Ophthalmology Flashcards

Question

strabismus

Answer 1

Any complaint of a 'turning eye' should be taken seriously even if this cannot be reproduced in a consultation, as the squint may be intermittent. Intermittent deviation of the eyes is common in healthy neonates and should not cause undue concern in an otherwise healthy baby. However, any constant squint, even in neonates, is significant. Normal binocular coordination is established at about 3 months, and any squint after this age is significant use corneal light reflex, cover, and cover/uncover tests Assess for the presence of the red reflex and exclude leukocoria (white or grey pupil) Squints that may give rise to particular concern about the underlying cause include: Constant unilateral exotropias. Any acquired incomitant squint. Sudden, late-onset (over 3–4 years) esotropia, particularly if there is no family history and no significant hypermetropia Refer any child with a suspected or confirmed squint to the local paediatric eye service. A routine referral is indicated for most children. However, the earlier treatment for a squint can be initiated, the better the outcome to prevent amblyopia Urgent referral if red flags which include: Limited abduction. Double vision. Headaches. Nystagmus a child with acquired strabismus or reduced vision may have a primary neurological disorder such as optic nerve glioma, medulloblastoma, craniopharyngioma or hydrocephalus. This is more likely in the presence of features such as persistently reduced visual acuity, resistant to amblyopia therapy, deteriorating visual acuity or an ocular muscle under action. A careful examination should be performed to exclude an afferent pupil defect, papilloedema, optic atrophy or other cranial nerve abnormality. The finding of any abnormal neurological signs should prompt referral to a paediatrician +/- MRI In many cases, the management of strabismus in children commences with glasses to address any refractive error leading to squint; In all forms of esotropia, full correction of hypermetropia is the treatment of choice, leaving it uncorrected might help in exotropia; A period of refractive adaption is recommended after glasses have been prescribed which may be followed by occlusive therapy managed by orthoptist botulinum injections and surgical correction are later mx steps

Answer 2

amblyopia refers to the reduction of best-corrected visual acuity (BCVA ie glasses worn if required) in one or both eyes that cannot be exclusively attributed to a structural abnormality of the eye It is often referred to as ‘lazy eye’. This is usually a result of an interruption in the visual development during early childhood, from birth to seven years can be caused by strabismus, hyperetropia, myopia, astigmatism, obstacle obscuring vision (cataract, ptosis, haemangioma etc) Glasses will be prescribed if there is any significant long or short sightedness, or astigmatism; if the vision remains reduced in the “lazy” eye after glasses have been worn for up to 16 weeks, the usual treatment for amblyopia is to wear a patch over the good eye that will, in turn, stimulate the vision in the poorer sighted eye Occasionally atropine drops/ointment may be used in the good eye instead. This blurs the vision in the good eye and encourages the vision in the weaker eye to develop. This treatment is usually only used if patching fails.

Answer 3

a. acute angle closure glaucoma b. (infective) endophthalmitis c. orbital cellulitis d. trauma i. corneal abrasion ii. corneal / subtarsal foreign body iii. hyphaema iv. chemical injury v. penetrating eye injury e. “-itises” i. conjunctivitis (viral, bacterial or allergic) ii. anterior uveitis iii. keratitis (herpetic or bacterial) iv. scleritis endophthalmitis is rare, usually days to weeks postop (for eg cornea) or post trauma; generally if the globe has opened creating a path for infection; pain, red eye, dec'd vision, quite sudden; acute needs emergency admission; vitreous antibiotics needed

Answer 4

severe pain: may be ocular or headache decreased visual acuity symptoms worse with mydriasis (e.g. watching TV in a dark room) hard, red-eye haloes around lights semi-dilated non-reacting pupil corneal oedema results in dull or hazy cornea systemic upset may be seen, such as nausea and vomiting and even abdominal pain an emergency and should prompt urgent referral to an ophthalmologist. no guidelines for the initial medical treatment emergency treatment. An example regime would be: combination of eye drops, for example: a direct parasympathomimetic (e.g. pilocarpine, causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour) a beta-blocker (e.g. timolol, decreases aqueous humour production) an alpha-2 agonist (e.g. apraclonidine, dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow) intravenous acetazolamide reduces aqueous secretions Definitive management laser peripheral iridotomy

