hours, often related to vascular causes.
Q: What are common causes of sudden painless loss of vision?
Ischaemic/vascular: Central retinal artery occlusion, central retinal vein occlusion, temporal arteritis.
Vitreous haemorrhage.
Retinal detachment.
Retinal migraine.
Q: How does central retinal artery occlusion present?
A: Presents with afferent pupillary defect and a “cherry red spot” on a pale retina on fundoscopy.
Q: How does central retinal vein occlusion present?
A: Presents with severe retinal haemorrhages on fundoscopy and is associated with conditions like hypertension, glaucoma, and polycythaemia.
Q: How can posterior vitreous detachment be differentiated from retinal detachment and vitreous haemorrhage?
Posterior vitreous detachment: Flashes of light, floaters (temporal side).
Retinal detachment: Dense shadow, curtain effect, central visual loss.
Vitreous haemorrhage: Dark spots, sudden visual loss if large bleed.
Q: What is the management of ischaemic causes like TMVL?
A: Treat as a TIA with aspirin 300 mg and investigate for vascular pathology.
Q: What is tunnel vision?
A: Tunnel vision is the concentric diminution of the visual fields, where peripheral vision is lost while central vision remains intact.
Q: What are the causes of tunnel vision?
Papilloedema
Glaucoma (especially advanced stages)
Retinitis pigmentosa
Choroidoretinitis
Optic atrophy secondary to tabes dorsalis
Hysteria (functional vision loss)
Q: What is vitreous haemorrhage?
A: Vitreous haemorrhage is bleeding into the vitreous humour, often causing sudden painless visual loss, ranging from floaters to complete vision loss.
Q: What are the common causes of vitreous haemorrhage?
Proliferative diabetic retinopathy (over 50%)
Posterior vitreous detachment
Ocular trauma (most common in children and young adults)
Q: What are the symptoms of vitreous haemorrhage?
Painless visual loss or haze (most common)
Red hue in vision
Floaters or dark spots in vision
Q: What investigations are used for vitreous haemorrhage?
Dilated fundoscopy: May reveal haemorrhage in the vitreous cavity
Slit-lamp examination: Shows red blood cells in anterior vitreous
Ultrasound: Rules out retinal tear/detachment
Fluorescein angiography: Identifies neovascularization
Orbital CT: Used if open globe injury is suspected
What are cotton wool spots in diabetic retinopathy
areas of infarction
What are features of ocular migraine
Ocular migraines are more prevalent in children and young adults, which aligns with the age of this patient. Scintillating phenomena are common and patients may describe distortions as shimmering, kaleidoscope or swimming in appearance. In other cases they may have a scotoma or even total monocular visual loss. Crucially these changes develop gradually over at least five minutes and last less than one hour.
Which eye drug can cause eyelashes to lengthen
prostaglandin analogues eg latanoprost