Answer 5

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 and carries a high mortality rate. Orbital cellulitis is a medical emergency requiring hospital admission and urgent senior review. periorb cellulitis can progress to orbital cellulitis; also this is mostly kids, mean age 7-12yo; periorb cellulitis, ear/face infection, sinus infection, lack of HiB vaccine are risk factors Presentation Redness and swelling around the eye Severe ocular pain Visual disturbance Proptosis Ophthalmoplegia/pain with eye movements Eyelid oedema and ptosis Drowsiness +/- Nausea/vomiting in meningeal involvement (Rare) Differentiating orbital from preseptal cellulitis reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements are NOT consistent with preseptal cellulitis Investigations Full blood count – WBC elevated, raised inflammatory markers. Clinical examination involving complete ophthalmological assessment – Decreased vision, afferent pupillary defect, proptosis, dysmotility, oedema, erythema. CT with contrast – Inflammation of the orbital tissues deep to the septum, sinusitis. Blood culture and microbiological swab to determine the organism. Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B. Management admission to hospital for IV antibiotics

Answer 6

Hyphema (blood in the anterior chamber of the eye) - especially in the context of trauma warrants urgent referral to an ophthalmic specialist for assessment and management. The main risk to sight comes from raised intraocular pressure which can develop due to the blockage of the angle and trabecular meshwork with erythrocytes. Strict bed rest is required as excessive movement can redisperse blood that had previously settled; therefore high-risk cases are often admitted. Even isolated hyphema will require daily ophthalmic review and pressure checks initially as an outpatient

Answer 7

foreign body: Features eye pain foreign body sensation photophobia watering eye red eye Indications for referral to ophthalmology Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns) Significant orbital or peri-ocular trauma has occurred. A chemical injury has occurred (irrigate for 20-30 mins before referring) Foreign bodies composed of organic material (such as seeds, soil) should be referred to ophthalmology as these are associated with a higher risk of infection and complications Foreign bodies in or near the centre of the cornea Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity corneal ulcer: more common in contact lens users Features eye pain photophobia watering of eye focal fluorescein staining of the cornea

Answer 8

allergic: may occur alone but is often seen in the context of hay fever Features Bilateral symptoms conjunctival erythema, conjunctival swelling (chemosis) Itch is prominent the eyelids may also be swollen May be a history of atopy May be seasonal (due to pollen) or perennial (due to dust mite, washing powder or other allergens) Management of allergic conjunctivitis first-line: topical or systemic antihistamines second-line: topical mast-cell stabilisers infective: most common eye problem presenting to primary care. It is characterised by sore, red eyes associated with a sticky discharge bacti is purulent, eyes may be stuck together; viral has serous discharge, maybe recent urti and preauric lymph nodes mx: normally a self-limiting condition that usually settles without treatment within 1-2 weeks topical antibiotic therapy is commonly offered to patients, e.g. Chloramphenicol. Chloramphenicol drops are given 2-3 hourly initially where as chloramphenicol ointment is given qds initially topical fusidic acid is an alternative and should be used for pregnant women. Treatment is twice daily contact lens should not be worn during an episode of conjunctivitis advice should be given not to share towels school exclusion is not necessary

Answer 9

epi: red eye classically not painful (in comparison to scleritis), but mild pain may be present watering and mild photophobia may be present in episcleritis, the injected vessels are mobile when gentle pressure is applied on the sclera. In scleritis, vessels are deeper, hence do not move phenylephrine drops may be used to differentiate between episcleritis and scleritis. Phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels. If the eye redness improves after phenylephrine a diagnosis of episcleritis can be made Approximately 50% of cases are bilateral. Management conservative artificial tears may sometimes be used scleritis: red eye classically painful (in comparison to episcleritis), but sometimes only mild pain/discomfort is present watering and photophobia are common gradual decrease in vision associated with autoimmune, msk conditions, hla-B27 conditions, TB, local infection spread from corneal ulcer should be referred to optho, cause will be identified and managed as well as NSAIDs given

Answer 10

inflammation of the anterior portion of the uvea - iris and ciliary body. It is associated with HLA-B27 and may be seen in association with other HLA-B27 linked conditions (see below). Features acute onset ocular discomfort & pain (may increase with use) pupil may be small +/- irregular due to sphincter muscle contraction photophobia (often intense) blurred vision red eye lacrimation ciliary flush: a ring of red spreading outwards hypopyon; describes pus and inflammatory cells in the anterior chamber, often resulting in a visible fluid level visual acuity initially normal → impaired Associated conditions ankylosing spondylitis reactive arthritis ulcerative colitis, Crohn's disease Behcet's disease sarcoidosis: bilateral disease may be seen Management urgent review by ophthalmology cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate steroid eye drops longer term steroid sparing agent may be needed eg methotrexate, mycophenolate mofetil, and azathioprine, TNFa inhibitors

Answer 11

inflammation of the cornea. Microbial keratitis is not like conjunctivitis - it is potentially sight threatening and should therefore be urgently evaluated and treated Causes bacterial typically Staphylococcus aureus Pseudomonas aeruginosa is seen in contact lens wearers fungal amoebic acanthamoebic keratitis accounts for around 5% of cases increased incidence if eye exposure to soil or contaminated water parasitic: onchocercal keratitis ('river blindness') Remember, other factors may causes keratitis: viral: herpes simplex keratitis environmental photokeratitis: e.g. welder's arc eye exposure keratitis contact lens acute red eye (CLARE) Features red eye: pain and erythema photophobia foreign body, gritty sensation hypopyon may be seen contact lens wearers assessing contact lens wearers who present with a painful red eye is difficult an accurate diagnosis can only usually be made with a slit-lamp, meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis Management stop using contact lens until the symptoms have fully resolved topical antibiotics typically quinolones are used first-line cycloplegic for pain relief e.g. cyclopentolate Complications may include: corneal scarring perforation endophthalmitis visual loss diff from conjunctivitis can be hard: may be more painful, have cloudy cornea, some photophobia, some blurring of vision; pupil will be normal unlike acute glauc

Answer 12

a. cataract i. age-related ii. pre-senile (steroids, diabetes, trauma, uveitis) b. age-related macular degeneration i. dry / atrophic ii. wet / neovascular / exudative c. primary open angle glaucoma d. diabetic eye disease i. retinopathy (nonproliferative, proliferative) ii. maculopathy (oedematous, ischaemic) e. presbyopia

Answer 13

Normal ageing process: most common cause Other possible causes Smoking Increased alcohol consumption Trauma Diabetes mellitus Long-term corticosteroids Radiation exposure Myotonic dystrophy Metabolic disorders: hypocalcaemia Patients typically present with a gradual onset of: Reduced vision Faded colour vision: making it more difficult to distinguish different colours Glare: lights appear brighter than usual Halos around lights Signs: A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex. Investigations: Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve Slit-lamp examination. Findings: visible cataract Management Non-surgical: In the early stages, age-related cataracts can be managed conservatively by prescribing stronger glasses/contact lens, or by encouraging the use of brighter lighting. These options help optimise vision but do not actually slow down the progression of cataracts, therefore surgery will eventually be needed. Surgery: Surgery is the only effective treatment for cataracts. This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice. Also whether both eyes are affected and the possible risks and benefits of surgery should be taken into account subtypes: Nuclear: change lens refractive index, common in old age Polar: localized, commonly inherited, lie in the visual axis Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy any vision impairment is sufficient for an op!

Answer 14

Risk factors advancing age itself is the greatest risk factor for ARMD the risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74. smoking current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13). family history is also a strong risk factor for developing ARMD first degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition. other risk factors for developing the condition include those associated with increased risk of ischaemic cardiovascular disease Traditionally two forms of macular degeneration are seen: dry macular degeneration 90% of cases also known as atrophic characterised by drusen - yellow round spots in Bruch's membrane wet macular degeneration 10% of cases also know as exudative or neovascular macular degeneration characterised by choroidal neovascularisation leakage of serous fluid and blood can subsequently result in a rapid loss of vision carries worst prognosis Recently there has been a move to a more updated classification: early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE) late age-related macular degeneration (neovascularisation, exudative) Patients typically present with a subacute onset of visual loss with: a reduction in visual acuity, particularly for near field objects difficulties in dark adaptation with an overall deterioration in vision at night fluctuations in visual disturbance which may vary significantly from day to day they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects Signs: distortion of line perception may be noted on Amsler grid testing fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar. in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage. Investigations: slit-lamp microscopy is the initial investigation of choice fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therap combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD. vascular endothelial growth factor (VEGF) VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.

Answer 15

POAG may present insidiously and for this reason is often detected during routine optometry appointments. Features may include peripheral visual field loss - nasal scotomas progressing to 'tunnel vision' decreased visual acuity optic disc cupping Fundoscopy signs of primary open-angle glaucoma (POAG): 1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen 2. Optic disc pallor - indicating optic atrophy 3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base 4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages Investigations: automated perimetry to assess visual field slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline applanation tonometry to measure IOP central corneal thickness measurement FH is a big risk factor!

Answer 16

NICE guidelines: first line: prostaglandin analogue (PGA) eyedrop second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop if more advanced: surgery or laser treatment can be tried Reassessment important to exclude progression and visual field loss prost analogue like latanoprost incs uveoscleral outflow, iris may gain brown pigment and eyelashes grow longer b blocke like timolol reduces aqueous production - avoid in asthmatic/heart block sympathomimetics do both above mechanisms, avoid if on MAOI/TCAs carb anyhdrase inhibs reduce aqueous production

Answer 17

Diabetic retinopathy is the most common cause of blindness in adults aged 35-65 years-old. Hyperglycaemia is thought to cause increased retinal blood flow and abnormal metabolism in the retinal vessel walls. This precipitates damage Mild NPDR 1 or more microaneurysm Moderate NPDR microaneurysms blot haemorrhages hard exudates cotton wool spots (retinal infarction), venous beading/looping and intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR Severe NPDR aka preprolif blot haemorrhages and microaneurysms in 4 quadrants venous beading in at least 2 quadrants IRMA in at least 1 quadrant Proliferative retinopathy retinal neovascularisation - may lead to vitrous haemorrhage fibrous tissue forming anterior to retinal disc more common in Type I DM, Maculopathy based on location rather than severity, anything is potentially serious hard exudates and other 'background' changes on macula check visual acuity more common in Type II DM Chronic hyperglycaemia causes blood vessels, including those supplying the retina, to weaken and rupture; the vessel walls may dilate resulting in microaneurysms or small haemorrhages. The damaged pericytes and erythrocytes increase vascular permeability. Lipoproteins, lipids and other products carried by blood are therefore able to leak out and cluster onto the retina as hard exudates. As blood flow becomes increasingly compromised, regions of the retina are starved of oxygen. This hypoxia is thought to stimulate the release of mediators such as vascular endothelial growth factor (VEGF) which promotes neovascularization. However, these new vessels are poorly formed and easily rupture resulting in bleeding. Neovascularization into the vitreous humour may culminate in widespread vitreous haemorrhage causing sudden and complete visual loss. Fibrovascular bundles can lead to fibrosis and, in turn, retinal traction. This can result in retinal detachment and recurrent vitreous haemorrhage. visual acuity assessed, slit-lamp or fundus photography to classify severity; fluorescein angiography can help you see unclear ischaemia, optical coherence tomography if diabetic macular oedema lifestyle, glycemic, and BP control; photocoagulation if proliferative or severe nonprolif and high risk eg one eye, pregnant, frequent flyer In focal photocoagulation, a specific point of leakage is identified and targeted with the laser. comps include worse central vision or scotoma Pan-retinal photocoagulation (PRP) The periphery of the retina is targeted with the aim of achieving a global reduction in oxygen demand. so less VEGF; Complications of PRP include a restricted peripheral vision, reduced quality of night vision, ocular pain, worsening macular oedema Anti-VEGF injections focus on minimising neovascularization and thus are used in proliferative diabetic retinopathy. Aflibercept (Eylea) and Ranibizumab (Lucentis) are two commonly used anti-VEGF agents in the treatment of DR. Although the mechanism of action is not completely understood, trials have shown intravitreal corticosteroids can also be effective in improving visual acuity and reducing maculopathy. anti-vegf contra'd if stroke or MI in last 3mo A potential complication of proliferative DR is bleeding into the vitreous humour, which further increases the risk of retinal detachment. In many cases, waiting for the haemorrhage to settle can allow sufficient view to perform laser therapy. However, in persistent haemorrhage or in central, sight-threatening tractional retinal detachment a vitrectomy may be performed. This allows for the removal of the vitreous and repair of any scarring/detachment of the retina. Photocoagulation may be used intra-operatively annual screening once >12yo retinal detachment/vitreous h+ are main complications, also neovascular glaucoma: Neovascularization can occur within the iris and its trabecular meshwork (rubeosis) causing a narrowing and closure of the drainage angle and therefore increased intraocular pressure. The typical presentation may include a patient complaining of an acutely painful, red eye If left untreated, approximately 50% of patients with proliferative DR will lose their vision in 2 years. Around 90% of affected patients will have lost most of their vision within 10 years. Those with proliferative DR that undergo treatment can reduce their risk of severe vision loss by 50%.

Answer 18

a. central retinal artery occlusion (CRAO) b. anterior ischaemic optic neuropathy i) non arteritic ii) arteritic (i.e. giant cell / temporal arteritis) c. vitreous haemorrhage d. wet age related macular degeneration e. retinal vein occlusion f. retinal detachment g. optic neuritis

Answer 19

art: sudden unilateral visual loss due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis) features include afferent pupillary defect, 'cherry red' spot on a pale retina vein: differential for sudden painless loss of vision. Risk factors increasing age glaucoma polycythaemia Features sudden, painless reduction or loss of visual acuity, usually unilaterally severe retinal haemorrhages are usually seen on fundoscopy

Answer 20

Common causes (collectively account for 90% of cases): proliferative diabetic retinopathy (over 50%) posterior vitreous detachment ocular trauma: the most common cause in children and young adults Patients typically present with an acute or subacute onset of: painless visual loss or haze (commonest) red hue in the vision floaters or shadows/dark spots in the vision Signs: decreased visual acuity: variable depending on the location, size and degree of vitreous haemorrhage visual field defect if severe haemorrhage Investigations: dilated fundoscopy: may show haemorrhage in the vitreous cavity slit-lamp examination: red blood cells in the anterior vitreous ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina fluorescein angiography: to identify neovascularization orbital CT: used if open globe injury

Answer 21

reversible cause of visual loss, provided it is recognised and treated before the macula is affected. If left untreated and symptomatic, retinal detachment will inevitably lead to permanent visual loss should be suspected if patients complain of new onset floaters or flashes, as these indicate pigment cells entering the vitreous space or traction on the retina respectively. Sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery should also raise suspicion of detachment Any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage Retinal tears or breaks are treated by laser therapy or cryotherapy detachment is treated with various surgical approaches

Answer 22

multiple sclerosis: the commonest associated disease diabetes syphilis Features unilateral decrease in visual acuity over hours or days poor discrimination of colours, 'red desaturation' pain worse on eye movement relative afferent pupillary defect central scotoma Management high-dose steroids recovery usually takes 4-6 weeks MRI is investigation of choice

Answer 23

a. third cranial nerve palsy b. fourth cranial nerve palsy c. sixth cranial nerve palsy d. blow out fracture e. thyroid eye disease f. myasthenia gravis +hypophos and misc others

Answer 24

a. migraine aura but also retinal migraine: symptoms of retinal migraine may include: partial or total loss of vision in 1 eye – this usually lasts 10 to 20 minutes before vision gradually returns headache – this may happen before, during or after the vision attack It's unusual for an episode of vision loss to last longer than an hour. The same eye is affected every time in almost all cases. Vision may slowly become blurred or dimmed, or there may be flashes of light. Some people see a mosaic-like pattern of blank spots (scotomas), which enlarge to cause total loss of vision. b. amaurosis fugax c. papilloedema

Answer 25

wide differential including large artery disease (atherothrombosis, embolus, dissection), small artery occlusive disease (anterior ischemic optic neuropathy, vasculitis e.g. temporal arteritis), venous disease and hypoperfusion may represent a form of transient ischaemic attack (TIA). It should therefore be treated in a similar fashion, with aspirin 300mg being given altitudinal field defects are often seen: 'curtain coming down' ischaemic optic neuropathy is due to occlusion of the short posterior ciliary arteries, causing damage to the optic nerve can think of amaurosis fugax as transient form of central retinal artery occlusion (as TIA is to stroke)

Answer 26

a sign of raised icp Fleeting vision changes—blurred vision, double vision, flickering, or complete loss of vision—typically lasting seconds are characteristic of papilledema. Other symptoms may be caused by the elevated icp following features may be observed during fundoscopy: venous engorgement: usually the first sign loss of venous pulsation: although many normal patients do not have normal pulsation blurring of the optic disc margin elevation of optic disc loss of the optic cup Causes of papilloedema space-occupying lesion: neoplastic, vascular malignant hypertension idiopathic intracranial hypertension hydrocephalus hypercapnia Rare causes include hypoparathyroidism and hypocalcaemia vitamin A toxicity

Answer 27

inflammation of the eyelid margins. It may due to either meibomian gland dysfunction (common, posterior blepharitis) or seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis) symptoms are usually bilateral grittiness and discomfort, particularly around the eyelid margins eyes may be sticky in the morning eyelid margins may be red. Swollen eyelids may be seen in staphylococcal blepharitis styes and chalazions are more common in patients with blepharitis secondary conjunctivitis may occur Management softening of the lid margin using hot compresses twice a day 'lid hygiene' - mechanical removal of the debris from lid margins cotton wool buds dipped in a mixture of cooled boiled water and baby shampoo is often used artificial tears if dry eyes

Answer 28

Different types of stye are recognised: external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands). internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst) management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis A chalazion (Meibomian cyst) is a retention cyst of the Meibomian gland. It presents as a firm painless lump in the eyelid. The majority of cases resolve spontaneously but some require surgical drainage if the mebomium cyst is persistent, recurrent, causing significant astigmatism, cosmetically unacceptable, or there is uncertainty about the diagnosis, refer the person to an ophthalmologist for further management. An opthalmologist may consider incision and curettage where appropriate, or intra-lesion injection of steroid (may be preferred in children). For recurrent lesions, biopsy may be indicated to rule out meibomium gland carcinoma. Otherwise, if the person is being managed in primary care, reassure them that a meibomian cyst is usually self-limiting and rarely causes serious complications. Advise the person to: Apply a warm compress (for example, a clean flannel that has been rinsed with warm water) to the affected eye for 10–15 minutes up to five times a day. Explain that this will encourage drainage of the cyst contents. Gently massage the meibomian cyst after application of the warm compress (to aid expression of the cyst contents). (also random note: remember basal cell carcinoma can be on eyelid, dont mistake that for a stye/chalazion) stye is on the eyelid margin, chalazion is a bit further away and often central

Answer 29

reactivation of the varicella-zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve. It accounts for around 10% of case of shingles. Features vesicular rash around the eye, which may or may not involve the actual eye itself Hutchinson's sign: rash on the tip or side of the nose. Indicates nasociliary involvement and is a strong risk factor for ocular involvement Management oral antiviral treatment for 7-10 days ideally started within 72 hours intravenous antivirals may be given for very severe infection or if the patient is immunocompromised ocular involvement requires urgent ophthalmology review Complications ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis ptosis post-herpetic neuralgia

Answer 30

separation of the vitreous membrane from the retina. This occurs due to natural changes to the vitreous fluid of the eye with ageing. Posterior vitreous detachment is a common condition that does not cause any pain or loss of vision. However, rarely the separation of the vitreous membrane can lead to tears and detachment of the retina. It is important to rule out retinal tears or retinal detachment in anyone with suspected posterior vitreous detachment The sudden appearance of floaters (occasionally a ring of floaters temporal to central vision) Flashes of light in vision Blurred vision Cobweb across vision The appearance of a dark curtain descending down vision (means that there is also retinal detachment) All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment. Management: Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary. If there is an associated retinal tear or detachment the patient will require surgery to fix this

Answer 31

Subconjunctival haemorrhage — this is due to a bleed into the subconjunctival space. There may or may not be a history of a contributory factor, such as straining with coughing or constipation. It may be associated with hypertension. On examination, there is an area of localized, well-demarcated haemorrhage in one eye, in the absence of pain, no reduction of visual acuity, normal pupil reactions, and no corneal staining. usually harmless!

Answer 32

Choroidal nevi are benign melanocytic lesions of the posterior uvea. In the United States, their prevalence ranges from 4.6 percent to 7.9 percent in Caucasians.1 By comparison, choroidal melanoma is rare, manifesting in approximately six in 1 million Caucasian individuals. Choroidal nevi tend to have clearly defined margins and to be flat or slightly elevated, and they remain stable in size. Over time, choroidal nevi display features such as overlying drusen as well as retinal pigment epithelial atrophy, hyperplasia or fibrous metaplasia. In contrast, choroidal melanomas are more likely to show signs of activity such as relatively indiscrete margins, irregular or oblong configuration, overlying subretinal fluid and orange pigment, and abruptly elevated edges. Documentation of growth. Most authorities agree that documentation of growth over a relatively short period of time, such as one to two years, is a convincing characteristic of a mitotically active melanoma. However, it is ideal to detect choroidal melanoma before the recognition of growth Patients with choroidal nevi who show no suspicious features require no treatment. During the first year, they should be monitored twice; subsequently, they should be evaluated annually as long as the nevi remain stable

Answer 33

papilloedema (tho more often enlarged blind spot) glaucoma (open angle) retinitis pigmentosa choroidoretinitis optic atrophy secondary to tabes dorsalis hysteria

Answer 34

vast majority of patients with blurred vision will have long-term refractive errors Causes refractive error: most common cataracts retinal detachment age-related macular degeneration acute angle closure glaucoma optic neuritis amaurosis fugax Assessment visual acuity with a Snellen chart pinhole occluders are a useful way to check for whether the blurred vision is due to a refractive error or not if the blurring improves with a pinhole occluder then likely cause is a refractive error visual fields fundoscopy if gradual onset, corrected by pinhole occluder and no other associated symptoms then an optician review would be the next step other patients should be seen by ophthalmology. If there are associated symptoms such as visual loss or pain this should be urgent

Answer 35

Also known as the Marcus-Gunn pupil, a relative afferent pupillary defect is found by the 'swinging light test'. It is caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina Finding the affected and normal eye appears to dilate when light is shone on the affected causes: optic neuritis. ischemic optic disease or retinal disease. severe glaucoma causing trauma to optic nerve. direct optic nerve damage (trauma, radiation, tumor) retinal detachment. very severe macular degeneration. retinal infection (CMV, herpes)

Answer 36

miosis, ptosis, anhidrosis central has anhidrosis of face/arm/trunk and inc stroke, syringomyelia, MS, tumours pregang has anhidrosis of face only and inc pancoast tumour, thyroidectomy or other trauma, cervical rib postgang has no anhidrosis and incs carotid art dissestion or aneurysm, cavernous sinus thrombosis, cluster headache

Answer 37

Causes of mydriasis (large pupil) third nerve palsy Holmes-Adie pupil traumatic iridoplegia phaeochromocytoma congenital Drug causes of mydriasis topical mydriatics: tropicamide, atropine sympathomimetic drugs: amphetamines, cocaine anticholinergic drugs: tricyclic antidepressants Holmes-Adie pupil is a benign condition most commonly seen in women. It is one of the differentials of a dilated pupil. Overview unilateral in 80% of cases dilated pupil once the pupil has constricted it remains small for an abnormally long time slowly reactive to accommodation but very poorly (if at all) to light Holmes-Adie syndrome association of Holmes-Adie pupil with reduced/absent ankle/knee reflexes

Answer 38

lacrimal gland is located anteriorly in the superolateral aspect of the orbit, within the lacrimal fossa – a depression in the orbital plate of the frontal bone. lacrimal fluid produced by the gland is secreted into excretory ducts, which empty into the superior conjunctival fornix. The fluid is then ‘spread’ over the cornea by the process of blinking After secretion, lacrimal fluid circulates across the eye, and accumulates in the lacrimal lake – located in the medial canthus of the eye. From here, it drains into the lacrimal sac via a series of canals. The lacrimal sac is the dilated end of the nasolacrimal duct, and is located in a groove formed by the lacrimal bone and frontal process of the maxilla. Lacrimal fluid drains down the nasolacrimal duct and empties into the inferior meatus of the nasal cavity Parasympathetic: Preganglionic fibres are carried in the greater petrosal nerve (branch of the facial nerve) and then the nerve of pterygoid canal, before synapsing at the pterygopalatine ganglion. Postganglionic fibres travel with the maxillary nerve, and finally the zygomatic nerve. Stimulates fluid secretion from the lacrimal gland

Answer 39

most common cause of watering eyes of new-borns is a delay in the normal development of the nasolacrimal system. It can affect one or both eyes. NLD is usually developed by the age of 12 months and the symptoms will often settle by this time. You can encourage tear flow and tear duct development by massaging the area on the inside of the upper lid(s) by firm pressure every day. Stickiness and discharge can be cleared away using clean water and cotton wool. Antibiotics are not needed unless the eye itself becomes red If the symptoms do not get better by 12-18 months of age, then ophtho may perform syringe and probing under general anaesthetic. This procedure uses a very thin instrument which is passed into the tear duct to open it. a few infants with NLDO present within the first few weeks of life with a more severe infection: acute dacryocystitis. Clinical findings include edema and erythema with distension of the lacrimal sac below the medial canthal tendon, and patients may have systemic signs of infection such as fever and irritability. This is a rare complication of isolated congenital NLDO. Acute dacryocystitis can be complicated by preseptal or orbital cellulitis, sepsis, or meningitis and should be treated promptly with systemic antibiotics - will need ophtho discussion ?surgery

Answer 40

Dacryoceles, also known as lacrimal sac mucocele are a rare form of congenital nasolacrimal duct obstruction with both proximal and distal obstruction resulting in lacrimal sac enlargement. Usually presenting at birth, there is significant risk for infection. Probing and excision of an associated intranasal cyst under general anesthesia may be needed may present in 3% of infants with NLDO Exam reveals a bluish, cystic mass that is located below the medial canthal tendon in the area of the nasolacrimal sac. The medial canthus can be displaced superiorly. Gentle pressure over the mass can produce mucopurulent discharge from the eyelid puncta

Answer 41

aka epiphora most commonly due to NLDO most important ddx is infantile glaucoma: it is important for ophthalmic evaluation of infants who have photophobia and other signs of ocular irritation (eg, excessive eye rubbing) to rule out this possibility also consider allergic and infectious conjunctivitis, entropion, corneal infection, corneal abrasion, foreign body (inc under eyelid)

Answer 42

Ophthalmia neonatorum is conjunctivitis of the newborn occurring within the first 28 days of life. A sticky eye is a relatively common problem in infancy. It is often simply due to a blocked lacrimal duct but may also be caused by a variety of bacterial and viral pathogens Causes associated with potentially severe outcomes, and which are not detected by routine bacterial eye swabs:  Neisseria gonorrhoeae  Chlamydia trachomatis  Herpes simplex virus Ask for maternal Sexually Transmitted Infection’s in history taking sx: * Redness (conjunctiva +/- lids) * Discharge (may be profuse in gonococcal infection) * Swelling of lids (may be severe) Symptoms usually bilateral (but may be sequential with few days between onset of each eye) gono: Hyperacute conjunctival injection and chemosis, lid oedema and severe purulent discharge (incubation 1-3 days), complications corneal ulceration and perforation Rarely, disseminated infection chlam: Unilateral/bilateral watery discharge which becomes copious and purulent later on, 5-28 days incubation, Chlamydial pneumonia (10- 20% chance in infants of untreated mothers) discuss cases with ophtho, take 3 swabs (routine, NAAT, viral) and start chloramphenicol eye drops for all, adding on below if needed for chlam - PO erythro for 14 days, assess for pneumonitis and admit if any resp involvement, otherwise senior review and discharge for gon - assess for sepsis; Cefotaxime 100mg/kg IV single dose (max 1g). IM stat dose can be given if baby is difficult to cannulate; if well home after senior review for HSV - admit, IV aciclovir If gonococcal or chlamydial infection confirmed, parent(s) should be referred to Genito-Urinary Medicine (GUM) clinic

Answer 43

pathogenesis of primary congenital glaucoma is unknown and is currently described as a developmental defect with obstruction at the trabecular meshwork characterized by the clinical triad of epiphora, blepharospasm and photophobia, but these symptoms are often missed. For example, epiphora may be mistaken for congenital nasolacrimal duct obstruction. The patient usually presents because of corneal clouding and ocular enlargement: glaucoma should be suspected in any child with a corneal diameter greater than 13.0 mm. needs urgent ophtho referral for IOP measurement, inspection of optic nerve etc Most infants with primary congenital glaucoma who present between 3 months and 1 year of age will have their IOP controlled by one or two angle surgeries

Answer 44

To function properly, the retina needs a constant supply of blood to provide oxygen. The blood vessels that supply this blood usually develop between weeks 16 and 36 of pregnancy. If a baby is born early, and the development of these blood vessels is incomplete, there will be areas on the retina that do not receive enough oxygen. This triggers the production of chemicals to produce new blood vessels. These new blood vessels are fragile and can leak blood causing scarring. This pulls the retina out of position, affecting the baby’s ability to see properly All babies less than 31 weeks gestational age (up to 30 weeks and 6 days) or less than 1501g birth weight should be screened for retinopathy of prematurity For infants born before 31+0 book the first screen as soon as both the criteria below are met Babies must be at least 4 weeks old Babies must be 31+0 weeks corrected gestational age or more For infants born from 31+0 (who weight 1500g or less) book the first screen as soon as the infant is: 4 weeks old OR Is 36 weeks corrected gestational age Usually then screen every 1-2 weeks screening can be stopped when retinal vascularization has extended into Zone 3 If the baby has a mild form of retinopathy, they will not need any treatment as their condition will resolve itself and the retinopathy will not affect their vision as they grow older Treat infants in whom a screening examination has detected: * Zone I any stage ROP with plus disease * Zone I stage 3 ROP without plus disease * Zone II stage 2 or 3 with plus disease ROP in zone I should be treated with an intravitreous injection of an anti-VEGF agent ROP in zone II should be treated with transpupillary laser

Ophthalmology Flashcards

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